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Institute","doi-asserted-by":"publisher","award":["AI149754"],"award-info":[{"award-number":["AI149754"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2023,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>CC16 is a protein mainly produced by nonciliated bronchial epithelial cells (BECs) that participates in host defense. Reduced CC16 protein concentrations in BAL and serum are associated with asthma susceptibility.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Few studies have investigated the relationship between CC16 and asthma progression, and none has focused on BECs. In this study, we sought to determine if CC16 mRNA expression levels in BECs are associated with asthma severity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Association analyses between CC16 mRNA expression levels in BECs (242 asthmatics and 69 control subjects) and asthma-related phenotypes in Severe Asthma Research Program were performed using a generalized linear model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Low CC16 mRNA expression levels in BECs were significantly associated with asthma susceptibility and asthma severity, high systemic corticosteroids use, high retrospective and prospective asthma exacerbations, and low pulmonary function. Low CC16 mRNA expression levels were significantly associated with high T2 inflammation biomarkers (fractional exhaled nitric oxide and sputum eosinophils). CC16 mRNA expression levels were negatively correlated with expression levels of Th2 genes (IL1RL1, POSTN, SERPINB2, CLCA1, NOS2, and MUC5AC) and positively correlated with expression levels of Th1 and inflammation genes (IL12A and MUC5B). A combination of two nontraditional T2 biomarkers (CC16 and IL-6) revealed four asthma endotypes with different characteristics of T2 inflammation, obesity, and asthma severity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings indicate that low CC16 mRNA expression levels in BECs are associated with asthma susceptibility, severity, and exacerbations, partially through immunomodulation of T2 inflammation. CC16 is a potential nontraditional T2 biomarker for asthma development and progression.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202206-1230oc","type":"journal-article","created":{"date-parts":[[2022,9,6]],"date-time":"2022-09-06T11:19:29Z","timestamp":1662463169000},"page":"438-451","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":38,"title":["Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity"],"prefix":"10.1093","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1208-8658","authenticated-orcid":false,"given":"Xingnan","family":"Li","sequence":"first","affiliation":[{"name":"Division of Genetics, Genomics, and Precision Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7218-3246","authenticated-orcid":false,"given":"Stefano","family":"Guerra","sequence":"additional","affiliation":[{"name":"Asthma and Airway Disease Research Center, Department of Medicine, University of Arizona, Tucson, Arizona"}]},{"given":"Julie G.","family":"Ledford","sequence":"additional","affiliation":[{"name":"Asthma and Airway Disease Research Center, Department of Medicine, University of Arizona, Tucson, Arizona"}]},{"given":"Monica","family":"Kraft","sequence":"additional","affiliation":[{"name":"Asthma and Airway Disease Research Center, Department of Medicine, University of Arizona, Tucson, Arizona"}]},{"given":"Huashi","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Genetics, Genomics, and Precision Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6607-7797","authenticated-orcid":false,"given":"Annette T.","family":"Hastie","sequence":"additional","affiliation":[{"name":"Department of Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina"}]},{"given":"Mario","family":"Castro","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, and Sleep Medicine, University of Kansas School of Medicine, Kansas City, Kansas"}]},{"given":"Loren C.","family":"Denlinger","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Wisconsin School of Medicine & Public Health, Madison, Wisconsin"}]},{"given":"Serpil C.","family":"Erzurum","sequence":"additional","affiliation":[{"name":"Lerner Research Institute and the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio"}]},{"given":"John V.","family":"Fahy","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of California at San Francisco, San Francisco, California"}]},{"given":"Benjamin","family":"Gaston","sequence":"additional","affiliation":[{"name":"Wells Center for Pediatric Research and Riley Hospital for Children, Indiana University, Indianapolis, Indiana"}]},{"given":"Elliot","family":"Israel","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Nizar N.","family":"Jarjour","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Wisconsin School of Medicine & Public Health, Madison, Wisconsin"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9515-5731","authenticated-orcid":false,"given":"Bruce D.","family":"Levy","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"David T.","family":"Mauger","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, College of Medicine, Penn State University, Hershey, Pennsylvania"}]},{"given":"Wendy C.","family":"Moore","sequence":"additional","affiliation":[{"name":"Department of Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina"}]},{"given":"Joe","family":"Zein","sequence":"additional","affiliation":[{"name":"Lerner Research Institute and the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5917-4601","authenticated-orcid":false,"given":"Naftali","family":"Kaminski","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut; and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4242-0164","authenticated-orcid":false,"given":"Sally E.","family":"Wenzel","sequence":"additional","affiliation":[{"name":"Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Prescott G.","family":"Woodruff","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of California at San Francisco, San 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Institute","doi-asserted-by":"publisher","award":["75N92020D00001"],"award-info":[{"award-number":["75N92020D00001"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01AG023629"],"award-info":[{"award-number":["R01AG023629"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"published-print":{"date-parts":[[2022,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Circulating inflammatory markers are associated with incident heart failure (HF), but prospective data on associations of immune cell subsets with incident HF are lacking. We determined the associations of immune cell subsets with incident HF as well as HF subtypes [with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF)].<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Peripheral blood immune cell subsets were measured in adults from the Multi-Ethnic Study of Atherosclerosis (MESA) and Cardiovascular Health Study (CHS). Cox proportional hazard models adjusted for demographics, HF risk factors, and cytomegalovirus serostatus were used to evaluate the association of the immune cell subsets with incident HF. The average age of the MESA cohort at the time of immune cell measurements was 63.0 \u00b1 10.4 years with 51% women, and in the CHS cohort, it was 79.6 \u00b1 4.4 years with 62% women. In the meta-analysis of CHS and MESA, a higher proportion of CD4+ T helper (Th) 1 cells (per one standard deviation) was associated with a lower risk of incident HF [hazard ratio (HR) 0.91, (95% CI 0.83\u20130.99), P = 0.03]. Specifically, higher proportion of CD4+ Th1 cells was significantly associated with a lower risk of HFrEF [HR 0.73, (95% CI 0.62\u20130.85), &amp;lt;0.001] after correction for multiple testing. No association was observed with HFpEF. No other cell subsets were associated with incident HF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We observed that higher proportions of CD4+ Th1 cells were associated with a lower risk of incident HFrEF in two distinct population-based cohorts, with similar effect sizes in both cohorts demonstrating replicability. Although unexpected, the consistency of this finding across cohorts merits further investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.14140","type":"journal-article","created":{"date-parts":[[2022,9,12]],"date-time":"2022-09-12T23:55:10Z","timestamp":1663026910000},"page":"4177-4188","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Association of Immune Cell Subsets with Incident Heart Failure in Two Population-Based Cohorts"],"prefix":"10.1093","volume":"9","author":[{"given":"Arjun","family":"Sinha","sequence":"first","affiliation":[{"name":"Department of Medicine, Feinberg School of Medicine, Northwestern University , Chicago, IL ,","place":["USA"]},{"name":"Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University , Chicago, IL ,","place":["USA"]}]},{"given":"Colleen M.","family":"Sitlani","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Margaret F.","family":"Doyle","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of Vermont , Burlington, VT ,","place":["USA"]}]},{"given":"Alison E.","family":"Fohner","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Petra","family":"Buzkova","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"James S.","family":"Floyd","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Sally A.","family":"Huber","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of Vermont , Burlington, VT ,","place":["USA"]}]},{"given":"Nels C.","family":"Olson","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of Vermont , Burlington, VT ,","place":["USA"]}]},{"given":"Joyce N.","family":"Njoroge","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California at San Francisco , San Francisco, CA ,","place":["USA"]}]},{"given":"Jorge R.","family":"Kizer","sequence":"additional","affiliation":[{"name":"Cardiology Section, San Francisco Veterans Affairs Health Care System and Departments of Medicine, Epidemiology and Biostatistics, University of California San Francisco , San Francisco, CA ,","place":["USA"]}]},{"given":"Joseph A.","family":"Delaney","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"College of Pharmacy, University of Manitoba , Winnipeg, Manitoba ,","place":["Canada"]}]},{"given":"Sanjiv S.","family":"Shah","sequence":"additional","affiliation":[{"name":"Department of Medicine, Feinberg School of Medicine, Northwestern University , Chicago, IL ,","place":["USA"]}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of Vermont , Burlington, VT ,","place":["USA"]},{"name":"Department of Biochemistry, Robert Larner M.D. College of Medicine, University of Vermont , Burlington, VT ,","place":["USA"]}]},{"given":"Bruce","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of 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Pharmaceutical Company","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"Novartis","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"Regeneron Pharmaceuticals","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"Sanofi","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2025,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>High-attenuation area (HAA) is a computed tomography (CT) tool that correlates with lung inflammation and fibrosis. Systemic molecular correlates of HAA (e.g., plasma proteins) may inform biological processes involved in interstitial lung disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To identify plasma proteins that associate with HAA and correlate with a higher probability of developing new-onset fibrotic or subpleural interstitial lung abnormalities (ILAs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Plasma protein levels were measured using a semiquantitative aptamer-based platform in MESA (the Multi-Ethnic Study of Atherosclerosis; N\u2009=\u20095,486) and SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study; N\u2009=\u20091,781). Linear regression models identified HAA-associated proteins after adjustment for demographic and socioeconomic factors, CT scanner parameters, study center, and batch. Associations of HAA-related proteins with new-onset fibrotic or subpleural ILAs were examined in MESA participants with ILA assessments on full-lung CT 10 years later. Immunohistochemical staining of select proteins was performed in lung tissue from pulmonary fibrosis cases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>There were 75 proteins detected that were significantly associated with HAA in MESA and SPIROMICS. Gene Ontology analysis of these proteins identified processes involved in immune cell chemotaxis and cellular growth and apoptosis. Seven proteins were associated with a higher probability of new-onset fibrotic or subpleural ILAs in MESA, and two of these, junctional adhesion molecule-like protein and GTP cyclohydrolase 1 feedback regulatory protein, stained in areas of fibrosis in lung tissue from patients with interstitial lung disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Plasma proteins associated with more HAA are involved in immune and cellular processes and associate with new-onset fibrotic-subpleural ILA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202503-0610oc","type":"journal-article","created":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T20:45:47Z","timestamp":1755895547000},"page":"1811-1822","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":2,"title":["Associations of High Attenuation Area\u2013Related Proteomic Biomarkers with Fibrotic or Subpleural Interstitial Lung Abnormalities"],"prefix":"10.1093","volume":"211","author":[{"given":"John S.","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"given":"Catherine L.","family":"Debban","sequence":"additional","affiliation":[{"name":"Department of Genome Sciences, and"}]},{"given":"Daniel E.","family":"Guzman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0403-792X","authenticated-orcid":false,"given":"Riley T.","family":"Hannan","sequence":"additional","affiliation":[{"name":"Department of Medicine"}]},{"given":"Mary","family":"Salvatore","sequence":"additional","affiliation":[{"name":"Department of Radiology, Jacobi Medical Center, Bronx, New York, New York"}]},{"given":"Claire","family":"McGroder","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2983-9796","authenticated-orcid":false,"given":"David","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9559-1485","authenticated-orcid":false,"given":"Anna J.","family":"Podolanczuk","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical Center, New York, New York"}]},{"given":"Daniel A.","family":"Duprez","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, Department of Medicine, School of Medicine, University of Minnesota, Minneapolis, 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Philadelphia, Pennsylvania"}]},{"given":"Ruth F.","family":"Dubin","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8889-2757","authenticated-orcid":false,"given":"Janelle Vu","family":"Pugashetti","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Michigan, Ann Arbor, Michigan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4670-7549","authenticated-orcid":false,"given":"Jennifer M.","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Michigan, Ann Arbor, Michigan"}]},{"given":"MeiLan K.","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Michigan, Ann Arbor, Michigan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4957-8869","authenticated-orcid":false,"given":"Justin M.","family":"Oldham","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Michigan, Ann Arbor, Michigan"}]},{"given":"Imre","family":"Noth","sequence":"additional","affiliation":[{"name":"Department of Medicine"}]},{"given":"Prescott G.","family":"Woodruff","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California, San Francisco, San Francisco, California"}]},{"given":"Victor E.","family":"Ortega","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mayo Clinic, Phoenix, Arizona"}]},{"given":"Julie C.","family":"Fanburg-Smith","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia"}]},{"given":"Edward B.","family":"Stelow","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia"}]},{"given":"Christopher 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Institute","doi-asserted-by":"crossref","award":["U01HL130114"],"award-info":[{"award-number":["U01HL130114"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"crossref","award":["R01AG023629"],"award-info":[{"award-number":["R01AG023629"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2025,3]]},"abstract":"<jats:sec>\n            <jats:title>Key Points<\/jats:title>\n            <jats:p>\n                                 <jats:list list-type=\"bullet\"><jats:list-item><jats:p>Evaluation of cardiac mechanics through two-dimensional speckle tracking echocardiography can identify early alterations in cardiac function.<\/jats:p><\/jats:list-item><jats:list-item><jats:p>In a subset of the Cardiovascular Health Study, c-terminal and intact fibroblast growth factor 23 were not independently associated with cardiac mechanic indices.<\/jats:p><\/jats:list-item><\/jats:list>\n                              <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Elevated levels of fibroblast growth factor 23 (FGF23) are associated with left ventricular hypertrophy and heart failure in individuals with and without kidney disease. Prior studies investigated the association of FGF23 and structural cardiac changes using conventional echocardiography, which is limited in its ability to detect early cardiac dysfunction. We investigated the relationship between FGF23 levels and cardiac dynamics using two-dimensional speckle tracking echocardiography (2D-STE), a novel imaging modality.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>This was a cross-sectional analysis of data from the Cardiovascular Health Study (CHS), an ongoing prospective, population-based cohort study. The study population included 506 participants from CHS with available c-terminal FGF23 (cFGF23) and intact FGF23 (iFGF23) measurements from 1996 to 1997 and 2D-STE images from 1994 to 1995. Forty-two percent of the study population had CKD, defined as an eGFR &lt;60 ml\/min per 1.73 m<jats:sup>2<\/jats:sup>, and the mean eGFR was 63 ml\/min per 1.73 m<jats:sup>2<\/jats:sup>. The primary exposures were cFGF23 and iFGF23. The primary outcomes were six 2D-STE parameters performed at the 1994\u20131995 study visit. Linear regression models were used to examine the independent associations of FGF23 with six cardiac 2D-STE indices adjusting for demographics, cardiovascular risk factors, markers of kidney disease severity, and inflammation.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>cFGF23 levels were moderately correlated with iFGF23 levels in the CHS population. In fully adjusted models, cFGF23 was associated with left atrial dysfunction, but no other cardiac imaging parameter (<jats:italic toggle=\"yes\">\u03b2<\/jats:italic> estimate, \u22122.47; 95% confidence interval, \u22124.68 to \u22120.25; Table 2). iFGF23 was not associated with any of the six 2D-STE indices. Limitations include small sample size and noncurrent FGF23 measurements and 2D-STE imaging.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>In a limited sample of individuals enrolled in the CHS with cFGF23 and iFGF23 measurements, we did not find consistent associations between FGF23 levels and 2D-STE parameters. Further investigations in a larger population with concurrent 2D-STE are needed to better understand the associations of FGF23 with early changes in cardiac mechanics.<\/jats:p>\n          <\/jats:sec>","DOI":"10.34067\/kid.0000000643","type":"journal-article","created":{"date-parts":[[2024,11,19]],"date-time":"2024-11-19T17:06:17Z","timestamp":1732035977000},"page":"391-399","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Association of Fibroblast Growth Factor 23 and Cardiac Mechanics in the Cardiovascular Health Study"],"prefix":"10.34067","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4950-5846","authenticated-orcid":false,"given":"Keertana","family":"Jain","sequence":"first","affiliation":[{"name":"Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7723-7469","authenticated-orcid":false,"given":"Ronit","family":"Katz","sequence":"additional","affiliation":[{"name":"Collaborative Health Studies Coordinating Center, Department of Biostatistics, University of Washington, Seattle, Washington"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9763-2367","authenticated-orcid":false,"given":"Tamara","family":"Isakova","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9936-7803","authenticated-orcid":false,"given":"Jorge R.","family":"Kizer","sequence":"additional","affiliation":[{"name":"Cardiology Section, San Francisco Veterans Affairs Health Care System, Departments of Medicine, Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9011-0163","authenticated-orcid":false,"given":"Shilpa","family":"Sharma","sequence":"additional","affiliation":[{"name":"Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California"}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Epidemiology, and Health Systems and Population Health, University of Washington, Seattle, Washington"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5655-8201","authenticated-orcid":false,"given":"Sanjiv J.","family":"Shah","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Northwestern University, Feinberg School of Medicine, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8084-9869","authenticated-orcid":false,"given":"Joachim","family":"Ix","sequence":"additional","affiliation":[{"name":"Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5848-4325","authenticated-orcid":false,"given":"Rupal","family":"Mehta","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"},{"name":"Division of Nephrology, Department of Medicine, Jesse Brown Veterans Affairs Health Administration, Chicago, Illinois"}]}],"member":"276","published-online":{"date-parts":[[2024,11,19]]},"reference":[{"issue":"5","key":"B2-20250327","doi-asserted-by":"crossref","first-page":"671","DOI":"10.1161\/CIRCULATIONAHA.105.580506","article-title":"Renal function as a predictor of outcome in a broad spectrum of patients with heart failure","volume":"113","author":"Hillege","year":"2006","journal-title":"Circulation."},{"issue":"1","key":"B3-20250327","doi-asserted-by":"crossref","first-page":"8","DOI":"10.1016\/j.jjcc.2010.09.004","article-title":"Chronic kidney disease and heart 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<jats:p>Proteomic profiling offers an expansive approach to biomarker discovery and mechanistic hypothesis generation for LV remodelling, a critical component of heart failure (HF). We sought to identify plasma proteins cross-sectionally associated with left ventricular (LV) size and geometry in a diverse population-based cohort without known cardiovascular disease (CVD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Among participants of the Multi-Ethnic Study of Atherosclerosis (MESA), we quantified plasma abundances of 1305 proteins using an aptamer-based platform at exam 1 (2000\u20132002) and exam 5 (2010\u20132011) and assessed LV structure by cardiac magnetic resonance (CMR) at the same time points. We used multivariable linear regression with robust variance to assess cross-sectional associations between plasma protein abundances and LV structural characteristics at exam 1, reproduced findings in later-life at exam 5, and explored relationships of associated proteins using annotated enrichment analysis. We studied 763 participants (mean age 60 \u00b1 10 years at exam 1; 53% female; 19% Black race; 31% Hispanic ethnicity). Following adjustment for renal function and traditional CVD risk factors, plasma levels of 3 proteins were associated with LV mass index at both time points with the same directionality (FDR &amp;lt; 0.05): leptin (LEP), renin (REN), and cathepsin-D (CTSD); 20 with LV end-diastolic volume index: LEP, NT-proBNP, histone-lysine N-methyltransferase (EHMT2), chordin-like protein 1 (CHRDL1), tumour necrosis factor-inducible gene 6 protein (TNFAIP6), NT-3 growth factor receptor (NTRK3), c5a anaphylatoxin (C5), neurogenic locus notch homologue protein 3 (NOTCH3), ephrin-B2 (EFNB2), osteomodulin (OMD), contactin-4 (CNTN4), gelsolin (GSN), stromal cell-derived factor 1 (CXCL12), calcineurin subunit B type 1 (PPP3R1), insulin-like growth factor 1 receptor (IGF1R), bone sialoprotein 2 (IBSP), interleukin-11 (IL-11), follistatin-related protein 1 (FSTL1), periostin (POSTN), and biglycan (BGN); and 4 with LV mass-to-volume ratio: RGM domain family member B (RGMB), transforming growth factor beta receptor type 3 (TGFBR3), ephrin-A2 (EFNA2), and cell adhesion molecule 3 (CADM3). Functional annotation implicated regulation of the PI3K-Akt pathway, bone morphogenic protein signalling, and cGMP-mediated signalling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We report proteomic profiling of LV size and geometry, which identified novel associations and reinforced previous findings on biomarker candidates for LV remodelling and HF. If validated, these proteins may help refine risk prediction and identify novel therapeutic targets for HF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.15073","type":"journal-article","created":{"date-parts":[[2024,9,12]],"date-time":"2024-09-12T09:33:55Z","timestamp":1726133635000},"page":"239-249","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Proteomics of Left Ventricular Structure in the Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"12","author":[{"given":"Tess E.","family":"Peterson","sequence":"first","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University , Baltimore, Maryland ,","place":["USA"]}]},{"given":"Joao A.C.","family":"Lima","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University , Baltimore, Maryland ,","place":["USA"]}]},{"given":"Sanjiv 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,","place":["USA"]}]},{"given":"Vinithra","family":"Varadarajan","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University , Baltimore, Maryland ,","place":["USA"]}]},{"given":"Josyf C.","family":"Mychaleckyj","sequence":"additional","affiliation":[{"name":"Department of Genome Sciences, University of Virginia , Charlottesville, Virginia ,","place":["USA"]}]},{"given":"Craig W.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington , Seattle, Washington ,","place":["USA"]}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Systems and Population Health, University of Washington , Seattle, Washington ,","place":["USA"]}]},{"given":"Clary B.","family":"Clish","sequence":"additional","affiliation":[{"name":"Metabolomics Platform, Broad Institute of Massachusetts Institute of Technology and Harvard , Cambridge, Washington ,","place":["USA"]}]},{"given":"Kent D.","family":"Taylor","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center , Torrance, California ,","place":["USA"]}]},{"given":"Peter","family":"Durda","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Vermont , Colchester, Vermont ,","place":["USA"]}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"Department of Pathology & Laboratory Medicine, University of Vermont , Colchester, Vermont ,","place":["USA"]}]},{"given":"Robert E.","family":"Gerszten","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Beth Israel Deaconess Hospital , Boston, Massachusetts ,","place":["USA"]}]},{"given":"Stephen S.","family":"Rich","sequence":"additional","affiliation":[{"name":"Department of Genome Sciences, University of Virginia , Charlottesville, Virginia ,","place":["USA"]}]},{"given":"Jerome I.","family":"Rotter","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center , Torrance, California ,","place":["USA"]}]},{"given":"Wendy S.","family":"Post","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University , Baltimore, Maryland ,","place":["USA"]}]},{"given":"James S.","family":"Pankow","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, School of Public Health, University of Minnesota , Minneapolis, Minnesota 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As blood donors are generally considered as the healthy population, assessing the risk of these silent killers in the blood donors can overall help in understanding the potential impact of these infections on the general population.  Objective: As the TTI prevalence is increasing rapidly in our region, it is much needed to take necessary actions for its prevention. The first step should be the actual frequency of these TTI\u2019s in healthy blood donors, so our study aimed to identify the positive ratio of Hep B, Hep C, HIV, malaria and syphilis in exchange and voluntary blood donors, their comparison and need of effective testing. Materials and Methods: It is a retrospective analysis in which all the data is taken from BBMIS software and analyzed by SPSS version 23. We included 56732 donors from 2020-2022. Screening of Hepatitis B, Hepatitis C and HIV was done by Chemoimmunoliscence (CLIA) whereas ICT based screening was done for Syphilis and Malaria. Result: Among donors, 50147 (88.4%) were exchange while 6585 (11.6%) were voluntary donors. The frequency of HCV was 3.1% followed by HbsAg (2.3%) and syphilis (1.6%), HIV 0.3% and the least was malaria 0.2%. As 88% of the donors were exchange, TTI positivity was also more in them. Conclusion: The prevalence of TTI in donors of RBC Karachi is worrysome. It highlights the fact of Nucleic Acid testing significance. Though CLIA is a sensitive technique, 100% safety of blood products requires the implication of Nucleic Acid testing, moreover the implication of voluntary blood donation should also be considered significantly.<\/jats:p>","DOI":"10.21089\/njhs.93.0204","type":"journal-article","created":{"date-parts":[[2024,10,4]],"date-time":"2024-10-04T02:49:43Z","timestamp":1728010183000},"page":"204-208","source":"Crossref","is-referenced-by-count":1,"title":["Trend of Infectious Disease Positivity in Exchange and Voluntary Blood Donors at Regional Blood Centre, Karachi"],"prefix":"10.21089","volume":"9","author":[{"name":"Blood Transfusion Department, Regional Blood Centre, Karachi, Pakistan.","sequence":"first","affiliation":[]},{"given":"Samra","family":"Waheed","sequence":"first","affiliation":[]},{"given":"Muhammad Sarwar","family":"Khan","sequence":"additional","affiliation":[]},{"name":"Administration Department, Regional Blood Centre, Karachi, Pakistan.","sequence":"additional","affiliation":[]},{"given":"Shumaila","family":"Qamar","sequence":"additional","affiliation":[]},{"name":"Quality Control Department, Regional Blood Centre, Karachi, Pakistan.","sequence":"additional","affiliation":[]},{"given":"Syeda Madiha","family":"Shah","sequence":"additional","affiliation":[]},{"name":"Blood Transfusion Department, Regional Blood Centre, Karachi, Pakistan.","sequence":"additional","affiliation":[]},{"given":"Erum","family":"Rafiq","sequence":"additional","affiliation":[]},{"name":"Blood Transfusion Department, Regional Blood Centre, Karachi, Pakistan.","sequence":"additional","affiliation":[]}],"member":"8719","published-online":{"date-parts":[[2024,9,24]]},"container-title":["National Journal of Health 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Methodology: Methodological study of technological innovation, developed with financial resources from the information technology law: Law No. 8.387\/1991 (13), by the Laboratory of Technology in Health and Education of the School of Health Sciences of the University of the State of Amazonas. Results: For the development of the BLOOD mobile application, the basic structure of technological product development was used. The mobile application development lifecycle used was the Scrum Agile model, divided into three phases: planning, development, closing. In the planning phase, the functional and non-functional requirements of the product were defined. The construction phase involved the development of the visual identity, and the development of the product\u2019s features, as well as the integration with existing systems in the healthcare facility. In the closing phase, the tests developed, licenses for use and the product validation process were described. 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We used dual-energy-X-ray-absorptiometry- (DXA-) derived measures of body fat obtained in the Women\u2019s Health Initiative to examine the association between body fat and breast cancer risk; we compared these risk estimates with those for conventional anthropometric measurements. The study included 10,960 postmenopausal women aged 50\u201379 years at recruitment, with baseline DXA measurements and no history of breast cancer. During followup (median: 12.9 years), 503 incident breast cancer cases were diagnosed. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models. All baseline DXA-derived body fat measures showed strong positive associations with breast cancer risk. The multivariable-adjusted HR for the uppermost quintile level (versus lowest) ranged from 1.53 (95% CI 1.14\u20132.07) for fat mass of the right leg to 2.05 (1.50\u20132.79) for fat mass of the trunk. Anthropometric indices (categorized by quintiles) of obesity (BMI (1.97, 1.45\u20132.68), waist circumference (1.97, 1.46\u20132.65), and waist\u2009:\u2009hip ratio (1.91, 1.41\u20132.58)) were all strongly, positively associated with risk and did not differ from DXA-derived measures in prediction of risk.<\/jats:p>","DOI":"10.1155\/2013\/754815","type":"journal-article","created":{"date-parts":[[2013,4,7]],"date-time":"2013-04-07T21:00:39Z","timestamp":1365368439000},"page":"1-13","source":"Crossref","is-referenced-by-count":44,"title":["Body Fat and Breast Cancer Risk in Postmenopausal Women: A Longitudinal Study"],"prefix":"10.1155","volume":"2013","author":[{"given":"Thomas E.","family":"Rohan","sequence":"first","affiliation":[{"name":"Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA"}]},{"given":"Moonseong","family":"Heo","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Population Health, 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Aging","doi-asserted-by":"publisher","award":["R01AG023629"],"award-info":[{"award-number":["R01AG023629"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"published-print":{"date-parts":[[2024,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Heart failure (HF) has shared genetic architecture with its risk factors: atrial fibrillation (AF), body mass index (BMI), coronary heart disease (CHD), systolic blood pressure (SBP), and type 2 diabetes (T2D). We aim to assess the association and risk prediction performance of risk-factor polygenic risk scores (PRSs) for incident HF and its subtypes in bi-racial populations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Five PRSs were constructed for AF, BMI, CHD, SBP, and T2D in White participants of the Atherosclerosis Risk in Communities (ARIC) study. The associations between PRSs and incident HF and its subtypes were assessed using Cox models, and the risk prediction performance of PRSs was assessed using C statistics. Replication was performed in the ARIC study Black and Cardiovascular Health Study (CHS) White participants. In 8624 ARIC study Whites, 1922 (31% cumulative incidence) HF cases developed over 30 years of follow-up. PRSs of AF, BMI, and CHD were associated with incident HF (P &amp;lt; 0.001), where PRSAF showed the strongest association [hazard ratio (HR): 1.47, 95% confidence interval (CI): 1.41\u20131.53]. Only the addition of PRSAF to the ARIC study HF risk equation improved C statistics for 10 year risk prediction from 0.812 to 0.829 (\u2206C: 0.017, 95% CI: 0.009\u20130.026). The PRSAF was associated with both incident HF with reduced ejection fraction (HR: 1.43, 95% CI: 1.27\u20131.60) and incident HF with preserved ejection fraction (HR: 1.46, 95% CI: 1.33\u20131.62). The associations between PRSAF and incident HF and its subtypes, as well as the improved risk prediction, were replicated in the ARIC study Blacks and the CHS Whites (P &amp;lt; 0.050). Protein analyses revealed that N-terminal pro-brain natriuretic peptide and other 98 proteins were associated with PRSAF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The PRSAF was associated with incident HF and its subtypes and had significant incremental value over an established HF risk prediction equation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.14665","type":"journal-article","created":{"date-parts":[[2024,1,23]],"date-time":"2024-01-23T01:54:40Z","timestamp":1705974880000},"page":"1086-1096","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["A Polygenic Risk Score of Atrial Fibrillation Improves Prediction of Lifetime Risk for Heart Failure"],"prefix":"10.1093","volume":"11","author":[{"given":"Taryn","family":"Alkis","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX ,","place":["USA"]}]},{"given":"Xi","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Data Science, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX ,","place":["USA"]}]},{"given":"Katherine","family":"Wall","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Data Science, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX ,","place":["USA"]}]},{"given":"Jennifer","family":"Brody","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Medicine, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Traci","family":"Bartz","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Departments of Medicine and Biostatistics, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Patricia P.","family":"Chang","sequence":"additional","affiliation":[{"name":"Division of Cardiology, University of North Carolina School of Medicine , Chapel Hill, NC ,","place":["USA"]}]},{"given":"Faye L.","family":"Norby","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, University of Minnesota , Minneapolis, MN ,","place":["USA"]}]},{"given":"Ron C.","family":"Hoogeveen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine , Houston, TX ,","place":["USA"]}]},{"given":"Alanna C.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX ,","place":["USA"]}]},{"given":"Christie M.","family":"Ballantyne","sequence":"additional","affiliation":[{"name":"Department of Medicine, Baylor College of Medicine , Houston, TX ,","place":["USA"]}]},{"given":"Josef","family":"Coresh","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health , Baltimore, MD ,","place":["USA"]}]},{"given":"Eric","family":"Boerwinkle","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX ,","place":["USA"]},{"name":"Human Genome Sequencing Center, Baylor College of Medicine , Houston, TX ,","place":["USA"]}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Medicine, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["USA"]},{"name":"Department of Health Systems and Population Health, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Amil M.","family":"Shah","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, UT Southwestern Medical Center , Dallas, TX ,","place":["USA"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4818-1077","authenticated-orcid":false,"given":"Bing","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston , Houston, TX 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We conducted a meta\u2010analysis of 11 studies comprising 8,332 cases and 16,087 controls of European ancestry and 382 cases and 1,476 controls of African American ancestry genotyped with the Illumina HumanExome BeadChip. We used the seqMeta package in R to conduct single variant and gene\u2010based rare variant tests. In the single variant analysis, we limited our analysis to the 64,794 variants with at least 40 minor alleles across studies (minor allele frequency [MAF] ~0.08%). We confirmed associations with previously identified VTE loci, including <jats:italic>ABO<\/jats:italic>, \n<jats:italic>F5<\/jats:italic>, \n<jats:italic>F11<\/jats:italic>, and \n<jats:italic>FGA<\/jats:italic>. After adjusting for multiple testing, we observed no novel significant findings in single variant or gene\u2010based analysis. Given our sample size, we had greater than 80% power to detect minimum odds ratios greater than 1.5 and 1.8 for a single variant with MAF of 0.01 and 0.005, respectively. Larger studies and sequence data may be needed to identify novel low\u2010frequency and rare variants associated with VTE risk.<\/jats:p>","DOI":"10.1002\/gepi.22187","type":"journal-article","created":{"date-parts":[[2019,1,19]],"date-time":"2019-01-19T19:53:00Z","timestamp":1547927580000},"page":"449-457","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["A large\u2010scale exome array analysis of venous thromboembolism"],"prefix":"10.1002","volume":"43","author":[{"given":"Sara","family":"Lindstr\u00f6m","sequence":"first","affiliation":[{"name":"Department of Epidemiology University of Washington Seattle Washington"},{"name":"Division of Public Health Sciences Fred Hutchinson Cancer Research Center Seattle Washington"}]},{"given":"Jennifer A.","family":"Brody","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Washington Seattle Washington"}]},{"given":"Constance","family":"Turman","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Harvard TH Chan School of Public Health Boston Massachusetts"}]},{"given":"Marine","family":"Germain","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm 1219, Bordeaux Population Health Research Center Bordeaux France"}]},{"given":"Traci M.","family":"Bartz","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Washington Seattle Washington"},{"name":"Department of Biostatistics University of Washington Seattle Washington"}]},{"given":"Erin N.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Rady Children\u2019s Hospital, University of California San Diego California"},{"name":"Department of Clinical Medicine UiT\u2014The Arctic University of Norway, K.G. 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Here we describe a novel intravital imaging approach based on the computer-vision stabilization algorithm, Computer-Vision Stabilized Intravital Imaging. This method corrects lung movements and deformations at submicron precision in respiring mouse lungs. The precision enables high-throughput quantitative analysis of intravital pulmonary polymorphonuclear neutrophil (PMN) dynamics in lungs. We quantified real-time PMN patrolling dynamics of microvessels in the basal state and PMN recruitment resulting from sequestration in a model of endotoxemia in mice. We focused on determining the marginated pool of PMNs in the lung. Direct visualization of marginated PMNs revealed that they are not static but highly dynamic and undergo repeated cycles of \u201ccatch and release.\u201d PMNs briefly arrest in larger diameter capillary junction (\u223c10 \u03bcm) and then squeeze into narrower, approximately 5-\u03bcm diameter vessels through PMN deformation. We also observed that the sequestered PMNs in lung microvessels lost their migratory capabilities in association with cell morphological change following prolonged endotoxemia. These observations underscore the value of direct visualization and quantitative analysis of PMN dynamics in lungs to study PMN physiology and pathophysiology and role in inflammatory lung injury.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0318ma","type":"journal-article","created":{"date-parts":[[2021,9,23]],"date-time":"2021-09-23T17:28:43Z","timestamp":1632418123000},"page":"12-22","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":10,"title":["Quantitative Pulmonary Neutrophil Dynamics Using Computer-Vision Stabilized Intravital Imaging"],"prefix":"10.1093","volume":"66","author":[{"given":"Yoshikazu","family":"Tsukasaki","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Regenerative Medicine and The Center for Lung and Vascular Biology"}]},{"given":"Peter T.","family":"Toth","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Regenerative Medicine and The Center for Lung and 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Institute","doi-asserted-by":"publisher","award":["UL1TR000040"],"award-info":[{"award-number":["UL1TR000040"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["UL1TR001079"],"award-info":[{"award-number":["UL1TR001079"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["UL1TR001420"],"award-info":[{"award-number":["UL1TR001420"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R24HL114473"],"award-info":[{"award-number":["R24HL114473"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92019R002"],"award-info":[{"award-number":["75N92019R002"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2022,9,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Study Objectives<\/jats:title>\n                  <jats:p>Obstructive sleep apnea (OSA) is characterized by multiple \u201cendotypic traits,\u201d including pharyngeal collapsibility, muscle compensation, loop gain, and arousal threshold. Here, we examined (1) within-night repeatability, (2) long-term consistency, and (3) influences of body position and sleep state, of endotypic traits estimated from in-home polysomnography in mild-to-severe OSA (apnea-hypopnea index, AHI &amp;gt; 5 events\/h).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Within-night repeatability was assessed using Multi-Ethnic Study of Atherosclerosis (MESA): Traits derived separately from \u201codd\u201d and \u201ceven\u201d 30-min periods were correlated and regression (error vs. N windows available) provided a recommended amount of data for acceptable repeatability (Rthreshold = 0.7). Long-term consistency was assessed using the Osteoporotic Fractures in Men Study (MrOS) at two time points 6.5 \u00b1 0.7 years apart, before and after accounting for across-year body position and sleep state differences. Within-night dependence of traits on position and state (MESA plus MrOS data) was estimated using bootstrapping.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Within-night repeatability for traits ranged from R = 0.62\u20130.79 and improved to R = 0.69\u20130.83 when recommended amounts of data were available (20\u201335 7-min windows, available in 94%\u201398% of participants); repeatability was similar for collapsibility, loop gain, and arousal threshold (R = 0.79\u20130.83), but lower for compensation (R = 0.69). Long-term consistency was modest (R = 0.30\u20130.61) and improved (R = 0.36\u20130.63) after accounting for position and state differences. Position\/state analysis revealed reduced loop gain in REM and reduced collapsibility in N3.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Endotypic traits can be obtained with acceptable repeatability. Long-term consistency was modest but improved after accounting for position and state changes. These data support the use of endotypic assessments in large-scale epidemiological studies.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Clinical Trial Information<\/jats:title>\n                  <jats:p>The data used in the manuscript are from observational cohort studies and are not a part of the clinical trial.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/sleep\/zsac129","type":"journal-article","created":{"date-parts":[[2022,6,11]],"date-time":"2022-06-11T22:11:40Z","timestamp":1654985500000},"source":"Crossref","is-referenced-by-count":41,"title":["Within-night repeatability and long-term consistency of sleep apnea endotypes: the Multi-Ethnic Study of Atherosclerosis and Osteoporotic Fractures in Men Study"],"prefix":"10.1093","volume":"45","author":[{"given":"Raichel M","family":"Alex","sequence":"first","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8520-8860","authenticated-orcid":false,"given":"Tamar","family":"Sofer","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4986-4753","authenticated-orcid":false,"given":"Ali","family":"Azarbarzin","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1740-8777","authenticated-orcid":false,"given":"Daniel","family":"Vena","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"given":"Laura K","family":"Gell","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"given":"Andrew","family":"Wellman","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"given":"David P","family":"White","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"given":"Susan","family":"Redline","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]},{"given":"Scott A","family":"Sands","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA , USA"}]}],"member":"286","published-online":{"date-parts":[[2022,6,11]]},"reference":[{"key":"2022090808591209400_CIT0001","doi-asserted-by":"crossref","first-page":"45","DOI":"10.1016\/j.smrv.2016.12.003","article-title":"Phenotypic approaches to obstructive sleep apnoea\u2014new pathways for targeted therapy","volume":"37","author":"Eckert","year":"2018","journal-title":"Sleep Med Rev."},{"issue":"1","key":"2022090808591209400_CIT0002","doi-asserted-by":"crossref","first-page":"179","DOI":"10.1213\/ANE.0000000000001546","article-title":"Understanding phenotypes of obstructive sleep apneasapplications in anesthesia, surgery, and perioperative medicine","volume":"124","author":"Subramani","year":"2017","journal-title":"Anesth Analg."},{"issue":"8","key":"2022090808591209400_CIT0003","doi-asserted-by":"crossref","first-page":"996","DOI":"10.1164\/rccm.201303-0448OC","article-title":"Defining phenotypic causes of obstructive sleep apnea. 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The WHI consisted of three overlapping clinical trials of hormone therapy, diet modification to reduce total dietary fat, and calcium\/vitamin D supplementation. Women who were ineligible for the hormone therapy or diet modification trials or not interested were invited to participate in the observational study. Women were recruited into WHI from 1993 to 1998 at 40 US clinical centers. WHI enrolled 26,046 underrepresented minority women and 135,762 white women. Women could participate in each trial if eligible. The final enrollment included 27,347 women in the hormone trial; 48,835 women in the diet modification trial; 36,282 women in the calcium\/vitamin D trial, and 93,676 in the observational study. After the main study ended in 2005, women were invited to continue follow-up for exposures and outcomes through two extensions to 2020. Proposals were recently submitted to continue follow-up through 2027. Information was collected on an extensive number of risk factors for fractures at baseline and over the follow-up, including fall and fracture history, weight patterns, comorbidities, diet, reproductive history, medications, anthropometry, and biomarkers. Bone mineral density was measured at three WHI clinical centers (n = 11,020) chosen to maximize race\/ethnic diversity. WHI encourages outside investigators to make use of the publicly available WHI data and to access the biobank of specimens (www.whi.org). \u00a9 2020 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.4026","type":"journal-article","created":{"date-parts":[[2020,4,14]],"date-time":"2020-04-14T08:53:05Z","timestamp":1586854385000},"page":"845-860","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["The Women's Health Initiative: A Landmark Resource for Skeletal Research Since 1992"],"prefix":"10.1093","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0752-4408","authenticated-orcid":false,"given":"Jane A","family":"Cauley","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Graduate School of Public Health University of Pittsburgh Pittsburgh PA 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Cox proportional hazard regression analyses were performed using a general model, with the major homozygote as the reference category. For 9,865 whites, a significant increase in the risk of CHD was seen only among lean (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>BMI<\/mml:mtext><mml:mo>&lt;<\/mml:mo><mml:mn>25<\/mml:mn><\/mml:mrow><\/mml:math>\u2009kg\/<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:msup><mml:mtext>m<\/mml:mtext><mml:mn>2<\/mml:mn><\/mml:msup><\/mml:mrow><\/mml:math>) individuals homozygous for the<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mi>T<\/mml:mi><\/mml:math>allele of the<jats:italic>TCF7L2<\/jats:italic>rs7903146 gene risk variant (hazard ratio 1.42; 95% CI 1.03,1.97;<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>.01<\/mml:mn><\/mml:mrow><\/mml:math>). No association was found among 3,631 blacks, regardless of BMI status. An attenuated hazard ratio was observed among the nondiabetic ARIC cohort members. This study suggests that body mass modifies the association of the<jats:italic>TCF7L2<\/jats:italic>rs7903146 T allele with CHD risk.<\/jats:p>","DOI":"10.1155\/2010\/651903","type":"journal-article","created":{"date-parts":[[2010,2,22]],"date-time":"2010-02-22T10:31:31Z","timestamp":1266834691000},"page":"1-5","source":"Crossref","is-referenced-by-count":5,"title":["Role of BMI in the Association of the<i>TCF7L2<\/i>rs7903146 Variant with Coronary Heart Disease: The Atherosclerosis Risk in Communities (ARIC) Study"],"prefix":"10.1155","volume":"2010","author":[{"given":"Anna M.","family":"Kucharska-Newton","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA"}]},{"given":"Keri L.","family":"Monda","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 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Patients with microvascular angina are at higher risk for major adverse cardiac events including MI, stroke, heart failure with preserved ejection fraction and death but to date there are no clear evidence-based guidelines for diagnosis and treatment. Recently, the Coronary Vasomotion Disorders International Study Group proposed standardised criteria for diagnosis of microvascular angina using invasive and non-invasive approaches. The management strategy for remains empirical, largely due to the lack of high-level-evidence-based guidelines and clinical trials. In this review, the authors will illustrate the updated approach to diagnosis of microvascular angina and address evidence-based pharmacological and non-pharmacological treatments for patients with the condition.<\/jats:p>","DOI":"10.15420\/ecr.2021.15","type":"journal-article","created":{"date-parts":[[2021,12,4]],"date-time":"2021-12-04T11:39:51Z","timestamp":1638617991000},"source":"Crossref","is-referenced-by-count":26,"title":["Microvascular Angina: Diagnosis and Management"],"prefix":"10.15420","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3785-2755","authenticated-orcid":false,"given":"Haider","family":"Aldiwani","sequence":"first","affiliation":[{"name":"Barbra Streisand Women\u2019s Heart Center, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, US;  Scripps Health Institution Chula Vista Hospital, Department of Internal Medicine, San Diego, US"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1210-6585","authenticated-orcid":false,"given":"Suzan","family":"Mahdai","sequence":"additional","affiliation":[{"name":"Scripps Health Institution Chula Vista Hospital, Department of Internal Medicine, San Diego, US"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5568-840X","authenticated-orcid":false,"given":"Ghaith","family":"Alhatemi","sequence":"additional","affiliation":[{"name":"St Mary Mercy Hospital, Department of Internal Medicine, Livonia, Michigan, US"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9933-5155","authenticated-orcid":false,"given":"C Noel","family":"Bairey Merz","sequence":"additional","affiliation":[{"name":"Barbra Streisand Women\u2019s Heart Center, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, US"}]}],"member":"6096","published-online":{"date-parts":[[2021,12,2]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"AlBadri A, Lai K, Wei J, et al. 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Institute","doi-asserted-by":"publisher","award":["U01HL089856"],"award-info":[{"award-number":["U01HL089856"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"name":"NIH","award":["75N92023D00011"],"award-info":[{"award-number":["75N92023D00011"]}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2025,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Interstitial lung abnormalities (ILAs) are visually identified changes on chest computed tomography (CT) scans that may represent early or mild pulmonary fibrosis. Quantitative interstitial abnormalities (QIAs) measure potential parenchymal lung injury on chest CT scans using an automated algorithm. It is not known if combining these visual and quantitative assessments improves prediction of imaging progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To assess the utility of quantitative imaging to predict imaging progression of ILAs and adverse clinical outcomes in a cohort of smokers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>ILA presence, subtypes, and progression, as well as QIAs, were assessed on chest CT scans from participants \u223c5 years apart in the COPDGene (Genetic Epidemiology of COPD) study. Multivariable logistic regression assessed associations with ILA progression, and Cox proportional hazards assessed the relationship between ILA progression and mortality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>A total of 4,373 participants had serial CT scans, and 544 (12%) had ILAs on at least one; of those, 391 (72%) had imaging visual progression, and 153 (28%) did not. Specific imaging features were associated progression (e.g., traction bronchiectasis; odds ratio, 3.1; 95% confidence interval [CI], 1.3\u20137.3; P\u2009=\u20090.003). Among those with ILAs, baseline quantitative measures (QIAs and FVC) were not associated with progression; however, visual imaging progression was associated with increased longitudinal change of QIAs (mean difference, 6.5%; 95% CI, 4.9\u20138.1%; P\u2009&amp;lt;\u20090.0001). In ILAs, QIA increase was associated with an increased rate of mortality independent of FVC decline (hazard ratio, 1.05; 95% CI, 1.01\u20131.09; P\u2009=\u20090.009).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Baseline quantitative measures (QIAs and FVC) were not associated with visual ILA progression; however, longitudinal change in QIAs was correlated with imaging progression and adverse clinical outcomes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202501-0247oc","type":"journal-article","created":{"date-parts":[[2025,7,28]],"date-time":"2025-07-28T20:41:37Z","timestamp":1753735297000},"page":"1794-1801","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":2,"title":["Visual and Quantitative Interstitial Lung Abnormality Progression in COPDGene"],"prefix":"10.1093","volume":"211","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8027-7450","authenticated-orcid":false,"given":"Rachel K.","family":"Putman","sequence":"first","affiliation":[{"name":"Pulmonary and Critical Care Division"}]},{"given":"Jonathan A.","family":"Rose","sequence":"additional","affiliation":[{"name":"Pulmonary and Critical Care Division"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7095-2432","authenticated-orcid":false,"given":"Ruben","family":"San Jos\u00e9 Estepar","sequence":"additional","affiliation":[{"name":"Department of Radiology"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2877-6535","authenticated-orcid":false,"given":"Ann-Marcia C.","family":"Tukpah","sequence":"additional","affiliation":[{"name":"Pulmonary and Critical Care Division"}]},{"given":"Claire C.","family":"Cutting","sequence":"additional","affiliation":[{"name":"Pulmonary and Critical Care Division"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8225-0737","authenticated-orcid":false,"given":"Takuya","family":"Hino","sequence":"additional","affiliation":[{"name":"Department of Radiology"},{"name":"Center for Pulmonary Functional Imaging, and"}]},{"given":"Akinori","family":"Hata","sequence":"additional","affiliation":[{"name":"Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, Osaka, Japan"}]},{"given":"Mizuki","family":"Nishino","sequence":"additional","affiliation":[{"name":"Department of Radiology"},{"name":"Center for Pulmonary Functional Imaging, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5113-4530","authenticated-orcid":false,"given":"Stephen M.","family":"Humphries","sequence":"additional","affiliation":[{"name":"Department of Radiology, National Jewish Health, Denver, Colorado; and"}]},{"given":"David A.","family":"Lynch","sequence":"additional","affiliation":[{"name":"Department of Radiology, National Jewish Health, Denver, 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We assessed the associations between BP and selected polysomnography (PSG) traits: sleep depth, airflow limitation measurements and OSA-specific hypoxic burden.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This cross-sectional analysis included 2055 participants from the Multi-Ethnic Study of Atherosclerosis who underwent PSG and BP measurements in 2010\u20132013. Sleep depth was assessed using the \u2018OR product\u2019, a continuous measure of arousability. Airflow limitation was assessed by duty cycle (T<jats:sub>i<\/jats:sub>\/T<jats:sub>t<\/jats:sub>) and % of breaths with flow limitation, and hypoxia by \u2018hypoxic burden\u2019. Primary outcomes were medication-adjusted systolic BP (SBP) and diastolic BP (DBP). We used generalised linear models adjusted for age, sex, race\/ethnicity, smoking, education, body mass index, alcohol use, periodic limb movements and alternative physiological disturbances.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The sample had a mean age of 68.4 years and apnoea\u2013hypopnoea index of 14.8 events\/hour. Sleep depth was not significantly associated with BP. Every 1 SD increment in log-transformed non-rapid eye movement duty cycle was associated with 0.9% decrease in SBP (95%\u2009CI: 0.1% to 1.6%), even after adjusting for sleep depth and hypoxic burden. Every 1 SD increment in log-transformed hypoxic burden was associated with a 1.1% increase in SBP (95%\u2009CI: 0.1% to 2.1%) and 1.9% increase in DBP (95%\u2009CI: 1.0% to 2.8%) among those not using hypertension medications.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Higher duty cycle was associated with lower SBP overall and hypoxic burden with higher SBP and DBP among non-BP medication users. These findings suggest changes in both respiratory effort and oxygenation during sleep influence BP.<\/jats:p><\/jats:sec>","DOI":"10.1136\/thoraxjnl-2019-213533","type":"journal-article","created":{"date-parts":[[2019,8,22]],"date-time":"2019-08-22T21:20:05Z","timestamp":1566508805000},"page":"57-63","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":47,"title":["Association of novel measures of sleep disturbances with blood pressure: the Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1136","volume":"75","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8887-150X","authenticated-orcid":false,"given":"John S.","family":"Kim","sequence":"first","affiliation":[]},{"given":"Ali","family":"Azarbarzin","sequence":"additional","affiliation":[]},{"given":"Rui","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Ina E.","family":"Djonlagic","sequence":"additional","affiliation":[]},{"given":"Naresh M.","family":"Punjabi","sequence":"additional","affiliation":[]},{"given":"Phyllis C.","family":"Zee","sequence":"additional","affiliation":[]},{"given":"Brian B.","family":"Koo","sequence":"additional","affiliation":[]},{"given":"Elsayed Z.","family":"Soliman","sequence":"additional","affiliation":[]},{"given":"Magdy","family":"Younes","sequence":"additional","affiliation":[]},{"given":"Susan","family":"Redline","sequence":"additional","affiliation":[]}],"member":"239","published-online":{"date-parts":[[2019,8,22]]},"reference":[{"key":"2024092103201713000_75.1.57.1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.117.032582"},{"key":"2024092103201713000_75.1.57.2","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.2109080"},{"key":"2024092103201713000_75.1.57.3","doi-asserted-by":"crossref","first-page":"587","DOI":"10.5665\/sleep.4576","article-title":"A systematic assessment of the association of polysomnographic indices with blood pressure: the multi-ethnic study of atherosclerosis (MESA)","volume":"38","author":"Dean","year":"2015","journal-title":"Sleep"},{"key":"2024092103201713000_75.1.57.4","doi-asserted-by":"crossref","DOI":"10.1093\/sleep\/zsx179","article-title":"Slow-Wave sleep is associated with incident hypertension: the sleep heart health study","volume":"41","author":"Javaheri","year":"2018","journal-title":"Sleep"},{"key":"2024092103201713000_75.1.57.5","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200302-201OC"},{"key":"2024092103201713000_75.1.57.6","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.164.4.406"},{"key":"2024092103201713000_75.1.57.7","doi-asserted-by":"crossref","first-page":"896","DOI":"10.1016\/S0873-2159(15)30387-1","article-title":"Daytime sleepiness and polysomnographic variables in sleep apnoea patients","volume":"13","author":"Mediano","year":"2007","journal-title":"Rev Port Pneumol"},{"key":"2024092103201713000_75.1.57.8","doi-asserted-by":"crossref","first-page":"167","DOI":"10.1016\/j.jsmc.2017.01.005","article-title":"The effects of insomnia and sleep loss on cardiovascular disease","volume":"12","author":"Khan","year":"2017","journal-title":"Sleep Med Clin"},{"key":"2024092103201713000_75.1.57.9","doi-asserted-by":"crossref","first-page":"44","DOI":"10.1016\/j.resp.2013.10.014","article-title":"Transcutaneous CO(2) plateau as set-point for respiratory drive during upper airway flow-limitation","volume":"191","author":"Rimpil\u00e4","year":"2014","journal-title":"Respir Physiol Neurobiol"},{"key":"2024092103201713000_75.1.57.10","doi-asserted-by":"crossref","first-page":"641","DOI":"10.5665\/sleep.4588","article-title":"Odds ratio product of sleep EEG as a continuous measure of sleep state","volume":"38","author":"Younes","year":"2015","journal-title":"Sleep"},{"key":"2024092103201713000_75.1.57.11","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.90408.2008"},{"key":"2024092103201713000_75.1.57.12","doi-asserted-by":"crossref","first-page":"134","DOI":"10.1016\/j.slsci.2015.08.003","article-title":"The role of flow limitation as an important diagnostic tool and clinical finding in mild sleep-disordered breathing","volume":"8","author":"Arora","year":"2015","journal-title":"Sleep Sci"},{"key":"2024092103201713000_75.1.57.13","doi-asserted-by":"crossref","first-page":"1149","DOI":"10.1093\/eurheartj\/ehy624","article-title":"The hypoxic burden of sleep apnoea predicts cardiovascular disease-related mortality: the osteoporotic fractures in men study and the sleep heart health study","volume":"40","author":"Azarbarzin","year":"2019","journal-title":"Eur Heart J"},{"key":"2024092103201713000_75.1.57.14","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1994.00420190121014"},{"key":"2024092103201713000_75.1.57.15","doi-asserted-by":"crossref","unstructured":"Hackshaw A , Morris JK , Boniface S , et al . 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This paper centers on the omnipresent motif of \"blood\" that permeates the entire text, employing close textual analysis and symbolic interpretation to examine how it simultaneously embodies themes of survival, emotional turmoil, and resistance through symbolism, suggestion, and connotation. The ebb and flow of blood vividly mirror the arduous struggle of the underprivileged class to exchange their own bodies for livelihood amid destitution; the distortion of blood kinship under economic strain reflects the alienation and fracture of familial bonds; meanwhile, acts of \"yi xue huan xue (blood-debt repayment, lit. blood for blood)\" manifest a powerless defiance constrained by corporeal limitations and systemic oppression. As a pivotal emblem, blood not only structures the novel\u2019s narrative framework but also offers a vital lens through which to comprehend grassroots experiences and societal inequities.<\/jats:p>","DOI":"10.62381\/e254b01","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T17:22:05Z","timestamp":1770225725000},"page":"1-6","source":"Crossref","is-referenced-by-count":0,"title":["Blood Coagulates, Blood Scatters: The Reality Beneath the \"Blood\" Imagery in Chronicle of a Blood Merchant"],"prefix":"10.62381","volume":"2","author":[{"given":"Xiyi","family":"Chen","sequence":"first","affiliation":[]}],"member":"48889","published-online":{"date-parts":[[2025,11]]},"reference":[{"key":"1","unstructured":"Wang Yi. Multidimensional Challenges \u2014 On the Writing of \"Blood\" in Yu Hua\u2019s Novels. Shanghai: East China Normal University, 2020."},{"key":"2","unstructured":"Zhang Lianyi, Tu Chunxia. The Symbolic Meaning of \"Selling Blood\" in Chronicle of a Blood Merchant. Journal of Language and Literature, 2005(9): 102-104."},{"key":"3","unstructured":"Ma Zheng. The Coldness and Warmth of Life \u2014 Analysis of the Blood Imagery in Chronicle of a Blood Merchant. Journal of Zaozhuang University, 2005(3): 51-52."},{"key":"4","unstructured":"Liang Shuang. Warm Blood Donation \u2014 A Cultural Interpretation of the Blood Imagery in Chronicle of a Blood Merchant. Journal of Kaifeng Education Institute, 2014(5): 32-33."},{"key":"5","unstructured":"Huang Zihan. Exploration of Life Consciousness in Cultural Works \u2014 Taking Yu Hua\u2019s Chronicle of a Blood Merchant as an Example. Mangzhong, 2024(08): 82-84."},{"key":"6","unstructured":"Yu Hua. Chronicle of a Blood Merchant. Beijing: Writers Publishing House, 2012."},{"key":"7","unstructured":"Zhao Ruisi. The View of Fate in Yu Hua\u2019s Creations. Delta, 2025(04): 75-77."},{"key":"8","unstructured":"Shu Qi. Cultural Reflections on the Blood Imagery in Yu Hua\u2019s Novels. New Curriculum (Mid-month), 2012(7): 41."},{"key":"9","unstructured":"Chen Linghui. The Philosophy of Survival in Chronicle of a Blood Merchant. Zhongyuan Literature, 2025(04): 17-19."},{"key":"10","unstructured":"Duan Yuhui. Ordinary Greatness, Stubborn Warmth \u2014 Interpreting Chronicle of a Blood Merchant through \"Blood\". Delta, 2025(16): 55-57."},{"key":"11","unstructured":"Wu Yiqin. Farewell to \"False Forms\" \u2014 The Significance of Chronicle of a Blood Merchant to Yu Hua. Literary Contention, 2000(01): 71-77."},{"key":"12","unstructured":"Fei Hao. The Multiple Meanings of \"Selling Blood\" in Chronicle of a Blood Merchant. 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    <jats:p>Some with interstitial lung abnormalities (ILA) are suspected to have interstitial lung disease (ILD), a subgroup with adverse outcomes. Rates of development and progression of suspected ILD and their effect on mortality are unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine rates of development, progression, and mortality in those with suspected ILD and assess effects of individual ILD and progression criteria.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Participants from COPDGene (Genetic Epidemiology of Chronic Obstructive Pulmonary Disease) with ILA characterization and FVC at enrollment and 5-year follow-up were included. ILD was defined as ILA and fibrosis and\/or FVC\u2009&amp;lt;\u200980% predicted. Prevalent ILD was assessed at enrollment and incident ILD and progression were assessed at 5-year follow-up. Computed tomography (CT) progression was assessed visually and FVC decline as relative change. Multivariable Cox regression tested associations between mortality and prevalent ILD, incident ILD, and progression groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Of 9,588 participants at enrollment, 268 (2.8%; 51% of ILA) had prevalent ILD. Those with prevalent ILD had 51% mortality after median 10.6 years, which was higher than those with ILA without prevalent ILD (henceforth ILA) (33%; hazard ratio [HR], 2.0; P\u2009&amp;lt;\u20090.001). The subgroup of prevalent ILD with only fibrosis criteria (FVC\u2009\u2265\u200980%) had worse mortality (58%) than ILA (HR, 2.2; P\u2009&amp;lt;\u20090.001). A total of 98 participants with prevalent ILD completed 5-year follow-up: 33% had stable CT and relative FVC decline &amp;lt;10%, 6% had FVC decline \u226510% only, 39% had CT progression only, and 22% had both CT progression and FVC decline \u226510%. Mortality rates were 31%, 50%, 45%, and 45%, respectively; those with only CT progression had worse mortality than those with ILA (HR, 2.6; P\u2009=\u20090.005). At 5-year follow-up, incident ILD occurred in 148\/4,842 participants without prevalent ILD (5.5\/1,000 person-years) and had worse mortality than ILA (HR, 2.4; P\u2009&amp;lt;\u20090.001).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Rates of mortality and progression are high among those with suspected ILD in COPDGene; fibrosis and radiologic progression are important predictors of mortality.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202402-0313oc","type":"journal-article","created":{"date-parts":[[2024,8,12]],"date-time":"2024-08-12T11:20:25Z","timestamp":1723461625000},"page":"1453-1460","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":11,"title":["Development, Progression, and Mortality of Suspected Interstitial Lung Disease in COPDGene"],"prefix":"10.1093","volume":"210","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3024-8309","authenticated-orcid":false,"given":"Jonathan A.","family":"Rose","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2877-6535","authenticated-orcid":false,"given":"Ann-Marcia C.","family":"Tukpah","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine"}]},{"given":"Claire","family":"Cutting","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine"}]},{"given":"Noriaki","family":"Wada","sequence":"additional","affiliation":[{"name":"Department of Radiology, and"}]},{"given":"Mizuki","family":"Nishino","sequence":"additional","affiliation":[{"name":"Department of Radiology, and"},{"name":"Department of Imaging, Dana-Farber Cancer Institute, Boston, 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This practice tends to inflate the apparent benefits of interventions with a high risk of mortality. Assessing a composite QoL-death outcome is a potential solution to this problem.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine the effect of lung volume reduction surgery (LVRS) on a composite endpoint consisting of the occurrence of death or a clinically meaningful decline in QoL defined as an increase of at least eight points in the St. George's Respiratory Questionnaire total score from the National Emphysema Treatment Trial.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In patients with chronic obstructive pulmonary disease and emphysema randomized to receive medical treatment (n = 610) or LVRS (n = 608), we analyzed the survival to the composite endpoint, the hazard functions and constructed prediction models of the slope of QoL decline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>The time to the composite endpoint was longer in the LVRS group (2 years) than the medical treatment group (1 year) (P &amp;lt; 0.0001). It was even longer in the subsets of patients undergoing LVRS without a high risk for perioperative death and with upper-lobe-predominant emphysema. The hazard for the composite event significantly favored the LVRS group, although it was most significant in patients with predominantly upper-lobe emphysema. The beneficial impact of LVRS on QoL decline was most significant during the 2 years after LVRS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>LVRS has a significant effect on the composite QoL-survival endpoint tested, indicating its meaningful palliative role, particularly in patients with upper-lobe\u2013predominant emphysema.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.200809-1383oc","type":"journal-article","created":{"date-parts":[[2009,5,29]],"date-time":"2009-05-29T21:47:56Z","timestamp":1243633676000},"page":"239-246","source":"Crossref","is-referenced-by-count":25,"title":["Integrating Health Status and Survival Data: The Palliative Effect of Lung Volume Reduction Surgery"],"prefix":"10.1093","volume":"180","author":[{"given":"Roberto","family":"Benzo","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, 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aged 52\u00a0years and more from the <jats:styled-content style=\"fixed-case\">ARIC<\/jats:styled-content> cohort were included. Retinal vascular diameters were measured and summarized as central retinal arteriolar\/venular equivalents (<jats:styled-content style=\"fixed-case\">CRAE<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">CRVE<\/jats:styled-content>). Periodontitis was determined by using the <jats:styled-content style=\"fixed-case\">CDC<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">AAP<\/jats:styled-content> definition. Multivariable linear regression models were used to estimate the relationships between <jats:styled-content style=\"fixed-case\">CRAE<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> CRVE<\/jats:styled-content> and periodontitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>No association was found between <jats:styled-content style=\"fixed-case\">CRAE<\/jats:styled-content> and periodontal status. However, <jats:styled-content style=\"fixed-case\">CRVE<\/jats:styled-content> and severe periodontitis were positively and significantly associated. Mean <jats:styled-content style=\"fixed-case\">CRVE<\/jats:styled-content> (\u00b1SD) was 187.0\u00a0\u00b1\u00a017.2\u00a0<jats:italic>\u03bc<\/jats:italic>m in the health\u2010gingivitis group, and, respectively, 188.5\u00a0\u00b1\u00a016.3\u00a0<jats:italic>\u03bc<\/jats:italic>m (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.39) and 191.6\u00a0\u00b1\u00a016.8\u00a0<jats:italic>\u03bc<\/jats:italic>m (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.04) in moderate and severe periodontitis groups, after adjustment for a propensity score based on confounders. Results were consistent when analyses were restricted to participants with diabetes mellitus (<jats:italic>n<\/jats:italic>\u00a0=\u00a066), but not diabetes\u2010free subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Severe periodontitis is associated with larger retinal venular diameter in patients with type 2 diabetes. Further studies are needed to explore the impact of diabetes mellitus on the association between periodontitis and retinal microcirculation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jcpe.12388","type":"journal-article","created":{"date-parts":[[2015,2,28]],"date-time":"2015-02-28T07:18:55Z","timestamp":1425107935000},"page":"342-349","source":"Crossref","is-referenced-by-count":20,"title":["Periodontitis and retinal microcirculation in the Atherosclerosis Risk in Communities study"],"prefix":"10.1111","volume":"42","author":[{"given":"Adrien","family":"Boillot","sequence":"first","affiliation":[{"name":"Department of Periodontology Rothschild Hospital (AP\u2010HP) UFR of Odontology University of Paris Diderot Paris France"},{"name":"INSERM UMS 011 Population\u2010Based Cohort Platform Villejuif France"}]},{"given":"Philippe","family":"Bouchard","sequence":"additional","affiliation":[{"name":"Department of Periodontology Rothschild Hospital (AP\u2010HP) UFR of Odontology University of 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Here, blood indexed a past and present colonial violence, as well as the future possibility for an ascetic transcendence of both politics and the body. The chapter then goes on to discuss how past, present, and future bloodsheds are evoked simultaneously in the iconography of fallen freedom-fighter martyrs. In this genre, heroes of India's independence struggle who shed their blood for the nation are depicted in portraits composed of human blood in the present. This aimed to inspire others to willingness to shed their blood, and that of others, in the future for the nation.<\/p>","DOI":"10.7591\/cornell\/9781501745096.003.0002","type":"book-chapter","created":{"date-parts":[[2020,5,22]],"date-time":"2020-05-22T14:50:50Z","timestamp":1590159050000},"page":"46-85","source":"Crossref","is-referenced-by-count":0,"title":["Sovereignty and Blood"],"prefix":"10.7591","author":[{"given":"Jacob","family":"Copeman","sequence":"first","affiliation":[]},{"given":"Dwaipayan","family":"Banerjee","sequence":"additional","affiliation":[]}],"member":"4434","published-online":{"date-parts":[[2020,5,21]]},"container-title":["Hematologies"],"original-title":["Sovereignty and 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Although AF affects both men and women at a similar rate, accumulating experimental and clinical evidence indicates that its underlying mechanisms, disease progression, and treatment responses differ by sex. However, current antiarrhythmic drug development and clinical management of AF remains largely sex neutral, likely contributing to limited efficacy and increased adverse effects. To address this gap, we developed a computational drug-screening pipeline based on experimentally constrained, sex-specific human atrial cardiomyocyte models to predict and evaluate sex-specific pharmacological strategies for AF. The pipeline integrates multivariable regression with mechanistic modeling to systematically test multi-target combinations of ion channel inhibitors and Ca\n                  <jats:sup>2+<\/jats:sup>\n                  handling modulators and identify interventions that reduce arrhythmia vulnerability by restoring sex-specific electrophysiological and Ca\n                  <jats:sup>2+<\/jats:sup>\n                  handling properties toward normal sinus rhythm (nSR). Application of this approach revealed a greater number of successful inhibitory drug combinations in males than in females. In males, optimal recovery to nSR primarily required inhibition of Na\n                  <jats:sup>+<\/jats:sup>\n                  and K\n                  <jats:sup>+<\/jats:sup>\n                  channels to prolong repolarization and refractoriness, increase Ca\n                  <jats:sup>2+<\/jats:sup>\n                  transient amplitude (CaT\n                  <jats:sub>Amp<\/jats:sub>\n                  ), and reduce susceptibility to action potential duration (APD) alternans. In females, modulation of Ca\n                  <jats:sup>2+<\/jats:sup>\n                  -related pathways was additionally required to suppress delayed afterdepolarizations (DADs). Forward single-cell simulations confirmed the predictions of the drug-analysis pipeline, demonstrating recovery of APD, CaT\n                  <jats:sub>Amp<\/jats:sub>\n                  , and arrhythmia vulnerability indices without introducing instabilities. Importantly, extension of these interventions to two-dimensional atrial tissue simulations demonstrated that sex-specific drug strategies reduce vulnerability to triggered activity, while suppression of reentry was most effective when combined with partial recovery of cell-cell coupling. Our results establish a multiscale computational pipeline for identifying sex-informed, multi-target antiarrhythmic therapies, amenable to experimental validation and translation to the clinic.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Clinical Perspective<\/jats:title>\n                  <jats:sec>\n                    <jats:title>What is Known<\/jats:title>\n                    <jats:list list-type=\"bullet\">\n                      <jats:list-item>\n                        <jats:p>Atrial fibrillation arises from multiple interacting multiscale mechanisms, which limit the effectiveness of single-target therapies.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Current single-target antiarrhythmic drugs for atrial fibrillation show more limited efficacy and higher adverse event rates in women than in men<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>What the Study Adds<\/jats:title>\n                    <jats:list list-type=\"bullet\">\n                      <jats:list-item>\n                        <jats:p>This study demonstrates that effective pharmacologic strategies require different combinations of ion channel and calcium handling modulation in males versus females with persistent (chronic) atrial fibrillation.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          In males, coordinated Na\n                          <jats:sup>+<\/jats:sup>\n                          and K\n                          <jats:sup>+<\/jats:sup>\n                          channel inhibition most effectively improves electrical stability, whereas in females additional targeting of Ca\n                          <jats:sup>2+<\/jats:sup>\n                          handling is required to suppress triggered activity.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Sex-specific multi-target drug strategies including partial recovery of intercellular coupling suppress triggered activity and reentry in atrial tissue while preserving conduction.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:sec>\n                <\/jats:sec>","DOI":"10.64898\/2026.02.06.704432","type":"posted-content","created":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T06:45:37Z","timestamp":1770705937000},"source":"Crossref","is-referenced-by-count":0,"title":["Predicting Sex-Specific Antiarrhythmic Strategies for Atrial Fibrillation through a Regression-Guided Computational Modeling Pipeline"],"prefix":"10.64898","author":[{"given":"Nathaniel T.","family":"Herrera","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of California Davis, Davis, California, United States"}]},{"given":"Haibo","family":"Ni","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of California Davis, Davis, California, United States"}]},{"given":"Charlotte E. 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Institute","doi-asserted-by":"publisher","award":["U10 HL110312"],"award-info":[{"award-number":["U10 HL110312"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U01 HL084861"],"award-info":[{"award-number":["U01 HL084861"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U10 HL084904"],"award-info":[{"award-number":["U10 HL084904"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Obesity is present in up to 45% of patients with heart failure (HF). Liraglutide, a glucagon-like peptide-1 (GLP-1) receptor antagonist, facilitates weight loss in obese patients. The efficacy of liraglutide as a weight loss agent among patients with HF and reduced ejection fraction (HFrEF) and a recent acute HF hospitalization remains unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>The Functional Impact of GLP-1 for Heart Failure Treatment study randomized 300 patients with HFrEF (ejection fraction \u2264 40%), both with and without diabetes and a recent HF hospitalization to liraglutide or placebo. The primary outcome for this post hoc analysis was the change in weight from baseline to last study visit. We conducted an \u2018on-treatment\u2019 analysis of patients with at least one follow-up visit on study drug (123 on liraglutide and 124 on placebo). The median age was 61 years, 21% were female, and 69% of patients had New York Heart Association functional Class III or IV symptoms. The median ejection fraction was 25% (25th, 75th percentile 19\u201332%). Liraglutide use was associated with a significant weight reduction [liraglutide \u22121.00 lbs vs. placebo 2.00 lbs; treatment difference \u22124.10 lbs; 95% confidence interval (CI) \u22127.94, \u22120.25; P = 0.0367; percentage treatment difference \u22122.07%, 95% CI \u22123.86, \u22120.28; P = 0.0237]. Similar results were seen after multivariable adjustments. Liraglutide also significantly reduced triglyceride levels (liraglutide 7.5 mg\/dL vs. placebo 12.0 mg\/dL; treatment difference \u221233.1 mg\/dL; 95% CI \u221260.7, \u22125.6; P = 0.019).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Liraglutide is an efficacious weight loss agent in patients with HFrEF. These findings will require further exploration in a well-powered cardiovascular outcomes trial.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.12334","type":"journal-article","created":{"date-parts":[[2018,8,18]],"date-time":"2018-08-18T00:08:58Z","timestamp":1534550938000},"page":"1035-1043","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Liraglutide and Weight Loss Among Patients with Advanced Heart Failure and a Reduced Ejection Fraction: Insights from the FIGHT Trial"],"prefix":"10.1093","volume":"5","author":[{"given":"Abhinav","family":"Sharma","sequence":"first","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]},{"name":"Mazankowski Alberta Heart Institute, University of Alberta , Edmonton, Alberta ,","place":["Canada"]}]},{"given":"Andrew P.","family":"Ambrosy","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Adam D.","family":"DeVore","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Kenneth B.","family":"Margulies","sequence":"additional","affiliation":[{"name":"Perelman School of Medicine, University of Pennsylvania , Philadelphia, PA ,","place":["USA"]}]},{"given":"Steven E.","family":"McNulty","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Robert J.","family":"Mentz","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Adrian F.","family":"Hernandez","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Gary","family":"Michael Felker","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]},{"given":"Lauren B.","family":"Cooper","sequence":"additional","affiliation":[{"name":"Inova Heart and Vascular Institute , Fall Church, VA ,","place":["USA"]}]},{"given":"Anuradha","family":"Lala","sequence":"additional","affiliation":[{"name":"The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Hospital , New York, NY ,","place":["USA"]}]},{"given":"Justin","family":"Vader","sequence":"additional","affiliation":[{"name":"Washington University School of Medicine , St. Louis, MO ,","place":["USA"]}]},{"given":"John D.","family":"Groake","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard University , Boston, MA ,","place":["USA"]}]},{"given":"Barry A.","family":"Borlaug","sequence":"additional","affiliation":[{"name":"Mayo Clinic , Rochester, MN ,","place":["USA"]}]},{"given":"Eric J.","family":"Velazquez","sequence":"additional","affiliation":[{"name":"Duke Clinical Research Institute, Duke University , 2400 Pratt Street, Durham, NC, 27705 ,","place":["USA"]}]}],"member":"286","published-online":{"date-parts":[[2018,8,17]]},"reference":[{"key":"2026012115110225200_ehf212334-bib-0001","doi-asserted-by":"crossref","first-page":"1754","DOI":"10.1016\/j.amjcard.2011.07.051","article-title":"Relation 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AF is accompanied by extensive structural remodelling of atria, including extracellular matrix expansion (fibrosis), which affects both AF maintenance and treatment outcomes. However, no fibrosis\u2010specific therapies are currently available for AF. To identify the prominent pathways in atrial fibroblasts (Fb) that modulate atrial fibrosis and arrhythmogenesis, we developed the first atrial Fb signalling network model. This expands on the well\u2010established ventricular model by integrating atrial\u2010relevant elements involved in fibrogenesis and\/or differentially expressed in chronic AF (<jats:italic>vs<\/jats:italic>. normal sinus rhythm) patients and connections based on experimental evidence in an Fb\u2010related context. Our findings indicate that under high profibrotic signals, e.g. angiotensin\u2010II (AngII) and transforming growth factor \u03b2, inhibition of Ca<jats:sup>2+<\/jats:sup> fluxes reduced the abundance of key fibrotic markers such as collagen I, collagen III, periostin, plasminogen activator inhibitor\u20101, connective tissue growth factor and \u03b1\u2010smooth muscle actin, via modulation of the Ca<jats:sup>2+<\/jats:sup>\/calmodulin\u2010dependent protein kinase II\/Smad3 pathway and extra domain A of fibronectin via the calcineurin pathway. Mechanistically, we found that the Ca<jats:sup>2+<\/jats:sup>\u2010dependent regulation of collagen I and III is primarily at the level of gene transcription, with collagen I and collagen III exhibiting similar dynamics in the Fb model. Overall, our study highlights the pivotal role of Ca<jats:sup>2+<\/jats:sup> signalling in the evolution of AF\u2010associated fibrogenesis and provides novel insights into potential anti\u2010AF therapeutic strategies targeting fibrotic responses. Future work will investigate in greater detail the upstream mechanisms driving Ca<jats:sup>2+<\/jats:sup> increases in atrial Fbs during AF.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16821-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>A fibroblast signalling network was developed incorporating new atrial\u2010informed elements and reactions to identify the prominent pathways that modulate atrial fibrosis and associated arrhythmogenesis, including atrial fibrillation (AF).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The model was validated against experimental data in cardiac fibroblasts. For atrial\u2010specific validation, we focused on the model responses to AF\u2010relevant profibrotic inputs, i.e. angiotensin\u2010II (AngII) and transforming growth factor \u03b2 (TGF\u03b2).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The analysis underscores the critical role of Ca<jats:sup>2+<\/jats:sup> signalling in mediating profibrotic responses under AF\u2010relevant stimuli, AngII and TGF\u03b2 and shows that Ca<jats:sup>2+<\/jats:sup>\/calmodulin\u2010dependent protein kinase II\/Smad3 and calcineurin mediate the Ca<jats:sup>2+<\/jats:sup>\u2010dependent upregulation of key fibrotic markers.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp289040","type":"journal-article","created":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T06:29:14Z","timestamp":1750400954000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Computational modelling of cardiac fibroblast signalling reveals a key role for Ca<sup>2+<\/sup> in driving atrial fibrillation\u2010associated fibrosis"],"prefix":"10.1113","author":[{"given":"Najme","family":"Khorasani","sequence":"first","affiliation":[{"name":"Department of Pharmacology University of California Davis  Davis CA USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0083-4286","authenticated-orcid":false,"given":"Haibo","family":"Ni","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of California Davis  Davis CA USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9464-8374","authenticated-orcid":false,"given":"Jeffrey J","family":"Saucerman","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering University of Virginia  Charlottesville VA USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4612-117X","authenticated-orcid":false,"given":"Dobromir","family":"Dobrev","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology, Faculty of Medicine University Duisburg\u2010Essen  Essen Germany"},{"name":"Department of Medicine and Research Center Montreal Heart Institute and Universit\u00e9 de Montr\u00e9al  Montr\u00e9al Canada"},{"name":"Department of Molecular Physiology and Biophysics Baylor College of Medicine  Houston TX USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8679-665X","authenticated-orcid":false,"given":"Stefano","family":"Morotti","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of California Davis  Davis CA USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4401-8857","authenticated-orcid":false,"given":"Eleonora","family":"Grandi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of California Davis  Davis CA USA"}]}],"member":"311","published-online":{"date-parts":[[2025,6,19]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"crossref","first-page":"45","DOI":"10.1016\/j.yjmcc.2012.10.016","article-title":"TRPV4 channels mediate cardiac fibroblast differentiation by integrating mechanical and soluble signals","volume":"54","author":"Adapala R. 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Institute","doi-asserted-by":"publisher","award":["HHSN268201100009C"],"award-info":[{"award-number":["HHSN268201100009C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201100010C"],"award-info":[{"award-number":["HHSN268201100010C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201100011C"],"award-info":[{"award-number":["HHSN268201100011C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201100012C"],"award-info":[{"award-number":["HHSN268201100012C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U01HL075572-01"],"award-info":[{"award-number":["U01HL075572-01"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["T32HL007024"],"award-info":[{"award-number":["T32HL007024"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["K01 DK076595"],"award-info":[{"award-number":["K01 DK076595"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01 DK089174"],"award-info":[{"award-number":["R01 DK089174"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2012,12,1]]},"abstract":"<jats:sec>\n                  <jats:title>BACKGROUND<\/jats:title>\n                  <jats:p>1,5-Anhydroglucitol (1,5-AG), fructosamine, and glycated albumin are of increasing interest as alternative measures of hyperglycemia. We characterize the associations of these nontraditional glycemic markers with hemoglobin A1c (Hb A1c) and fasting glucose and assess their ability to identify people with diabetes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>We conducted a cross-sectional comparison of 1,5-AG, fructosamine, and glycated albumin with Hb A1c and fasting glucose measurements in 1719 participants from the Atherosclerosis Risk in Communities Study. We evaluated nonlinear relationships using R2 and F-statistics. Performance for identification of cases of diabetes was determined using the area under the curve (AUC). Diabetes was defined by Hb A1c \u22656.5%, fasting glucose \u2265126 mg\/dL (\u22656.99 mmol\/L), and\/or a self-reported history of diagnosed diabetes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>Median values of Hb A1c and fasting glucose were 5.8% and 109 mg\/dL (6.05 mmol\/L), respectively; 17.3% of the study population had diagnosed diabetes. Glycated albumin, fructosamine, and 1,5-AG were more strongly correlated with Hb A1c compared with fasting glucose (all P values &amp;lt;0.05). Nonlinear models provided the best fit for describing the relationships of the alternative markers to Hb A1c. When diabetes was defined by an Hb A1c \u22656.5%, fructosamine (AUC 0.83; 95% CI, 0.79\u20130.87) and glycated albumin (AUC 0.87; 95% CI, 0.83\u20130.90) performed comparably to fasting glucose (AUC 0.83; 95% CI, 0.79\u20130.87), while 1,5-AG performed worse (AUC 0.74; 95% CI, 0.69\u20130.78) for identifying cases of undiagnosed diabetes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Fructosamine and glycated albumin may be useful adjuncts to Hb A1c and fasting glucose. Future studies should examine these markers in situations in which fasting glucose or Hb A1c measurements are invalid or not available.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1373\/clinchem.2012.188367","type":"journal-article","created":{"date-parts":[[2012,9,28]],"date-time":"2012-09-28T14:54:20Z","timestamp":1348844060000},"page":"1648-1655","source":"Crossref","is-referenced-by-count":86,"title":["Associations of Alternative Markers of Glycemia with Hemoglobin A1c and Fasting Glucose"],"prefix":"10.1093","volume":"58","author":[{"given":"Stephen P","family":"Juraschek","sequence":"first","affiliation":[{"name":"Johns Hopkins School of Medicine, Johns Hopkins Bloomberg School of Public Health, and Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD"}]},{"given":"Michael W","family":"Steffes","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN"}]},{"given":"Elizabeth","family":"Selvin","sequence":"first","affiliation":[{"name":"Johns Hopkins School of Medicine, Johns Hopkins Bloomberg School of Public Health, and Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD"}]}],"member":"286","published-online":{"date-parts":[[2012,12,1]]},"reference":[{"key":"2020022705231763600_B1","doi-asserted-by":"crossref","first-page":"S106","DOI":"10.2337\/diacare.26.2007.S106","article-title":"Tests of glycemia in diabetes","volume":"26","author":"Goldstein","year":"2003","journal-title":"Diabetes Care"},{"key":"2020022705231763600_B2","doi-asserted-by":"crossref","first-page":"355","DOI":"10.1089\/152091503765691839","article-title":"Serum 1,5-anhydroglucitol (GlycoMark): a short-term glycemic marker","volume":"5","author":"Buse","year":"2003","journal-title":"Diabetes Technol Ther"},{"key":"2020022705231763600_B3","doi-asserted-by":"crossref","first-page":"2153","DOI":"10.1093\/clinchem\/33.12.2153","article-title":"Fructosamine: structure, analysis, and clinical usefulness","volume":"33","author":"Armbruster","year":"1987","journal-title":"Clin Chem"},{"key":"2020022705231763600_B4","doi-asserted-by":"crossref","first-page":"645","DOI":"10.1016\/j.biochi.2010.12.003","article-title":"The glycation of albumin: structural and functional impacts","volume":"93","author":"Rondeau","year":"2011","journal-title":"Biochimie"},{"key":"2020022705231763600_B5","doi-asserted-by":"crossref","first-page":"1688","DOI":"10.1001\/jama.295.14.1688","article-title":"Assessing glycemia in diabetes using self-monitoring blood glucose and hemoglobin A1c","volume":"295","author":"Saudek","year":"2006","journal-title":"JAMA"},{"key":"2020022705231763600_B6","doi-asserted-by":"crossref","first-page":"264","DOI":"10.1373\/clinchem.2010.144949","article-title":"Progression of nephropathy in type 2 diabetes: the glycation gap is a significant predictor after adjustment for glycohemoglobin (Hb A1c)","volume":"57","author":"Rodr\u00edguez-Segade","year":"2011","journal-title":"Clin Chem"},{"key":"2020022705231763600_B7","doi-asserted-by":"crossref","first-page":"1712","DOI":"10.2337\/dc10-1767","article-title":"Evidence for consistency of the glycation gap in diabetes","volume":"34","author":"Nayak","year":"2011","journal-title":"Diabetes Care"},{"key":"2020022705231763600_B8","doi-asserted-by":"crossref","first-page":"687","DOI":"10.1093\/oxfordjournals.aje.a115184","article-title":"The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. 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Institutet","license":[{"start":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T00:00:00Z","timestamp":1754870400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/rightsstatements.org\/page\/InC\/1.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"abstract":"<jats:p>&lt;p dir=\"ltr\"&gt;Blood transfusion therapy is a cornerstone of modern obstetric care, commonly administered during childbirth to manage acute hemorrhage. Meanwhile, blood donation represents a vital public health act sustained by healthy individuals, many of whom are women of reproductive age. This thesis examines red-cell transfusion and whole blood donation from multiple perspectives, including clinical patterns, recurrence, long-term outcomes, and the effects of pre- pregnancy donation on maternal and offspring health. It combines four register- based cohort studies using Swedish health data and blood donation data integrated within the SCANDAT3-S database to evaluate how blood, both received and given, intersects with maternal and neonatal health.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Aims . To describe the patterns and temporal trends of red-cell transfusion use in obstetric care in Sweden.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To assess the risk of recurrent transfusion in delivery.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To investigate whether red-cell transfusion during childbirth is associated with long-term risks of autoimmune disease and non-Hodgkin lymphoma.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To evaluate whether blood donation before pregnancy is associated with adverse maternal or neonatal outcomes.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study I. Transfusion practices in obstetric care in Sweden have evolved, but national-level data on usage patterns remain limited. This study analyzed a nationwide cohort of 1.6 million deliveries in Sweden between 2003 and 2017. In addition to describing overall transfusion patterns, we examined temporal trends and volume using logistic regression. For analyses of inter-hospital variations in transfusion rates, we used direct standardization to the year 2003, adjusting for parity and maternal age. Overall, 3 percent of women were transfused annually, and there were no considerable changes over the study period. We saw an increasing proportion of low-volume and a decline in high-volume transfusions. The most common number of red-cell units transfused per delivery was two, reflecting a broader pattern where even-numbered transfusions-particularly two or four units-dominated clinical practice. We saw substantial variation in the proportion of transfused deliveries across hospitals.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: While overall transfusion rates remained stable, hospital-level variation and the use of paired units may signal inappropriate use and warrant further investigation.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study II. Although transfusion during childbirth is typically viewed as an event determined by the specific circumstances of each delivery, some women experience repeated transfusions across deliveries. We analyzed a nationwide cohort of 825,000 women with deliveries between 2000 and 2017 to investigate the recurrence of transfusion. We used logistic regression to estimate the odds ratios of requiring a repeated transfusion in relation to specific risk factors. Women transfused in their first delivery were overall approximately five times more likely to be transfused in their second delivery (adjusted odds ratio [aOR] 5.4, 95% confidence intervals [CI]; 5.0-5.8) than non-transfused, non- hemorrhaged women. The overall odds of repeat transfusion were similar regardless of hemorrhage diagnosis in the first delivery. When considering specific subtypes, we saw the most pronounced recurrence risk associated with prior diagnoses of atony (aOR 6.7; 95% CI 6.1-7.4), placental retention (aOR 4.4; 95% CI, 3.8-5.1), and caesarian section with hemorrhage (aOR 6.8; 95% CI, 5.8- 8.0). Certain conditions in the second pregnancy (e.g., preeclampsia, placenta previa, iron deficiency anemia) increased the odds of recurrence. Having a sister transfused in childbirth was associated with higher odds of transfusion in childbirth (aOR 1.8; 95% CI, 1.5-2.1).&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: A prior transfusion is a strong risk factor for future transfusion, underscoring the importance of individualized risk management.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study III. The long-term effects of obstetric transfusion on immune-mediated conditions remain poorly understood. In this study, we followed a large register- based cohort of over one million women, starting in 1987, for up to 25 years to assess the risk of autoimmune disease and non-Hodgkin lymphoma. Cox proportional hazard models were used, adjusting for both fixed and time- dependent maternal factors. To reduce the risk of reverse causation, a six-month lag period was applied before the start of follow-up after each delivery. Transfusion in childbirth was modestly associated with increased risks for later diagnosis of systemic lupus erythematosus (SLE) (adjusted hazard ratio [aHR] 1.38; 95% CI, 1.01-1.87) and systemic sclerosis (aHR 1.89; 95% CI, 1.21-3.21), but not associated with risk of non-Hodgkin lymphoma or rheumatoid arthritis. However, the absolute risk difference at 25 years was slight. Sensitivity analyses, applying various stratifications and restrictions, generally supported the main findings.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: Although the absolute risk difference was small, transfusion in childbirth was associated with an increased risk of developing SLE and systemic sclerosis.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study IV. While blood donors are typically healthier than the general population, frequent donation may deplete iron stores and influence pregnancy outcomes. We analyzed a register-based cohort of 2.5 million deliveries between 1985 and 2017 to investigate any potential adverse effects of blood donations on pregnancy and childbirth. We used mixed-effects linear models to estimate birth weight by donation intensity, and logistic regression was applied to assess maternal and neonatal outcomes. When comparing births to non-donors to those to women who donated at least once within five years of delivery, we found that donors were less likely to experience adverse pregnancy outcomes and that the birth weight of their offspring was slightly higher. However, when considering only donors, high-frequency donors (29 donations within five years of delivery) had lower birth weight babies and higher risks of preeclampsia (aOR 1.18; 95% CI, 1.06-1.31), preterm birth (aOR 1.33; 95% CI, 1.22-1.45), and SGA infants (aOR 1.17; 95% CI, 1.03-1.34) than low-frequency donors (1-2 donations). Specific temporal analyses using interaction terms supported the notion of a biological effect. Sensitivity analyses confirmed the main findings.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: High-frequency whole blood donation before pregnancy may have adverse effects on maternal health and neonatal outcomes.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;In conclusion, the thesis reveals that transfusion and donation intersect with maternal health. It underscores the need for consistent transfusion practices, monitoring for recurrence risk, awareness of potential long-term immune effects, and cautious iron management in frequent female donors.&lt;\/p&gt;&lt;h3&gt;List of scientific papers&lt;\/h3&gt;&lt;p dir=\"ltr\"&gt;I. &lt;b&gt;Brynolf A.&lt;\/b&gt;, Zhao J., Wikman A., \u00d6berg S., Sandstr\u00f6m A., Edgren G. (2021), Patterns of red-cell transfusion use in obstetric practice in Sweden 2003-2017: A nationwide study. Vox Sang, 116: 821-830. Epub 2021 Feb 2. PMID: 33528029&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1111\/vox.13074\"&gt;https:\/\/doi.org\/10.1111\/vox.13074&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Il. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstrom A, Edgren G. Risk of recurrent red-cell transfusion in delivery: A nationwide longitudinal study. BJOG. 2024 Mar;131(4):455-462. doi: 10.1111\/1471-0528.17672. Epub 2023 Sep 25. PMID: 37749750.&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1111\/1471-0528.17672\"&gt;https:\/\/doi.org\/10.1111\/1471-0528.17672&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;III. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstr\u00f6m A, Hjalgrim H, Edgren G. Association Between Red-Cell Transfusion in Childbirth and Long-Term Risk of Lymphoma and Autoimmune Disease: A Swedish Nationwide Cohort Study. Am J Hematol. 2025 Apr;100(4):735-739. doi: 10.1002\/ajh.27610. Epub 2025 Jan 27. PMID: 39868856.&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1002\/ajh.27610\"&gt;https:\/\/doi.org\/10.1002\/ajh.27610&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;IV. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstr\u00f6m A, \u00d6berg S, Toss F, Edgren G. Whole blood donations before delivery and the risk of adverse pregnancy, delivery, and neonatal outcomes: A Swedish longitudinal cohort study. 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Sciences","doi-asserted-by":"publisher","award":["UL1\u2010TR\u2010001420"],"award-info":[{"award-number":["UL1\u2010TR\u2010001420"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"published-print":{"date-parts":[[2020,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Soluble tumour necrosis factor-\u03b1 receptor 1 (sTNF-\u03b1R1) and interleukin-2 receptor \u03b1 (sIL-2R\u03b1) predict incident heart failure (HF) in the elderly population. However, the association of these biomarkers with HF in a multi-ethnic asymptomatic population is unclear. We aimed to investigate the association of sTNF-\u03b1R1 and sIL-2R\u03b1 with incident HF in a multi-ethnic population of middle age and older participants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>The multi-ethnic study of atherosclerosis is a prospective population-based study of 6814 participants aged 45\u201384 years who were free of clinical cardiovascular disease at enrolment. We included 2869 participants with available sTNF-\u03b1R1 or sIL-2R\u03b1 level measurement at baseline multi-ethnic study of atherosclerosis exam (2000\u20132002). We used Cox proportional-hazards model to investigate the association between sTNF-\u03b1R1 and sIL-2R\u03b1 with incident HF after adjusting for traditional cardiovascular risk factors and coronary artery calcium score measured by cardiac computed tomography. Among the included participants, the mean (standard deviation) age was 61.6 (10.2) years and 46.7% were men. The median (interquartile range) sTNF-\u03b1R1 and sIL-2R\u03b1 were 1293 (1107\u20131547) and 901 (727\u20131154) pg\/mL. During a median follow-up of 14.2 (interquartile range: 11.7\u201314.8) years, 130 participants developed HF. In multivariable analysis, the hazard ratio (95% confidence interval, P value) of incident HF for each standard deviation increment of log-transformed sTNF-\u03b1R1 and sIL-2R\u03b1 was 1.43 (1.21\u20131.7, P \u2264 0.001) and 1.26 (1.04\u20131.53, P = 0.02), respectively. Excluding participants with interim coronary heart disease, we found a statistically significant association between sTNF-\u03b1R1 and HF with hazard ratio of 1.39 (95% confidence interval: 1.11 to 1.74, P = 0.005) and sIL-2R\u03b1 and HF showing a hazard ratio of 1.39 (95% confidence interval: 1.09 to 1.76, P = 0.007).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>sTNF-\u03b1R1 and sIL-2R\u03b1 are associated with a higher risk of incident HF in a multi-ethnic cohort without a previous history of cardiovascular disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.12623","type":"journal-article","created":{"date-parts":[[2020,3,10]],"date-time":"2020-03-10T16:09:56Z","timestamp":1583856596000},"page":"639-644","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Association of Soluble Interleukin-2 Receptor \u03b1 and Tumour Necrosis Factor Receptor 1 with Heart Failure: The Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"7","author":[{"given":"Hooman","family":"Bakhshi","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, Baltimore, MD, 21287 ,","place":["USA"]},{"name":"Inova Heart and Vascular Institute , Falls Church, Virginia ,","place":["USA"]}]},{"given":"Vinithra","family":"Varadarajan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, Baltimore, MD, 21287 ,","place":["USA"]}]},{"given":"Bharath","family":"Ambale-Venkatesh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, Baltimore, MD, 21287 ,","place":["USA"]}]},{"given":"Zahra","family":"Meyghani","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, Baltimore, MD, 21287 ,","place":["USA"]}]},{"given":"Mohammad R.","family":"Ostovaneh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, Baltimore, MD, 21287 ,","place":["USA"]}]},{"given":"Peter","family":"Durda","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont , Burlington, VT, 05405 ,","place":["USA"]}]},{"given":"Colin O.","family":"Wu","sequence":"additional","affiliation":[{"name":"Office of Biostatistics Research, National Heart Lung and Blood Institute , Bethesda, MD, 20892 ,","place":["USA"]}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont , Burlington, VT, 05405 ,","place":["USA"]}]},{"given":"Mary","family":"Cushman","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont , Burlington, VT, 05405 ,","place":["USA"]},{"name":"Department of Medicine, Larner College of Medicine at the University of Vermont , Burlington, VT, 05405 ,","place":["USA"]}]},{"given":"David A.","family":"Bluemke","sequence":"additional","affiliation":[{"name":"Department of Radiology, University of Wisconsin School of Medicine and Public Health , Madison, WI, 53726 ,","place":["USA"]}]},{"given":"Jo\u00e3o A.C.","family":"Lima","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, Johns Hopkins University , Wolfe Street\/Blalock 524, 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Institute","doi-asserted-by":"publisher","award":["N01-HC65237"],"award-info":[{"award-number":["N01-HC65237"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Obesity"],"published-print":{"date-parts":[[2015]]},"abstract":"<jats:p><jats:italic>Background.<\/jats:italic>The study examined the association of obesity with acculturation in a large and diverse sample of US Hispanic\/Latino adults.<jats:italic>Methods.<\/jats:italic>The Hispanic Community Health Study (HCHS)\/Study of Latinos (SOL) is a community-based cohort study of Hispanic\/Latino adults aged 18\u201374 years (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>N<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn fontstyle=\"italic\">16,415<\/mml:mn><\/mml:math>) from four urban areas. Height and weight were directly measured using a standardized protocol. Acculturation was assessed by the Short Acculturation Scale for Hispanics (SASH). Other immigration related variables included place of birth, length of residency in the US, and age at immigration. Odds ratios were calculated to assess the association of overweight, moderate obesity, and extreme obesity (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mo>\u2265<\/mml:mo><mml:mn fontstyle=\"italic\">40<\/mml:mn><\/mml:math>\u2009kg\/m<jats:sup>2<\/jats:sup>) with acculturation and sociodemographic variables.<jats:italic>Results.<\/jats:italic>The prevalence of obesity was 42.4% for women and 36.5% for men and varied by field center and Hispanic\/Latino background. The strongest predictor of moderate and extreme obesity was length of residency in mainland US. This association was consistent across Hispanic\/Latino backgrounds. Acculturation was not significantly associated with obesity.<jats:italic>Discussion.<\/jats:italic>The burden of obesity is high among Hispanic\/Latino adults. The study findings suggest that prolonged exposure to the environments in these communities, rather than acculturation, is an important risk factor for obesity in this population.<\/jats:p>","DOI":"10.1155\/2015\/186276","type":"journal-article","created":{"date-parts":[[2015,3,29]],"date-time":"2015-03-29T17:01:01Z","timestamp":1427648461000},"page":"1-8","source":"Crossref","is-referenced-by-count":99,"title":["Is Acculturation Related to Obesity in Hispanic\/Latino Adults? Results from the Hispanic Community Health Study\/Study of Latinos"],"prefix":"10.1155","volume":"2015","author":[{"given":"Carmen R.","family":"Isasi","sequence":"first","affiliation":[{"name":"Department of Epidemiology & Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA"}]},{"given":"Guadalupe X.","family":"Ayala","sequence":"additional","affiliation":[{"name":"Division of Health Promotion and Behavioral Science, Graduate School of Public Health, San Diego State University and the Institute for Behavioral and Community Health, San Diego State University Research Foundation, San Diego, CA 92123, USA"}]},{"given":"Daniela","family":"Sotres-Alvarez","sequence":"additional","affiliation":[{"name":"Collaborative Studies Coordinating Center, Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2547-2202","authenticated-orcid":true,"given":"Hala","family":"Madanat","sequence":"additional","affiliation":[{"name":"Division of Health Promotion and Behavioral Science, Graduate School of Public Health, San Diego State University and the Institute for Behavioral and Community Health, San Diego State University Research Foundation, San Diego, CA 92123, USA"}]},{"given":"Frank","family":"Penedo","sequence":"additional","affiliation":[{"name":"Department of Medical Social Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA"}]},{"given":"Catherine M.","family":"Loria","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD 20817, USA"}]},{"given":"John P.","family":"Elder","sequence":"additional","affiliation":[{"name":"Division of Health Promotion and Behavioral Science, Graduate School of Public Health, San Diego State University and the Institute for Behavioral and Community Health, San Diego State University Research Foundation, San Diego, CA 92123, USA"}]},{"given":"Martha L.","family":"Daviglus","sequence":"additional","affiliation":[{"name":"Institute for Minority Health Research, University of Illinois at Chicago, Chicago, IL 60612, USA"}]},{"given":"Janice","family":"Barnhart","sequence":"additional","affiliation":[{"name":"Department of Epidemiology & Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA"}]},{"given":"Anna Maria","family":"Siega-Riz","sequence":"additional","affiliation":[{"name":"Departments of Epidemiology and Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1362-5806","authenticated-orcid":true,"given":"Linda","family":"Van Horn","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60126, USA"}]},{"given":"Neil","family":"Schneiderman","sequence":"additional","affiliation":[{"name":"The Behavioral Research Center, Department of Psychology, University of Miami, Coral Gables, FL 33124, USA"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2012.39"},{"key":"2","year":"2005"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1007\/s10903-012-9665-8"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1016\/j.socscimed.2012.03.013"},{"key":"5","volume-title":"Conceptual approaches to acculturation","year":"2003"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.1016\/j.jada.2008.05.009"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.1038\/ijo.2012.159"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.1001\/jama.296.1.79"},{"key":"9","doi-asserted-by":"publisher","DOI":"10.1016\/j.annepidem.2010.03.015"},{"key":"10","doi-asserted-by":"publisher","DOI":"10.1016\/j.annepidem.2010.05.006"},{"key":"11","year":"1998"},{"key":"12","doi-asserted-by":"publisher","DOI":"10.1177\/07399863870092005"},{"key":"13","doi-asserted-by":"publisher","DOI":"10.1007\/s11135-007-9077-3"},{"key":"14","doi-asserted-by":"publisher","DOI":"10.1377\/hlthaff.21.2.245"},{"key":"15","year":"2010"},{"key":"16","doi-asserted-by":"publisher","DOI":"10.1136\/jech-2013-202354"},{"key":"17","doi-asserted-by":"publisher","DOI":"10.1001\/jama.292.23.2860"},{"key":"18","doi-asserted-by":"publisher","DOI":"10.1016\/j.whi.2004.07.003"},{"key":"19","doi-asserted-by":"publisher","DOI":"10.1016\/j.amepre.2004.07.005"},{"key":"20","doi-asserted-by":"publisher","DOI":"10.1016\/s0277-9536(03)00072-8"},{"key":"21","doi-asserted-by":"publisher","DOI":"10.1002\/ajpa.10367"},{"key":"22","doi-asserted-by":"publisher","DOI":"10.1016\/j.socscimed.2005.01.016"},{"issue":"1","key":"23","first-page":"A10","volume":"4","year":"2007","journal-title":"Preventing 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Obesity"],"language":"en","link":[{"URL":"http:\/\/downloads.hindawi.com\/journals\/jobe\/2015\/186276.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/downloads.hindawi.com\/journals\/jobe\/2015\/186276.xml","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/downloads.hindawi.com\/journals\/jobe\/2015\/186276.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2016,8,18]],"date-time":"2016-08-18T09:44:47Z","timestamp":1471513487000},"score":8.788315,"resource":{"primary":{"URL":"http:\/\/www.hindawi.com\/journals\/jobe\/2015\/186276\/"}},"issued":{"date-parts":[[2015]]},"references-count":34,"alternative-id":["186276","186276"],"URL":"https:\/\/doi.org\/10.1155\/2015\/186276","ISSN":["2090-0708","2090-0716"],"issn-type":[{"value":"2090-0708","type":"print"},{"value":"2090-0716","type":"electronic"}],"published":{"date-parts":[[2015]]}},{"institution":[{"name":"Karolinska Institutet"}],"indexed":{"date-parts":[[2025,8,15]],"date-time":"2025-08-15T01:55:42Z","timestamp":1755222942552,"version":"3.43.0"},"posted":{"date-parts":[[2025,8,11]]},"reference-count":0,"publisher":"Karolinska Institutet","license":[{"start":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T00:00:00Z","timestamp":1754870400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/rightsstatements.org\/page\/InC\/1.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"abstract":"<jats:p>&lt;p dir=\"ltr\"&gt;Blood transfusion therapy is a cornerstone of modern obstetric care, commonly administered during childbirth to manage acute hemorrhage. Meanwhile, blood donation represents a vital public health act sustained by healthy individuals, many of whom are women of reproductive age. This thesis examines red-cell transfusion and whole blood donation from multiple perspectives, including clinical patterns, recurrence, long-term outcomes, and the effects of pre- pregnancy donation on maternal and offspring health. It combines four register- based cohort studies using Swedish health data and blood donation data integrated within the SCANDAT3-S database to evaluate how blood, both received and given, intersects with maternal and neonatal health.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Aims . To describe the patterns and temporal trends of red-cell transfusion use in obstetric care in Sweden.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To assess the risk of recurrent transfusion in delivery.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To investigate whether red-cell transfusion during childbirth is associated with long-term risks of autoimmune disease and non-Hodgkin lymphoma.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;\u00b7 To evaluate whether blood donation before pregnancy is associated with adverse maternal or neonatal outcomes.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study I. Transfusion practices in obstetric care in Sweden have evolved, but national-level data on usage patterns remain limited. This study analyzed a nationwide cohort of 1.6 million deliveries in Sweden between 2003 and 2017. In addition to describing overall transfusion patterns, we examined temporal trends and volume using logistic regression. For analyses of inter-hospital variations in transfusion rates, we used direct standardization to the year 2003, adjusting for parity and maternal age. Overall, 3 percent of women were transfused annually, and there were no considerable changes over the study period. We saw an increasing proportion of low-volume and a decline in high-volume transfusions. The most common number of red-cell units transfused per delivery was two, reflecting a broader pattern where even-numbered transfusions-particularly two or four units-dominated clinical practice. We saw substantial variation in the proportion of transfused deliveries across hospitals.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: While overall transfusion rates remained stable, hospital-level variation and the use of paired units may signal inappropriate use and warrant further investigation.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study II. Although transfusion during childbirth is typically viewed as an event determined by the specific circumstances of each delivery, some women experience repeated transfusions across deliveries. We analyzed a nationwide cohort of 825,000 women with deliveries between 2000 and 2017 to investigate the recurrence of transfusion. We used logistic regression to estimate the odds ratios of requiring a repeated transfusion in relation to specific risk factors. Women transfused in their first delivery were overall approximately five times more likely to be transfused in their second delivery (adjusted odds ratio [aOR] 5.4, 95% confidence intervals [CI]; 5.0-5.8) than non-transfused, non- hemorrhaged women. The overall odds of repeat transfusion were similar regardless of hemorrhage diagnosis in the first delivery. When considering specific subtypes, we saw the most pronounced recurrence risk associated with prior diagnoses of atony (aOR 6.7; 95% CI 6.1-7.4), placental retention (aOR 4.4; 95% CI, 3.8-5.1), and caesarian section with hemorrhage (aOR 6.8; 95% CI, 5.8- 8.0). Certain conditions in the second pregnancy (e.g., preeclampsia, placenta previa, iron deficiency anemia) increased the odds of recurrence. Having a sister transfused in childbirth was associated with higher odds of transfusion in childbirth (aOR 1.8; 95% CI, 1.5-2.1).&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: A prior transfusion is a strong risk factor for future transfusion, underscoring the importance of individualized risk management.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study III. The long-term effects of obstetric transfusion on immune-mediated conditions remain poorly understood. In this study, we followed a large register- based cohort of over one million women, starting in 1987, for up to 25 years to assess the risk of autoimmune disease and non-Hodgkin lymphoma. Cox proportional hazard models were used, adjusting for both fixed and time- dependent maternal factors. To reduce the risk of reverse causation, a six-month lag period was applied before the start of follow-up after each delivery. Transfusion in childbirth was modestly associated with increased risks for later diagnosis of systemic lupus erythematosus (SLE) (adjusted hazard ratio [aHR] 1.38; 95% CI, 1.01-1.87) and systemic sclerosis (aHR 1.89; 95% CI, 1.21-3.21), but not associated with risk of non-Hodgkin lymphoma or rheumatoid arthritis. However, the absolute risk difference at 25 years was slight. Sensitivity analyses, applying various stratifications and restrictions, generally supported the main findings.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: Although the absolute risk difference was small, transfusion in childbirth was associated with an increased risk of developing SLE and systemic sclerosis.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Study IV. While blood donors are typically healthier than the general population, frequent donation may deplete iron stores and influence pregnancy outcomes. We analyzed a register-based cohort of 2.5 million deliveries between 1985 and 2017 to investigate any potential adverse effects of blood donations on pregnancy and childbirth. We used mixed-effects linear models to estimate birth weight by donation intensity, and logistic regression was applied to assess maternal and neonatal outcomes. When comparing births to non-donors to those to women who donated at least once within five years of delivery, we found that donors were less likely to experience adverse pregnancy outcomes and that the birth weight of their offspring was slightly higher. However, when considering only donors, high-frequency donors (29 donations within five years of delivery) had lower birth weight babies and higher risks of preeclampsia (aOR 1.18; 95% CI, 1.06-1.31), preterm birth (aOR 1.33; 95% CI, 1.22-1.45), and SGA infants (aOR 1.17; 95% CI, 1.03-1.34) than low-frequency donors (1-2 donations). Specific temporal analyses using interaction terms supported the notion of a biological effect. Sensitivity analyses confirmed the main findings.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Summary: High-frequency whole blood donation before pregnancy may have adverse effects on maternal health and neonatal outcomes.&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;In conclusion, the thesis reveals that transfusion and donation intersect with maternal health. It underscores the need for consistent transfusion practices, monitoring for recurrence risk, awareness of potential long-term immune effects, and cautious iron management in frequent female donors.&lt;\/p&gt;&lt;h3&gt;List of scientific papers&lt;\/h3&gt;&lt;p dir=\"ltr\"&gt;I. &lt;b&gt;Brynolf A.&lt;\/b&gt;, Zhao J., Wikman A., \u00d6berg S., Sandstr\u00f6m A., Edgren G. (2021), Patterns of red-cell transfusion use in obstetric practice in Sweden 2003-2017: A nationwide study. Vox Sang, 116: 821-830. Epub 2021 Feb 2. PMID: 33528029&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1111\/vox.13074\"&gt;https:\/\/doi.org\/10.1111\/vox.13074&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;Il. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstrom A, Edgren G. Risk of recurrent red-cell transfusion in delivery: A nationwide longitudinal study. BJOG. 2024 Mar;131(4):455-462. doi: 10.1111\/1471-0528.17672. Epub 2023 Sep 25. PMID: 37749750.&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1111\/1471-0528.17672\"&gt;https:\/\/doi.org\/10.1111\/1471-0528.17672&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;III. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstr\u00f6m A, Hjalgrim H, Edgren G. Association Between Red-Cell Transfusion in Childbirth and Long-Term Risk of Lymphoma and Autoimmune Disease: A Swedish Nationwide Cohort Study. Am J Hematol. 2025 Apr;100(4):735-739. doi: 10.1002\/ajh.27610. Epub 2025 Jan 27. PMID: 39868856.&lt;br&gt;&lt;a href=\"https:\/\/doi.org\/10.1002\/ajh.27610\"&gt;https:\/\/doi.org\/10.1002\/ajh.27610&lt;\/a&gt;&lt;br&gt;&lt;br&gt;&lt;\/p&gt;&lt;p dir=\"ltr\"&gt;IV. &lt;b&gt;Brynolf A,&lt;\/b&gt; Sandstr\u00f6m A, \u00d6berg S, Toss F, Edgren G. Whole blood donations before delivery and the risk of adverse pregnancy, delivery, and neonatal outcomes: A Swedish longitudinal cohort study. [Manuscript]&lt;\/p&gt;<\/jats:p>","DOI":"10.69622\/28929593","type":"posted-content","created":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T09:31:01Z","timestamp":1754904661000},"source":"Crossref","is-referenced-by-count":0,"title":["Blood in, blood out : aspects of blood transfusions and donations in the realms of obstetric care and beyond"],"prefix":"10.69622","author":[{"given":"Anne","family":"Brynolf","sequence":"first","affiliation":[]}],"member":"12730","deposited":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T09:31:01Z","timestamp":1754904661000},"score":8.786484,"resource":{"primary":{"URL":"https:\/\/openarchive.ki.se\/articles\/thesis\/Blood_in_blood_out_aspects_of_blood_transfusions_and_donations_in_the_realms_of_obstetric_care_and_beyond\/28929593"}},"issued":{"date-parts":[[2025,8,11]]},"references-count":0,"URL":"https:\/\/doi.org\/10.69622\/28929593","relation":{"has-part":[{"id-type":"pmid","id":"33528029","asserted-by":"subject"},{"id-type":"pmid","id":"37749750","asserted-by":"subject"},{"id-type":"pmid","id":"39868856","asserted-by":"subject"}]},"published":{"date-parts":[[2025,8,11]]},"subtype":"dissertation"},{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T08:38:46Z","timestamp":1772267926294,"version":"3.50.1"},"publisher-location":"Ithaca, NY","reference-count":0,"publisher":"Cornell University Press","isbn-type":[{"value":"9781501745102","type":"electronic"}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2019,12,15]]},"DOI":"10.7591\/9781501745102-005","type":"book-chapter","created":{"date-parts":[[2019,12,14]],"date-time":"2019-12-14T13:04:19Z","timestamp":1576328659000},"page":"127-151","source":"Crossref","is-referenced-by-count":0,"title":["4. Hemo Economicus: From Blood Sacrifice to Blood 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Institute","doi-asserted-by":"crossref","award":["HHSN268201600003C"],"award-info":[{"award-number":["HHSN268201600003C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"crossref","award":["HHSN268201600004C"],"award-info":[{"award-number":["HHSN268201600004C"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            We aimed to elucidate potential methylation, proteomic, and metabolomic mechanisms by which\n                            <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                            variants may be linked to kidney disease.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            We report distinct methylation profiling between\n                            <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                            risk allele carriers and noncarriers, many near\n                            <jats:italic toggle=\"yes\">APOL<\/jats:italic>\n                            gene family.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We report higher APOL1 protein and lower C18:1 cholesteryl ester in two risk allele carriers.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      The\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      high-risk haplotype has been associated with CKD and the deterioration of kidney function, particularly in populations with West African ancestry. However, the mechanisms by which\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      risk variants increase the risk for kidney disease and its progression have not been fully elucidated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We compared methylation (\n                      <jats:italic toggle=\"yes\">N<\/jats:italic>\n                      =3191; 715 [22%] carriers), proteomic (\n                      <jats:italic toggle=\"yes\">N<\/jats:italic>\n                      =1240; 169 [14%] carriers), and metabolomic (\n                      <jats:italic toggle=\"yes\">N<\/jats:italic>\n                      =6309; 674 [11%] carriers) profiles in African and Hispanic\/Latino carriers of two\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      high-risk alleles (G1\/G1, G2\/G2, G1\/G2) and noncarriers (G0\/G0), excluding heterozygotes (G0\/G1, G0\/G2), from the Population Architecture using Genomics and Epidemiology Consortium and UK Biobank. In each study, the associations between the\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      high-risk haplotype and up to 722,719 cytosine-phosphate-guanine (CpG) sites, 2923 proteins, or 836 metabolites were estimated using covariate-adjusted linear regression models, followed by fixed-effects sample size\u2013weighted meta-analyses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Significant associations were observed between\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      high-risk haplotype and methylation at 52 CpG sites, with 48 located on chromosome 22 and 18 in the vicinity of\n                      <jats:italic toggle=\"yes\">APOL1\u20134<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">MYH9<\/jats:italic>\n                      . All significant CpG sites near\n                      <jats:italic toggle=\"yes\">APOL2<\/jats:italic>\n                      were hypomethylated, whereas those near\n                      <jats:italic toggle=\"yes\">APOL3<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">APOL4<\/jats:italic>\n                      were hypermethylated.\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      -associated CpG sites were also identified in genes involved in ion transport and mitochondrial stress pathways. Sensitivity analyses indicated consistent yet attenuated effects among heterozygotes, supporting an additive effect of\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      risk alleles. Further analyses of the 52 CpG sites identified two near\n                      <jats:italic toggle=\"yes\">APOL4<\/jats:italic>\n                      exhibiting G1-specific effects, eight associated with CKD but none with eGFR, and three showing heterogeneity by CKD status. In addition, carrying two\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      risk alleles was associated with higher plasma APOL1 protein (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =1.12,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      <jats:sub>FDR<\/jats:sub>\n                      = 2.26e-70) and lower C18:1 cholesteryl ester metabolite (Z=\u22124.50,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      <jats:sub>FDR<\/jats:sub>\n                      = 4.83e-3).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our results demonstrate differential methylation, proteomic, and metabolomic profiles associated with\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      high-risk haplotypes.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000000688","type":"journal-article","created":{"date-parts":[[2025,4,7]],"date-time":"2025-04-07T16:12:33Z","timestamp":1744042353000},"page":"1490-1504","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Alterations in DNA Methylation, Proteomic, and Metabolomic Profiles in African Ancestry Populations with APOL1 Risk Alleles"],"prefix":"10.1681","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5789-4592","authenticated-orcid":false,"given":"Xinruo","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North 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Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5937-3811","authenticated-orcid":false,"given":"Yishu","family":"Qu","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8813-6871","authenticated-orcid":false,"given":"Kendra R.","family":"Ferrier","sequence":"additional","affiliation":[{"name":"Department of Biomedical Informatics, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-5590-8637","authenticated-orcid":false,"given":"Brian D.","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North 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We evaluated the effect of maintaining systolic blood pressure (SBP) below clinical thresholds on dementia incidence.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>We included 6806 Multi\u2010Ethnic Study of Atherosclerosis participants (44 to 84 years old). We implemented the parametric g\u2010formula to simulate the hypothetical interventions to reduce SBP below 120 and 140\u00a0mmHg over time, accounting for time\u2010varying confounding. We estimated risk ratios (RRs) and risk differences for dementia incidence at 19 years.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>The RRs (95% confidence intervals [CIs]) comparing an intervention reducing SBP below 120\u00a0mmHg to no intervention were 0.93 (0.87 to 0.99) for total sample, 0.95 (0.88 to 1.02) for White, 0.90 (0.79 to 1.02) for Black, 0.90 (0.78 to 1.05) for Latino, and 1.16 (0.83 to 1.55) for Chinese American participants. Results for lowering SBP below 140\u00a0mmHg and with death as competing event were attenuated.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>The reduction of SBP below 120\u00a0mmHg over time has modest effects on reducing dementia incidence. More work is needed to understand the heterogeneity across racial and ethnic groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>There is a potential beneficial effect in lowering SBP to reduce the risk of dementia, which may vary by race and ethnicity.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The percentage of participants who would need intervention on blood pressure to meet clinical thresholds is greater for Black and Latino communities.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Results are sensitive to the way that death is specified in the research question and analysis.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.13894","type":"journal-article","created":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T07:01:59Z","timestamp":1720594919000},"page":"5271-5280","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Racial and ethnic differences in the risk of dementia diagnosis under hypothetical blood pressure\u2013lowering interventions: The Multi\u2010Ethnic Study of Atherosclerosis"],"prefix":"10.1002","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0875-5737","authenticated-orcid":false,"given":"L. 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Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2021,6,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Previous studies have demonstrated an association between gait speed and cognitive function. However, the relationship between balance and cognition remains less well explored. This study examined the cross-sectional and longitudinal relationship of balance and cognitive decline in older adults.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>A cohort of 4,811 adults, aged \u226565\u00a0years, participating in the Cardiovascular Health Study was followed for 6\u00a0years. Modified Mini-Mental State Examination (3MSE) and Digit Symbol Substitution Test (DSST) were used to measure cognition. Tandem balance measures were used to evaluate balance. Regression models were adjusted for demographics, behavioural and disease factors.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Worse balance was independently associated with worse cognition in cross-sectional analysis. Longitudinally, participants aged \u226576\u00a0years with poorer balance had a faster rate of decline after adjustment for co-variates: \u22120.97 points faster decline in 3MSE per year (95% confidence interval (CI): \u22121.32, \u22120.63) compared to the participants with good balance. There was no association of balance and change in 3MSE among adults aged &amp;lt;76\u00a0years (P value for balance and age interaction &amp;lt; 0.0001). DSST scores reflected \u22120.21 (95% CI: \u22120.37, \u22120.05) points greater decline when adjusted for co-variates. In Cox proportional hazard models, participants with worse balance had a higher risk of being cognitively impaired over the 6 years of follow-up visits (adjusted HR:1.72, 95% CI: 1.30, 2.29).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Future studies should evaluate standing balance as a potential screening technique to identify individuals at risk of cognitive decline. Furthermore, a better understanding of the pathophysiological link between balance and cognition may inform strategies to prevent cognitive decline.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ageing\/afab038","type":"journal-article","created":{"date-parts":[[2021,2,7]],"date-time":"2021-02-07T20:07:35Z","timestamp":1612728455000},"page":"1342-1348","source":"Crossref","is-referenced-by-count":26,"title":["Balance and cognitive decline in older adults in the cardiovascular health study"],"prefix":"10.1093","volume":"50","author":[{"given":"Claire C","family":"Meunier","sequence":"first","affiliation":[{"name":"School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA"}]},{"given":"Ellen","family":"Smit","sequence":"additional","affiliation":[{"name":"School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA"}]},{"given":"Annette L","family":"Fitzpatrick","sequence":"additional","affiliation":[{"name":"Departments of Family Medicine, Epidemiology, and Global Health, University of Washington, Seattle, WA, USA"}]},{"given":"Michelle C","family":"Odden","sequence":"additional","affiliation":[{"name":"School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR, USA"},{"name":"Department of Epidemiology and Population Health, Stanford University, Stanford, CA, USA"}]}],"member":"286","published-online":{"date-parts":[[2021,3,10]]},"reference":[{"key":"2021091504005347800_ref1"},{"key":"2021091504005347800_ref2","doi-asserted-by":"crossref","first-page":"731","DOI":"10.1016\/j.jamda.2015.06.017","article-title":"Brain health: the importance of recognizing cognitive impairment: an IAGG consensus conference","volume":"16","author":"Morley","year":"2015","journal-title":"J Am Med Dir Assoc"},{"key":"2021091504005347800_ref3","doi-asserted-by":"publisher","first-page":"e0119075","DOI":"10.1371\/journal.pone.0119075","article-title":"Predicting cognitive function from clinical measures of physical function and health status in older adults","volume":"10","author":"Bolandzadeh","year":"2015","journal-title":"PLoS One"},{"key":"2021091504005347800_ref4","doi-asserted-by":"crossref","first-page":"14","DOI":"10.1111\/ggi.13034","article-title":"Slow gait speed as a predictor of 1-year cognitive decline in a veterans\u2019 retirement community in southern Taiwan","volume":"17","author":"Hsu","year":"2017","journal-title":"Geriatr Gerontol Int"},{"key":"2021091504005347800_ref5","doi-asserted-by":"crossref","first-page":"165","DOI":"10.1111\/psyg.12133","article-title":"Gait speed in older people: an easy test for detecting cognitive impairment, functional independence, and health state","volume":"16","author":"Garcia-Pinillos","year":"2016","journal-title":"Psychogeriatrics"},{"key":"2021091504005347800_ref6","first-page":"50","article-title":"Mild cognitive impairment in older adults with pre-dialysis patients with chronic kidney disease: prevalence and association with physical function","volume":"24","author":"Otobe","year":"2019","journal-title":"Nephrol Ther"},{"key":"2021091504005347800_ref7","doi-asserted-by":"crossref","first-page":"1055","DOI":"10.1111\/jgs.12255","article-title":"Mild physical impairment predicts future diagnosis of dementia of the Alzheimer type","volume":"61","author":"Wilkins","year":"2013","journal-title":"J Am Geriatr Soc"},{"key":"2021091504005347800_ref8","doi-asserted-by":"crossref","first-page":"471","DOI":"10.1080\/00016489.2017.1408142","article-title":"Relationship between cognitive function and balance in a community-dwelling population in Japan","volume":"138","author":"Goto","year":"2018","journal-title":"Acta Otolaryngol (Stockh)"},{"key":"2021091504005347800_ref9","doi-asserted-by":"crossref","first-page":"67","DOI":"10.1159\/000445831","article-title":"The impact of mild cognitive impairment on gait and balance: a systematic review and meta-analysis of studies using instrumented assessment","volume":"63","author":"Bahureksa","year":"2017","journal-title":"Gerontology"},{"key":"2021091504005347800_ref10","doi-asserted-by":"crossref","first-page":"1408","DOI":"10.1111\/jgs.14224","article-title":"Sound body sound mind? 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Disease","doi-asserted-by":"crossref","award":["DK063491"],"award-info":[{"award-number":["DK063491"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Disease","doi-asserted-by":"crossref","award":["DK063491"],"award-info":[{"award-number":["DK063491"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01AG023629"],"award-info":[{"award-number":["R01AG023629"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Merck Foundation\/Society of Epidemiologic Research"},{"DOI":"10.13039\/100005644","name":"Alpha Phi Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005644","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Locke Charitable Foundation"},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Southern California Diabetes Endocrinology Research Center"}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2019,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Study Objectives<\/jats:title>\n                    <jats:p>Daytime sleepiness is a consequence of inadequate sleep, sleep\u2013wake control disorder, or other medical conditions. Population variability in prevalence of daytime sleepiness is likely due to genetic and biological factors as well as social and environmental influences. DNA methylation (DNAm) potentially influences multiple health outcomes. Here, we explored the association between DNAm and daytime sleepiness quantified by the Epworth Sleepiness Scale (ESS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed multi-ethnic and ethnic-specific epigenome-wide association studies for DNAm and ESS in the Multi-Ethnic Study of Atherosclerosis (MESA; n = 619) and the Cardiovascular Health Study (n = 483), with cross-study replication and meta-analysis. Genetic variants near ESS-associated DNAm were analyzed for methylation quantitative trait loci and followed with replication of genotype-sleepiness associations in the UK Biobank.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In MESA only, we detected four DNAm-ESS associations: one across all race\/ethnic groups; three in African-Americans (AA) only. Two of the MESA AA associations, in genes KCTD5 and RXRA, nominally replicated in CHS (p-value &lt; 0.05). In the AA meta-analysis, we detected 14 DNAm-ESS associations (FDR q-value &lt; 0.05, top association p-value = 4.26 \u00d7 10\u22128). Three DNAm sites mapped to genes (CPLX3, GFAP, and C7orf50) with biological relevance. We also found evidence for associations with DNAm sites in RAI1, a gene associated with sleep and circadian phenotypes. UK Biobank follow-up analyses detected SNPs in RAI1, RXRA, and CPLX3 with nominal sleepiness associations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We identified methylation sites in multiple genes possibly implicated in daytime sleepiness. Most significant DNAm-ESS associations were specific to AA. Future work is needed to identify mechanisms driving ancestry-specific methylation effects.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/sleep\/zsz101","type":"journal-article","created":{"date-parts":[[2019,5,29]],"date-time":"2019-05-29T01:10:19Z","timestamp":1559092219000},"source":"Crossref","is-referenced-by-count":38,"title":["Epigenome-wide association analysis of daytime sleepiness in the Multi-Ethnic Study of Atherosclerosis reveals African-American-specific associations"],"prefix":"10.1093","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6276-7704","authenticated-orcid":false,"given":"Richard","family":"Barfield","sequence":"first","affiliation":[{"name":"Department of Epidemiology, University of Washington, Seattle, WA"},{"name":"Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1486-7495","authenticated-orcid":false,"given":"Heming","family":"Wang","sequence":"additional","affiliation":[{"name":"Program in Medical and Population Genetics, Broad Institute, Cambridge, MA"},{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA"}]},{"given":"Yongmei","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Prevention, Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8509-148X","authenticated-orcid":false,"given":"Jennifer A","family":"Brody","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"}]},{"given":"Brenton","family":"Swenson","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"},{"name":"Institute for Public Health Genetics, University of Washington, Seattle, WA"}]},{"given":"Ruitong","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA"}]},{"given":"Traci M","family":"Bartz","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"},{"name":"Institute for Public Health Genetics, University of Washington, Seattle, WA"}]},{"given":"Nona","family":"Sotoodehnia","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"}]},{"given":"Yii-der I","family":"Chen","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Departments of Pediatrics and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1424-0673","authenticated-orcid":false,"given":"Brian E","family":"Cade","sequence":"additional","affiliation":[{"name":"Program in Medical and Population Genetics, Broad Institute, Cambridge, MA"},{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9510-4923","authenticated-orcid":false,"given":"Han","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA"},{"name":"Human Genetics Center, Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX"},{"name":"Center for Precision Health, School of Public Health & School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9142-5172","authenticated-orcid":false,"given":"Sanjay R","family":"Patel","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA"}]},{"given":"Xiaofeng","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Population and Quantitative Health Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2480-4367","authenticated-orcid":false,"given":"Sina A","family":"Gharib","sequence":"additional","affiliation":[{"name":"Computational Medicine Core, Center for Lung Biology, University of Washington Medicine Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, WA"}]},{"given":"W Craig","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington, Seattle, WA"}]},{"given":"Jerome I","family":"Rotter","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Departments of Pediatrics and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2233-1065","authenticated-orcid":false,"given":"Richa","family":"Saxena","sequence":"additional","affiliation":[{"name":"Program in Medical and Population Genetics, Broad Institute, Cambridge, MA"},{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA"},{"name":"Center for Genomic Medicine and Department of Anesthesia, Pain, and Critical Care Medicine, Massachusetts General Hospital, Boston, MA"}]},{"given":"Shaun","family":"Purcell","sequence":"additional","affiliation":[{"name":"Program in Medical and Population Genetics, Broad Institute, Cambridge, MA"},{"name":"Department of Psychiatry, Brigham & Women\u2019s Hospital, Harvard Medical School, Boston, MA"}]},{"given":"Xihong","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA"},{"name":"Department of Statistics, Harvard University, Cambridge, MA"}]},{"given":"Susan","family":"Redline","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA"},{"name":"Division of Pulmonary, Critical Care, and Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8520-8860","authenticated-orcid":false,"given":"Tamar","family":"Sofer","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA"},{"name":"Department of Biostatistics, Harvard T. H. 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apnea is the manifestation of key endotypic traits, including greater pharyngeal collapsibility, reduced dilator muscle compensation, and elevated chemoreflex loop gain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We investigated how endotypic traits vary with obesity, age, sex, and race\/ethnicity to influence sleep apnea disease severity (apnea\u2013hypopnea index [AHI]).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Endotypic traits were estimated from polysomnography in a diverse community-based cohort study (Multi-Ethnic Study of Atherosclerosis, N\u2009=\u20091,971; age range, 54\u201393 yr). Regression models assessed associations between each exposure (continuous variables per 2 standard deviations [SDs]) and endotypic traits (per SD) or AHI (events\/h), independent of other exposures. Generalizability was assessed in two independent cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Greater AHI was associated with obesity (+19 events\/h per 11 kg\/m2 [2 SD]), male sex (+13 events\/h vs. female), older age (+7 events\/h per 20 yr), and Chinese ancestry (+5 events\/h vs. White, obesity adjusted). Obesity-related increase in AHI was best explained by elevated collapsibility (+0.40 SD) and greater loop gain (+0.38 SD; percentage mediated, 26% [95% confidence interval (CI), 20\u201332%]). Male-related increase in AHI was explained by elevated collapsibility (+0.86 SD) and reduced compensation (\u22120.40 SD; percentage mediated, 57% [95% CI, 50\u201366%]). Age-related AHI increase was explained by elevated collapsibility (+0.37 SD) and greater loop gain (+0.15 SD; percentage mediated, 48% [95% CI, 34\u201363%]). Increased AHI with Chinese ancestry was explained by collapsibility (+0.57 SD; percentage mediated, 87% [95% CI, 57\u2013100]). Black race was associated with reduced collapsibility (\u22120.30 SD) and elevated loop gain (+0.29 SD). Similar patterns were observed in the other cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Different subgroups exhibit different underlying pathophysiological pathways to sleep apnea, highlighting the variability in mechanisms that could be targeted for intervention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1513\/annalsats.202203-271oc","type":"journal-article","created":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T11:59:59Z","timestamp":1666785599000},"page":"440-449","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":58,"title":["Pathophysiology Underlying Demographic and Obesity Determinants of Sleep Apnea Severity"],"prefix":"10.1093","volume":"20","author":[{"given":"Scott A.","family":"Sands","sequence":"first","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Raichel M.","family":"Alex","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Dwayne","family":"Mann","sequence":"additional","affiliation":[{"name":"Institute for Social Science Research and"},{"name":"School of Information Technology and Electrical Engineering, The University of Queensland, Brisbane, Queensland, Australia"}]},{"given":"Daniel","family":"Vena","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Philip I.","family":"Terrill","sequence":"additional","affiliation":[{"name":"School of Information Technology and Electrical Engineering, The University of Queensland, Brisbane, Queensland, Australia"}]},{"given":"Laura K.","family":"Gell","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0488-9778","authenticated-orcid":false,"given":"Andrey","family":"Zinchuk","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yale University School of Medicine, New Haven, Connecticut"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8520-8860","authenticated-orcid":false,"given":"Tamar","family":"Sofer","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9142-5172","authenticated-orcid":false,"given":"Sanjay R.","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Medicine, Center for Sleep and Cardiovascular Outcomes Research, and"},{"name":"Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania"}]},{"given":"Luigi","family":"Taranto-Montemurro","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Ali","family":"Azarbarzin","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Michael","family":"Rueschman","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"David P.","family":"White","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Andrew","family":"Wellman","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"given":"Susan","family":"Redline","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]}],"member":"286","published-online":{"date-parts":[[2023,3,1]]},"reference":[{"key":"2026012203262742600_bib1","doi-asserted-by":"crossref","first-page":"1006","DOI":"10.1093\/aje\/kws342","article-title":"Increased prevalence of sleep-disordered breathing in adults","volume":"177","author":"Peppard","year":"2013","journal-title":"Am J Epidemiol"},{"key":"2026012203262742600_bib2","doi-asserted-by":"crossref","first-page":"1800674","DOI":"10.1183\/13993003.00674-2018","article-title":"Identifying obstructive sleep apnoea patients 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We use a case-crossover analysis to explore the association between incident cardiovascular events and residential relocation to a new home address.<jats:italic>Methods<\/jats:italic>. We conducted an ambidirectional case-crossover analysis to explore the association between incident cardiovascular events and residential relocation to a new address using data from the Cardiovascular Health Study (CHS), a community-based prospective cohort study of 5,888 older adults from four U.S. sites beginning in 1989. Relocation was assessed twice a year during follow-up. Event occurrences were classified as present or absent for the period preceding the first reported move, as compared with an equal length of time immediately prior to and following this period.<jats:italic>Results<\/jats:italic>. Older adults (65+) that experience incident cardiovascular disease had an increased probability of reporting a change of residence during the following year (OR 1.6, 95% confidence interval (CI) = 1.2\u20132.1). Clinical conditions associated with relocation included stroke (OR: 2.0, 95% CI: 1.2\u20133.3), angina (OR: 1.6, 95% CI: 1.0\u20132.6), and congestive heart failure (OR: 1.5, 95% CI: 1.0\u20132.1).<jats:italic>Conclusions<\/jats:italic>. Major incident cardiovascular disease may increase the probability of residential relocation in older adults. Case-crossover analyses represent an opportunity to investigate triggering events, but finer temporal resolution would be crucial for future research on residential relocations.<\/jats:p>","DOI":"10.1155\/2014\/951971","type":"journal-article","created":{"date-parts":[[2014,3,23]],"date-time":"2014-03-23T17:03:43Z","timestamp":1395594223000},"page":"1-7","source":"Crossref","is-referenced-by-count":5,"title":["Residential Relocation by Older Adults in Response to Incident Cardiovascular Health Events: A Case-Crossover Analysis"],"prefix":"10.1155","volume":"2014","author":[{"given":"Gina S.","family":"Lovasi","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Columbia University, 722 West 168th Street, New York, NY 10032, USA"}]},{"given":"John M.","family":"Richardson","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Columbia University, 722 West 168th Street, New York, NY 10032, USA"}]},{"given":"Carlos 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Health","doi-asserted-by":"publisher","award":["R01HL097357"],"award-info":[{"award-number":["R01HL097357"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32HL007895"],"award-info":[{"award-number":["T32HL007895"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"published-print":{"date-parts":[[2022,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Resistin is a circulating inflammatory biomarker that is associated with cardiovascular disease. We investigated the associations of resistin and incident heart failure (HF) and its subtypes, as well as specific measures of subclinical HF (myocardial fibrosis and relevant biomarkers).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analysed data from 1968 participants in the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels at clinic visits from 2002 to 2005. Participants were subsequently followed for a median of 10.5 years for HF events. The associations between resistin levels and incident HF, HF with reduced ejection fraction (HFrEF), and HF with preserved ejection fraction (HFpEF) were examined using multivariable Cox proportional hazards models. Linear regression models assessed the associations between resistin levels and myocardial fibrosis from cardiac magnetic resonance imaging, as well as hs-cTnT and NT-proBNP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The mean age of the cohort was 64.7 years, and 50.0% were female. Seventy-four participants (4%) developed incident HF during follow-up. In a Cox proportional hazards model adjusted for age, gender, education level, race\/ethnicity, and traditional risk factors, higher resistin levels were significantly associated with incident HF (HR 1.44, CI 1.18\u20131.75, P = 0.001) and HFrEF (HR 1.47, CI 1.07\u20132.02, P = 0.016), but not with HFpEF (HR 1.25, CI 0.89\u20131.75, P = 0.195). Resistin levels showed no significant associations with myocardial fibrosis, NT-proBNP, or hs-cTnT levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In a multi-ethnic cohort free of cardiovascular disease at baseline, elevated resistin levels were associated with incident HF, more prominently with incident HFrEF than HFpEF, but not with subclinical myocardial fibrosis or biomarkers of HF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.14064","type":"journal-article","created":{"date-parts":[[2022,7,21]],"date-time":"2022-07-21T02:45:11Z","timestamp":1658371511000},"page":"3452-3460","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Resistin and Risks of Incident Heart Failure Subtypes and Cardiac Fibrosis: The Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8933-7133","authenticated-orcid":false,"given":"Xinjiang","family":"Cai","sequence":"first","affiliation":[{"name":"Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Icahn School of Medicine at Mount Sinai , New York, NY ,","place":["USA"]},{"name":"Specialty Training and Advanced Research (STAR) program, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA , Los Angeles, CA ,","place":["USA"]}]},{"given":"Matthew A.","family":"Allison","sequence":"additional","affiliation":[{"name":"Department of Family Medicine, University of California, San Diego , La Jolla, CA ,","place":["USA"]}]},{"given":"Bharath","family":"Ambale-Venkatesh","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins School of Medicine , Baltimore, MD ,","place":["USA"]}]},{"given":"Neal W.","family":"Jorgensen","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington School of Public Health , Seattle, WA ,","place":["USA"]}]},{"given":"Joao A.C.","family":"Lima","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins School of Medicine , Baltimore, MD ,","place":["USA"]}]},{"given":"Evan D.","family":"Muse","sequence":"additional","affiliation":[{"name":"Scripps Research Translational Institute and Division of Cardiovascular Diseases, Scripps Clinic , La Jolla, CA ,","place":["USA"]}]},{"given":"Robyn L.","family":"McClelland","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington School of Public Health , Seattle, WA ,","place":["USA"]}]},{"given":"Steven","family":"Shea","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, Columbia University Irving Medical Center , New York, NY ,","place":["USA"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7911-2923","authenticated-orcid":false,"given":"Djamel","family":"Lebeche","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Icahn School of Medicine at Mount Sinai , New York, NY ,","place":["USA"]},{"name":"Diabetes, Obesity and Metabolism Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai , New York, NY ,","place":["USA"]},{"name":"Department of Physiology, University of Tennessee Health Science Center , 318H Translational Research Building, Memphis, TN, 38163 ,","place":["USA"]}]}],"member":"286","published-online":{"date-parts":[[2022,7,20]]},"reference":[{"key":"2026012114160652200_ehf214064-bib-0001","doi-asserted-by":"crossref","first-page":"e139","DOI":"10.1161\/CIR.0000000000000757","article-title":"Heart disease and stroke statistics-2020 update: A report from the American Heart 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remain unclear. We examined the plasma proteomic profile associated with longitudinal changes in physical function measured by gait speed and grip strength in community\u2010dwelling adults. We applied an aptamer\u2010based platform to assay 1154 plasma proteins on 2854 participants (60% women, aged 76\u2009years) in the Cardiovascular Health Study (CHS) in 1992\u20131993 and 1130 participants (55% women, aged 54\u2009years) in the Framingham Offspring Study (FOS) in 1991\u20131995. Gait speed and grip strength were measured annually for 7\u2009years in CHS and at cycles 7 (1998\u20132001) and 8 (2005\u20132008) in FOS. The associations of individual protein levels (log\u2010transformed and standardized) with longitudinal changes in gait speed and grip strength in two populations were examined separately by linear mixed\u2010effects models. Meta\u2010analyses were implemented using random\u2010effects models and corrected for multiple testing. We found that plasma levels of 14 and 18 proteins were associated with changes in gait speed and grip strength, respectively (corrected <jats:italic>p<\/jats:italic>\u00a0&lt;\u20090.05). The proteins most strongly associated with gait speed decline were GDF\u201015 (Meta\u2010analytic <jats:italic>p<\/jats:italic>\u00a0=\u20091.58\u2009\u00d7\u200910<jats:sup>\u221215<\/jats:sup>), pleiotrophin (1.23\u2009\u00d7\u200910<jats:sup>\u22129<\/jats:sup>)<jats:italic>,<\/jats:italic> and TIMP\u20101 (5.97\u2009\u00d7\u200910<jats:sup>\u22128<\/jats:sup>). For grip strength decline, the strongest associations were for carbonic anhydrase III (1.09\u2009\u00d7\u200910<jats:sup>\u22127<\/jats:sup>), CDON (2.38\u2009\u00d7\u200910<jats:sup>\u22127<\/jats:sup>), and SMOC1 (7.47\u2009\u00d7\u200910<jats:sup>\u22127<\/jats:sup>). Several statistically significant proteins are involved in the inflammatory responses or antagonism of activin by follistatin pathway. These novel proteomic biomarkers and pathways should be further explored as future mechanisms and targets for age\u2010related functional decline.<\/jats:p>","DOI":"10.1111\/acel.13736","type":"journal-article","created":{"date-parts":[[2022,11,5]],"date-time":"2022-11-05T04:34:37Z","timestamp":1667622877000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Plasma proteomic signature of decline in gait speed and grip strength"],"prefix":"10.1111","volume":"21","author":[{"given":"Xiaojuan","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Epidemiology and Population Health Stanford University School of Medicine  Stanford California USA"}]},{"given":"Stephanie","family":"Pan","sequence":"additional","affiliation":[{"name":"Framingham Heart Study and Section of Preventive Medicine and Epidemiology Boston University School of Medicine  Boston Massachusetts USA"},{"name":"Department of 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of 264 participants in the Multi-Ethnic Study of Atherosclerosis (MESA). Urinary arsenic species, including inorganic arsenic (iAs), monomethylarsonate (MMA), dimethylarsinate (DMA), and arsenobetaine (Ab), were measured using high performance liquid chromatography-inductively coupled plasma mass spectrometry (HPLC-ICPMS) and corrected for organic sources from seafood consumption by regressing Ab on arsenic species using a validated method. Principal components of arsenic metabolism were also used as independent phenotypes. We conducted linear regression of arsenic traits with allelic dosage of candidate single nucleotide polymorphisms (SNPs) rs12768205 (G &gt; A), rs3740394 (A &gt; G), and rs3740393 (G &gt; C) measured using Illumina MetaboChip. Models were stratified by non-Hispanic white vs. all other race\/ethnicity and adjusted for age, sex, arsenic exposure, study site, and population stratification. Consistent with previous studies, rs12768205 showed evidence for strongest association (non-Hispanic white: iAs% \u22120.14 (P 0.83), MMA% \u22120.66 (0.49), DMA% 0.81(0.49); other race\/ethnicity: 0.13 (0.71), \u22121.21 (0.09), 1.08 (0.20)). No association, however, passed the strict Bonferroni p-value. 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major risk factor for vertebral compression fractures. Although sarcopenia has been shown to be associated with low bone mineral density (BMD), it is not known whether trunk musculature is directly associated with lumbar BMD, and whether exercise modifies this association. Using data from the Multi-Ethnic Study of Atherosclerosis (MESA), we sought to determine the association of muscle density and fat fraction of the psoas, paraspinal, and oblique muscle groups with L3 lumbar volumetric BMD, and whether these associations were modified by exercise. We obtained L3 vBMD measurements, and fat and muscle measurements (in Hounsfield units [HU]) from abdominal computed tomography (CT) scans spanning the L2\u2013L4 intervertebral disc spaces. Muscle density was defined as the mean HU value for a muscle group area. Fat fraction was calculated as the mean HU value for the muscle group fat area\/total muscle group area (cm2). Exercise data were self-reported (MET-minute\/week). We utilized multivariable linear regression to evaluate these associations, stratified by gender, and adjusting for demographics, body mass index (BMI), smoking status, impaired fasting glucose, and corticosteroid and anti-resorptive medication use. Among 1923 MESA participants, mean \u00b1 standard deviation (SD) age was 62\u2009\u00b1\u200910\u2009years, 49% were female, 40% white, 21% black, 26% Hispanic\/Latino, and 13% Chinese. In fully adjusted analysis, for every 1-SD higher psoas fat fraction, there was a 3.19-SD lower L3 vBMD in men and 4.3-SD lower L3 vBMD in women (p\u2009&amp;lt;\u20090.001). For every 1-SD higher psoas density, there was a 0.2-SD higher L3 vBMD (p\u2009&amp;lt;\u20090.001) in men and 0.19-SD higher L3 vBMD (p\u2009&amp;lt;\u20090.001) in women. Findings were similar for paraspinal and oblique muscles. Intentional exercise did not modify these associations. In men and women, trunk muscle density was positively associated with higher lumbar BMD, suggesting a local association. Future studies are warranted to determine the temporality of this association. \u00a9 2022 American Society for Bone and Mineral Research (ASBMR).<\/jats:p>","DOI":"10.1002\/jbmr.4634","type":"journal-article","created":{"date-parts":[[2022,6,12]],"date-time":"2022-06-12T08:53:54Z","timestamp":1655024034000},"page":"1537-1544","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Density and Fat Fraction of the Psoas, Paraspinal, and Oblique Muscle Groups Are Associated With Lumbar Vertebral Bone Mineral Density in a Multi-Ethnic Community-Living Population: The Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"37","author":[{"given":"Pradyumna","family":"Gurusamy","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery, School of Medicine University of California, San Diego La Jolla CA USA"}]},{"given":"Britta A.","family":"Larsen","sequence":"additional","affiliation":[{"name":"Herbert Wertheim School of Public Health and Human Longevity Science University of California, San Diego La Jolla CA USA"}]},{"given":"Richard T.","family":"Allen","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic Surgery, School of Medicine University of California, San Diego La Jolla CA USA"}]},{"given":"Samuel R.","family":"Ward","sequence":"additional","affiliation":[{"name":"Department of Radiology, School of Medicine University of California, San Diego La Jolla CA USA"},{"name":"Department of Orthopaedic Surgery, School of Medicine University of California, San Diego La Jolla CA USA"}]},{"given":"Matthew A.","family":"Allison","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, Department of Family Medicine and Public Health University of California, San Diego La Jolla CA USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7255-274X","authenticated-orcid":false,"given":"Jan M.","family":"Hughes-Austin","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic Surgery, School of Medicine University of California, San Diego La Jolla CA USA"}]}],"member":"286","published-online":{"date-parts":[[2022,6,12]]},"reference":[{"key":"2024012713545733500_jbmr4634-bib-0001","doi-asserted-by":"crossref","first-page":"1479","DOI":"10.2106\/JBJS.G.00675","article-title":"Mortality following the diagnosis of a vertebral compression fracture in the Medicare population","volume":"90","author":"Lau","year":"2008","journal-title":"J Bone Joint Surg Am"},{"key":"2024012713545733500_jbmr4634-bib-0002","doi-asserted-by":"crossref","first-page":"324","DOI":"10.1186\/s12889-015-1684-7","article-title":"Disability-adjusted-life-years losses in postmenopausal women with osteoporosis: a burden of illness 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We conducted proteomic association studies of incident type 2 diabetes and physiologic responses to an intravenous glucose tolerance test (IVGTT) to identify novel protein contributors to glucose homeostasis and diabetes risk. We tested 4,776 SomaScan proteins measured in relation to 18-year incident diabetes risk in participants from the Cardiovascular Health Study (N = 2,631) and IVGTT-derived measures in participants from the HERITAGE Family Study (N = 752). We characterize 51 proteins that were associated with longitudinal diabetes risk, using their respective 39, 9, and 8 concurrent associations with insulin sensitivity index (SI), acute insulin response to glucose (AIRG), and glucose effectiveness (SG). Twelve of the 51 diabetes associations appear to be novel, including \u03b2-glucuronidase, which was associated with increased diabetes risk and lower SG, suggesting an alternative pathway to insulin for glucose disposal; and plexin-B2, which also was associated with increased diabetes risk, but with lower AIRG, and not with SI, indicating a mechanism related instead to pancreatic dysfunction. Other novel protein associations included alcohol dehydrogenase-1C, fructose-bisphosphate aldolase-B, sorbitol dehydrogenase with elevated type 2 diabetes risk, and a leucine-rich repeat containing protein-15 and myocilin with decreased risk.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Article Highlights<\/jats:title>\n                  <jats:p>Plasma proteins are associated with the risk of incident diabetes in older adults independent of various demographic, lifestyle, and biochemical risk factors. These same proteins are associated with subtle differences in measures of glucose homeostasis earlier in life. Proteins that are associated with lower insulin sensitivity in individuals without diabetes tend to be associated with appropriate compensatory mechanisms, such as a stronger acute insulin response or higher glucose effectiveness. Proteins that are associated with future diabetes risk, but not with insulin insensitivity, tend to be associated with lower glucose effectiveness and\/or impaired acute insulin response.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/db22-0628","type":"journal-article","created":{"date-parts":[[2023,2,7]],"date-time":"2023-02-07T21:16:21Z","timestamp":1675804581000},"page":"666-673","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":18,"title":["Plasma Proteomic Risk Markers of Incident Type 2 Diabetes Reflect Physiologically Distinct Components of Glucose-Insulin Homeostasis"],"prefix":"10.2337","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6855-8324","authenticated-orcid":false,"given":"H\u00e9l\u00e9ne T.","family":"Cronj\u00e9","sequence":"first","affiliation":[{"name":"1Department of Public Health, Section of Epidemiology, University of Copenhagen, Copenhagen, Denmark"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8031-8948","authenticated-orcid":false,"given":"Michael Y.","family":"Mi","sequence":"additional","affiliation":[{"name":"2Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"given":"Thomas R.","family":"Austin","sequence":"additional","affiliation":[{"name":"3Department of Epidemiology, University of Washington, Seattle, WA"}]},{"given":"Mary L.","family":"Biggs","sequence":"additional","affiliation":[{"name":"4Department of Biostatistics, University of Washington, Seattle, WA"}]},{"given":"David S.","family":"Siscovick","sequence":"additional","affiliation":[{"name":"5New York Academy of Medicine, New York, NY"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7038-1844","authenticated-orcid":false,"given":"Rozenn N.","family":"Lemaitre","sequence":"additional","affiliation":[{"name":"6Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"6Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA"},{"name":"7Department of Epidemiology, Health Systems and Population Health, University of Washington, Seattle, WA"}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"8Department of Pathology Laboratory Medicine, Larner College of Medicine, University of Vermont, Burlington, VT"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9902-3047","authenticated-orcid":false,"given":"Luc","family":"Djouss\u00e9","sequence":"additional","affiliation":[{"name":"9Division of Aging, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, MA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9936-7803","authenticated-orcid":false,"given":"Jorge R.","family":"Kizer","sequence":"additional","affiliation":[{"name":"10Cardiology Section San Francisco Veterans Affairs Health Care System, San Francisco, CA"},{"name":"11Department of Medicine, Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA"}]},{"given":"Joachim H.","family":"Ix","sequence":"additional","affiliation":[{"name":"12Division of Nephrology-Hypertension, University of California, San Diego, La Jolla, CA"}]},{"given":"Prashant","family":"Rao","sequence":"additional","affiliation":[{"name":"2Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"given":"Jeremy M.","family":"Robbins","sequence":"additional","affiliation":[{"name":"2Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"given":"Jacob L.","family":"Barber","sequence":"additional","affiliation":[{"name":"13Department of Exercise Science, University of South Carolina, Columbia, SC"}]},{"given":"Mark A.","family":"Sarzynski","sequence":"additional","affiliation":[{"name":"13Department of Exercise Science, University of South Carolina, Columbia, SC"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8259-9245","authenticated-orcid":false,"given":"Clary B.","family":"Clish","sequence":"additional","affiliation":[{"name":"14Broad Institute of MIT and Harvard, Cambridge, MA"}]},{"given":"Claude","family":"Bouchard","sequence":"additional","affiliation":[{"name":"15Pennington Biomedical Research Center, Baton Rouge, LA"}]},{"given":"Kenneth J.","family":"Mukamal","sequence":"additional","affiliation":[{"name":"16Division of General Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6767-7687","authenticated-orcid":false,"given":"Robert E.","family":"Gerszten","sequence":"additional","affiliation":[{"name":"2Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA"}]},{"given":"Majken K.","family":"Jensen","sequence":"additional","affiliation":[{"name":"1Department of Public Health, Section of Epidemiology, University of Copenhagen, Copenhagen, Denmark"},{"name":"17Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA"}]}],"member":"1167","published-online":{"date-parts":[[2023,2,7]]},"reference":[{"key":"2023050519170244000_B1","doi-asserted-by":"crossref","first-page":"14790","DOI":"10.1038\/s41598-020-71908-9","article-title":"Global, regional, and national burden and trend of diabetes in 195 countries and territories: an analysis from 1990 to 2025","volume":"10","author":"Lin","year":"2020","journal-title":"Sci Rep"},{"key":"2023050519170244000_B2","doi-asserted-by":"crossref","first-page":"1534","DOI":"10.1038\/s41588-021-00948-2","article-title":"Genome-wide association analyses highlight etiological differences underlying newly defined subtypes of diabetes","volume":"53","author":"Mansour Aly","year":"2021","journal-title":"Nat Genet"},{"key":"2023050519170244000_B3","doi-asserted-by":"crossref","first-page":"1851","DOI":"10.1038\/s41591-019-0665-2","article-title":"Plasma protein patterns as comprehensive indicators of health","volume":"25","author":"Williams","year":"2019","journal-title":"Nat Med"},{"key":"2023050519170244000_B4","doi-asserted-by":"crossref","first-page":"2766","DOI":"10.2337\/db20-0296","article-title":"Deciphering the plasma proteome of type 2 diabetes","volume":"69","author":"Elhadad","year":"2020","journal-title":"Diabetes"},{"key":"2023050519170244000_B5","doi-asserted-by":"crossref","first-page":"1843","DOI":"10.2337\/db19-1070","article-title":"Circulating protein signatures and causal candidates for type 2 diabetes","volume":"69","author":"Gudmundsdottir","year":"2020","journal-title":"Diabetes"},{"key":"2023050519170244000_B6","doi-asserted-by":"crossref","first-page":"e144392","DOI":"10.1172\/jci.insight.144392","article-title":"Proteomic profiling reveals biomarkers and pathways in type 2 diabetes risk","volume":"6","author":"Ngo","year":"2021","journal-title":"JCI Insight"},{"key":"2023050519170244000_B7","doi-asserted-by":"crossref","first-page":"263","DOI":"10.1016\/1047-2797(91)90005-W","article-title":"The cardiovascular health study: design and rationale","volume":"1","author":"Fried","year":"1991","journal-title":"Ann Epidemiol"},{"key":"2023050519170244000_B8","doi-asserted-by":"crossref","first-page":"755","DOI":"10.1007\/s10654-022-00888-z","article-title":"Proteomics and population biology in the Cardiovascular Health Study (CHS): design of a study with mentored access and active data sharing","volume":"37","author":"Austin","year":"2022","journal-title":"Eur J Epidemiol"},{"key":"2023050519170244000_B9","doi-asserted-by":"crossref","first-page":"415","DOI":"10.2337\/dc11-1519","article-title":"Total and high-molecular-weight adiponectin and risk of incident diabetes in older people","volume":"35","author":"Kizer","year":"2012","journal-title":"Diabetes Care"},{"key":"2023050519170244000_B10","doi-asserted-by":"crossref","first-page":"721","DOI":"10.1249\/00005768-199505000-00015","article-title":"The HERITAGE family study. 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Due to overlapping clinical risk factors, identifying high\u2010risk patients with OSA who are likely to develop CVD remains challenging. We aimed to identify baseline clinical factors associated with the future development of CVD in patients with OSA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Study Design<\/jats:title>\n                    <jats:p>Retrospective analysis of prospectively collected data.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed a retrospective analysis of 967 adults aged 45 to 84\u2009years and enrolled in the Multi\u2010Ethnic Study of Atherosclerosis. Six machine learning models were created using baseline clinical factors initially identified by stepwise variable selection. The performance of these models for the prediction of additional risk of CVD in OSA was calculated. Additionally, these models were evaluated for interpretability using locally interpretable model\u2010agnostic explanations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Of the 967 adults without baseline OSA or CVD, 116 were diagnosed with OSA and CVD and 851 with OSA alone 10\u2009years after enrollment. The best performing models included random forest (sensitivity 84%, specificity 99%, balanced accuracy 91%) and bootstrap aggregation (sensitivity 84%, specificity 100%, balanced accuracy 92%). The strongest predictors of OSA and CVD versus OSA alone were fasting glucose &gt;91\u2009mg\/dL, diastolic pressure &gt;73\u2009mm Hg, and age &gt;59\u2009years.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In the selected study population of adults without OSA or CVD at baseline, the strongest predictors of CVD in patients with OSA include fasting glucose, diastolic pressure, and age. These results may shape a strategy for cardiovascular risk stratification in patients with OSA and early intervention to mitigate CVD\u2010related morbidity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Level of Evidence<\/jats:title>\n                    <jats:p>\n                      3\n                      <jats:italic>Laryngoscope<\/jats:italic>\n                      , 132:234\u2013241, 2022\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/lary.29852","type":"journal-article","created":{"date-parts":[[2021,9,6]],"date-time":"2021-09-06T14:31:12Z","timestamp":1630938672000},"page":"234-241","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Stratifying the Risk of Cardiovascular Disease in Obstructive Sleep Apnea Using Machine Learning"],"prefix":"10.1002","volume":"132","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7812-4087","authenticated-orcid":false,"given":"Saikrishna C.","family":"Gourishetti","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology\u2014Head and Neck Surgery University of Maryland School of Medicine Baltimore  Baltimore Maryland U.S.A."}]},{"given":"Rodney","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology\u2014Head and Neck Surgery University of Maryland School of Medicine Baltimore  Baltimore Maryland U.S.A."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3064-6964","authenticated-orcid":false,"given":"Amal","family":"Isaiah","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology\u2014Head and Neck Surgery University of Maryland School of Medicine Baltimore  Baltimore Maryland U.S.A."},{"name":"Department of Pediatrics University of Maryland School of Medicine Baltimore  Baltimore Maryland U.S.A."}]}],"member":"311","published-online":{"date-parts":[[2021,9,6]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000485"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.118.010440"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2008.05.002"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.291.16.2013"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.2147\/VHRM.S74703"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1056\/nejmoa043104"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(05)71141-7"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1586\/ERC.10.55"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.5664\/jcsm.27191"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.5665\/sleep.5774"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1093\/jamia\/ocy064"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.5665\/sleep.4732"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1093\/aje\/kwf113"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2011.08.021"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.5664\/jcsm.6506"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.2202\/1544-6115.1730"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1109\/TAC.1974.1100705"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1037\/a0016973"},{"key":"e_1_2_6_20_1","first-page":"220","article-title":"On the asymptotic theory of permutation statistics","volume":"8","author":"Strasser H","year":"1999","journal-title":"Math Methods Stat"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1023\/A:1010933404324"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1201\/9780429246593"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1023\/A:1018628609742"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1532-0464(03)00034-0"},{"key":"e_1_2_6_25_1","doi-asserted-by":"crossref","unstructured":"YadavS ShuklaS.Analysis of k\u2010fold cross\u2010validation over hold\u2010out validation on colossal datasets for quality classification. 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Prior studies have been limited by their cross-sectional design and potential confounding by body habitus.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To test the hypothesis that OSA severity is associated with more high-attenuation areas (HAAs) on computed tomography and worse lung function over time among older community-dwelling adults.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used data from participants in the MESA (Multi-Ethnic Study of Atherosclerosis) who had apnea\u2013hypopnea index (AHI) measured from polysomnography (2010\u20132013), high attenuation areas (HAAs, \u2212600 to \u2212250 Hounsfield units, n\u2009=\u2009784), assessments from exams 5 (2010\u20132012) and 6 (2016\u20132018) full-lung computed tomography scans, and spirometry assessments (n\u2009=\u2009677). Linear mixed-effects models with random intercept were used to examine associations of OSA severity (i.e., AHI and hypoxic burden) with changes in HAAs, total lung volumes, and forced vital capacity (FVC) between exams 5 and 6. Potential confounders were adjusted for in the model, including age, sex, smoking history, height, and weight.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Among those with a higher AHI there were more men and a higher body mass index. Participants with AHI\u2009\u2a7e\u200915 events\/h and in the highest hypoxic burden quartile each had increases in HAAs of 11.30% (95% confidence interval [CI], 3.74\u201319.35%) and 9.85% (95% CI, 1.40\u201319.01%) per 10 years, respectively. There was a more rapid decline in total lung volumes imaged and FVC among those with AHI\u2009\u2a7e\u200915 events\/h of 220.2 ml (95% CI, 47.8\u2013392.5 ml) and 3.63% (95% CI, 0.43\u20136.83%) per 10 years, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>A greater burden of hypoxia related to obstructive events during sleep was associated with increased lung densities over time and a more rapid decline in lung volumes regardless of body habitus. Our findings suggest OSA may be a contributing factor in the early stages of ILD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1513\/annalsats.202208-719oc","type":"journal-article","created":{"date-parts":[[2023,2,15]],"date-time":"2023-02-15T12:26:59Z","timestamp":1676464019000},"page":"728-737","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":13,"title":["Obstructive Sleep Apnea and Longitudinal Changes in Interstitial Lung Imaging and Lung Function: The MESA Study"],"prefix":"10.1093","volume":"20","author":[{"given":"John S.","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Virginia School of Medicine, Charlottesville, Virginia"},{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"given":"Ali","family":"Azarbarzin","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Sleep Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9559-1485","authenticated-orcid":false,"given":"Anna J.","family":"Podolanczuk","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical Center, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9274-7643","authenticated-orcid":false,"given":"Michaela R.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Perelman School of Medicine, Philadelphia, Pennsylvania"}]},{"given":"Brian E.","family":"Cade","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Sleep Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, Massachusetts"},{"name":"Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts"}]},{"given":"Steven M.","family":"Kawut","sequence":"additional","affiliation":[{"name":"Department of Medicine, Perelman School of Medicine, Philadelphia, Pennsylvania"}]},{"given":"Artur","family":"Wysoczanski","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"given":"Andrew F.","family":"Laine","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Columbia University, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8456-9437","authenticated-orcid":false,"given":"Eric A.","family":"Hoffman","sequence":"additional","affiliation":[{"name":"Department of Radiology"},{"name":"Department of Medicine, and"},{"name":"Department of Biomedical Engineering, University of Iowa Carver College of Medicine, Iowa City, Iowa"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8812-8751","authenticated-orcid":false,"given":"Daniel J.","family":"Gottlieb","sequence":"additional","affiliation":[{"name":"Veterans Affairs Boston Healthcare System, Brigham and Women\u2019s Hospital, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0771-1249","authenticated-orcid":false,"given":"Christine Kim","family":"Garcia","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"}]},{"given":"R. Graham","family":"Barr","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York"},{"name":"Department of Epidemiology, Mailman School of Public Health, New York, New York; and"}]},{"given":"Susan","family":"Redline","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Sleep Disorders, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"},{"name":"Division of Pulmonary, Critical Care, and Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts"}]}],"member":"286","published-online":{"date-parts":[[2023,5,1]]},"reference":[{"key":"2026012203265943600_bib1","doi-asserted-by":"crossref","first-page":"958","DOI":"10.1056\/NEJMra2005230","article-title":"Spectrum of fibrotic lung diseases","volume":"383","author":"Wijsenbeek","year":"2020","journal-title":"N Engl J 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The discovery that the Koblenz based company UB Plasma had used blood and plasma that had been improperly screened for HIV antibody shocked the German public and led the federal minister of health, Horst Seehofer, to open an official inquiry into what was widely per ceived as a \u201cscandal.\u201d1 Such reactions were late in coming, given the fact that press accounts of the effect of HIV contamination of the blood supply had appeared years earlier. 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Medicine","doi-asserted-by":"publisher","award":["5T15LM007359"],"award-info":[{"award-number":["5T15LM007359"]}],"id":[{"id":"10.13039\/100000092","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Genetic Epidemiology"],"published-print":{"date-parts":[[2020,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    25\u2010Hydroxyvitamin D (25(OH)D) concentration is a complex trait with genetic and environmental predictors that may determine how much vitamin D exposure is required to reach optimal concentration. Interactions between continuous measures of a polygenic score (PGS) and vitamin D intake (PGS*intake) or available ultraviolet (UV) radiation (PGS*UV) were evaluated in individuals of African (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20091,099) or European (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20098,569) ancestries. Interaction terms and joint effects (main and interaction terms) were tested using one\u2010degree of freedom (1\u2010DF) and 2\u2010DF models, respectively. Models controlled for age, sex, body mass index, cohort, and dietary intake\/available UV. In addition, in participants achieving Institute of Medicine (IOM) vitamin D intake recommendations, 25(OH)D was evaluated by level PGS. The 2\u2010DF PGS*intake, 1\u2010DF PGS*UV, and 2\u2010DF PGS*UV results were statistically significant in participants of European ancestry (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20093.3\u2009\u00d7\u200910\n                    <jats:sup>\u221218<\/jats:sup>\n                    ,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u2009\u20092.1\u2009\u00d7\u200910\n                    <jats:sup>\u22122<\/jats:sup>\n                    , and\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u2009\u20092.4\u2009\u00d7\u200910\n                    <jats:sup>\u221219<\/jats:sup>\n                    , respectively), but not in those of African ancestry. In European\u2010ancestry participants reaching IOM vitamin D intake guidelines, the percent of participants achieving adequate 25(OH)D (\n                    <jats:styled-content>&gt;<\/jats:styled-content>\n                    20\u2009ng\/ml) increased as genetic risk decreased (72% vs. 89% in highest vs. lowest risk;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u2009.018). Available UV radiation and vitamin D intake interact with genetics to influence 25(OH)D. Individuals with higher genetic risk may require more vitamin D exposure to maintain optimal 25(OH)D concentrations.\n                  <\/jats:p>","DOI":"10.1002\/gepi.22272","type":"journal-article","created":{"date-parts":[[2019,12,12]],"date-time":"2019-12-12T08:31:29Z","timestamp":1576139489000},"page":"208-217","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Multi\u2010ethnic analysis shows genetic risk and environmental predictors interact to influence 25(OH)D concentration and optimal vitamin D intake"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0849-7018","authenticated-orcid":false,"given":"Kathryn E.","family":"Hatchell","sequence":"first","affiliation":[{"name":"Department of Population Health Sciences, School of Medicine and Public Health University of Wisconsin\u2010Madison Madison Wisconsin"}]},{"given":"Qiongshi","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Medical Informatics, School of Medicine and Public Health University of Wisconsin\u2010Madison Madison Wisconsin"}]},{"given":"Julie A.","family":"Mares","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences University of Wisconsin\u2010Madison Madison Wisconsin"}]},{"given":"Erin D.","family":"Michos","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Ciccarone Center for the Prevention of Cardiovascular Disease School of Medicine Johns Hopkins University Baltimore Maryland"}]},{"given":"Alexis C.","family":"Wood","sequence":"additional","affiliation":[{"name":"Children's Nutrition Research Center USDA\/ARS Children's Nutrition Research Center Baylor College of Medicine Houston Texas"}]},{"given":"Corinne D.","family":"Engelman","sequence":"additional","affiliation":[{"name":"Department of Population Health Sciences, School of Medicine and Public Health University of Wisconsin\u2010Madison Madison Wisconsin"}]}],"member":"311","published-online":{"date-parts":[[2019,12,12]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.g6330"},{"key":"e_1_2_9_3_1","unstructured":"Anderson G.WHI harmonized and imputed GWAS data. dbGaP study accession: phs000746.v2.p3"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1047-2797(03)00043-7"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.anai.2014.07.005"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.3945\/jn.113.183541"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/gepi.20492"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/bioinformatics\/btr330"},{"key":"e_1_2_9_9_1","unstructured":"dbGaP. 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Retrieved fromhttps:\/\/www.ncbi.nlm.nih.gov\/gap"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/mp.2017.77"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2007-2702"},{"key":"e_1_2_9_12_1","doi-asserted-by":"publisher","DOI":"10.3945\/jn.112.169482"},{"key":"e_1_2_9_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nutres.2010.12.001"},{"issue":"5","key":"e_1_2_9_14_1","first-page":"1","article-title":"Wanted: 1 million people to help transform precision medicine: All of Us program open for enrollment","volume":"48","author":"Haskins J.","year":"2018","journal-title":"The Nation's 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randomization studies do not support a role for vitamin d in coronary artery disease","volume":"9","author":"Manousaki D.","year":"2016","journal-title":"Circulation Genomic and Precision Medicine"},{"key":"e_1_2_9_27_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1809944"},{"key":"e_1_2_9_28_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41588-019-0379-x"},{"key":"e_1_2_9_29_1","doi-asserted-by":"publisher","DOI":"10.1093\/aje\/kwr160"},{"key":"e_1_2_9_30_1","volume-title":"Dietary reference intakes for calcium and vitamin D","author":"Institute of 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Epidemiology"],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fgepi.22272","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/gepi.22272","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/full-xml\/10.1002\/gepi.22272","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/gepi.22272","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,9,5]],"date-time":"2023-09-05T21:11:29Z","timestamp":1693948289000},"score":8.670449,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/gepi.22272"}},"issued":{"date-parts":[[2019,12,12]]},"references-count":45,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2020,3]]}},"alternative-id":["10.1002\/gepi.22272"],"URL":"https:\/\/doi.org\/10.1002\/gepi.22272","archive":["Portico"],"relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/652941","asserted-by":"object"}]},"ISSN":["0741-0395","1098-2272"],"issn-type":[{"value":"0741-0395","type":"print"},{"value":"1098-2272","type":"electronic"}],"published":{"date-parts":[[2019,12,12]]},"assertion":[{"value":"2019-10-13","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication 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This paper evaluates available conditional and marginal models and establishes the relationship between the conditional and marginal parameters with the primary objective of comparing the treatment mean effects. We perform extensive simulation studies to investigate these models under complete data and the selection models under missing data with different parametric distributions and missingness patterns and mechanisms. The generalized estimating equations and the generalized linear mixed-effects models with pseudo-likelihood estimation are advocated for valid and robust inference. We also propose a controlled multiple imputation method as a sensitivity analysis of the missing data assumption. Lastly, we implement the proposed models and the sensitivity analysis in two real data examples with binary data. <\/jats:p>","DOI":"10.1177\/09622802211047177","type":"journal-article","created":{"date-parts":[[2021,11,15]],"date-time":"2021-11-15T15:21:46Z","timestamp":1636989706000},"page":"119-138","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Analysis of crossover designs for longitudinal binary data with ignorable and nonignorable dropout"],"prefix":"10.1177","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9478-0199","authenticated-orcid":false,"given":"Xi","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Public Health Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA, USA"}]},{"given":"Vernon M.","family":"Chinchilli","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA, USA"}]}],"member":"179","published-online":{"date-parts":[[2021,11,15]]},"reference":[{"key":"bibr1-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1186\/1745-6215-15-237"},{"key":"bibr2-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1201\/9781420011180"},{"key":"bibr3-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1214\/cbms\/1462106075"},{"key":"bibr4-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1177\/096228029400300403"},{"key":"bibr5-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/73.1.13"},{"key":"bibr6-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1080\/01621459.1993.10594284"},{"key":"bibr7-09622802211047177","doi-asserted-by":"publisher","DOI":"10.2307\/2531248"},{"key":"bibr8-09622802211047177","volume-title":"A representation of the joint distribution of responses to n dichotomous items","author":"Bahadur RR","year":"1959"},{"key":"bibr9-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/80.1.141"},{"key":"bibr10-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/90.4.765"},{"key":"bibr11-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/63.3.581"},{"key":"bibr12-09622802211047177","volume-title":"Statistical analysis with missing data","volume":"793","author":"Little RJ","year":"2019"},{"key":"bibr13-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/82.2.277"},{"key":"bibr14-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1002\/sim.4497"},{"key":"bibr15-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1016\/j.jspi.2004.06.005"},{"key":"bibr16-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1080\/03610920903427800"},{"key":"bibr17-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biostatistics\/kxt009"},{"key":"bibr18-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1177\/0962280212445838"},{"key":"bibr19-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1093\/biomet\/72.2.411"},{"key":"bibr20-09622802211047177","first-page":"589","volume":"22","author":"Kyoung Y","year":"2015","journal-title":"Commun Stat Appl Methods"},{"key":"bibr21-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1002\/bimj.201400064"},{"key":"bibr22-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1002\/sim.7583"},{"key":"bibr23-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1002\/hed.10317"},{"key":"bibr24-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1111\/ppe.12382"},{"key":"bibr25-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1905560"},{"key":"bibr26-09622802211047177","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1008770"},{"key":"bibr27-09622802211047177","unstructured":"Ich C. 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<jats:p>Criteria for progressive pulmonary fibrosis (PPF) have been proposed, but their prognostic value beyond categorical decline in FVC remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine whether proposed PPF criteria predict transplant-free survival (TFS) in patients with non\u2013idiopathic pulmonary fibrosis (IPF) forms of interstitial lung disease (ILD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A retrospective, multicenter cohort analysis was performed. Patients with diagnoses of fibrotic connective tissue disease\u2013associated ILD, fibrotic hypersensitivity pneumonitis, and non-IPF idiopathic interstitial pneumonia from three U.S. centers and one UK center constituted the test and validation cohorts, respectively. Cox proportional hazards regression was used to test the association between 5-year TFS and \u226510% FVC decline, followed by 13 additional PPF criteria satisfied in the absence of \u226510% FVC decline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>One thousand three hundred forty-one patients met the inclusion criteria. A \u226510% relative FVC decline was the strongest predictor of reduced TFS and showed consistent TFS association across cohorts, ILD subtypes, and treatment groups, resulting in a phenotype that closely resembled IPF. Ten additional PPF criteria satisfied in the absence of 10% relative FVC decline were also associated with reduced TFS in the U.S. test cohort, with 6 maintaining TFS associations in the UK validation cohort. Validated PPF criteria requiring a combination of physiologic, radiologic, and symptomatic worsening performed similarly to their stand-alone components but captured a smaller number of patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>An FVC decline of \u226510% and six additional PPF criteria satisfied in the absence of such decline identify patients with non-IPF ILD at increased risk for death or lung transplantation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202201-0124oc","type":"journal-article","created":{"date-parts":[[2022,8,9]],"date-time":"2022-08-09T12:42:35Z","timestamp":1660048955000},"page":"69-76","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":124,"title":["Validation of Proposed Criteria for Progressive Pulmonary 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and St. Thomas\u2019 NHS Foundation Trust, London, United Kingdom"}]},{"given":"Athol U.","family":"Wells","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute, Imperial College London, London, United Kingdom"},{"name":"Royal Brompton and Harefield Hospitals, Guy\u2019s and St. Thomas\u2019 NHS Foundation Trust, London, United Kingdom"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0771-1249","authenticated-orcid":false,"given":"Christine Kim","family":"Garcia","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Columbia University, New York, New York"}]},{"given":"Felix","family":"Chua","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute, Imperial College London, London, United Kingdom"},{"name":"Royal Brompton and Harefield Hospitals, Guy\u2019s and St. Thomas\u2019 NHS Foundation Trust, London, United Kingdom"}]},{"given":"Chad 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Pipe and cigar use remains common among US adults, yet its risks remain insufficiently understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We analysed data from five pooled cohorts with adults enrolled from 1971 to 2011 with follow-up through 2018. Pipe\/cigar use was defined by baseline self-report. Forced expiratory volume in 1\u2009s (FEV\n                      <jats:sub>1<\/jats:sub>\n                      ), forced vital capacity (FVC) and FEV\n                      <jats:sub>1<\/jats:sub>\n                      \/FVC ratio were measured by spirometry. All-cause mortality, coronary heart disease mortality and hospitalisation, respiratory-related mortality, and chronic obstructive pulmonary disease (COPD) mortality and hospitalisation were classified via adjudication or validated algorithms. Associations were estimated with linear mixed models and Fine-Gray subdistribution hazards models adjusted for sociodemographic and clinical factors.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 22\u2009823 participants (mean (SD) age 48.0 (15.7) years; 44.9% male sex; 70.5% white, 25.4% black, 2.4% Hispanic\/Latino), 2621 (11.5%) reported ever pipe\/cigar use, including 518 (2.3%) exclusive users without cigarette history. Compared with never tobacco users (n=9931), exclusive pipe\/cigar use was associated with faster decline in FEV\n                      <jats:sub>1<\/jats:sub>\n                      (3.36\u2009mL\/year; 95%\u2009CI 1.99 to 4.72), FVC (3.73\u2009mL\/year; 95%\u2009CI 2.05 to 5.42) and FEV\n                      <jats:sub>1<\/jats:sub>\n                      \/FVC (0.031 per year; 95%\u2009CI 0.008 to 0.054). Exclusive users had higher all-cause mortality (adjusted HR (aHR) 1.24; 95% CI 1.08 to 1.41), COPD hospitalisation\/mortality (aHR 2.02; 95%\u2009CI 1.41 to 2.90) and preserved ratio impaired spirometry (aHR 1.83; 95%\u2009CI 1.24 to 2.71).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Pipe and cigar use was associated with accelerated lung function decline and increased mortality and cardiopulmonary events, including among never cigarette users. These findings underscore the need for prevention and cessation efforts targeting non-cigarette tobacco.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/thorax-2025-224461","type":"journal-article","created":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T18:20:32Z","timestamp":1772562032000},"page":"thorax-2025-224461","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Pipe and cigar use, lung function decline and clinical outcomes: an analysis of the NHLBI Pooled Cohorts Study"],"prefix":"10.1136","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7607-3586","authenticated-orcid":false,"given":"William M","family":"Gardner","sequence":"first","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, USA"}]},{"given":"Pallavi P","family":"Balte","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3249-926X","authenticated-orcid":false,"given":"Christina M","family":"Eckhardt","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, USA"}]},{"given":"Jack E","family":"Morris","sequence":"additional","affiliation":[{"name":"Columbia University Mailman School of Public Health, New York, New York, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8418-4497","authenticated-orcid":false,"given":"Surya P","family":"Bhatt","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama At Birmingham, Birmingham, Alabama, USA"}]},{"given":"David J","family":"Couper","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA"}]},{"given":"Neal D","family":"Freedman","sequence":"additional","affiliation":[{"name":"Tobacco Control Research Branch, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, Maryland, USA"}]},{"given":"David R","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA"}]},{"given":"Ravi","family":"Kalhan","sequence":"additional","affiliation":[{"name":"Division of Pulmonary\/Critical Care, Northwestern University, Chicago, Illinois, USA"}]},{"given":"Laura R","family":"Loehr","sequence":"additional","affiliation":[{"name":"Department of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4911-5290","authenticated-orcid":false,"given":"Stephanie J","family":"London","sequence":"additional","affiliation":[{"name":"National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1572-1340","authenticated-orcid":false,"given":"Pamela L","family":"Lutsey","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota, USA"}]},{"given":"Joseph E","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, USA"},{"name":"Department of Psychiatry, Stony Brook University Renaissance School of Medicine, Stony Brook, New York, USA"}]},{"given":"Wendy","family":"White","sequence":"additional","affiliation":[{"name":"Undergraduate Training and Education Center, Tougaloo College, Jackson, Mississippi, 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Yes, it is totally safe to consume the supplement accordingly. One  just needs to consume the supplement on regular basis in order to gain  the positive results. If you face any kind of trouble or hindrance while  consuming this solution then you can immediately stop the consumption  as well.  We will advise you to make the purchase from the online market only.  If you will place the order from any of the offline market then you  might get some copied product to your door. So, it would be good for you  if you make the purchase from the guardian blood balance Australia.  Final Words on Guardian Blood Balance Australia  This is an amazing blood boost formula with potent weight loss  benefits as well. It is a reliable solution that counters various issues  in the human body. Guardian blood balance Australia helps the person to  recover from all kinds of diabetes issues and blood-related problems  with ease. Any single person can try out this supplement to counter the  problems from the root.  If you want to develop good health results then guardian blood boost  formula is here for you. The herbal and powerful ingredients of this  supplement will easily deliver various positive outcomes in your body  tone. It will amaze your life in no time and allow you to counter the  problems from the root with ease.  Lastly, it is your choice whether you want to reduce your health  issues or not. If you are looking for some private treatment then the  choice is totally yours. Feel free to place the order today to enable  good health results. Enjoy the positive working of this blood boost  formula if you don\u2019t want to rip your bank account.   <\/p>","DOI":"10.17504\/protocols.io.q26g741m3gwz\/v1","type":"posted-content","created":{"date-parts":[[2022,3,16]],"date-time":"2022-03-16T17:45:28Z","timestamp":1647452728000},"source":"Crossref","is-referenced-by-count":0,"title":["[RETRACTED] Guardian Blood Balance Australia- Reviews - Guardian Botanicals Blood Balance [AU] SCAM ALERT! Read Real Critical Reports.. 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Sciences","doi-asserted-by":"publisher","award":["KL2TR001882"],"award-info":[{"award-number":["KL2TR001882"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2022,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Chronic obstructive pulmonary disease (COPD) is defined by fixed spirometric ratio, FEV1\/FVC\u2009&amp;lt;\u20090.70 after inhaled bronchodilators. However, the implications of variable obstruction (VO), in which the prebronchodilator FEV1\/FVC ratio is less than 0.70 but increases to 0.70 or more after inhaled bronchodilators, have not been determined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We explored differences in physiology, exacerbations, and health status in participants with VO compared with reference participants without obstruction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Data from the SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) cohort were obtained. Participants with VO were compared with reference participants without obstruction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>We assessed differences in baseline radiographic emphysema and small airway disease at study entry, baseline, and change in lung function by spirometry, functional capacity by 6-minute walk, health status using standard questionnaires, exacerbation rates, and progression to COPD between the two groups. All models were adjusted for participant characteristics, asthma history, and tobacco exposure. We assessed 175 participants with VO and 603 reference participants without obstruction. Participants with VO had 6.2 times the hazard of future development of COPD controlling for other factors (95% confidence interval, 4.6\u20138.3; P\u2009&amp;lt;\u20090.001). Compared with reference participants, the VO group had significantly lower baseline pre- and post-bronchodilator (BD) FEV1, and greater decline over time in post-BD FEV1, and pre- and post-BD FVC. There were no significant differences in exacerbations between groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Significant risk for future COPD development exists for those with pre- but not post-BD airflow obstruction. These findings support consideration of expanding spirometric criteria defining COPD to include pre-BD obstruction.<\/jats:p>\n                    <jats:p>Clinical trial registered with www.clinicaltrials.gov (NCT 01969344).<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202201-0094oc","type":"journal-article","created":{"date-parts":[[2022,5,12]],"date-time":"2022-05-12T13:15:32Z","timestamp":1652361332000},"page":"554-562","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":43,"title":["Reversible Airflow Obstruction Predicts Future Chronic Obstructive Pulmonary Disease Development in the SPIROMICS Cohort: An Observational Cohort Study"],"prefix":"10.1093","volume":"206","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6159-7435","authenticated-orcid":false,"given":"Russell G.","family":"Buhr","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, and"},{"name":"Center for the Study of Healthcare Innovation, Implementation, and Policy, Health Services Research and Development, Greater Los Angeles Veterans Affairs Healthcare System, Los Angeles, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8096-0858","authenticated-orcid":false,"given":"Igor Z.","family":"Barjaktarevic","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, and"}]},{"given":"P. Miguel","family":"Quibrera","sequence":"additional","affiliation":[{"name":"Collaborative Studies Coordinating Center, Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina"}]},{"given":"Lori A.","family":"Bateman","sequence":"additional","affiliation":[{"name":"Collaborative Studies Coordinating Center, Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4767-3494","authenticated-orcid":false,"given":"Eugene R.","family":"Bleecker","sequence":"additional","affiliation":[{"name":"Division of Genetics, Genomics, and Precision Medicine, University of Arizona, Tucson, Arizona"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4313-9235","authenticated-orcid":false,"given":"David J.","family":"Couper","sequence":"additional","affiliation":[{"name":"Collaborative Studies Coordinating Center, Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5191-4847","authenticated-orcid":false,"given":"Jeffrey L.","family":"Curtis","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan"},{"name":"Medical Service, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Michigan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0405-608X","authenticated-orcid":false,"given":"Brett A.","family":"Dolezal","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9095-4419","authenticated-orcid":false,"given":"MeiLan K.","family":"Han","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8740-9751","authenticated-orcid":false,"given":"Nadia N.","family":"Hansel","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5525-4778","authenticated-orcid":false,"given":"Jerry A.","family":"Krishnan","sequence":"additional","affiliation":[{"name":"Breathe Chicago Center, Division of Pulmonary and Critical Care Medicine, University of Illinois at Chicago College of Medicine, Chicago, Illinois"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2412-3182","authenticated-orcid":false,"given":"Fernando J.","family":"Martinez","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3184-9256","authenticated-orcid":false,"given":"William","family":"McKleroy","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4511-4437","authenticated-orcid":false,"suffix":"III","given":"Robert","family":"Paine","sequence":"additional","affiliation":[{"name":"Division of Respiratory, Critical Care, and Occupational Medicine, University of Utah School of Medicine, Salt Lake City, Utah"},{"name":"Veterans Affairs Salt Lake City Healthcare System, Salt Lake City, Utah; and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7909-0253","authenticated-orcid":false,"given":"Stephen I.","family":"Rennard","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5607-4872","authenticated-orcid":false,"given":"Donald P.","family":"Tashkin","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3176-0603","authenticated-orcid":false,"given":"Prescott G.","family":"Woodruff","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6915-599X","authenticated-orcid":false,"given":"Richard E.","family":"Kanner","sequence":"additional","affiliation":[{"name":"Division of Respiratory, Critical Care, and Occupational Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6314-0903","authenticated-orcid":false,"given":"Christopher B.","family":"Cooper","sequence":"additional","affiliation":[{"name":"Division of 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unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used data from participants in the Multi-Ethnic Study of Atherosclerosis with high-attenuation areas (HAAs, Examinations 1\u20136 (2000\u20132018)) and<jats:italic>MUC5B<\/jats:italic>genotype (n=4552) and telomere length (n=4488) assessments. HAA was defined as the per cent of imaged lung with attenuation of \u2212600 to \u2212250 Hounsfield units. We used linear mixed-effects models to examine associations of<jats:italic>MUC5B<\/jats:italic>risk allele (T) and telomere length with longitudinal changes in HAAs. Joint models were used to examine associations of longitudinal changes in HAAs with death and interstitial lung disease (ILD).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The<jats:italic>MUC5B<\/jats:italic>risk allele (T) was associated with an absolute change in HAAs of 2.60% (95% CI 0.36% to 4.86%) per 10 years overall. This association was stronger among those with a telomere length below an age-adjusted percentile of 5% (p value for interaction=0.008). A 1% increase in HAAs per year was associated with 7% increase in mortality risk (rate ratio (RR)=1.07, 95%\u2009CI 1.02 to 1.12) for overall death and 34% increase in ILD (RR=1.34, 95%\u2009CI 1.20 to 1.50). Longer baseline telomere length was cross-sectionally associated with less HAAs from baseline scans, but not with longitudinal changes in HAAs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Longitudinal increases in HAAs were associated with the<jats:italic>MUC5B<\/jats:italic>risk allele and a higher risk of death and ILD.<\/jats:p><\/jats:sec>","DOI":"10.1136\/thorax-2021-218139","type":"journal-article","created":{"date-parts":[[2022,8,25]],"date-time":"2022-08-25T15:30:24Z","timestamp":1661441424000},"page":"566-573","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["<i>MUC5B<\/i>, telomere length and longitudinal quantitative interstitial lung changes: the MESA Lung Study"],"prefix":"10.1136","volume":"78","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8887-150X","authenticated-orcid":false,"given":"John 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PA has been shown to substantially reduce cardiovascular and cardiometabolic risk through mechanisms such as favorable cardiac remodeling, improved endothelial function, and enhanced metabolic regulation. This review explores the broad cardiovascular benefits of PA across both general and diabetic populations, highlighting its impact on reducing disease incidence, improving cardiac function, and lowering cardiovascular mortality. Various forms of PA\u2014including aerobic, resistance, and flexibility and balance training\u2014demonstrate differing but complementary roles in promoting cardiovascular health. Despite strong evidence and guideline endorsements, participation rates remain low, with fewer than a quarter of US adults meeting the minimum PA recommendations. Barriers to PA\u2014personal, environmental, and health\u2010related\u2014remain significant and underaddressed. Enhanced patient education, clinician engagement, and tailored intervention strategies are essential to improve adherence and outcomes. Overall, PA is a critical, evidence\u2010based strategy for reducing CVD risk.<\/jats:p>","DOI":"10.1155\/jdr\/3341765","type":"journal-article","created":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T13:30:43Z","timestamp":1774963843000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Physical Activity and Cardiovascular Health"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0282-4850","authenticated-orcid":false,"given":"Alexander","family":"Polyak","sequence":"first","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0009-0005-0736-7686","authenticated-orcid":false,"given":"Alexander","family":"Lee","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0735-9756","authenticated-orcid":false,"given":"Martha","family":"Gulati","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2026,3,31]]},"reference":[{"key":"e_1_2_11_1_2","unstructured":"Cardiovascular Diseases (CVDs) published July 31 2025 https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/cardiovascular-diseases-(cvds)."},{"key":"e_1_2_11_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.115.002495"},{"key":"e_1_2_11_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.115.002014"},{"key":"e_1_2_11_4_2","doi-asserted-by":"publisher","DOI":"10.15167\/2421-4248\/jpmh2022.63.2S3.2756"},{"key":"e_1_2_11_5_2","doi-asserted-by":"publisher","DOI":"10.2337\/dc16-1728"},{"key":"e_1_2_11_6_2","volume-title":"StatPearls","author":"Patel R.","year":"2024"},{"key":"e_1_2_11_7_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12933-018-0728-6"},{"key":"e_1_2_11_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/s40273-015-0268-9"},{"key":"e_1_2_11_9_2","doi-asserted-by":"publisher","DOI":"10.2337\/dc17-1962"},{"key":"e_1_2_11_10_2","first-page":"1","article-title":"Physical Activity Among Adults Aged 18 and Over: United States, 2020","volume":"443","author":"Elgaddal N.","year":"2022","journal-title":"NCHS Data Brief"},{"key":"e_1_2_11_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.109.192703"},{"key":"e_1_2_11_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000001078"},{"key":"e_1_2_11_13_2","doi-asserted-by":"publisher","DOI":"10.1136\/bjsports-2014-306596rep"},{"key":"e_1_2_11_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2017.04.025"},{"key":"e_1_2_11_15_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00130.2018"},{"key":"e_1_2_11_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000559"},{"key":"e_1_2_11_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2021.11.002"},{"key":"e_1_2_11_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacl.2014.10.002"},{"key":"e_1_2_11_19_2","doi-asserted-by":"publisher","DOI":"10.1249\/MSS.0000000000002800"},{"key":"e_1_2_11_20_2","doi-asserted-by":"publisher","DOI":"10.2337\/dc19-0538"},{"key":"e_1_2_11_21_2","doi-asserted-by":"publisher","DOI":"10.2337\/db16-1327"},{"key":"e_1_2_11_22_2","doi-asserted-by":"publisher","DOI":"10.1080\/14779072.2024.2328644"},{"key":"e_1_2_11_23_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000312"},{"key":"e_1_2_11_24_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000001168"},{"key":"e_1_2_11_25_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000678"},{"key":"e_1_2_11_26_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000001062"},{"key":"e_1_2_11_27_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYP.0000000000000066"},{"key":"e_1_2_11_28_2","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2012-303461"},{"key":"e_1_2_11_29_2","first-page":"126","article-title":"Physical Activity, Exercise, and Physical Fitness: Definitions and Distinctions for Health-Related Research","volume":"100","author":"Caspersen C. 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Healthy Living 2019 https:\/\/www.cardiosmart.org\/topics\/healthy-living\/move-more."},{"key":"e_1_2_11_73_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12966-017-0509-8"},{"key":"e_1_2_11_74_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12889-024-20134-3"},{"key":"e_1_2_11_75_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijerph182010659"},{"key":"e_1_2_11_76_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12875-022-01866-w"},{"key":"e_1_2_11_77_2","doi-asserted-by":"publisher","DOI":"10.1080\/09638288.2020.1844315"},{"key":"e_1_2_11_78_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10067-023-06518-7"},{"key":"e_1_2_11_79_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.apmr.2014.09.013"},{"key":"e_1_2_11_80_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0239244"}],"container-title":["Journal of Diabetes 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Stroke","doi-asserted-by":"publisher","award":["R01AG023629"],"award-info":[{"award-number":["R01AG023629"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2019,9,24]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>High-sensitivity cardiac troponin T (hs-cTnT) is individually associated with incident hypertension (HTN) and cardiovascular disease (CVD) events. We hypothesize that the increases in hs-cTnT with increases in blood pressure will be related to higher incidence of CVD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>The Cardiovascular Health Study is a longitudinal cohort of older adults. Those with hs-cTnT data and CVD risk factors at baseline and follow-up (2\u20133 years later) were stratified based on systolic blood pressure (SBP; optimal: &amp;lt;120 mm Hg, intermediate: 120\u2013139 mm Hg, elevated: \u2265140 mm Hg) and hs-cTnT (undetectable: &amp;lt;5 ng\/l, detectable: 5\u201313 ng\/l, elevated: \u226514 ng\/l) categories. SBP and hs-cTnT were classified as increased or decreased if they changed categories between exams, and stable if they did not. Cox regression evaluated incident CVD events over an average 9-year follow-up.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>Among 2,219 adults, 510 (23.0 %) had decreased hs-cTnT, 1,279 (57.6 %) had stable hs-cTnT, and 430 (19.4 %) had increased hs-cTnT. Those with increased hs-cTnT had a higher CVD risk with stable SBP (hazard ratio [HR]: 1.28 [1.04\u20131.57], P = 0.02) or decreased SBP (HR: 1.57 [1.08\u20132.28], P = 0.02) compared to those within the same SBP group but a stable hs-cTnT. In those with lower SBP at follow-up, there was an inverse relation between diastolic blood pressure (DBP) and risk of CVD events in those with increased hs-cTnT (HR: 0.44 per 10 mm Hg increase, P &amp;lt; 0.01).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSION<\/jats:title>\n                  <jats:p>An increase in hs-cTnT over time is associated with a higher risk of CVD even when the blood pressure is stable or decreases over time.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ajh\/hpz102","type":"journal-article","created":{"date-parts":[[2019,6,20]],"date-time":"2019-06-20T03:13:27Z","timestamp":1561000407000},"page":"1013-1020","source":"Crossref","is-referenced-by-count":13,"title":["Trends in Blood Pressure and High-Sensitivity Cardiac Troponin-T With Cardiovascular Disease: The Cardiovascular Health Study"],"prefix":"10.1093","volume":"32","author":[{"given":"David 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Our understanding of the pathophysiology of RV dysfunction is limited but improving. Methods to better diagnose RV dysfunction earlier and treatments specifically designed to minimize or reverse the remodeling process are likely to improve outcomes. We review the current understanding of RV dysfunction in chronic pressure overload and introduce some novel insights based on recent investigations into pathophysiology, diagnosis, and treatment.<\/jats:p>","DOI":"10.4061\/2011\/568095","type":"journal-article","created":{"date-parts":[[2011,3,23]],"date-time":"2011-03-23T13:31:40Z","timestamp":1300887100000},"page":"1-7","source":"Crossref","is-referenced-by-count":43,"title":["Right Ventricular Dysfunction and Failure in Chronic Pressure Overload"],"prefix":"10.1155","volume":"2011","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3080-3675","authenticated-orcid":true,"given":"Marc A.","family":"Simon","sequence":"first","affiliation":[{"name":"Cardiovascular Institute, University of Pittsburgh, Scaife Hall S-554, 200 Lothrop Street, Pittsburgh, PA 15213, USA"},{"name":"Department of Critical Care Medicine, University of Pittsburgh, Scaife Hall S-554, 200 Lothrop Street, Pittsburgh, PA 15213, USA"}]},{"given":"Michael 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<jats:p>Acute exacerbations of chronic obstructive pulmonary disease (AE-COPDs) are associated with a significant disease burden. Blood immune phenotyping may improve our understanding of a COPD endotype at increased risk of exacerbations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To determine the relationship between the transcriptome of circulating leukocytes and COPD exacerbations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Blood RNA sequencing data (n\u2009=\u20093,618) from the COPDGene (Genetic Epidemiology of COPD) study were analyzed. Blood microarray data (n\u2009=\u2009646) from the ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) study were used for validation. We tested the association between blood gene expression and AE-COPDs. We imputed the abundance of leukocyte subtypes and tested their association with prospective AE-COPDs. Flow cytometry was performed on blood in SPIROMICS (Subpopulations and Intermediate Outcomes in COPD Study) (n\u2009=\u2009127), and activation markers for T cells were tested for association with prospective AE-COPDs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Exacerbations were reported 4,030 and 2,368 times during follow-up in COPDGene (5.3\u2009\u00b1\u20091.7\u2009yr) and ECLIPSE (3\u2009yr), respectively. We identified 890, 675, and 3,217 genes associated with a history of AE-COPDs, persistent exacerbations (at least one exacerbation per year), and prospective exacerbation rate, respectively. In COPDGene, the number of prospective exacerbations in patients with COPD (Global Initiative for Chronic Obstructive Lung Disease stage \u22652) was negatively associated with circulating CD8+ T cells, CD4+ T cells, and resting natural killer cells. The negative association with naive CD4+ T cells was replicated in ECLIPSE. In the flow-cytometry study, an increase in CTLA4 on CD4+ T cells was positively associated with AE-COPDs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Individuals with COPD with lower circulating lymphocyte counts, particularly decreased CD4+ T cells, are more susceptible to AE-COPDs, including persistent exacerbations.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202301-0085oc","type":"journal-article","created":{"date-parts":[[2023,6,7]],"date-time":"2023-06-07T20:56:45Z","timestamp":1686171405000},"page":"247-255","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":23,"title":["Blood Gene Expression and Immune Cell Subtypes Associated with Chronic Obstructive Pulmonary Disease Exacerbations"],"prefix":"10.1093","volume":"208","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3071-7363","authenticated-orcid":false,"given":"Min Hyung","family":"Ryu","sequence":"first","affiliation":[{"name":"Channing Division of Network Medicine and"},{"name":"Department of Medicine, Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4361-8295","authenticated-orcid":false,"given":"Jeong H.","family":"Yun","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"},{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women\u2019s Hospital, Boston, Massachusetts"},{"name":"Department of Medicine, Harvard Medical School, Boston, Massachusetts"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5670-5865","authenticated-orcid":false,"given":"Jarrett D.","family":"Morrow","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"},{"name":"Department of Medicine, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Aabida","family":"Saferali","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"},{"name":"Department of Medicine, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Peter","family":"Castaldi","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"},{"name":"Department of Medicine, Harvard Medical School, Boston, Massachusetts"}]},{"given":"Robert","family":"Chase","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"}]},{"given":"Meryl","family":"Stav","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"}]},{"given":"Zhonghui","family":"Xu","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine and"}]},{"given":"Igor","family":"Barjaktarevic","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California"}]},{"given":"MeiLan","family":"Han","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"}]},{"given":"Wassim","family":"Labaki","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7497-6597","authenticated-orcid":false,"given":"Yvonne J.","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"},{"name":"Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan"}]},{"given":"Stephanie","family":"Christenson","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, California"}]},{"given":"Wanda","family":"O\u2019Neal","sequence":"additional","affiliation":[{"name":"Marsico Lung Institute, School of Medicine, University of North Carolina, Chapel Hill, North Carolina"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4651-363X","authenticated-orcid":false,"given":"Russell","family":"Bowler","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, National Jewish Health, Denver, Colorado"}]},{"given":"Don D.","family":"Sin","sequence":"additional","affiliation":[{"name":"Centre for Heart and Lung Innovation, St. Paul\u2019s Hospital, Vancouver, British Columbia, Canada"},{"name":"Division of Respiratory Medicine, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; 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Understanding the basis for heterogeneity has led to major advances in therapy for many cancers and pulmonary diseases such as cystic fibrosis and asthma. Although heterogeneity of risk factors, disease severity, and outcomes in survivors are common features of the acute respiratory distress syndrome (ARDS), many challenges exist in understanding the clinical and molecular basis for disease heterogeneity and using heterogeneity to tailor therapy for individual patients. This report summarizes the proceedings of the 2021 Aspen Lung Conference, which was organized to review key issues related to understanding clinical and molecular heterogeneity in ARDS. The goals were to review new information about ARDS phenotypes, to explore multicellular and multisystem mechanisms responsible for heterogeneity, and to review how best to account for clinical and molecular heterogeneity in clinical trial design and assessment of outcomes. 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Obesity is the major cause of concern  that creates of these problems within the body. Pills and medicines are  there to counter the issues of blood sugar and diabetes but still people  are not getting the good results. The treatment of diabetes &amp; blood  sugar can easily rip one\u2019s bank account.  Guardian Blood balance Australia  is here to help all those individuals who are looking for a healthy  lifestyle. This is a blood boost formula that counters all the problems  that are related to blood. It is an amazing solution that provides a  wide range of benefits to the human body and allows the person to  counter the problems with ease. We will discuss all the information  about guardian Blood balance Australia in this article. You can read all  the information in this page to know more about it.  Visit the Official Website:- Click Here..!!  To Learn More: Go To the Official Website Guardian Blood Balance (AUSTRALIA) !!!       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Customers Point of View  It is good for you to know about the reviews from the old customers.  This will help you out in dealing with all the questions with ease. You  can check some of the reviews of our customers in this page as well.  Have a look on them for once only to know more about it.  Willy Jackson: \u2013 guardian blood balance is the  best solution for me to counter my diabetes. I am a true fan of this  product after consuming it for several weeks. It just improved my  positive wellness and helped me out in generating positive results in  life. I am really thankful to guardian\u2019s blood balance for giving the  hope of a healthy lifestyle.  Daren martin: \u2013 I would love to suggest this blood  sugar solution to all those individuals who are willing to counter all  these issues and problems. This is the best solution that I tried till  now. There are no more issues left behind in my body as my blood  circulation has been improved. I am literally thankful to this solution  for giving me the positive benefits.   {DON\u2019T WASTE TIME} Grab The Best Deal Of Guardian Blood Balance Till Date!!!  Describe The Money Refund Policy of Guardian Blood Balance Australia  This supplement comes under the 30 days money refund policy. One can  easily ask for a refund by clicking on any of the information portals of  the company. If you didn\u2019t find the supplement effective then you can  easily ask for your money back. Do tap on any of the links in order to  place the order for yourself.  You just need to place the order from the online market so that all  your problems and issues will be easily sorted out for sure. The refund  policy will not only help you out in making the purchase but also allow  you to get it to deliver to the doorstep. Feel free to click on the link  today in order to achieve healthy results. 3 1 Is It Safe to Use Guardian Blood Balance Australia?  Yes, it is totally safe to consume the supplement accordingly. One  just needs to consume the supplement on regular basis in order to gain  the positive results. If you face any kind of trouble or hindrance while  consuming this solution then you can immediately stop the consumption  as well.  We will advise you to make the purchase from the online market only.  If you will place the order from any of the offline market then you  might get some copied product to your door. So, it would be good for you  if you make the purchase from the guardian blood balance Australia.  Final Words on Guardian Blood Balance Australia  This is an amazing blood boost formula with potent weight loss  benefits as well. It is a reliable solution that counters various issues  in the human body. Guardian blood balance Australia helps the person to  recover from all kinds of diabetes issues and blood-related problems  with ease. Any single person can try out this supplement to counter the  problems from the root.  If you want to develop good health results then guardian blood boost  formula is here for you. The herbal and powerful ingredients of this  supplement will easily deliver various positive outcomes in your body  tone. It will amaze your life in no time and allow you to counter the  problems from the root with ease.  Lastly, it is your choice whether you want to reduce your health  issues or not. If you are looking for some private treatment then the  choice is totally yours. Feel free to place the order today to enable  good health results. Enjoy the positive working of this blood boost  formula if you don\u2019t want to rip your bank account.   <\/p>","DOI":"10.17504\/protocols.io.b6djra4n","type":"posted-content","created":{"date-parts":[[2022,5,13]],"date-time":"2022-05-13T13:52:35Z","timestamp":1652449955000},"source":"Crossref","is-referenced-by-count":0,"title":["[RETRACTED] Guardian Blood Balance Australia- Reviews - Guardian Botanicals Blood Balance [AU] SCAM ALERT! Read Real Critical Reports.. 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We hypothesize that outcomes following continuous-flow LVAD (CF-LVAD) implantation in those with anthracycline-induced cardiomyopathy are comparable with other aetiologies of cardiomyopathy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Using the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) from 2008 to 2017, we identified patients with anthracycline-induced cardiomyopathy who received a CF-LVAD and compared them with those with idiopathic dilated (IDM) and ischaemic cardiomyopathies (ICM). Mortality was studied using the Cox proportional hazards model. Other adverse events were evaluated using competing risk models. Overall, 248 anthracycline-induced cardiomyopathy patients underwent CF-LVAD implantation, with a median survival of 48 months, an improvement compared with those before 2012 [adjusted hazards ratio (aHR): 0.53; confidence interval (CI): 0.33\u20130.86]. At 12 months, 85.1% of anthracycline-induced cardiomyopathy, 86.0% of IDM, and 80.2% of ICM patients were alive (anthracycline-induced cardiomyopathy vs. IDM: aHR: 1.12; CI: 0.88\u20131.43 and anthracycline-induced cardiomyopathy vs. ICM: aHR: 0.98; CI: 0.76\u20131.28). Anthracycline-induced cardiomyopathy patients had a higher major bleeding risk compared with IDM patients (aHR: 1.23; CI: 1.01\u20131.50), and a lower risk of stroke and prolonged respiratory support compared to ICM patients (aHR: 0.31 and 0.67 respectively; both P &amp;lt; 0.05). There was no difference in the risk of major infection, acute kidney injury, and venous thromboembolism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>After receiving a CF-LVAD, survival in patients with anthracycline-induced cardiomyopathy is similar to those with ICM or IDM. Further research into differential secondary endpoints-related disparities is warranted.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ehf2.13362","type":"journal-article","created":{"date-parts":[[2021,5,13]],"date-time":"2021-05-13T06:40:31Z","timestamp":1620888031000},"page":"2866-2875","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Outcomes in Patients with Anthracycline-Induced Cardiomyopathy Undergoing Left Ventricular Assist Devices Implantation"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0253-1174","authenticated-orcid":false,"given":"Avirup","family":"Guha","sequence":"first","affiliation":[{"name":"Harrington Heart and Vascular Institute, Case Western Reserve University , Cleveland, OH ,","place":["USA"]},{"name":"Cardio-Oncology Program, Division of Cardiology, The Ohio State University Medical Center , Columbus, OH ,","place":["USA"]}]},{"given":"Cesar","family":"Caraballo","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]},{"name":"Center for Outcomes Research and Evaluation , New Haven, CT ,","place":["USA"]}]},{"given":"Prantesh","family":"Jain","sequence":"additional","affiliation":[{"name":"Division of Hematology and Medical Oncology, University Hospitals Cleveland Medical Center, Seidman Cancer Center at Case Comprehensive Cancer Center, Case Western Reserve University , Cleveland, OH ,","place":["USA"]}]},{"given":"P. Elliott","family":"Miller","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]},{"name":"Yale National Clinician Scholars Program , New Haven, CT ,","place":["USA"]}]},{"given":"Jocelyn","family":"Owusu-Guha","sequence":"additional","affiliation":[{"name":"Pharmacy Department, OhioHealth Riverside Methodist Hospital , Columbus, OH ,","place":["USA"]}]},{"given":"Katherine A.A.","family":"Clark","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]}]},{"given":"Eric J.","family":"Velazquez","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]}]},{"given":"Tariq","family":"Ahmad","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]},{"name":"Center for Outcomes Research and Evaluation , New Haven, CT ,","place":["USA"]}]},{"given":"Lauren A.","family":"Baldassarre","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]}]},{"given":"Daniel","family":"Addison","sequence":"additional","affiliation":[{"name":"Cardio-Oncology Program, Division of Cardiology, The Ohio State University Medical Center , Columbus, OH ,","place":["USA"]},{"name":"Cancer Control Program, Department of Medicine, Ohio State University Comprehensive Cancer Center , Columbus, OH ,","place":["USA"]}]},{"given":"Neal L.","family":"Weintraub","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology, and Vascular Biology Center, Medical College of Georgia at Augusta University , Augusta, GA ,","place":["USA"]}]},{"given":"Nihar R.","family":"Desai","sequence":"additional","affiliation":[{"name":"Section of Cardiovascular Medicine, Yale School of Medicine , New Haven, CT ,","place":["USA"]},{"name":"Center for Outcomes Research and Evaluation , New Haven, CT ,","place":["USA"]}]}],"member":"286","published-online":{"date-parts":[[2021,5,13]]},"reference":[{"key":"2026012114205636500_ehf213362-bib-0001","doi-asserted-by":"crossref","first-page":"278","DOI":"10.1056\/NEJM197902083000603","article-title":"Serial assessment of doxorubicin cardiotoxicity with quantitative radionuclide angiocardiography","volume":"300","author":"Alexander","year":"1979","journal-title":"N Engl J Med"},{"key":"2026012114205636500_ehf213362-bib-0002","doi-asserted-by":"crossref","first-page":"2231","DOI":"10.1016\/j.jacc.2009.02.050","article-title":"Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management","volume":"53","author":"Yeh","year":"2009","journal-title":"J Am Coll Cardiol"},{"key":"2026012114205636500_ehf213362-bib-0003","doi-asserted-by":"crossref","first-page":"1077","DOI":"10.1056\/NEJM200004133421502","article-title":"Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy","volume":"342","author":"Felker","year":"2000","journal-title":"N Engl J Med"},{"key":"2026012114205636500_ehf213362-bib-0004","doi-asserted-by":"crossref","first-page":"898","DOI":"10.1002\/ejhf.1049","article-title":"Comparison of long-term outcome in anthracycline-related versus idiopathic dilated cardiomyopathy: a single centre experience","volume":"20","author":"Fornaro","year":"2018","journal-title":"Eur J Heart Fail"},{"key":"2026012114205636500_ehf213362-bib-0005","doi-asserted-by":"crossref","first-page":"776","DOI":"10.1016\/j.jacc.2017.04.025","article-title":"2017 ACC\/AHA\/HFSA Focused Update of the 2013 ACCF\/AHA Guideline for the Management of Heart Failure. 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We tested the hypothesis that higher circulating brain injury markers were associated with increased risk of hip fracture and fall hospitalizations. Brain injury markers were measured in 2141 participants (mean age 77.9\u00a0yr; 60% women). Brain injury markers included neurofilament light chain (NfL), a marker of axonal injury; glial fibrillary acidic protein (GFAP), a marker of astrocytic injury; total Tau, whose many functions include neuron microtubule stabilization; and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), a major protein of neurons. Incident hip fractures and hospitalizations for falls were identified through participant report and confirmed with medical records or medicare claims. Hazard ratios were computed for a doubling exposure (log2 transformed brain injury marker) using multivariable-adjusted Cox models. After a median follow-up of 11\u00a0yr, 304 incident hip fractures and 284 incident fall hospitalizations occurred. Doubling of GFAP and NfL were associated with a 22% (p\u2009=\u2009.048) and 42% (p\u2009&amp;lt;\u2009.001) higher risk of hip fracture, respectively. Additional adjustment for cognitive function, gait speed, grip strength, inflammatory markers, and depressive symptoms had no effect on results. Models that adjusted for all 4 brain markers showed that only NfL was independent of the other markers. Neurofilament light chain was also associated with a 47% increase risk of hospitalization for falls. There was no association of total Tau or UCH-L1 with hip fracture or falls. GFAP was also unrelated to fall hospitalizations. Neurofilament light chain was independently associated with an incident risk of hip fracture and fall hospitalizations. These results suggest that subclinical degrees of brain injury may contribute to falls and hip fracture. Future research is needed to test whether the association between NfL and hip fracture is independent of falls.<\/jats:p>","DOI":"10.1093\/jbmr\/zjaf155","type":"journal-article","created":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T12:04:28Z","timestamp":1761307468000},"page":"38-45","source":"Crossref","is-referenced-by-count":0,"title":["Circulating neurodegenerative brain injury markers and hip fracture and fall hospitalizations: the Cardiovascular Health Study"],"prefix":"10.1093","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0752-4408","authenticated-orcid":false,"given":"Jane A","family":"Cauley","sequence":"first","affiliation":[{"name":"Department of Epidemiology, School of Public Health, University of Pittsburgh , Pittsburgh, PA 15261 ,","place":["United States"]}]},{"given":"Petra","family":"Buzkova","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington , Seattle, WA 98195 ,","place":["United 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L","family":"Lopez","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Pittsburgh , Pittsburgh, PA 15261 ,","place":["United States"]}]},{"given":"Lauren","family":"Carlson","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, School of Public Health, University of Pittsburgh , Pittsburgh, PA 15261 ,","place":["United States"]}]},{"given":"John A","family":"Robbins","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California , Davis, CA 94143 ,","place":["United States"]}]},{"given":"Luc","family":"Djousse","sequence":"additional","affiliation":[{"name":"Division of Aging, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School , Boston, MA 02115 ,","place":["United States"]}]},{"given":"Kenneth J","family":"Mukamal","sequence":"additional","affiliation":[{"name":"Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA 02115 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This study was undertaken to investigate the risk of ischemic stroke associated with occlusive and nonocclusive carotid atherosclerotic\u00a0disease in patients with AF in the prospective population\u2010based Cardiovascular Health Study.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We included participants aged \u226565\u2009years with AF. We used multivariable Cox regression analysis to explore the risk of ischemic stroke associated with the percentage of carotid stenosis, plaque irregularity, echogenicity, and vulnerability (markedly irregular, ulcerated, or hypoechoic plaques).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A total of 1398 participants were included (55.2% female, 61.7% aged 65\u201374\u2009years). The maximum carotid stenosis was &lt;50%, 50%\u201399%, and 100% in 94.5%, 5%, and 0.5% of participants, respectively. High\u2010risk plaques based on echogenicity and plaque irregularity were found in 25.6% and 8.9% of participants, respectively. After a median follow\u2010up of 10.9\u2009years (interquartile range\u2009=\u20097.5\u201315.6), 298 ischemic strokes were recorded. There was no difference in the incidence of ischemic stroke according to the degree of carotid artery stenosis (<jats:italic>p<\/jats:italic>\u2009=\u20090.44), plaque echogenicity (low vs. high risk, <jats:italic>p<\/jats:italic>\u2009=\u20090.68), plaque irregularity (low vs. high risk, <jats:italic>p<\/jats:italic>\u2009=\u20090.55), and plaque vulnerability (<jats:italic>p<\/jats:italic>\u2009=\u20090.86). The CHA\u2082DS\u2082\u2010VASc score was associated with an increased risk of ischemic stroke (adjusted hazard ratio\u2009=\u20091.28, 95% confidence interval\u2009=\u20091.18\u20131.40, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). Both maximum grade of stenosis and plaque vulnerability were not associated with incident ischemic stroke (all <jats:italic>p<\/jats:italic>\u2009&gt;\u20090.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Neither the degree of carotid stenosis nor the presence of vulnerable plaques was associated with incident ischemic stroke in this cohort\u00a0of individuals with AF. This suggests that carotid disease was probably not a significant contributor to ischemic stroke in this population.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ene.15817","type":"journal-article","created":{"date-parts":[[2023,4,11]],"date-time":"2023-04-11T05:17:35Z","timestamp":1681190255000},"page":"2042-2050","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["High\u2010risk carotid plaques and incident ischemic stroke in patients with atrial fibrillation in the Cardiovascular Health Study"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7722-9757","authenticated-orcid":false,"given":"Jean Jacques","family":"Noubiap","sequence":"first","affiliation":[{"name":"Centre for Heart Rhythm Disorders University of Adelaide  Adelaide South Australia Australia"},{"name":"Division of Cardiology, Department of Medicine University of California\u2010San Francisco  San Francisco California 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HL159246"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart Lung and Blood Institute","doi-asserted-by":"publisher","award":["R35HL1358181"],"award-info":[{"award-number":["R35HL1358181"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart Lung and Blood Institute","doi-asserted-by":"publisher","award":["R01AG070867"],"award-info":[{"award-number":["R01AG070867"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Cardiovascular Health Across Ethnic Groups","award":["R01HL098433"],"award-info":[{"award-number":["R01HL098433"]}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1TR000040"],"award-info":[{"award-number":["UL1TR000040"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1TR001079"],"award-info":[{"award-number":["UL1TR001079"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1TR001420"],"award-info":[{"award-number":["UL1TR001420"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2023,9,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Study Objectives<\/jats:title>\n                  <jats:p>Multiple sleep characteristics are informative of health, sleep characteristics cluster, and sleep health can be described as a composite of positive sleep attributes. We assessed the association between a sleep score reflecting multiple sleep dimensions, and mortality. We tested the hypothesis that more favorable sleep (higher sleep scores) is associated with lower mortality.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>The Multi-Ethnic Study of Atherosclerosis (MESA) is a racially and ethnically-diverse multi-site, prospective cohort study of US adults. Sleep was measured using unattended polysomnography, 7-day wrist actigraphy, and validated questionnaires (2010\u20132013). 1726 participants were followed for a median of 6.9 years (Q1\u2013Q3, 6.4\u20137.4 years) until death (171 deaths) or last contact. Survival models were used to estimate the association between the exposure of sleep scores and the outcome of all-cause mortality, adjusting for socio-demographics, lifestyle, and medical comorbidities; follow-up analyses examined associations between individual metrics and mortality. The exposure, a sleep score, was constructed by an empirically-based Principal Components Analysis on 13 sleep metrics, selected a priori.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>After adjusting for multiple confounders, a 1 standard deviation (sd) higher sleep score was associated with 25% lower hazard of mortality (Hazard Ratio [HR]: 0.75; 95% Confidence interval: [0.65, 0.87]). The largest drivers of this association were: night-to-night sleep regularity, total sleep time, and the Apnea-Hypopnea Index.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>More favorable sleep across multiple characteristics, operationalized by a sleep score, is associated with lower risk of death in a diverse US cohort of adults. Results suggest that interventions that address multiple dimensions may provide novel approaches for improving health.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/sleep\/zsad048","type":"journal-article","created":{"date-parts":[[2023,7,31]],"date-time":"2023-07-31T20:37:50Z","timestamp":1690835870000},"source":"Crossref","is-referenced-by-count":21,"title":["Multi-dimensional sleep and mortality: The Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"46","author":[{"given":"Joon","family":"Chung","sequence":"first","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital , Boston, MA , USA"},{"name":"Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3982-7940","authenticated-orcid":false,"given":"Matthew","family":"Goodman","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital , Boston, MA , USA"},{"name":"Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8420-9167","authenticated-orcid":false,"given":"Tianyi","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital , Boston, MA , USA"},{"name":"Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3951-890X","authenticated-orcid":false,"given":"Meredith L","family":"Wallace","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of Pittsburgh , Pittsburgh, PA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1572-1340","authenticated-orcid":false,"given":"Pamela L","family":"Lutsey","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, School of Public Health, the University of Minnesota , Minneapolis, MN , USA"}]},{"given":"Jarvis T","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health , Boston, MA , USA"}]},{"given":"Cecilia","family":"Castro-Diehl","sequence":"additional","affiliation":[{"name":"Harvard Medical School , Boston, MA , USA"}]},{"given":"Suzanne","family":"Bertisch","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital , Boston, MA , USA"},{"name":"Harvard Medical School , Boston, MA , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6585-1610","authenticated-orcid":false,"given":"Susan","family":"Redline","sequence":"additional","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Brigham and Women\u2019s Hospital , Boston, MA , USA"},{"name":"Harvard Medical School , Boston, MA , USA"}]}],"member":"286","published-online":{"date-parts":[[2023,7,31]]},"reference":[{"issue":"6","key":"2024022609021527100_CIT0001","doi-asserted-by":"crossref","first-page":"zsy047","DOI":"10.1093\/sleep\/zsy047","article-title":"Insomnia with objective short sleep duration and risk of incident cardiovascular disease and all-cause mortality: Sleep Heart Health Study","volume":"41","author":"Bertisch","year":"2018","journal-title":"Sleep."},{"issue":"5","key":"2024022609021527100_CIT0002","doi-asserted-by":"crossref","first-page":"585","DOI":"10.1093\/sleep\/33.5.585","article-title":"Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies","volume":"33","author":"Cappuccio","year":"2010","journal-title":"Sleep."},{"issue":"14","key":"2024022609021527100_CIT0003","doi-asserted-by":"crossref","first-page":"1149","DOI":"10.1093\/eurheartj\/ehy624","article-title":"The hypoxic burden of sleep apnoea predicts cardiovascular disease-related mortality: the Osteoporotic Fractures in Men Study and the Sleep Heart Health Study","volume":"40","author":"Azarbarzin","year":"2019","journal-title":"Eur Heart J."},{"issue":"1","key":"2024022609021527100_CIT0004","doi-asserted-by":"crossref","first-page":"63","DOI":"10.1097\/01.PSY.0000039756.23250.7C","article-title":"Healthy older adults\u2019 sleep predicts all-cause mortality at 4 to 19 years of follow-up","volume":"65","author":"Dew","year":"2003","journal-title":"Psychosom Med."},{"issue":"2","key":"2024022609021527100_CIT0005","doi-asserted-by":"crossref","first-page":"87","DOI":"10.2188\/jea.10.87","article-title":"Sleep patterns and total mortality: a 12-year follow-up study in Japan","volume":"10","author":"Kojima","year":"2000","journal-title":"J Epidemiol."},{"issue":"1","key":"2024022609021527100_CIT0006","doi-asserted-by":"crossref","first-page":"28","DOI":"10.1016\/j.sleep.2010.04.016","article-title":"Mortality related to actigraphic long and short sleep","volume":"12","author":"Kripke","year":"2011","journal-title":"Sleep Med."},{"issue":"3","key":"2024022609021527100_CIT0007","doi-asserted-by":"crossref","first-page":"207","DOI":"10.1046\/j.1365-2796.2002.00941.x","article-title":"Sleep complaints predict coronary artery disease mortality in males: a 12-year follow-up study of a middle-aged Swedish population","volume":"251","author":"Mallon","year":"2002","journal-title":"J Intern Med."},{"issue":"4","key":"2024022609021527100_CIT0008","doi-asserted-by":"crossref","first-page":"e91965","DOI":"10.1371\/journal.pone.0091965","article-title":"The joint effect of sleep duration and disturbed sleep on cause-specific mortality: results from the Whitehall II cohort study","volume":"9","author":"Rod","year":"2014","journal-title":"PLoS One."},{"issue":"3","key":"2024022609021527100_CIT0009","doi-asserted-by":"crossref","first-page":"300","DOI":"10.1093\/aje\/kwq371","article-title":"Sleep disturbances and cause-specific mortality: results from the GAZEL cohort study","volume":"173","author":"Rod","year":"2011","journal-title":"Am J Epidemiol."},{"issue":"6","key":"2024022609021527100_CIT0010","doi-asserted-by":"crossref","first-page":"e13386","DOI":"10.1111\/jsr.13386","article-title":"Physiological sleep measures predict time to 15-year mortality in community adults: application of a novel machine learning framework","volume":"30","author":"Wallace","year":"2021","journal-title":"J Sleep Res."},{"issue":"4","key":"2024022609021527100_CIT0011","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1093\/sleep\/zsac015","article-title":"Actigraphy-derived sleep health profiles and mortality in older men and women","volume":"45","author":"Wallace","year":"2022","journal-title":"Sleep."},{"issue":"1","key":"2024022609021527100_CIT0012","doi-asserted-by":"crossref","first-page":"zsx189","DOI":"10.1093\/sleep\/zsx189","article-title":"Which sleep health characteristics predict all-cause mortality in older men? 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 <jats:p>This study explores the association between psychosocial stressors and current e-cigarette use among adolescents in the United States.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used data from 12,767 participants in the 2019 National Youth Risk Behavioral Survey to examine the association between psychosocial stressors (bullying, sexual assault, safety-related absence from school, depressive symptoms, suicidal ideation, physical altercation, and weapon threats) and past-30-day e-cigarette use using multivariable-adjusted logistic regression models. We examined the association for each stressor and then as a burden score (0\u20137). To compare the strength of the association between stressors and current e-cigarette use to current combustible cigarette use, we additionally examined the association between each stressor and current combustible cigarette use.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Approximately 32.7% reported current e-cigarette use. The weighted prevalence of current e-cigarette use was higher among individuals who experienced stressors than those who did not. For example, bullying (43.9% vs. 29.0%). Similar prevalence patterns were seen among other stressors. Individuals who experienced stressors had significantly higher adjusted odds of current e-cigarette use than those who did not (OR [Odds Ratio] range: 1.47\u20131.75). Similarly, individuals with higher burden scores had a higher prevalence (zero [20.5%], one [32.8%], two [41.4%], three [49.6%], four to seven [60.9%]) and higher odds of current e-cigarette use (OR range: 1.43\u20132.73) than those with a score of zero. The strength of the association between the stressors and e-cigarette use was similar to that between the stressors and combustible cigarette use.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The study demonstrates a significant association between psychosocial stressors and adolescent e-cigarette use, highlighting the potential importance of interventions, such as targeted school-based programs that address stressors and promote stress management, as possible means of reducing adolescent e-cigarette use. Future research directions include exploring underlying mechanisms linking stressors to e-cigarette use and evaluating the effectiveness of interventions addressing stressors in reducing adolescent e-cigarette use.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12889-023-16031-w","type":"journal-article","created":{"date-parts":[[2023,6,6]],"date-time":"2023-06-06T02:02:10Z","timestamp":1686016930000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Psychosocial stressors and current e-cigarette use in the youth risk behavior survey"],"prefix":"10.1186","volume":"23","author":[{"given":"John","family":"Erhabor","sequence":"first","affiliation":[]},{"given":"Ellen","family":"Boakye","sequence":"additional","affiliation":[]},{"given":"Ngozi","family":"Osuji","sequence":"additional","affiliation":[]},{"given":"Olufunmilayo","family":"Obisesan","sequence":"additional","affiliation":[]},{"given":"Albert D.","family":"Osei","sequence":"additional","affiliation":[]},{"given":"Hassan","family":"Mirbolouk","sequence":"additional","affiliation":[]},{"given":"Andrew C.","family":"Stokes","sequence":"additional","affiliation":[]},{"given":"Omar","family":"Dzaye","sequence":"additional","affiliation":[]},{"given":"Omar","family":"El-Shahawy","sequence":"additional","affiliation":[]},{"given":"Carlos J.","family":"Rodriguez","sequence":"additional","affiliation":[]},{"given":"Glenn A.","family":"Hirsch","sequence":"additional","affiliation":[]},{"given":"Emelia J.","family":"Benjamin","sequence":"additional","affiliation":[]},{"given":"Andrew P.","family":"DeFilippis","sequence":"additional","affiliation":[]},{"given":"Rose Marie","family":"Robertson","sequence":"additional","affiliation":[]},{"given":"Aruni","family":"Bhatnagar","sequence":"additional","affiliation":[]},{"given":"Michael J.","family":"Blaha","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2023,6,6]]},"reference":[{"key":"16031_CR1","unstructured":"WHO global report on trends in prevalence of tobacco use, 2000\u20132025, fourth edition ISBN 978\u201392\u20134\u2013003932\u20132 (electronic version). 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We investigated the prognostic significance of 24\u2010hour cumulative postdiuretic urine sodium concentration in a multicenter clinical trial population.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The Renal Optimization Strategies Evaluation AHF (ROSE AHF) trial randomized 360 patients with AHF and renal dysfunction receiving intravenous diuretic to dopamine, nesiritide, or placebo. Sodium concentration was measured in cumulative urine sample collected during the first 24\u2009hours after randomization in 298 patients. Based on prior studies, lower <jats:italic>U<\/jats:italic><jats:sub>Na<\/jats:sub> was defined as \u226460\u2009mmol\/L.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Lower <jats:italic>U<\/jats:italic><jats:sub>Na<\/jats:sub> was present in 142 (48%) patients, who had longer LOS (7\u2009days vs 5\u2009days, <jats:italic>P<\/jats:italic>\u2009&lt;\u2009.001) and less 72\u2010hour weight loss (5.7 lb vs 9.0 lb, <jats:italic>P<\/jats:italic>\u2009&lt;\u2009.001). These associations persisted after controlling for baseline estimated glomerular filtration rate and outpatient furosemide dose. Lower <jats:italic>U<\/jats:italic><jats:sub>Na<\/jats:sub> did not modify the null effects of dopamine or nesiritide on clinical outcomes. Results were similar for spot rather than cumulative 24\u2010hour <jats:italic>U<\/jats:italic><jats:sub>Na<\/jats:sub> concentration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In patients hospitalized for AHF and renal dysfunction, <jats:italic>U<\/jats:italic><jats:sub>Na<\/jats:sub>\u2009\u2264\u200960\u2009mmol\/L during the first 24\u2009hours of diuresis identifies patients at risk for prolonged hospitalization but does not provide an indication for adjunctive dopamine or nesiritide.<\/jats:p><\/jats:sec>","DOI":"10.1002\/clc.23286","type":"journal-article","created":{"date-parts":[[2019,11,13]],"date-time":"2019-11-13T06:23:15Z","timestamp":1573626195000},"page":"43-49","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Lower urine sodium predicts longer length of stay in acute heart failure patients: Insights from the ROSE AHF 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This study aimed to examine the relationship between the supine sleep position and the frequency of angina pectoris (angina), a common symptom of ischemic heart disease, and to explore whether body mass index (BMI) or sex moderate this relationship.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Data from the Sleep Heart Health Study (SHHS) were used. Supine sleep position was quantified as the percentage of total sleep duration spent in the supine position, measured by unattended home polysomnography (PSG) during the first SHHS visit. Angina frequency was defined by the number of episodes over a 15-year follow-up period. Multiple Poisson regression was conducted, adjusting for various conventional cardiovascular disease (CVD) risk factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The study included 5,804 participants (52% female), with a mean age of 63 years and an average BMI of 28.16\u00a0kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      . The average time spent in the supine position was 32.4%, and the mean number of angina episodes was 0.48. Longer time in the supine sleep position was independently associated with an increased risk of angina (IRR\u2009=\u20091.003,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u2009.0001); a 10% increase in supine sleep time was associated with a 3% increase in angina risk. BMI (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.189) and sex (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.117) did not significantly moderate this association.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Sleeping in the supine position was significantly associated with more angina episodes. The study lacked information on other sleep positions. Identifying optimal sleep positions to support cardiovascular health could significantly contribute to CVD prevention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11325-025-03501-1","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T09:46:49Z","timestamp":1761126409000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Supine sleep position and angina frequency: an analysis from the sleep heart health study"],"prefix":"10.1007","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6599-6975","authenticated-orcid":false,"given":"Jeongok G.","family":"Logan","sequence":"first","affiliation":[]},{"given":"Ha Do","family":"Byon","sequence":"additional","affiliation":[]},{"given":"Yeajoo","family":"Lee","sequence":"additional","affiliation":[]},{"given":"Yeonsu","family":"Kim","sequence":"additional","affiliation":[]},{"given":"Sunbok","family":"Park","sequence":"additional","affiliation":[]},{"given":"Younghoon","family":"Kwon","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2025,10,22]]},"reference":[{"key":"3501_CR1","doi-asserted-by":"publisher","first-page":"199","DOI":"10.1177\/1074248416679733","volume":"22","author":"RA Kloner","year":"2017","unstructured":"Kloner RA, Chaitman B (2017) Angina and its management. 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Environmental stressors which, like air pollution, generate oxidative stress at the cellular level, may induce somatic mutations and some mutations may provide a selection advantage for persistence and expansion of specific clones.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) N = 4,379 and the Women's Health Initiative (WHI) N = 7,701 to estimate cross-sectional associations between annual average air pollution concentrations at participant address the year before blood draw using validated spatiotemporal models. We used covariate-adjusted logistic regression to estimate risk of CHIP per interquartile range increases in particulate matter (PM2.5; 4 \u03bcg\/m3) and nitrogen dioxide (NO2; 10 ppb) as ORs (95% confidence intervals).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Prevalence of CHIP at blood draw (variant allele fraction &amp;gt; 2%) was 4.4% and 8.7% in MESA and WHI, respectively. The most common CHIP driver mutation was in DNMT3A. Neither pollutant was associated with CHIP: ORMESA PM2.5 = 1.00 (0.68\u20131.45), ORMESA NO2 = 1.05 (0.69\u20131.61), ORWHI PM2.5 = 0.97 (0.86\u20131.09), ORWHI NO2 = 0.98 (0.88\u20131.10); or with DNMT3A-driven CHIP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>We did not find evidence that air pollution contributes to CHIP prevalence in two large observational cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Impact:<\/jats:title>\n                    <jats:p>This is the first study to estimate associations between air pollution and CHIP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/1055-9965.epi-23-0305","type":"journal-article","created":{"date-parts":[[2023,7,19]],"date-time":"2023-07-19T11:05:05Z","timestamp":1689764705000},"page":"1470-1473","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Associations between Ambient Air Pollutants and Clonal Hematopoiesis of Indeterminate Potential"],"prefix":"10.1158","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9998-5481","authenticated-orcid":false,"given":"Claire L.","family":"Leiser","sequence":"first","affiliation":[{"name":"1Department of Epidemiology, University of Washington, Seattle, Washington."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4843-3641","authenticated-orcid":false,"given":"Eric A.","family":"Whitsel","sequence":"additional","affiliation":[{"name":"2Departments of Epidemiology and Medicine, University of North Carolina Chapel Hill, Chapel Hill, North Carolina."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1427-4470","authenticated-orcid":false,"given":"Alexander","family":"Reiner","sequence":"additional","affiliation":[{"name":"1Department of Epidemiology, University of Washington, Seattle, Washington."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3872-7793","authenticated-orcid":false,"given":"Stephen S.","family":"Rich","sequence":"additional","affiliation":[{"name":"3Center for Public Health Genomics, Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia."}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7191-1723","authenticated-orcid":false,"given":"Jerome I.","family":"Rotter","sequence":"additional","affiliation":[{"name":"4The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2756-4370","authenticated-orcid":false,"given":"Kent D.","family":"Taylor","sequence":"additional","affiliation":[{"name":"4The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0080-2420","authenticated-orcid":false,"given":"Russel P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"5Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7986-8560","authenticated-orcid":false,"given":"Charles","family":"Kooperberg","sequence":"additional","affiliation":[{"name":"6Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1942-5845","authenticated-orcid":false,"given":"Albert Vernon","family":"Smith","sequence":"additional","affiliation":[{"name":"7Department of Biostatistics, University of Michigan, Ann Arbor, Michigan."}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9426-7595","authenticated-orcid":false,"given":"JoAnn E.","family":"Manson","sequence":"additional","affiliation":[{"name":"8Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2595-0005","authenticated-orcid":false,"given":"Josyf C.","family":"Mychaleckyj","sequence":"additional","affiliation":[{"name":"3Center for Public Health Genomics, Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia."}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5824-9595","authenticated-orcid":false,"given":"Alexander G.","family":"Bick","sequence":"additional","affiliation":[{"name":"9School of Medicine, Vanderbilt University, Nashville, Tennessee."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4995-238X","authenticated-orcid":false,"given":"Adam A.","family":"Szpiro","sequence":"additional","affiliation":[{"name":"10Department of Biostatistics, University of Washington, Seattle, Washington."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4174-9037","authenticated-orcid":false,"given":"Joel D.","family":"Kaufman","sequence":"additional","affiliation":[{"name":"1Department of Epidemiology, University of Washington, Seattle, Washington."},{"name":"11Department of Occupational and Environmental Health Sciences, Seattle, Washington."}]}],"member":"1086","published-online":{"date-parts":[[2023,7,19]]},"reference":[{"key":"2025112608183779600_bib1","doi-asserted-by":"crossref","first-page":"9","DOI":"10.1182\/blood-2015-03-631747","article-title":"Clonal hematopoiesis of indeterminate potential and its 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Whether senescent lymphocytes are associated with the future occurrence of DM is uncertain.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used cryopreserved peripheral blood mononuclear cells collected from 1860 Cardiovascular Health Study participants (average age 80.2\u2009years) and flow cytometry immunophenotyping to evaluate the longitudinal relationships of naive (CD45RA<jats:sup>+<\/jats:sup>), memory (CD45RO<jats:sup>+<\/jats:sup>), senescent (CD28<jats:sup>\u2212<\/jats:sup>), and T effector memory RA<jats:sup>+<\/jats:sup> (TEMRA) (CD28<jats:sup>\u2212<\/jats:sup>CD57<jats:sup>+<\/jats:sup>CD45RA<jats:sup>+<\/jats:sup>) CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells, and memory B cells (CD19<jats:sup>+<\/jats:sup>CD27<jats:sup>+<\/jats:sup>), with the risk of incident DM. In exploratory analyses we evaluated the relationships of 13 additional innate lymphocyte and CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> subsets with incident DM risk.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Over a median follow\u2010up time of 8.9\u2009years, 155 cases of incident DM occurred. In Cox models adjusted for demographic variables (age, sex, race, study site and flow cytometry analytical batch) or diabetes risk factors (demographic variables plus education, body mass index, smoking status, alcohol use, systolic blood pressure, hypertension medication use and physical activity), no significant associations were observed for any CD4<jats:sup>+<\/jats:sup>, CD8<jats:sup>+<\/jats:sup> or CD19<jats:sup>+<\/jats:sup> cell phenotypes with incident DM.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results suggest the frequencies of naive, memory and senescent T cells and memory B cells are not strongly associated with incident DM risk in older 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<\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We identified TBXA2R expression in lungs of patients with IPF and mice and studied primary mouse and human lung fibroblasts to determine the impact of TBXA2R signaling on fibroblast activation. We used TBXA2R-deficient mice and small-molecule inhibitors to investigate TBXA2R signaling in preclinical lung fibrosis models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>TBXA2R expression was upregulated in fibroblasts in the lungs of patients with IPF and in mouse lungs during experimental lung fibrosis. Genetic deletion of TBXA2R, but not inhibition of thromboxane synthase, protected mice from bleomycin-induced lung fibrosis, thereby suggesting that an alternative ligand activates profibrotic TBXA2R signaling. In contrast to thromboxane, F2-isoprostanes, which are nonenzymatic products of arachidonic acid induced by reactive oxygen species, were persistently elevated during fibrosis. F2-isoprostanes induced TBXA2R signaling in fibroblasts and mediated a myofibroblast activation profile due, at least in part, to potentiation of TGF-\u03b2 (transforming growth factor-\u03b2) signaling. In vivo treatment with the TBXA2R antagonist ifetroban reduced profibrotic signaling in the lungs, protected mice from lung fibrosis in three preclinical models (bleomycin, Hermansky-Pudlak mice, and radiation-induced fibrosis), and markedly enhanced fibrotic resolution after bleomycin treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>TBXA2R links oxidative stress to fibroblast activation during lung fibrosis. TBXA2R antagonists could have utility in treating pulmonary fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202106-1503oc","type":"journal-article","created":{"date-parts":[[2022,6,21]],"date-time":"2022-06-21T16:24:37Z","timestamp":1655828677000},"page":"596-607","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":25,"title":["Thromboxane\u2013Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis"],"prefix":"10.1093","volume":"206","author":[{"given":"Toshio","family":"Suzuki","sequence":"first","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"},{"name":"Department of Medical Oncology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan"}]},{"given":"Jonathan A.","family":"Kropski","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"},{"name":"Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee"},{"name":"Department of Medicine, Department of Veterans Affairs Medical Center, Nashville, Tennessee"}]},{"given":"Jingyuan","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Erica J.","family":"Carrier","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Xinping","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Taylor P.","family":"Sherrill","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Nichelle I.","family":"Winters","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Jane E.","family":"Camarata","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Vasiliy V.","family":"Polosukhin","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Wei","family":"Han","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3474-8063","authenticated-orcid":false,"given":"Anandharajan","family":"Rathinasabapathy","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4402-0516","authenticated-orcid":false,"given":"Sergey","family":"Gutor","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Peter","family":"Gulleman","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Carleen","family":"Sabusap","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Nicholas E.","family":"Banovich","sequence":"additional","affiliation":[{"name":"Translational Genomics Research Institute, Phoenix, Arizona"}]},{"given":"Harikrishna","family":"Tanjore","sequence":"additional","affiliation":[{"name":"Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, and"}]},{"given":"Michael 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However, no studies have focused on the presence and activity of fatty acid desaturases (FADS) in the mature RBC.<\/jats:p><\/jats:sec><jats:sec><jats:title>Study design and methods<\/jats:title><jats:p>Steady state metabolomics and isotope\u2010labeled tracing experiments, immunofluorescence approaches, and pharmacological interventions were used to determine the degree of fatty acid unsaturation, FADS activity as a function of storage, oxidant stress, and G6PD deficiency in human and mouse RBCs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In 250 blood units from the REDS III RBC Omics recalled donor population, we report a storage\u2010dependent accumulation of free mono\u2010, poly\u2010(PUFAs), and highly unsaturated fatty acids (HUFAs), which occur at a faster rate than saturated fatty acid accumulation. Through a combination of immunofluorescence, pharmacological inhibition, tracing experiments with stable isotope\u2010labeled fatty acids, and oxidant challenge with hydrogen peroxide, we demonstrate the presence and redox\u2010sensitive activity of FADS2, FADS1, and FADS5 in the mature RBC. Increases in PUFAs and HUFAs in human and mouse RBCs correlate negatively with storage hemolysis and positively with posttransfusion recovery. Inhibition of these enzymes decreases accumulation of free PUFAs and HUFAs in stored RBCs, concomitant to increases in pyruvate\/lactate ratios. Alterations of this ratio in G6PD deficient patients or units supplemented with pyruvate\u2010rich rejuvenation solutions corresponded to decreased PUFA and HUFA accumulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Fatty acid desaturases are present and active in mature RBCs. 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To date, proteomic studies of frailty are scarce, and few evaluated prefrailty as a separate state or examined predictors of incident frailty. Using plasma proteins measured by 4955 SOMAmers in the Atherosclerosis Risk in Community study, we identified 134 and 179 proteins cross\u2010sectionally associated with prefrailty and frailty, respectively, after Bonferroni correction (<jats:italic>p<\/jats:italic>\u2009&lt;\u20091\u2009\u00d7\u200910<jats:sup>\u22125<\/jats:sup>) among 3838 older adults aged \u226565\u2009years, adjusting for demographic and physiologic factors and chronic diseases. Among them, 23 (17%) and 82 (46%) were replicated in the Cardiovascular Health Study using the same models (FDR <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). Notably, higher odds of prefrailty and frailty were observed with higher levels of growth differentiation factor 15 (GDF15; <jats:italic>p<\/jats:italic><jats:sub>prefrailty<\/jats:sub>\u2009=\u20091\u2009\u00d7\u200910<jats:sup>\u221215<\/jats:sup>, <jats:italic>p<\/jats:italic><jats:sub>frailty<\/jats:sub>\u2009=\u20092\u2009\u00d7\u200910<jats:sup>\u221219<\/jats:sup>), transgelin (TAGLN; <jats:italic>p<\/jats:italic><jats:sub>prefrailty<\/jats:sub>\u2009=\u20092\u2009\u00d7\u200910<jats:sup>\u221212<\/jats:sup>, <jats:italic>p<\/jats:italic><jats:sub>frailty<\/jats:sub>\u2009=\u20096\u2009\u00d7\u200910<jats:sup>\u221222<\/jats:sup>), and insulin\u2010like growth factor\u2010binding protein 2 (IGFBP2; <jats:italic>p<\/jats:italic><jats:sub>prefrailty<\/jats:sub>\u2009=\u20095\u2009\u00d7\u200910<jats:sup>\u221215<\/jats:sup>, <jats:italic>p<\/jats:italic><jats:sub>frailty<\/jats:sub>\u2009=\u20091\u2009\u00d7\u200910<jats:sup>\u221215<\/jats:sup>) and with a lower level of growth hormone receptor (GHR, <jats:italic>p<\/jats:italic><jats:sub>prefrailty<\/jats:sub>\u2009=\u20093\u2009\u00d7\u200910<jats:sup>\u221216<\/jats:sup>, <jats:italic>p<\/jats:italic><jats:sub>frailty<\/jats:sub>\u2009=\u20092\u2009\u00d7\u200910<jats:sup>\u221218<\/jats:sup>). Longitudinally, we identified 4 proteins associated with incident frailty (<jats:italic>p<\/jats:italic>\u2009&lt;\u20091\u2009\u00d7\u200910<jats:sup>\u22125<\/jats:sup>). Higher levels of triggering receptor expressed on myeloid cells 1 (TREM1), TAGLN, and heart and adipocyte fatty\u2010acid binding proteins predicted incident frailty. Differentially regulated proteins were enriched in pathways and upstream regulators related to lipid metabolism, angiogenesis, inflammation, and cell senescence. Our findings provide a set of plasma proteins and biological mechanisms that were dysregulated in both the prodromal and the clinical stage of frailty, offering new insights into frailty etiology and targets for intervention.<\/jats:p>","DOI":"10.1111\/acel.13975","type":"journal-article","created":{"date-parts":[[2023,9,12]],"date-time":"2023-09-12T05:52:49Z","timestamp":1694497969000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Late\u2010life plasma proteins associated with prevalent and incident frailty: A proteomic analysis"],"prefix":"10.1111","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1554-1478","authenticated-orcid":false,"given":"Fangyu","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Epidemiology Johns Hopkins Bloomberg School of Public Health  Baltimore Maryland USA"}]},{"given":"Thomas R.","family":"Austin","sequence":"additional","affiliation":[{"name":"Department of Epidemiology University of Washington  Seattle Washington USA"}]},{"given":"Jennifer A.","family":"Schrack","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Johns Hopkins Bloomberg School of Public Health  Baltimore Maryland USA"},{"name":"Center on Aging and Health Johns Hopkins University  Baltimore Maryland USA"}]},{"given":"Jingsha","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Johns Hopkins Bloomberg School of Public Health  Baltimore Maryland USA"}]},{"given":"Jeremy","family":"Walston","sequence":"additional","affiliation":[{"name":"Department of Medicine Johns Hopkins University  Baltimore Maryland USA"}]},{"given":"Rasika A.","family":"Mathias","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Johns Hopkins Bloomberg School of Public Health  Baltimore Maryland USA"},{"name":"Department of Medicine Johns Hopkins University  Baltimore Maryland USA"}]},{"given":"Morgan","family":"Grams","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Johns Hopkins Bloomberg School of Public Health  Baltimore Maryland USA"},{"name":"Division of Precision Medicine New York University Grossman School of Medicine  New York New York USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5974-3648","authenticated-orcid":false,"given":"Michelle C.","family":"Odden","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Population Health Stanford University School of Medicine  Stanford California USA"}]},{"given":"Anne","family":"Newman","sequence":"additional","affiliation":[{"name":"Department of Epidemiology University of Pittsburgh  Pittsburgh Pennsylvania USA"}]},{"given":"Bruce M.","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Systems and Population Health University of Washington  Seattle Washington USA"}]},{"given":"Diego","family":"Ramonfaur","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard Medical School, Cardiovascular Medicine  Boston Massachusetts USA"}]},{"given":"Amil M.","family":"Shah","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard Medical School, Cardiovascular Medicine  Boston Massachusetts USA"}]},{"given":"B. 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All rights reserved.","name":"copyright","label":"Copyright"}]},{"indexed":{"date-parts":[[2024,5,5]],"date-time":"2024-05-05T13:42:15Z","timestamp":1714916535680},"reference-count":0,"publisher":"Jaypee Brothers Medical Publishers (P) Ltd.","isbn-type":[{"value":"9789380704524","type":"print"}],"content-domain":{"domain":[],"crossmark-restriction":false},"DOI":"10.5005\/jp\/books\/12163_14","type":"book-chapter","created":{"date-parts":[[2014,12,15]],"date-time":"2014-12-15T04:44:36Z","timestamp":1418618676000},"page":"80-80","source":"Crossref","is-referenced-by-count":0,"title":["Blood components"],"prefix":"10.5005","author":[{"given":"SR","family":"Mehdi","sequence":"first","affiliation":[]}],"member":"2914","published-online":{"date-parts":[[2013]]},"container-title":["Essentials of Blood Banking"],"language":"en","deposited":{"date-parts":[[2019,8,15]],"date-time":"2019-08-15T08:56:21Z","timestamp":1565859381000},"score":8.584476,"resource":{"primary":{"URL":"https:\/\/www.jaypeedigital.com\/book\/9789380704524\/chapter\/ch14"}},"issued":{"date-parts":[[2013]]},"ISBN":["9789380704524"],"references-count":0,"URL":"https:\/\/doi.org\/10.5005\/jp\/books\/12163_14","published":{"date-parts":[[2013]]}},{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:52:07Z","timestamp":1761155527678},"publisher-location":"Amsterdam","reference-count":0,"publisher":"Amsterdam University Press","isbn-type":[{"value":"9789087280314","type":"print"}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2007]]},"DOI":"10.5117\/9789087280314","type":"monograph","created":{"date-parts":[[2011,10,18]],"date-time":"2011-10-18T15:03:04Z","timestamp":1318950184000},"source":"Crossref","is-referenced-by-count":3,"title":["Red Blood Cell Alloimmunization after Blood Transfusion"],"prefix":"10.5117","author":[{"given":"Henk","family":"Schonewille","sequence":"first","affiliation":[]}],"member":"3180","language":"en","deposited":{"date-parts":[[2011,10,18]],"date-time":"2011-10-18T15:12:05Z","timestamp":1318950725000},"score":8.584476,"resource":{"primary":{"URL":"http:\/\/dare.uva.nl\/aup\/nl\/record\/332265"}},"issued":{"date-parts":[[2007]]},"ISBN":["9789087280314"],"references-count":0,"URL":"https:\/\/doi.org\/10.5117\/9789087280314","published":{"date-parts":[[2007]]}},{"indexed":{"date-parts":[[2025,8,2]],"date-time":"2025-08-02T19:22:40Z","timestamp":1754162560959,"version":"3.41.2"},"reference-count":0,"publisher":"Sciencedomain International","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int. Blood Res. Rev."],"abstract":"<jats:p>Background: Packed cell volume and blood group are two parameters which are key in blood transfusion services, and as such, reduced packed cell volume or incompatible blood group will affect the outcome of transfusion. Blood lead may or may not affect the concentration of blood, as has been demonstrated in studies in other parts. However, this association has not been confirmed in the blood of donors in Port Harcourt; likewise, the association between blood lead and blood group is also not known.\r\nAims: To identify if any relationship exists between blood lead levels, packed cell volume and blood group of blood donors in a tertiary hospital in Port Harcourt.\r\nStudy Design: A descriptive, cross-sectional study.\r\nPlace and Duration of Study: Blood bank of the department of Haematology and Blood Transfusion of the University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria, between March 2023 to May 2023.\r\nMethodology: We included 246 donors, all were male, aged 18-55 years. Biodata and other relevant information were obtained using a semi-structure questionnaire, after consent to participate in the study was obtained. 5mls of blood was drawn from the antecubital fossa and Packed Cell Volume and blood group was determined. Blood Lead concentration was measured using Solaar thermo elemental atomic absorption spectrophotometer. Statistical analysis was done by SPSS version 21. Ethical approval was obtained.\r\nResults: The relationship between donor blood lead levels, and packed cell volume and blood group were both statistically insignificant at P =0.238 and 0.061 respectively. However, the age of donors showed a significant relationship with blood lead levels, P = 0.013.\r\nConclusion: No statistically significant association was found to exist between blood lead levels, packed cell volume or the blood group of blood donors.<\/jats:p>","DOI":"10.9734\/ibrr\/2025\/v16i2356","type":"journal-article","created":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T08:29:44Z","timestamp":1753864184000},"page":"32-41","source":"Crossref","is-referenced-by-count":0,"title":["Analysis of Association between Blood Lead Levels, Packed Cell Volume and Blood Group in Blood Donors: An Experience from a Tertiary Healthcare Facility in Port Harcourt"],"prefix":"10.9734","volume":"16","author":[{"given":"Paxman Dandyson","family":"Uku","sequence":"first","affiliation":[]},{"given":"Eunice","family":"Belema","sequence":"additional","affiliation":[]},{"given":"Chimankpam Edison Okechukwu","family":"Omeodu","sequence":"additional","affiliation":[]}],"member":"4694","published-online":{"date-parts":[[2025,7,29]]},"container-title":["International Blood Research &amp; 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Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL049426"],"award-info":[{"award-number":["HL049426"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL086936"],"award-info":[{"award-number":["HL086936"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL114501"],"award-info":[{"award-number":["HL114501"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL115813"],"award-info":[{"award-number":["HL115813"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL130704"],"award-info":[{"award-number":["HL130704"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL160661"],"award-info":[{"award-number":["HL160661"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2022,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Patients with chronic obstructive pulmonary disease (COPD)\u2013pulmonary emphysema often develop locomotor muscle dysfunction, which entails reduced muscle mass and force-generation capacity and is associated with worse outcomes, including higher mortality. Myogenesis contributes to adult muscle integrity during injury\u2013repair cycles. Injurious events crucially occur in the skeletal muscles of patients with COPD in the setting of exacerbations and infections, which lead to acute decompensations for limited periods of time, after which patients typically fail to recover the baseline status they had before the acute event. Autophagy, which is dysregulated in muscles from patients with COPD, is a key regulator of muscle stem-satellite- cells activation and myogenesis, yet very little research has so far mechanistically investigated the role of autophagy dysregulation in COPD muscles. Using a genetically inducible interleukin-13\u2013driven pulmonary emphysema model leading to muscle dysfunction, and confirmed with a second genetic animal model, we found a significant myogenic dysfunction associated with the reduced proliferative capacity of satellite cells. Transplantation experiments followed by lineage tracing suggest that an intrinsic defect in satellite cells, and not in the COPD environment, plays a dominant role in the observed myogenic dysfunction. RNA sequencing analysis and direct observation of COPD mice satellite cells suggest dysregulated autophagy. Moreover, while autophagy flux experiments with bafilomycin demonstrated deacceleration of autophagosome turnover in COPD mice satellite cells, spermidine-induced autophagy stimulation leads to a higher replication rate and myogenesis in these animals. Our data suggest that pulmonary emphysema causes disrupted myogenesis, which could be improved with stimulation of autophagy and satellite cells activation, leading to an attenuated muscle dysfunction.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0351oc","type":"journal-article","created":{"date-parts":[[2022,3,14]],"date-time":"2022-03-14T17:58:57Z","timestamp":1647280737000},"page":"623-637","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":26,"title":["Deaccelerated Myogenesis and Autophagy in Genetically Induced Pulmonary Emphysema"],"prefix":"10.1093","volume":"66","author":[{"given":"Joseph","family":"Balnis","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"},{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Lisa A.","family":"Drake","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"},{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Diane V.","family":"Singer","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Catherine E.","family":"Vincent","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Tanner C.","family":"Korponay","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"},{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Jeanine","family":"D\u2019Armiento","sequence":"additional","affiliation":[{"name":"Departments of Anesthesiology and Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University Medical Center, New York, New York; and"}]},{"given":"Chun Geun","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island"}]},{"given":"Jack A.","family":"Elias","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island"}]},{"given":"Harold A.","family":"Singer","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]},{"given":"Ariel","family":"Jaitovich","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine and"},{"name":"Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York"}]}],"member":"286","published-online":{"date-parts":[[2022,6,1]]},"reference":[{"key":"2026012204020536200_bib1","doi-asserted-by":"crossref","first-page":"175","DOI":"10.1164\/rccm.201710-2140CI","article-title":"Skeletal muscle dysfunction in chronic obstructive pulmonary disease. 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The \u03b22AR (\u03b2-2-adrenoceptor), as well as the Gs-coupled EP2 and EP4 (E-prostanoid) receptor subtypes of the EP receptor subfamily, are effective regulators of multiple airway smooth muscle (ASM) cell functions whose dysregulation contributes to asthma pathobiology. Here, we identify specific roles of the AKAPs Ezrin and Gravin in differentially regulating PKA substrates downstream of the \u03b22AR, EP2R (EP2 receptor) and EP4R. Knockdown of Ezrin, Gravin, or both in primary human ASM cells caused differential phosphorylation of the PKA substrates VASP (vasodilator-stimulated phosphoprotein) and HSP20 (heat shock protein 20). Ezrin knockdown, as well as combined Ezrin and Gravin knockdown, significantly reduced the induction of phospho-VASP and phospho-HSP20 by \u03b22AR, EP2R, and EP4R agonists. Gravin knockdown inhibited the induction of phospho-HSP20 by \u03b22AR, EP2R, and EP4R agonists. Knockdown of Ezrin, Gravin, or both also attenuated histamine-induced phosphorylation of MLC20. Moreover, knockdown of Ezrin, Gravin, or both suppressed the inhibitory effects of Gs-coupled receptor agonists on cell migration in ASM cells. 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In the Trials of Hypertension Prevention (TOHP), individuals aged 30\u201054\u00a0years with high normal BP were randomized to weight loss, usual care or other intervention over 18\u00a0months (TOHP I) or 3\u20104\u00a0years (TOHP II), with average 23\u2010year mortality follow\u2010up. We examined mortality and (a) randomized weight loss and (b) observed weight change among all with high baseline weight. Among 2964 randomized participants, 227 deaths occurred, with no intervention difference (hazard ratio (HR)\u00a0=\u00a00.97, 95% confidence interval (CI)\u00a0=\u00a00.75\u20101.26, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.84). Among 3828 high\u2010weight participants, weight change was directly related to mortality (HR\u00a0=\u00a01.14 per 5% change, 95% CI\u00a0=\u00a01.02\u20101.28, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.019). During the trial 15% lost &gt;5% (HR\u00a0=\u00a00.82), 29% lost 0\u2010&lt;=5% (HR\u00a0=\u00a00.94), 41% gained 0\u2010&lt;5% (reference), and 16% gained &gt;5% (HR\u00a0=\u00a01.29) (<jats:italic>P<\/jats:italic>\u2010trend\u00a0=\u00a00.046). This is consistent with a long\u2010term beneficial effect of presumed intentional weight loss on mortality.<\/jats:p>","DOI":"10.1111\/jch.13418","type":"journal-article","created":{"date-parts":[[2018,11,3]],"date-time":"2018-11-03T05:47:24Z","timestamp":1541224044000},"page":"1666-1673","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Weight change and mortality: Long\u2010term results from the trials of hypertension prevention"],"prefix":"10.1111","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9705-0842","authenticated-orcid":false,"given":"Nancy R.","family":"Cook","sequence":"first","affiliation":[{"name":"Division of Preventive Medicine, Brigham and Women\u2019s Hospital Harvard Medical School Boston Massachusetts"}]},{"given":"Lawrence J.","family":"Appel","sequence":"additional","affiliation":[{"name":"Welch Center for Prevention, Epidemiology, and Clinical Research The Johns Hopkins University Baltimore Maryland"}]},{"given":"Paul K.","family":"Whelton","sequence":"additional","affiliation":[{"name":"Department of Epidemiology Tulane University School of Public Health and Tropical Medicine New Orleans Louisiana"}]}],"member":"311","published-online":{"date-parts":[[2018,11,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/1047-2797(91)90045-E"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1212914"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1990.00390130131021"},{"key":"e_1_2_7_5_1","doi-asserted-by":"crossref","first-page":"1801","DOI":"10.1001\/jama.1989.03430130077038","article-title":"Primary prevention of hypertension by nutritional\u2010hygienic means: final report of a randomized controlled trial","volume":"262","author":"Stamler R","year":"1989","journal-title":"J Amer Med Assoc"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198811033191801"},{"issue":"9","key":"e_1_2_7_7_1","doi-asserted-by":"crossref","first-page":"1213","DOI":"10.1001\/jama.1992.03480090061028","article-title":"The effects of nonpharmacologic interventions on blood pressure of persons with high normal levels. 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Patients with asthma are grouped into phenotypes with shared clinical features and biomarker profiles to help tailor specific therapies. However, factors driving development of specific phenotypes are poorly understood. Prenatal exposure to maternal asthma is a unique risk factor for childhood asthma. Here we tested whether maternal asthma skews asthma phenotypes in offspring. We compared airway hyperreactivity and inflammatory and neurotrophin lung signatures before and after allergen challenge in offspring born to mice exposed to house dust mite (HDM) or vehicle during pregnancy. Maternal HDM exposure potentiated offspring responses to HDM allergen, significantly increasing both airway hyperreactivity and airway eosinophilia compared with control mice. Maternal HDM exposure broadly skewed the offspring cytokine response from a classic allergen-induced T-helper cell type 2 (Th2)-predominant signature in HDM-treated offspring of vehicle-exposed mothers, toward a mixed Th17\/Th1 phenotype in HDM-treated offspring of HDM-exposed mothers. Morphologic analysis determined that maternal HDM exposure also increased airway epithelial sensory nerve density and induced distinct neurotrophin signatures to support airway hyperinnervation. Our results demonstrate that maternal allergen exposure alters fetal lung development and promotes a unique inflammatory phenotype at baseline and in response to allergen that persists into adulthood.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0535oc","type":"journal-article","created":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T17:17:40Z","timestamp":1648833460000},"page":"89-98","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":16,"title":["Unique Allergic Asthma Phenotypes in Offspring of House Dust Mite\u2013exposed Mice"],"prefix":"10.1093","volume":"67","author":[{"given":"Katie M.","family":"Lebold","sequence":"first","affiliation":[{"name":"Department of Emergency Medicine, Stanford University School of Medicine, Palo Alto, California; and"}]},{"given":"Matthew G.","family":"Drake","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, Oregon Health and 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to safe and effective blood and blood products remains a crucial public health challenge in low- and middle-income countries (LMICs), regardless of the essential role in treatment of several diseases, such as, major trauma, haemophilia and obstetric complications. This dissertation explores the diverse global and regional facets in the selection, registration, and regulation of blood products, highlighting the systemic gaps that limit access and emerging opportunities for data-driven approaches to strengthen access and safety.  \n\nThe first part of the research investigates the global selection of essential medicines on 105 NEMLs and their registration in 61 LMICs. Our findings showed a low uptake of essential blood products, especially, blood and blood components, and frequent registration of non-essential blood products like Albumin. LMICs from Africa, in particular, showed significant under-registration of WHO recommended blood and blood products. These insights suggest an urgent need for policy reforms that are guided by national health priorities and supported by evidence-based inclusion criteria, regulatory system strengthening and international collaboration to improve availability and accessibility. \n\nThe second section turns the focus to Africa and evaluates the regulatory landscape for blood and blood products using the WHO Global Benchmarking Tool (GBT)+ Blood. Data from 12 countries show better performance in regulating plasma-derived medicines compared to the regulation of blood components and plasma for fractionation, which remains weak. Similarly, haemovigilance systems across 10 countries show major gaps in the implementation of governance, legal frameworks, and human resource. It is evident from our findings that nascent blood regulatory frameworks exist in many countries and advocate for urgent, targeted support to build resilient regulatory systems capable of overseeing the entire blood value chain, from collection to patient use. \n\nFinally, this thesis explores how data-driven haemovigilance, using global tools such as the WHO\u2019s VigiBase, can support safety monitoring of blood products. By analysing over 111,000 reports from across the world, the study highlights the potential for improved global surveillance if systems are better harmonised. The work also showcases the impact of the BloodTrain initiative, which has strengthened blood regulation in African countries through tailored capacity building, system development, and stakeholder engagement. 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A comprehensive analysis was conducted on data of patients who were hospitalized and received transfusions at the Third Xiangya Hospital of Central South University from 2021 to 2023. The results indicated significant variations in ABO blood group distribution among various departments. Group A was predominant in gynecology (34.53%) and hepatobiliary surgery (35.60%), while group O was found to be the most frequent blood type in obstetrics (34.97%) and urology (34.53%). Blood component usage was also correlated with diseases: red blood cell (RBC) transfusions were predominantly administered to cancer patients (12.76%), liver disease patients receiving the highest amount of frozen plasma (FP) and cryoprecipitate (19.71%, 27.05%), and autoimmune hemolytic anemia patients receiving the highest amount of platelets (PLTs, 30.29%). Additionally, group O was more frequently used for RBCs (34.72%), FP (36.17%), and PLTs (36.84%), whereas group A showed predominant usage in RBCs (34.56%) and cryoprecipitate (34.21%). 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Institute","doi-asserted-by":"publisher","award":["5U01HL138635"],"award-info":[{"award-number":["5U01HL138635"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Health Serv Res"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>The growing burden of hypertension and diabetes is one of the major public health challenges being faced by the health system in India. Clinical Decision Support Systems (CDSS) that assist with tailoring evidence-based management approaches combined with task-shifting from more specialized to less specialized providers may together enhance the impact of a program. We sought to integrate a technology \u201cCDSS\u201d and a strategy \u201cTask-shifting\u201d within the Government of India\u2019s (GoI) Non-Communicable Diseases (NCD) System under the Comprehensive Primary Health Care (CPHC) initiative to enhance the program\u2019s impact to address the growing burden of hypertension and diabetes in India.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We developed a model of care \u201cI-TREC\u201d entirely calibrated for implementation within the current health system across all facility types (Primary Health Centre, Community Health Centre, and District Hospital) in a block in Shaheed Bhagat Singh (SBS) Nagar district of Punjab, India. We undertook an academic-community partnership to incorporate the combination of a CDSS with task-shifting into the GoI CPHC-NCD system, a platform that assists healthcare providers to record patient information for routine NCD care. Academic partners developed clinical algorithms, a revised clinic workflow, and provider training modules with iterative collaboration and consultation with government and technology partners to incorporate CDSS within the existing system.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Discussion<\/jats:title>\n                <jats:p>The CDSS-enabled GoI CPHC-NCD system provides evidence-based recommendations for hypertension and diabetes; threshold-based prompts to assure referral mechanism across health facilities; integrated patient database, and care coordination through workflow management and dashboard alerts. To enable efficient implementation, modifications were made in the patient workflow and the fulcrum of the use of technology shifted from physician to nurse.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Designed to be applicable nationwide, the I-TREC model of care is being piloted in a block in the state of Punjab, India. Learnings from I-TREC will provide a roadmap to other public health experts to integrate and adapt their interventions at the national level.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Trial registration<\/jats:title>\n                <jats:p>CTRI\/2020\/01\/022723.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12913-022-08025-y","type":"journal-article","created":{"date-parts":[[2022,5,23]],"date-time":"2022-05-23T10:03:58Z","timestamp":1653300238000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Improving care for hypertension and diabetes in india by addition of clinical decision support system and task shifting in the national NCD program: I-TREC model of care"],"prefix":"10.1186","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2384-7354","authenticated-orcid":false,"given":"Devraj","family":"Jindal","sequence":"first","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7590-160X","authenticated-orcid":false,"given":"Hanspria","family":"Sharma","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4345-717X","authenticated-orcid":false,"given":"Yashdeep","family":"Gupta","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4102-0505","authenticated-orcid":false,"given":"Vamadevan S.","family":"Ajay","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6418-4388","authenticated-orcid":false,"given":"Ambuj","family":"Roy","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3522-7945","authenticated-orcid":false,"given":"Rakshit","family":"Sharma","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9936-2962","authenticated-orcid":false,"given":"Mumtaj","family":"Ali","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5020-3995","authenticated-orcid":false,"given":"Prashant","family":"Jarhyan","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3929-235X","authenticated-orcid":false,"given":"Priti","family":"Gupta","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4037-6371","authenticated-orcid":false,"given":"Nikhil","family":"Srinivasapura Venkateshmurthy","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7266-2503","authenticated-orcid":false,"given":"Mohammed K.","family":"Ali","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8621-5405","authenticated-orcid":false,"given":"K M Venkat","family":"Narayan","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3172-834X","authenticated-orcid":false,"given":"Dorairaj","family":"Prabhakaran","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2804-3948","authenticated-orcid":false,"given":"Mary Beth","family":"Weber","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1853-3596","authenticated-orcid":false,"given":"Sailesh","family":"Mohan","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0082-5857","authenticated-orcid":false,"given":"Shivani A.","family":"Patel","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4604-1986","authenticated-orcid":false,"given":"Nikhil","family":"Tandon","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2022,5,23]]},"reference":[{"issue":"3","key":"8025_CR1","doi-asserted-by":"publisher","first-page":"363","DOI":"10.1001\/jamainternmed.2017.8094","volume":"178","author":"P Geldsetzer","year":"2018","unstructured":"Geldsetzer P, Manne-Goehler J, Theilmann M, Davies JI, Awasthi A, Vollmer S, et al. 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Research"],"published-print":{"date-parts":[[2012]]},"abstract":"<jats:p><jats:italic>Introduction<\/jats:italic>. Successful aging has many dimensions, which may manifest differently in men and women at different ages.<jats:italic>Methods<\/jats:italic>. We characterized one-year transitions among health states in 12 measures of successful aging among adults in the Cardiovascular Health Study. The measures included self-rated health, ADLs, IADLs, depression, cognition, timed walk, number of days spent in bed, number of blocks walked, extremity strength, recent hospitalizations, feelings about life as a whole, and life satisfaction. We dichotomized variables into \u201chealthy\u201d or \u201csick,\u201d states, and estimated the prevalence of the healthy state and the probability of transitioning from one state to another, or dying, during yearly intervals. We compared men and women and three age groups (65\u201374, 75\u201384, and 85\u201394).<jats:italic>Findings<\/jats:italic>. Measures of successful aging showed similar results by gender. Most participants remained healthy even into advanced ages, although health declined for all measures. Recuperation, although less common with age, still occurred frequently. Men had a higher death rate than women regardless of health status, and were also more likely to remain in the healthy state.<jats:italic>Discussion.<\/jats:italic>The results suggest a qualitatively different experience of successful aging between men and women. Men did not simply \u201cage faster\u201d than women.<\/jats:p>","DOI":"10.1155\/2012\/243263","type":"journal-article","created":{"date-parts":[[2012,10,21]],"date-time":"2012-10-21T17:00:28Z","timestamp":1350838828000},"page":"1-9","source":"Crossref","is-referenced-by-count":10,"title":["Transitions among Health States Using 12 Measures of Successful Aging in Men and Women: Results from the Cardiovascular Health Study"],"prefix":"10.1155","volume":"2012","author":[{"given":"Stephen","family":"Thielke","sequence":"first","affiliation":[{"name":"Department of Psychiatry, University of Washington, Seattle, WA 98195, USA"},{"name":"Geriatrics Research, Education, and Clinical Center, Puget Sound VA Medical Center and Psychiatry and Behavioral Sciences, University of Washington, P.O. Box 356560, Seattle, WA 98195, USA"}]},{"given":"Paula","family":"Diehr","sequence":"additional","affiliation":[{"name":"Departments of Biostastitics and Health Services, University of Washington, Seattle, WA 98195, USA"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1007\/s10654-010-9472-2"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1503\/cmaj.060674"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1016\/j.archger.2011.06.024"},{"issue":"4","key":"4","doi-asserted-by":"crossref","first-page":"393","DOI":"10.1089\/154099904323087088","volume":"13","year":"2004","journal-title":"Journal of Women's Health"},{"issue":"4","key":"5","doi-asserted-by":"crossref","first-page":"387","DOI":"10.2307\/2136716","volume":"17","year":"1976","journal-title":"Journal of Health and Social 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Stimula Blood Sugar Support is an all-normal blood sugar equation that assists you with dealing with a solid blood pressure level and blood sugar easily. This supplement incorporates all-regular fixings that are protected to use by anybody at whatever stage in life. The additional fixings in this supplement are absolutely obtained from nature's concentrate. This blood sugar support recipe can diminish blood sugar where you can likewise get thinner rapidly and successfully. Stimula Blood Sugar Support Supplement assists you with dealing with your blood sugar normally and in the most secure manner. This item is totally regular where it won't cause you any secondary effects.  Order Now -- https:\/\/dmocoz.com\/stimula-blood-sugar-support\/  Stimula Blood Sugar is a dietary enhancement that permits an individual to dispose of issues that occur because of ill-advised blood course. It contains all-normal parts which further develop numerous medical issues. 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Ltd.","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int J Blood Transfus Immunohematol"],"abstract":"<jats:p>Introduction: Severe acute reparatory syndrome coronavirus-2 (SARS-CoV-2) is a recently emerged coronavirus, and infection with SARS-CoV-2 can remain asymptomatic or lead to coronavirus infection disease. Clinical pictures range from a pre-clinical stage to severe pneumonia. The presence of this pre-clinical infection stage could pose a problem for the management of the transfusion chain as donors or employees may become infected during their travels or activities, and this may exponentially increase the number of infected but asymptomatic individuals. So, SARS-CoV-2 may pose a threat to blood safety.\n\n\t\t\t\t\t\t\t\tAim: In this study, we want to provide the necessary information about the real risk of transmission of SARS-CoV-2 via blood and blood products. It constitutes one of the most controversial topics with several critical questions for which both professionals in blood centers and health services seek apparent answers.\n\n\t\t\t\t\t\t\t\tMethods: It is a literature review where we have consulted relevant papers and articles about the real risk of transmission of SARS-CoV-2 through blood or blood products. For this purpose, scientific research sites were consulted using key terms search strategy. Thus, we compiled and presented the necessary information from (i) positions of international scientific societies and public bodies; (ii) available data to date on detecting SARS-CoV-2 RNA in the blood of COVID-19 patients and blood donors; and (iii) published cases of transfusion of blood products from donors confirmed COVID-19 positive after donation and the process in recipients of these products.\n\n\t\t\t\t\t\t\t\tResults: All papers published to date stipulated that SARS-CoV-2 is a new infectious agent. No sufficient information is available to exclude with certainty the risk of transfusion transmission, which remains a theoretical risk. SARS-CoV-2 RNA has been detected very lowly, but virus infectivity has not been confirmed in blood donors. Reported cases of product transfusion from COVID-19 positive donors after a donation have not provided any evidence of transmission of the virus to recipients. As a precautionary measure, blood transfusion centers have set up necessary measures to reduce the risk of transmission of SARS-CoV-2 through blood products and ensure the safety of donors and recipients. Strengthening the hemovigilance system and post-donation information is an essential link for blood safety during the COVID-19 pandemic.\n\n\t\t\t\t\t\t\t\tConclusion: All data available to date stipulated that SARS-CoV-2 is not transfusion-transmitted and that the risk of transmission of this new coronavirus through blood and blood products is still theoretical. This novel coronavirus may be no direct threat to blood safety but raises serious issues for general blood supply. All measures taken by blood centers to secure blood donation against this new virus are preventive measures that should consider the need to ensure the availability of blood products.<\/jats:p>","DOI":"10.5348\/100064z02sb2021rv","type":"journal-article","created":{"date-parts":[[2021,10,29]],"date-time":"2021-10-29T07:38:26Z","timestamp":1635493106000},"page":"1-11","source":"Crossref","is-referenced-by-count":0,"title":["The risk of transmission of SARS-CoV-2 through blood and blood products: The current state of knowledge (international review)"],"prefix":"10.5348","volume":"11","author":[{"given":"Sabah","family":"Bouhou","sequence":"first","affiliation":[{"name":"National Centre for Blood Transfusion and Hematology, Rabat, Morocco, Hematology Research Team, Hematology Laboratory, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco"}]},{"given":"Mohammed","family":"Benajiba","sequence":"first","affiliation":[{"name":"National Centre for Blood Transfusion and Hematology, Rabat, Morocco"}]},{"given":"Azlarab","family":"Masrar","sequence":"first","affiliation":[{"name":"Hematology Research Team, Hematology Laboratory, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco, Central Hematology Laboratory, Ibn Sina University Hospital Centre, Rabat, Morocco"}]}],"member":"3299","published-online":{"date-parts":[[2021,10,28]]},"reference":[{"key":"ref=1","doi-asserted-by":"crossref","unstructured":"Li H, Wang Y, Ji M, et al. 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Ltd.","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int J Blood Transfus Immunohematol"],"abstract":"<jats:p>Introduction: Transfusion systems worldwide have had to face many challenges against the emergence or the re-emergence of numerous infectious diseases. Some of those viruses have posed significant impacts on blood transfusion activities. Several scientific and transfusion experts consider the current COVID-19 pandemic to present a potential risk of reducing and compromising the supply of blood products. Blood establishments had to activate their emergency plans and to propose appropriate response measures. Method: It is an international review where we used key terms search strategy to identify necessary information about: (i) the impact of some previous emergent viruses on the availability and the safety of blood products and (ii) the impact of the current COVID-19 pandemic on the blood transfusion activities worldwide. Additionally, we presented the impact of the COVID-19 pandemic on the Moroccan transfusion system activities and the measures established by the Moroccan National Centre of Blood Transfusion and Hematology (MNCBTH) to ensure management of this health crisis on the availability and the safety of blood products in Morocco. Results: Viruses like Zika, Influenza A (H1N1), Chikungunya, SARS-CoV, MERS-CoV, and Ebola have been of great concern in terms of virulence, modes of transmission, and impact on blood transfusion activities. The COVID-19 pandemic has impacted the availability of blood products in blood establishments worldwide. In Morocco, the COVID-19 pandemic affected blood collections and caused a significant decrease in the number of blood donors nationally. Data provided from all regional blood transfusion centers and blood banks in Morocco show that the total number of blood donations made in 2020 was 297,841 blood donations nationally compared to 334,510 blood donations made in 2019, with a decrease of 36,669 blood donations. The number of LBP produced in 2020 was 455,805 units compared to 695,974 units produced in 2019, which corresponds to a reduction of 57,654 units. The number of Labile Blood Products (LBP) delivered in 2020 is 455,805 units against 451,736 delivered in 2019, with an increase of 4069 units. The pandemic impacted other activities of the blood transfusion system in Morocco like continuing education programs, meeting activities, technical missions, and the Moroccan plasma removal for the fractionation. Conclusion: The COVID-19 pandemic has had a significant impact on blood transfusion activities worldwide. The MNCBTH has expressed continued adaptability to ensure proper management of the impact of the COVID-19 pandemic on the availability and safety of blood products in Morocco.<\/jats:p>","DOI":"10.5348\/100065z02sb2021rv","type":"journal-article","created":{"date-parts":[[2022,2,23]],"date-time":"2022-02-23T08:41:53Z","timestamp":1645605713000},"page":"1-21","source":"Crossref","is-referenced-by-count":2,"title":["Impact of the COVID-19 pandemic on blood transfusion systems: International review and the Moroccan blood transfusion system experience"],"prefix":"10.5348","volume":"11","author":[{"given":"Sabah","family":"Bouhou","sequence":"first","affiliation":[{"name":"National Centre for Blood Transfusion and Hematology, Rabat, Morocco, Hematology Research Team, Hematology Laboratory, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco"}]},{"given":"Khadija","family":"Lahjouji","sequence":"first","affiliation":[{"name":"National Centre for Blood Transfusion and Hematology, Rabat, Morocco"}]},{"given":"Mohammed","family":"Benajiba","sequence":"first","affiliation":[{"name":"National Centre for Blood Transfusion and Hematology, Rabat, Morocco"}]},{"given":"Azlarab","family":"Masrar","sequence":"first","affiliation":[{"name":"Hematology Research Team, Hematology Laboratory, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco, Central Hematology Laboratory, Ibn Sina University Hospital Centre, Rabat, Morocco"}]}],"member":"3299","published-online":{"date-parts":[[2021,11,15]]},"reference":[{"key":"ref=1","doi-asserted-by":"crossref","unstructured":"Chidiac C, Ferry T. 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This is the first large cohort study to examine binge drinking as a risk factor for vascular brain injury (VBI). Methods: We used linear and Poisson regression to examine the association of self-reported binge drinking with VBI, measured via magnetic resonance imaging (MRI), in 817 older AIs who participated in the Strong Heart and Cerebrovascular Disease and Its Consequences in American Indians studies. Results: Any binge drinking at multiple time-points was associated with increased sulcal (\u03b2 = 0.360, 95% CI [0.079, 0.641]) and ventricle dilatation (\u03b2 = 0.512, 95% CI [0.174, 0.850]) compared to no binge drinking. Discussion: These observed associations are consistent with previous findings. Identifying how binge drinking may contribute to VBI in older AIs may suggest modifiable health behaviors for neurological risk reduction and disease prevention. <\/jats:p>","DOI":"10.1177\/08982643211013696","type":"journal-article","created":{"date-parts":[[2021,6,25]],"date-time":"2021-06-25T04:23:11Z","timestamp":1624594991000},"page":"51S-59S","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Associations of Binge Drinking With Vascular Brain Injury and Atrophy in Older American Indians: The Strong Heart Study"],"prefix":"10.1177","volume":"33","author":[{"given":"Jordan P.","family":"Lewis","sequence":"first","affiliation":[{"name":"WWAMI School of Medical Education, College of Health, University of Alaska Anchorage, Anchorage, AK, USA"}]},{"given":"Astrid M.","family":"Suchy-Dicey","sequence":"additional","affiliation":[{"name":"Institute for Research and Education to Advance Community Health, Washington State University, Seattle, WA, USA"},{"name":"Elson S Floyd College of Medicine, Washington State University, Seattle, WA, USA"}]},{"given":"Carolyn","family":"Noonan","sequence":"additional","affiliation":[{"name":"Institute for Research and Education to Advance Community Health, Washington State University, Seattle, WA, USA"},{"name":"Elson S Floyd College of Medicine, Washington State University, Seattle, WA, USA"}]},{"given":"Valarie","family":"Blue Bird Jernigan","sequence":"additional","affiliation":[{"name":"College of Public Health, Oklahoma State University Center for Health Sciences, Tulsa, OK, USA"}]},{"given":"Jason G.","family":"Umans","sequence":"additional","affiliation":[{"name":"MedStar Health Research Institute, Hyattsville, MD, USA"},{"name":"Georgetown-Howard Universities Center for Clinical and Translational Science, Washington, DC, USA"}]},{"given":"Kimiko","family":"Domoto-Reilly","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Washington, Seattle, WA, USA"}]},{"given":"Dedra S.","family":"Buchwald","sequence":"additional","affiliation":[{"name":"Institute for Research and Education to Advance Community Health, Washington State University, Seattle, WA, USA"},{"name":"Elson S Floyd College of Medicine, Washington State University, Seattle, WA, USA"}]},{"given":"Spero M.","family":"Manson","sequence":"additional","affiliation":[{"name":"Centers for American Indian and Alaska Native Health, University of Colorado Anschutz Medical Campus, Auraro, CO, USA"}]}],"member":"179","published-online":{"date-parts":[[2021,6,24]]},"reference":[{"key":"bibr1-08982643211013696","doi-asserted-by":"publisher","DOI":"10.1177\/0022042613491100"},{"key":"bibr2-08982643211013696","doi-asserted-by":"publisher","DOI":"10.1016\/j.tox.2013.03.001"},{"key":"bibr3-08982643211013696","doi-asserted-by":"publisher","DOI":"10.2105\/ajph.93.10.1683"},{"issue":"1","key":"bibr4-08982643211013696","first-page":"14","volume":"61","author":"Centers for Disease Control and Prevention CDC","year":"2012","journal-title":"MMWR. 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Pulsatile shear stress (PS) is defined by laminar flow and is predominantly located in straight vascular regions, while disturbed or oscillatory shear stress (OS) is localized to branch points and bifurcations. Such flow patterns have become a central focus of vascular diseases, such as atherosclerosis, because the focal distribution of endothelial dysfunction corresponds to regions exposed to OS, whereas endothelial homeostasis is maintained in regions defined by PS. Deciphering the mechanotransduction events that occur in ECs in response to differential flow patterns has required the innovation of multidisciplinary approaches in both in vitro and in vivo systems. The results from these studies have identified a multitude of shear stress-regulated molecular networks in the endothelium that are implicated in health and disease. This review outlines the significance of scientific findings generated in collaboration with Dr. Shu Chien.<\/jats:p>","DOI":"10.1063\/1.5129563","type":"journal-article","created":{"date-parts":[[2020,2,20]],"date-time":"2020-02-20T12:51:53Z","timestamp":1582203113000},"update-policy":"https:\/\/doi.org\/10.1063\/aip-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Endothelial mechanobiology"],"prefix":"10.1063","volume":"4","author":[{"given":"Ming","family":"He","sequence":"first","affiliation":[{"name":"Department of Medicine, University of California 1 , San Diego, California 92093, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0035-0185","authenticated-orcid":false,"given":"Marcy","family":"Martin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine 2 , Stanford, California 94305, USA"}]},{"given":"Traci","family":"Marin","sequence":"additional","affiliation":[{"name":"Department of Health Sciences, Victor Valley College 3 , Victorville, California 92395, USA"}]},{"given":"Zhen","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Diabetes Complications and Metabolism, Beckman Research Institute, City of Hope 4 , California 91010, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9627-613X","authenticated-orcid":false,"given":"Brendan","family":"Gongol","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California 1 , San Diego, California 92093, USA"}]}],"member":"317","published-online":{"date-parts":[[2020,2,20]]},"reference":[{"key":"2024061318161202100_c1","doi-asserted-by":"publisher","first-page":"113","DOI":"10.3233\/CH-2008-1074","article-title":"Endothelial dysfunction and monocyte recruitment in cells\n            exposed to non-uniform shear stress","volume":"39","year":"2008","journal-title":"Clin. 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However, previous work has not used statistical causal inference methods tailored to address bias from time-varying confounding. The objective of this study is to propose an analytical approach for estimating longitudinal health effects of air pollution while accounting for time-varying confounding using marginal structural models and to re-analyze data on air pollution and emphysema progression from the Multi-Ethnic Study of Atherosclerosis using this analytical approach. We estimate weights for continuous exposure levels using two techniques: quantile binning of the exposure and a semiparametric model for the requisite conditional densities. The latter approach incorporates flexible machine learning methods. We find evidence for the harmful effects of ambient ozone pollution during study follow-up on the progression of emphysema, consistent with previously reported results. We find no evidence of effects of NOx during study follow-up. 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DK089174"],"award-info":[{"award-number":["R01 DK089174"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2014,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>BACKGROUND<\/jats:title>\n                  <jats:p>1,5-Anhydroglucitol (1,5-AG) is inversely related to hyperglycemia and may be a useful indicator of short-term (1\u20132 weeks) hyperglycemia and glycemic excursions, but its prognostic value is unclear. We sought to evaluate the associations of 1,5-AG with risk of diabetes and microvascular disease.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>We measured 1,5-AG in blood samples from over 10 000 participants in the ARIC (Atherosclerosis Risk in Communities) Study (baseline, 1990\u20131992) and characterized the independent associations with prevalent retinopathy and with incident chronic kidney disease and incident diabetes during approximately 20 years of follow-up.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>We found that 1,5-AG was associated with prevalent retinopathy, driven primarily by the strong association in persons with diagnosed diabetes: adjusted odds ratio (OR) 11.26 (95% CI, 6.17\u201320.53) for &amp;lt;6 \u03bcg\/mL compared to 1,5-AG \u226510 \u03bcg\/mL. This result remained significant after further adjustment for hemoglobin A1c (Hb A1c) (OR, 4.85; 95% CI, 2.42\u20139.74). In persons with diagnosed diabetes, low 1,5-AG (&amp;lt;6 \u03bcg\/mL vs \u226510 \u03bcg\/mL) was also associated with a &amp;gt;2-fold increased risk of incident chronic kidney disease [adjusted hazard ratio (HR), 2.83; 95% CI, 2.15\u20133.74] and remained significant after adjustment for Hb A1c (HR, 1.43; 95% CI, 1.02\u20132.00). Nondiabetic participants with high 1,5-AG (\u226510 \u03bcg\/mL) had the lowest prevalence of retinopathy and lowest risk of kidney disease. In persons without diagnosed diabetes at baseline, 1,5-AG &amp;lt;10 \u03bcg\/mL was also associated with incident diabetes (adjusted HR, 2.29; 95% CI, 2.03\u20132.58).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>1,5-AG was associated with long-term risk of important microvascular outcomes, particularly in persons with diagnosed diabetes and even after adjustment for Hb A1c. Our results suggest 1,5-AG may capture risk information associated with hyperglycemic excursions.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1373\/clinchem.2014.229427","type":"journal-article","created":{"date-parts":[[2014,9,8]],"date-time":"2014-09-08T23:23:58Z","timestamp":1410218638000},"page":"1409-1418","source":"Crossref","is-referenced-by-count":59,"title":["Association of 1,5-Anhydroglucitol with Diabetes and Microvascular Conditions"],"prefix":"10.1093","volume":"60","author":[{"given":"Elizabeth","family":"Selvin","sequence":"first","affiliation":[{"name":"Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"},{"name":"Division of General Internal Medicine, Department of Medicine, Johns Hopkins University, Baltimore, MD"}]},{"given":"Andreea M","family":"Rawlings","sequence":"first","affiliation":[{"name":"Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]},{"given":"Morgan","family":"Grams","sequence":"first","affiliation":[{"name":"Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"},{"name":"Division of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, MD"}]},{"given":"Ronald","family":"Klein","sequence":"first","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health"}]},{"given":"Michael","family":"Steffes","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MD"}]},{"given":"Josef","family":"Coresh","sequence":"first","affiliation":[{"name":"Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"},{"name":"Division of General Internal Medicine, Department of Medicine, Johns Hopkins University, Baltimore, MD"}]}],"member":"286","published-online":{"date-parts":[[2014,11,1]]},"reference":[{"key":"2020022705524974000_B1","doi-asserted-by":"crossref","first-page":"S14","DOI":"10.2337\/dc14-S014","article-title":"Standards of medical care in diabetes\u20132014","volume":"37","author":"American Diabetes Association","year":"2014","journal-title":"Diabetes Care"},{"key":"2020022705524974000_B2","doi-asserted-by":"crossref","first-page":"1545","DOI":"10.1001\/archinte.167.14.1545","article-title":"Short-term variability in measures of glycemia and implications for the classification of diabetes","volume":"167","author":"Selvin","year":"2007","journal-title":"Arch Intern Med"},{"key":"2020022705524974000_B3","doi-asserted-by":"crossref","first-page":"1211","DOI":"10.1161\/01.CIR.0000027569.76671.A8","article-title":"Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial dysfunction and oxidative stress generation: effects of short- and long-term simvastatin treatment","volume":"106","author":"Ceriello","year":"2002","journal-title":"Circulation"},{"key":"2020022705524974000_B4","doi-asserted-by":"crossref","first-page":"775","DOI":"10.2337\/diacare.24.4.775","article-title":"Postprandial blood glucose. American diabetes association","volume":"24","author":"American Diabetes Association","year":"2001","journal-title":"Diabetes Care"},{"key":"2020022705524974000_B5","doi-asserted-by":"crossref","first-page":"1845","DOI":"10.2337\/diacare.25.10.1845","article-title":"Fasting and postchallenge glycemia and cardiovascular disease risk: the Framingham Offspring Study","volume":"25","author":"Meigs","year":"2002","journal-title":"Diabetes Care"},{"key":"2020022705524974000_B6","first-page":"E268","article-title":"Origin and disposal of 1,5-anhydroglucitol, a major polyol in the human body","volume":"263","author":"Yamanouchi","year":"1992","journal-title":"Am J Physiol"},{"key":"2020022705524974000_B7","doi-asserted-by":"crossref","first-page":"S261","DOI":"10.1016\/0168-8227(94)90259-3","article-title":"Serum 1,5-anhydroglucitol (1,5 ag): new clinical marker for glycemic control","volume":"24","author":"Yamanouchi","year":"1994","journal-title":"Diabetes Res Clin 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HL092577"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["18SFRN34110082"],"award-info":[{"award-number":["18SFRN34110082"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:sec id=\"sec001\">\n<jats:title>Background<\/jats:title>\n<jats:p>Both elevated and low resting heart rates are associated with atrial fibrillation (AF), suggesting a U-shaped relationship. However, evidence for a U-shaped causal association between genetically-determined resting heart rate and incident AF is limited. We investigated potential directional changes of the causal association between genetically-determined resting heart rate and incident AF.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec002\">\n<jats:title>Method and results<\/jats:title>\n<jats:p>Seven cohorts of the AFGen consortium contributed data to this meta-analysis. All participants were of European ancestry with known AF status, genotype information, and a heart rate measurement from a baseline electrocardiogram (ECG). Three strata of instrumental variable-free resting heart rate were used to assess possible non-linear associations between genetically-determined resting heart rate and the logarithm of the incident AF hazard rate: &lt;65; 65\u201375; and &gt;75 beats per minute (bpm). Mendelian randomization analyses using a weighted resting heart rate polygenic risk score were performed for each stratum.<\/jats:p>\n<jats:p>We studied 38,981 individuals (mean age 59\u00b110 years, 54% women) with a mean resting heart rate of 67\u00b111 bpm. During a mean follow-up of 13\u00b15 years, 4,779 (12%) individuals developed AF. A U-shaped association between the resting heart rate and the incident AF-hazard ratio was observed. Genetically-determined resting heart rate was inversely associated with incident AF for instrumental variable-free resting heart rates below 65 bpm (hazard ratio for genetically-determined resting heart rate, 0.96; 95% confidence interval, 0.94\u20130.99; p = 0.01). Genetically-determined resting heart rate was not associated with incident AF in the other two strata.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec003\">\n<jats:title>Conclusions<\/jats:title>\n<jats:p>For resting heart rates below 65 bpm, our results support an inverse causal association between genetically-determined resting heart rate and incident AF.<\/jats:p>\n<\/jats:sec>","DOI":"10.1371\/journal.pone.0268768","type":"journal-article","created":{"date-parts":[[2022,5,20]],"date-time":"2022-05-20T17:44:50Z","timestamp":1653068690000},"page":"e0268768","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":14,"title":["Resting heart rate and incident atrial fibrillation: A stratified Mendelian randomization in the AFGen consortium"],"prefix":"10.1371","volume":"17","author":[{"given":"J. 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Cells in granuloerythrocytic colonies that developed in such mixing experiments were either uniformly female by Y- chromatin analysis or contained Y-chromatin bodies in both the granulocytic and erythroid cells.<\/jats:p>","DOI":"10.1182\/blood.v52.6.1243.1243","type":"journal-article","created":{"date-parts":[[2019,10,13]],"date-time":"2019-10-13T00:16:36Z","timestamp":1570925796000},"page":"1243-1248","update-policy":"http:\/\/dx.doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":256,"title":["Granuloerythropoietic colonies in human bone marrow, peripheral blood, and cord blood"],"prefix":"10.1182","volume":"52","author":[{"given":"AA","family":"Fauser","sequence":"first","affiliation":[]},{"given":"HA","family":"Messner","sequence":"additional","affiliation":[]}],"member":"234","container-title":["Blood"],"language":"en","link":[{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/52\/6\/1243\/581447\/1243.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/52\/6\/1243\/581447\/1243.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,11,19]],"date-time":"2019-11-19T15:09:45Z","timestamp":1574176185000},"score":8.526369,"resource":{"primary":{"URL":"https:\/\/ashpublications.org\/blood\/article\/52\/6\/1243\/161089\/Granuloerythropoietic-colonies-in-human-bone"}},"issued":{"date-parts":[[1978,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1978,12,1]]}},"URL":"https:\/\/doi.org\/10.1182\/blood.v52.6.1243.1243","ISSN":["0006-4971","1528-0020"],"issn-type":[{"value":"0006-4971","type":"print"},{"value":"1528-0020","type":"electronic"}],"published":{"date-parts":[[1978,12,1]]}},{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T05:48:07Z","timestamp":1773380887143,"version":"3.50.1"},"reference-count":5,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Blood Res"],"published-print":{"date-parts":[[2015]]},"DOI":"10.5045\/br.2015.50.1.3","type":"journal-article","created":{"date-parts":[[2015,3,28]],"date-time":"2015-03-28T20:39:16Z","timestamp":1427575156000},"page":"3","source":"Crossref","is-referenced-by-count":2,"title":["Is cord blood worth saving for public or private banking?"],"prefix":"10.1007","volume":"50","author":[{"given":"Young-Ho","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Hanyang University Medical Center, Hanyang University College of Medicine, Seoul, Korea."}]}],"member":"297","reference":[{"key":"10.5045\/br.2015.50.1.3_ref1","doi-asserted-by":"crossref","first-page":"163","DOI":"10.1097\/MOP.0000000000000065","volume":"26","author":"Yoder","year":"2014","journal-title":"Curr Opin Pediatr"},{"key":"10.5045\/br.2015.50.1.3_ref2","doi-asserted-by":"crossref","first-page":"20","DOI":"10.1016\/j.bbmt.2013.09.010","volume":"20","author":"Iafolla","year":"2014","journal-title":"Biol Blood Marrow Transplant"},{"key":"10.5045\/br.2015.50.1.3_ref3","unstructured":"Number of shipments done globally for unrelated patients. 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Blood grouping ABO and Rhesus were determined using conventional blood typing procedures based on Beth-Vincent and Simonin-Michon methods.\n\n\t\t\t\t\t\t\tResults: Out of 266,055 blood donors included, 217,990 (81.9%) were male and 48,065 (18.1%) were female donors. Most donors were young adults, representing the age group of 18\u201330 (45%). The majority were replacement (62.4%) while the remainder was voluntary donors (37.6%). The most prevalent blood group was O (56.6%), followed by blood groups A (20.3%) and B (20.1%), whereas the least prevalent blood group was AB (2.9%). The majority 97.6% were Rh D positive, and 2.4% were Rh D negative.\n\n\t\t\t\t\t\t\tConclusion: The study has a significant implication regarding the inventory management of blood transfusion center in Republic of Congo.\n\t\t\t            \t<\/jats:p>","DOI":"10.5348\/100077z02ba2023ra","type":"journal-article","created":{"date-parts":[[2023,6,28]],"date-time":"2023-06-28T07:54:28Z","timestamp":1687938868000},"page":"9-14","source":"Crossref","is-referenced-by-count":0,"title":["Distribution of ABO and Rhesus (RHD) blood groups among blood donors in Republic of Congo"],"prefix":"10.5348","volume":"13","author":[{"given":"Brunel","family":"M Angounda","sequence":"first","affiliation":[{"name":"National Center of Blood Transfusion, Brazzaville, Republic of Congo, Faculty of Sciences and Technology, Marien NGOUABI University, Brazzaville, Republic of Congo"}]},{"given":"Serge","family":"O Mokono","sequence":"first","affiliation":[{"name":"National Center of Blood Transfusion, Brazzaville, Republic of Congo, Faculty of Health Sciences, Marien NGOUABI University, Brazzaville, Republic of Congo"}]},{"given":"Genevi\u00e8ve","family":"B Boukatou","sequence":"first","affiliation":[{"name":"National Center of Blood Transfusion, Brazzaville, Republic of Congo"}]},{"given":"Boris","family":"S Bakoua","sequence":"first","affiliation":[{"name":"National Center of Blood Transfusion, Brazzaville, Republic of Congo"}]},{"given":"Edwige","family":"PLC Nanitelamio","sequence":"first","affiliation":[{"name":"National Center of Blood Transfusion, Brazzaville, Republic of Congo"}]}],"member":"3299","published-online":{"date-parts":[[2023,6,28]]},"reference":[{"key":"ref=1","doi-asserted-by":"crossref","unstructured":"Shrestha L, Malla U, Mahotra NB. 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Diseases","doi-asserted-by":"publisher","award":["R01-DK-089174"],"award-info":[{"award-number":["R01-DK-089174"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01-HL-70825"],"award-info":[{"award-number":["R01-HL-70825"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"published-print":{"date-parts":[[2017,7,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>Hemoglobin A1c (HbA1c), a measure of average blood glucose level, is associated with the risk of dementia and cognitive impairment. However, the role of glycemic variability or glucose excursions in this association is unclear. We examined the association of glucose peaks in midlife, as determined by the measurement of 1,5-anhydroglucitol (1,5-AG) level, with the risk of dementia and 20-year cognitive decline.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>Nearly 13,000 participants from the Atherosclerosis Risk in Communities (ARIC) study were examined. Dementia was ascertained from surveillance, neuropsychological testing, telephone calls with participants or their proxies, or death certificate dementia codes. Cognitive function was assessed using three neuropsychological tests at three visits over 20 years and was summarized as z scores. We used Cox and linear mixed-effects models. 1,5-AG level was dichotomized at 10 \u03bcg\/mL and examined within clinical categories of HbA1c.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>Over a median time of 21 years, dementia developed in 1,105 participants. Among persons with diabetes, each 5 \u03bcg\/mL decrease in 1,5-AG increased the estimated risk of dementia by 16% (hazard ratio 1.16, P = 0.032). For cognitive decline among participants with diabetes and HbA1c &amp;lt;7% (53 mmol\/mol), those with glucose peaks had a 0.19 greater z score decline over 20 years (P = 0.162) compared with those without peaks. Among participants with diabetes and HbA1c \u22657% (53 mmol\/mol), those with glucose peaks had a 0.38 greater z score decline compared with persons without glucose peaks (P &amp;lt; 0.001). We found no significant associations in persons without diabetes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Among participants with diabetes, glucose peaks are a risk factor for cognitive decline and dementia. Targeting glucose peaks, in addition to average glycemia, may be an important avenue for prevention.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/dc16-2203","type":"journal-article","created":{"date-parts":[[2017,5,13]],"date-time":"2017-05-13T00:30:24Z","timestamp":1494635424000},"page":"879-886","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":95,"title":["Glucose Peaks and the Risk of Dementia and 20-Year Cognitive Decline"],"prefix":"10.2337","volume":"40","author":[{"given":"Andreea M.","family":"Rawlings","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]},{"given":"A. Richey","family":"Sharrett","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]},{"given":"Thomas H.","family":"Mosley","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Mississippi Medical Center, Jackson, MS"}]},{"given":"Shoshana H.","family":"Ballew","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]},{"given":"Jennifer A.","family":"Deal","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6923-7151","authenticated-orcid":false,"given":"Elizabeth","family":"Selvin","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD"}]}],"member":"1167","published-online":{"date-parts":[[2017,6,13]]},"reference":[{"key":"2022031219470566100_B1","doi-asserted-by":"crossref","first-page":"507","DOI":"10.1002\/dmrr.1112","article-title":"Cognitive dysfunction in patients with type 2 diabetes","volume":"26","author":"Reijmer","year":"2010","journal-title":"Diabetes Metab Res Rev"},{"key":"2022031219470566100_B2","doi-asserted-by":"crossref","first-page":"47","DOI":"10.1177\/0891988713516543","article-title":"Type 2 diabetes and cognitive impairment: contributions from neuroimaging","volume":"27","author":"Ryan","year":"2014","journal-title":"J Geriatr Psychiatry Neurol"},{"key":"2022031219470566100_B3","first-page":"S1","article-title":"Standards of medical care in diabetes\u20132016","volume":"39","author":"American Diabetes Association","year":"2016","journal-title":"Diabetes Care"},{"key":"2022031219470566100_B4","doi-asserted-by":"crossref","unstructured":"Tuligenga\u2008RH, Dugravot\u2008A, Tab\u00e1k\u2008AG, et al. 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Ltd.","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int J Blood Transfus Immunohematol"],"abstract":"<jats:p>\n\t\t\t\t    \t    Aims: The demand for blood and blood products in sub-Saharan Africa is occasioned by tropical infectious diseases and obstetric complications that cause anemia. We therefore need a well-organized blood transfusion service with sufficient resources to process blood and blood products, especially in the Western Kenya, where co-infections of tropical diseases are rampant. This study was aimed at determining the blood deficiency and challenges experienced by Eldoret Regional Blood Transfusion Center (ERBTC).\n\n\t\t\t\t\t\t\tMethods: A cross-sectional descriptive design was used to conduct the study. All the ERBTC staffs, donor records, and blood requisition and dispatch registers were studied. Self-administered questionnaires and data collection abstraction forms were used to collect data. The extracted data from ERBTC registers included those on demand and supply mismatches and blood discards. The obtained data were entered into Microsoft Excel and analyzed using descriptive statistics.\n\n\t\t\t\t\t\t\tResults: A total of 16 staffs, 230 donor records, and 9612 units of requested blood were reviewed. The ERBTC reported many challenges ranging from understaffing, limited funding, insufficient equipment, and irregular reagents and other laboratory supplies. During the study period, the blood bank only managed to supply 4740 units of blood against a demand of 9612 units, thus occasioning a 50.7% deficit. A discard rate of 7.8% after the screening was also reported due to insufficient volumes after collection and transfusion transmissible infections. However, there were no wastages during the study period.\n\n\t\t\t\t\t\t\tConclusion: The main challenges experienced by ERBTC were understaffing, insufficient funding, limited equipment, frequent reagent outages, and discards of unsuitable blood, resulting in very high deficits. We recommend hiring staff, increased funding, acquiring modern equipment and reagents, and recruiting known regular blood donors to alleviate frequent shortage.\n\t\t\t            \t<\/jats:p>","DOI":"10.5348\/100075z02km2022ra","type":"journal-article","created":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T15:44:54Z","timestamp":1665589494000},"page":"12-20","source":"Crossref","is-referenced-by-count":1,"title":["Challenges facing blood transfusion services at a regional blood transfusion center in Western Kenya"],"prefix":"10.5348","volume":"12","author":[{"given":"Kavulavu","family":"BM","sequence":"first","affiliation":[{"name":"Department of Medical Laboratory Sciences, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Bushuru","family":"BN","sequence":"first","affiliation":[{"name":"Department of Medical Laboratory Sciences, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Muendo","family":"NN","sequence":"first","affiliation":[{"name":"Department of Medical Laboratory Sciences, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Kumotia","family":"WO","sequence":"first","affiliation":[{"name":"Department of Medical Laboratory Sciences, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Kipkulei","family":"JC","sequence":"first","affiliation":[{"name":"Department of Pathology (Hematology and Blood Transfusion), School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Lotodo","family":"TC","sequence":"first","affiliation":[{"name":"Department of Pathology (Hematology and Blood Transfusion), School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Kirinyet","family":"JK","sequence":"first","affiliation":[{"name":"Department of Medical Laboratory Sciences, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]},{"given":"Tum","family":"F","sequence":"first","affiliation":[{"name":"Directorate of Pathology and Laboratory Services, Moi Teaching and Reference Hospital, PO Box 3-30100, Eldoret, Kenya"}]},{"given":"Obala","family":"A","sequence":"first","affiliation":[{"name":"Department of Microbiology and Parasitology, School of Medicine, Moi University, PO Box 4606-30100, Eldoret, Kenya"}]}],"member":"3299","published-online":{"date-parts":[[2022,10,12]]},"reference":[{"key":"ref=1","doi-asserted-by":"crossref","unstructured":"Chevalier MS, Kuehnert M, Basavaraju SV, Bjork A, Pitman JP. 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We analysed 1412 participants from the Multi\u2010Ethnic Study of Atherosclerosis who underwent both overnight polysomnography and cardiac magnetic resonance imaging. Subjects had been recruited 10\u00a0years earlier when free of cardiovascular disease. Our main exposure is the presence of central sleep apnea as defined by central apnea\u2013hypopnea index\u00a0=\u00a05 or the presence of Cheyne\u2013Stokes breathing. Outcome variables were left ventricular mass\/height, left ventricular ejection fraction, and left ventricular mass\/volume ratio. Multivariate linear regression models adjusted for age, gender, race, waist circumference, tobacco use, hypertension, and the obstructive apnea\u2013hypopnea index were fit for the outcomes. Of the 1412 participants, 27 (2%) individuals had central sleep apnea. 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Components of blood are described, including the blood cell types, their development and functions. Anaemias are discussed and their dental implications. Haemostasis and the coagulation pathway are described, followed by the bleeding disorders, how they are detected in blood tests and managed so as to avoid complications arising from dental treatment. The main malignancies of white blood cells are described in relation to dental care. 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Wonju: Korean Red Cross; 2024."},{"key":"ref3","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2017. Wonju: Korean Red Cross; 2018."},{"key":"ref4","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2018. Wonju: Korean Red Cross; 2019."},{"key":"ref5","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2019. Wonju: Korean Red Cross; 2020."},{"key":"ref6","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2020. Wonju: Korean Red Cross; 2021."},{"key":"ref7","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2021. Wonju: Korean Red Cross; 2022."},{"key":"ref8","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2022. Wonju: Korean Red Cross; 2023."},{"key":"ref9","unstructured":"Korean Red Cross Blood Services Headquarters. Blood services statistics 2023. Wonju: Korean Red Cross; 2024."},{"key":"ref10","unstructured":"Oh DJ. An experience of blood donor registry. Korean J Blood Transfus 2000;11:19-25."},{"key":"ref11","unstructured":"Oh DJ, Kim MH. Changes of hemoglobin and serum ferritin levels in whole blood donations. Korean J Blood Transfus 1998;9:1-7."},{"key":"ref12","unstructured":"Oh DJ, Lee JY. Repeat blood donors and iron deficiency anemia. 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Linear mixed\u2010effects and multistate models were adjusted for demographics, time\u2010varying covariates including blood pressure, and comorbidities these were used to examine associations of weight change and slow walking pace (&lt;2\u2009miles\/h) with (i) rate of annual estimated glomerular filtration rate (eGFR) decline and (ii) incident CKD, defined as eGFR<jats:sub>Cr\u2010Cys<\/jats:sub>\u2009&lt;\u200960\u2009mL\/min\/1.73 m<jats:sup>2<\/jats:sup>, and tested for interaction by baseline hypertension status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Among 1208 included MESA participants (median BMI 33.0\u2009kg\/m<jats:sup>2<\/jats:sup> [interquartile range 31.2\u201335.9]), 15% developed CKD. Slow walking pace was associated with eGFR decline (\u22120.27\u2009mL\/min\/1.73\u2009m<jats:sup>2<\/jats:sup>\/year; 95% CI: \u22120.42 to \u22120.12) and CKD risk (adjusted hazard ratio 1.48; 95% CI: 1.08 to 2.01). Weight gain was associated with CKD risk (adjusted hazard ratio 1.34; 95% CI: 1.02 to 1.78 per 5\u2009kg weight gain from baseline). There was no significant interaction by baseline hypertension status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Slow walking pace and weight gain were associated with CKD risk among adults with obesity who did not have diabetes at baseline.<\/jats:p><\/jats:sec>","DOI":"10.1002\/oby.23883","type":"journal-article","created":{"date-parts":[[2023,9,28]],"date-time":"2023-09-28T07:01:31Z","timestamp":1695884491000},"page":"3056-3065","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Modifiable kidney disease risk factors among nondiabetic adults with obesity from the Multi\u2010Ethnic Study of Atherosclerosis"],"prefix":"10.1002","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6500-2814","authenticated-orcid":false,"given":"Meera N.","family":"Harhay","sequence":"first","affiliation":[{"name":"Department of Medicine Drexel University College of Medicine  Philadelphia Pennsylvania USA"},{"name":"Department of Epidemiology and Biostatistics Drexel University Dornsife School of Public Health  Philadelphia Pennsylvania USA"},{"name":"Department of Medicine, Division of Nephrology University of Pennsylvania Health System  Philadelphia Pennsylvania USA"}]},{"given":"Yuna","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Biostatistics Drexel University Dornsife School of Public Health  Philadelphia Pennsylvania USA"}]},{"given":"Kari","family":"Moore","sequence":"additional","affiliation":[{"name":"Urban Health Collaborative Drexel University Dornsife School of Public Health  Philadelphia Pennsylvania USA"}]},{"given":"Michael O.","family":"Harhay","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine University of Pennsylvania  Philadelphia Pennsylvania USA"}]},{"given":"Ronit","family":"Katz","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Washington  Seattle Washington USA"}]},{"given":"Michael G.","family":"Shlipak","sequence":"additional","affiliation":[{"name":"Kidney Health Research Collaborative San Francisco VA Healthcare System and University of California  San Francisco California USA"}]},{"given":"Holly J.","family":"Mattix\u2010Kramer","sequence":"additional","affiliation":[{"name":"Departments of Public Health Science and Medicine, Division of Nephrology and Hypertension Loyola University Chicago  Maywood Illinois USA"}]}],"member":"311","published-online":{"date-parts":[[2023,9,28]]},"reference":[{"key":"e_1_2_9_2_1","unstructured":"United States Renal Data System.2020 Annual Data Report.2020Accessed May 1 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This is the first large scale attempt which uses transcriptomics, proteomics, and metabolomics (multi-omics) to determine whether there are molecularly defined clusters with distinct clinical phenotypes that may underlie the clinical heterogeneity. Subjects included 3,278 subjects from the COPDGene cohort with at least one of the following profiles: whole blood transcriptomes (2,650 subjects); plasma proteomes (1,013 subjects); and plasma metabolomes (1,136 subjects). 489 subjects had all three contemporaneous -omics profiles. Autoencoder embeddings were performed individually for each -omics dataset. Embeddings underwent subspace clustering using MineClus, either individually by -omics or combined, followed by recursive feature selection based on Support Vector Machines. Clusters were tested for associations with clinical variables. Optimal single -omics clustering typically resulted in two clusters. Although there was overlap for individual -omics cluster membership, each -omics cluster tended to be defined by unique molecular pathways. For example, prominent molecular features of the metabolome-based clustering included sphingomyelin, while key molecular features of the transcriptome-based clusters were related to immune and bacterial responses. We also found that when we integrated the -omics data at a later stage, we identified subtypes that varied based on age, severity of disease, in addition to diffusing capacity of the lungs for carbon monoxide, and precent on atrial fibrillation. In contrast, when we integrated the -omics data at an earlier stage by treating all data sets equally, there were no clinical differences between subtypes. Similar to clinical clustering, which has revealed multiple heterogenous clinical phenotypes, we show that transcriptomics, proteomics, and metabolomics tend to define clusters of COPD patients with different clinical characteristics. Thus, integrating these different -omics data sets affords additional insight into the molecular nature of COPD and its heterogeneity.<\/jats:p>","DOI":"10.1371\/journal.pone.0255337","type":"journal-article","created":{"date-parts":[[2021,8,25]],"date-time":"2021-08-25T17:26:28Z","timestamp":1629912388000},"page":"e0255337","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":35,"title":["Multi-omics subtyping pipeline for chronic obstructive pulmonary disease"],"prefix":"10.1371","volume":"16","author":[{"given":"Lucas A.","family":"Gillenwater","sequence":"first","affiliation":[]},{"given":"Shahab","family":"Helmi","sequence":"additional","affiliation":[]},{"given":"Evan","family":"Stene","sequence":"additional","affiliation":[]},{"given":"Katherine 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Sciences","doi-asserted-by":"publisher","award":["UL1-TR-001079"],"award-info":[{"award-number":["UL1-TR-001079"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1-TR-001420"],"award-info":[{"award-number":["UL1-TR-001420"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2023,5,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Ketone bodies (KB) are an important alternative metabolic fuel source for the myocardium. Experimental and human investigations suggest that KB may have protective effects in patients with heart failure. This study aimed to examine the association between KB and cardiovascular outcomes and mortality in an ethnically diverse population free from cardiovascular disease (CVD).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>This analysis included 6796 participants (mean age 62 \u00b1 10 years, 53% women) from the Multi-Ethnic Study of Atherosclerosis. Total KB was measured by nuclear magnetic resonance spectroscopy. Multivariable-adjusted Cox proportional hazard models were used to examine the association of total KB with cardiovascular outcomes. At a mean follow-up of 13.6 years, after adjusting for traditional CVD risk factors, increasing total KB was associated with a higher rate of hard CVD, defined as a composite of myocardial infarction, resuscitated cardiac arrest, stroke, and cardiovascular death, and all CVD (additionally included adjudicated angina) [hazard ratio, HR (95% confidence interval, CI): 1.54 (1.12\u20132.12) and 1.37 (1.04\u20131.80) per 10-fold increase in total KB, respectively]. Participants also experienced an 87% (95% CI: 1.17\u20132.97) increased rate of CVD mortality and an 81% (1.45\u20132.23) increased rate of all-cause mortality per 10-fold increase in total KB. Moreover, a higher rate of incident heart failure was observed with increasing total KB [1.68 (1.07\u20132.65), per 10-fold increase in total KB].<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>The study found that elevated endogenous KB in a healthy community-based population is associated with a higher rate of CVD and mortality. Ketone bodies could serve as a potential biomarker for cardiovascular risk assessment.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehad087","type":"journal-article","created":{"date-parts":[[2023,3,7]],"date-time":"2023-03-07T19:16:16Z","timestamp":1678216576000},"page":"1636-1646","source":"Crossref","is-referenced-by-count":40,"title":["Circulating ketone bodies and cardiovascular outcomes: the MESA study"],"prefix":"10.1093","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1162-2991","authenticated-orcid":false,"given":"Elad","family":"Shemesh","sequence":"first","affiliation":[{"name":"Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center , 6 Weizmann Street, Tel Aviv 6423906 , Israel"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4084-8175","authenticated-orcid":false,"given":"Parag Anilkumar","family":"Chevli","sequence":"additional","affiliation":[{"name":"Section on Hospital Medicine, Department of Internal Medicine, Wake Forest University School of Medicine , Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]},{"given":"Tareq","family":"Islam","sequence":"additional","affiliation":[{"name":"Section on Hospital Medicine, Department of Internal Medicine, Geisinger Medical Center , 100 N. Academy Ave, Danville, PA 17822 , USA"}]},{"given":"Charles A","family":"German","sequence":"additional","affiliation":[{"name":"Section of Cardiology, Department of Medicine, University of Chicago , 5841 S Maryland Ave, MC 6080, Chicago, IL 60637 , USA"}]},{"given":"James","family":"Otvos","sequence":"additional","affiliation":[{"name":"NMR Diagnostics , Morrisville, NC"}]},{"given":"Joseph","family":"Yeboah","sequence":"additional","affiliation":[{"name":"Section on Cardiovascular Medicine, Wake Forest University School of Medicine , Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]},{"given":"Fatima","family":"Rodriguez","sequence":"additional","affiliation":[{"name":"Section on Cardiovascular Medicine, Department of Internal Medicine, Stanford University School of Medicine , 300 Pasteur Drive, Stanford, CA 94305 , USA"}]},{"given":"Christopher","family":"deFilippi","sequence":"additional","affiliation":[{"name":"Inova Heart and Vascular Institute , 3300 Gallows Rd, Falls Church, VA 22042 , USA"}]},{"given":"Joao A C","family":"Lima","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Johns Hopkins University , 600 N. Wolfe Street, Baltimore, MD 21287 , USA"}]},{"given":"Michael","family":"Blaha","sequence":"additional","affiliation":[{"name":"The Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University , 600 N. Wolfe Street, Baltimore, MD 21287 , USA"}]},{"given":"Ambarish","family":"Pandey","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center , 5323 Harry Hines Blvd, Dallas, TX 75390 , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0885-1953","authenticated-orcid":false,"given":"Muthiah","family":"Vaduganathan","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School , MA75 Francis Street, Boston, MA 20115 , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9071-3287","authenticated-orcid":false,"given":"Michael D","family":"Shapiro","sequence":"additional","affiliation":[{"name":"Center for the Prevention of Cardiovascular Disease, Section on Cardiovascular Medicine, Wake Forest University School of Medicine , Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]}],"member":"286","published-online":{"date-parts":[[2023,3,6]]},"reference":[{"key":"2023080919094869400_ehad087-B1","doi-asserted-by":"crossref","first-page":"165739","DOI":"10.1016\/j.bbadis.2020.165739","article-title":"Cardiac ketone body metabolism","volume":"1866","author":"Abdul Kadir","year":"2020","journal-title":"Biochim Biophys Acta Mol Basis Dis"},{"key":"2023080919094869400_ehad087-B2","doi-asserted-by":"crossref","first-page":"262","DOI":"10.1016\/j.cmet.2016.12.022","article-title":"Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics","volume":"25","author":"Puchalska","year":"2017","journal-title":"Cell Metab"},{"key":"2023080919094869400_ehad087-B3","doi-asserted-by":"crossref","first-page":"706","DOI":"10.1161\/CIRCULATIONAHA.115.017545","article-title":"Evidence for intramyocardial disruption of lipid metabolism and increased myocardial ketone utilization in advanced human heart failure","volume":"133","author":"Bedi","year":"2016","journal-title":"Circulation"},{"key":"2023080919094869400_ehad087-B4","doi-asserted-by":"crossref","first-page":"698","DOI":"10.1161\/CIRCULATIONAHA.115.017355","article-title":"The failing heart relies on ketone bodies as a fuel","volume":"133","author":"Aubert","year":"2016","journal-title":"Circulation"},{"key":"2023080919094869400_ehad087-B5","doi-asserted-by":"crossref","first-page":"1800","DOI":"10.1161\/CIRCULATIONAHA.119.045033","article-title":"Implications of altered ketone metabolism and therapeutic ketosis in heart failure","volume":"141","author":"Selvaraj","year":"2020","journal-title":"Circulation"},{"key":"2023080919094869400_ehad087-B6","doi-asserted-by":"crossref","first-page":"689","DOI":"10.1161\/CIRCULATIONAHA.116.021230","article-title":"Ketones step to the plate A game changer for metabolic remodeling in heart failure?","volume":"133","author":"Kolwicz","year":"2016","journal-title":"Circulation"},{"key":"2023080919094869400_ehad087-B7","doi-asserted-by":"crossref","first-page":"211","DOI":"10.1126\/science.1227166","article-title":"Suppression of oxidative stress by beta-hydroxybutyrate, an endogenous histone deacetylase inhibitor","volume":"339","author":"Shimazu","year":"2013","journal-title":"Science"},{"key":"2023080919094869400_ehad087-B8","doi-asserted-by":"crossref","first-page":"e005066","DOI":"10.1161\/JAHA.116.005066","article-title":"Ketone body infusion with 3-hydroxybutyrate reduces myocardial glucose uptake and increases blood flow in humans: a positron emission tomography study","volume":"6","author":"Gormsen","year":"2017","journal-title":"J Am Heart Assoc"},{"key":"2023080919094869400_ehad087-B9","doi-asserted-by":"crossref","first-page":"e124079","DOI":"10.1172\/jci.insight.124079","article-title":"The failing heart utilizes 3-hydroxybutyrate as a metabolic stress defense","volume":"4","author":"Horton","year":"2019","journal-title":"JCI Insight"},{"key":"2023080919094869400_ehad087-B10","doi-asserted-by":"crossref","first-page":"2129","DOI":"10.1161\/CIRCULATIONAHA.118.036459","article-title":"Cardiovascular effects of treatment with the ketone body 3-hydroxybutyrate in chronic heart failure patients","volume":"139","author":"Nielsen","year":"2019","journal-title":"Circulation"},{"key":"2023080919094869400_ehad087-B11","doi-asserted-by":"crossref","first-page":"1573","DOI":"10.1007\/s00125-016-3987-3","article-title":"SGLT2 Inhibition and cardiovascular events: why did EMPA-REG outcomes surprise and what were the likely mechanisms? 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We investigated the relationship of LV longitudinal strain, LV early diastolic strain rate (SR) and left atrial (LA) reservoir strain with long-term CHD incidence in community-dwelling older adults.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>The association of all three strain measures with incidence of non-fatal and fatal CHD (primary outcome of revascularisation, non-fatal and fatal myocardial infarction) was examined in the population-based Cardiovascular Health Study using multivariable Cox proportional hazards models. Follow-up was truncated at 10 years.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>We included 3313 participants (mean (SD) age 72.6 (5.5) years). During a median follow-up of 10.0 (25th\u201375th percentile 7.7\u201310.0) years, 439 CHD events occurred. LV longitudinal strain (HR=1.25 per SD decrement, 95% CI 1.09 to 1.43) and LV early diastolic SR (HR=1.31 per SD decrement, 95% CI 1.14 to 1.50) were associated with a significantly greater risk of incident CHD after adjustment for potential confounders. By contrast, LA reservoir strain was not associated with incident CHD (HR=1.06 per SD decrement, 95% CI 0.94 to 1.19). Additional adjustment for biochemical and echocardiographic measures of myocardial stress, dysfunction and remodelling did not meaningfully alter these associations.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>We found an association between echocardiographic measures of subclinically altered LV mechanics and incident CHD. These findings inform the underlying biology of subclinical LV dysfunction and CHD. Early detection of asymptomatic myocardial dysfunction may offer an opportunity for prevention and early intervention.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/heartjnl-2021-319296","type":"journal-article","created":{"date-parts":[[2021,7,13]],"date-time":"2021-07-13T13:25:53Z","timestamp":1626182753000},"page":"529-535","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["Adverse cardiac mechanics and incident coronary heart disease in the Cardiovascular Health Study"],"prefix":"10.1136","volume":"108","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9499-6456","authenticated-orcid":false,"given":"Daniele","family":"Massera","sequence":"first","affiliation":[{"name":"Leon H. Charney Division of Cardiology, NYU Langone Health, New York, New York, USA"}]},{"given":"Mo","family":"Hu","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}]},{"given":"Joseph A","family":"Delaney","sequence":"additional","affiliation":[{"name":"College of Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada"}]},{"given":"Traci M","family":"Bartz","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington, Seattle, Washington, USA"}]},{"given":"Megan E","family":"Bach","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}]},{"given":"Stephen J","family":"Dvorak","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}]},{"given":"Christopher R","family":"DeFilippi","sequence":"additional","affiliation":[{"name":"Inova Heart and Vascular Institute, Falls Church, Virginia, USA"}]},{"given":"Bruce M","family":"Psaty","sequence":"additional","affiliation":[{"name":"Cardiovascular Health Research Unit, Departments of Epidemiology, Medicine, and Health Services, University of Washington, Seattle, Washington, USA"}]},{"given":"John S","family":"Gottdiener","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, University of Maryland, Baltimore, Maryland, USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9936-7803","authenticated-orcid":false,"given":"Jorge R","family":"Kizer","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA"}]},{"given":"Sanjiv J","family":"Shah","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}]}],"member":"239","published-online":{"date-parts":[[2021,7,13]]},"reference":[{"key":"2025091922021580000_108.7.529.1","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0000000000000558"},{"key":"2025091922021580000_108.7.529.2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCIMAGING.110.959817"},{"key":"2025091922021580000_108.7.529.3","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCIMAGING.115.004181"},{"key":"2025091922021580000_108.7.529.4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00642.2013"},{"key":"2025091922021580000_108.7.529.5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcmg.2011.02.018"},{"key":"2025091922021580000_108.7.529.6","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2019.01.059"},{"key":"2025091922021580000_108.7.529.7","doi-asserted-by":"publisher","DOI":"10.1002\/ejhf.154"},{"key":"2025091922021580000_108.7.529.8","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.115.002071"},{"key":"2025091922021580000_108.7.529.9","doi-asserted-by":"crossref","unstructured":"Biering-S\u00f8rensen T , Biering-S\u00f8rensen SR , Olsen FJ , et al . Global longitudinal strain by echocardiography predicts long-term risk of cardiovascular morbidity and mortality in a low-risk general population. 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The study originated and grew over many years of introspection from a series of value questions formulated within the context of attempts to distinguish the \u2018social\u2019 from the \u2018economic\u2019 in public policies and in those institutions and services with declared \u2018welfare\u2019 goals. As such, this book centres on human blood: the scientific, social, economic, and ethical issues involved in its procurement, processing, distribution, use, and benefit in Britain, the United States, the Soviet Union, South Africa, and other countries. Ultimately, it considers the role of altruism in modern society. It attempts to fuse the politics of welfare and the morality of individual wills.<\/p>","DOI":"10.1332\/policypress\/9781447349570.003.0001","type":"book-chapter","created":{"date-parts":[[2019,5,23]],"date-time":"2019-05-23T10:06:36Z","timestamp":1558605996000},"page":"1-4","source":"Crossref","is-referenced-by-count":1,"title":["Introduction: human blood and social policy"],"prefix":"10.1332","author":[{"given":"Richard M.","family":"Titmuss","sequence":"first","affiliation":[]}],"member":"165","published-online":{"date-parts":[[2019,5,23]]},"container-title":["The Gift Relationship"],"original-title":["Introduction: human blood and social policy"],"language":"en","deposited":{"date-parts":[[2022,7,28]],"date-time":"2022-07-28T19:22:37Z","timestamp":1659036157000},"score":8.509856,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/policy-press-scholarship-online\/book\/22093\/chapter\/182204278"}},"issued":{"date-parts":[[2018,10,31]]},"ISBN":["9781447349570","9781447349587"],"references-count":0,"URL":"https:\/\/doi.org\/10.1332\/policypress\/9781447349570.003.0001","published":{"date-parts":[[2018,10,31]]}},{"indexed":{"date-parts":[[2024,4,18]],"date-time":"2024-04-18T21:10:41Z","timestamp":1713474641554},"publisher-location":"London","standards-body":{"name":"BSI British Standards","acronym":"BSI"},"reference-count":0,"publisher":"BSI British Standards","content-domain":{"domain":[],"crossmark-restriction":false},"DOI":"10.3403\/30331654","type":"standard","created":{"date-parts":[[2020,4,22]],"date-time":"2020-04-22T20:30:34Z","timestamp":1587587434000},"approved":{"date-parts":[[2018,10,3]]},"source":"Crossref","is-referenced-by-count":0,"title":["Extracorporeal systems for blood purification"],"prefix":"10.3403","member":"1988","deposited":{"date-parts":[[2024,4,18]],"date-time":"2024-04-18T20:32:51Z","timestamp":1713472371000},"score":8.507828,"resource":{"primary":{"URL":"https:\/\/linkresolver.bsigroup.com\/junction\/resolve\/000000000030331654?restype=standard"}},"subtitle":["Extracorporeal blood circuit for haemodialysers, haemodiafilters and haemofilters"],"issued":{"date-parts":[[null]]},"references-count":0,"URL":"https:\/\/doi.org\/10.3403\/30331654"},{"indexed":{"date-parts":[[2025,6,28]],"date-time":"2025-06-28T04:06:33Z","timestamp":1751083593669,"version":"3.41.0"},"reference-count":0,"publisher":"S. 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Fasting and postload levels of glucose and non-esterified fatty acids (NEFAs) reflect different facets of metabolic regulation. We sought to study their respective contributions to AF risk concurrently.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>We assessed levels of fasting and postload glucose and NEFA in the Cardiovascular Health Study to identify associations with AF incidence and, secondarily, with ECG parameters of AF risk available at baseline. Linear and Cox regressions were performed.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The study included 1876 participants (age 77.7\u00b14.4). During the median follow-up of 11.4 years, 717 cases of incident AF occurred. After adjustment for potential confounders, postload glucose showed an association with incident AF (HR per SD increment of postload glucose=1.11, 95% CI 1.02 to 1.21, p=0.017). Both glucose measures, but not NEFA, were positively associated with higher P wave terminal force in V1 (PTFV1); the association remained significant only for postload glucose when the two measures were entered together (\u03b2 per SD increment=138 \u03bcV\u00b7ms, 95% CI 15 to 260, p=0.028). Exploratory analyses showed significant interaction by sex for fasting NEFA (p<jats:sub>interaction<\/jats:sub>=0.044) and postload glucose (p<jats:sub>interaction<\/jats:sub>=0.015) relative to AF, with relationships stronger in women. For postload glucose, the association with incident AF was observed among women but not among men.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Among older adults, postload glucose was positively associated with incident AF, with consistent findings for PTFV1. In exploratory analyses, the relationship with AF appeared specific to women. These findings require further study but suggest that interventions to address postprandial dysglycaemia late in life might reduce AF.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/heartjnl-2022-321633","type":"journal-article","created":{"date-parts":[[2022,12,22]],"date-time":"2022-12-22T13:20:39Z","timestamp":1671715239000},"page":"606-611","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":5,"title":["Dysregulated carbohydrate and lipid metabolism and risk of atrial fibrillation in advanced old age"],"prefix":"10.1136","volume":"109","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9136-3285","authenticated-orcid":false,"given":"Cara N","family":"Pellegrini","sequence":"first","affiliation":[{"name":"Medical Service, San Francisco VA Health Care System, San Francisco, CA, USA"},{"name":"Medicine, University of California, San Francisco, San Francisco, CA, 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overall brain function, little is known about how brain structural properties are associated with oscillatory activity, particularly during sleep. In this study, we analyzed whole-night sleep electroencephalography (EEG) and brain structural MRI data from a subset of 621 individuals in the Multi-Ethnic Study of Atherosclerosis to explore the relationship between brain structure and sleep EEG properties. We found that larger total white matter (WM) volume was associated with higher absolute broad-band power, regardless of sleep stage, likely reflecting WM contribution to enhanced synchronization across cortical regions and reduced activation attenuation via long-range myelinated fibers. Additionally, both WM fractional anisotropy and thalamic volume showed a negative association with relative slow power and a positive association with delta power during non-rapid eye movement sleep. This was mirrored in the duration of slow oscillations, both overall and when divided into slow-switching and fast-switching types, with their ratio additionally linked to total WM volume. Furthermore, we observed strong but largely independent effects of age and sex on sleep EEG and structural magnetic resonance imaging (MRI) metrics, suggesting that sleep EEG captures aging processes and sex-specific features that extend beyond the macro-scale brain morphology changes examined here. Overall, these findings deepen our understanding of how structural brain properties influence sleep-related oscillatory activity.<\/jats:p>","DOI":"10.1093\/sleep\/zsaf074","type":"journal-article","created":{"date-parts":[[2025,4,17]],"date-time":"2025-04-17T02:40:45Z","timestamp":1744857645000},"source":"Crossref","is-referenced-by-count":2,"title":["Mapping the relationships between structural brain MRI characteristics and sleep electroencephalography patterns: the Multi-Ethnic Study of atherosclerosis"],"prefix":"10.1093","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6450-4959","authenticated-orcid":false,"given":"Nataliia","family":"Kozhemiako","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Brigham and Women\u2019s Hospital , Boston, MA ,","place":["USA"]},{"name":"Department of Psychiatry, Harvard Medical School , Boston, MA ,","place":["USA"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7100-512X","authenticated-orcid":false,"given":"Susan 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            <jats:title>Aims<\/jats:title>\n                  <jats:p>Obesity, traditionally measured using body mass index (BMI), is considered a significant risk factor for the development of cardiovascular disease (CVD). However, there have been mixed findings regarding the association between obesity and cardiovascular events in part due to the way it is measured. Major limitations exist with the use of BMI as it cannot assess body composition or fat distribution, and thus fails to account for the separate roles of muscle and fat mass (FM). The objective is to examine the relationship between various measures of body composition including FM, fat-free mass (FFM), waist-to-height ratio, waist circumference, and BMI, and coronary heart disease (CHD) events, from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>MESA is a population-based cohort study of 6814 men and women, aged between 45 and 85 years, without clinically apparent CVD. FM and FFM at baseline (Exam 1) were estimated using multiplicative power equations formulated from bioelectrical impedance analysis (BIA) measurements. Multi-variable Cox regression models were used to estimate the hazard ratio (HR) and 95% confidence interval (CI) for 10-year incident hard CHD events (non-fatal myocardial infarction, resuscitated cardiac arrest, and death resulting from CHD) for FM\/FFM, waist-to-height ratio, waist circumference, and BMI. Higher FM was associated with higher risk of hard CHD events, with a HR of 1.64 (1.09\u20132.48) per standard deviation (SD) unit increase (P-value 0.019). FFM was associated with a lower risk of CHD, with a HR of 0.24 (0.08\u20130.76) per SD unit increase of FFM (P-value 0.014). The waist-to-height ratio had a HR of 1.21 (1.08\u20131.35) (P-value 0.001) per SD unit increase in the ratio and was significantly associated with a higher risk of hard CHD events, as was waist circumference with a HR of 1.14 (1.03\u20131.28) (P-value 0.016) per SD unit increase. BMI had a HR of 1.08 (0.97\u20131.21) (P-value 0.158) and was not significantly associated with a 10-year risk of hard CHD events.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Higher FM, waist-to-height ratio, and waist circumference were associated with increased risk for hard CHD events while higher FFM was associated with decreased risk. This highlights the potential importance of lifestyle interventions to build muscle and minimize adiposity for the prevention of CVD and strengthens the call for the inclusion of alternative methodologies to define obesity and measure body composition in the clinical setting.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/eurjpc\/zwaf212","type":"journal-article","created":{"date-parts":[[2025,4,8]],"date-time":"2025-04-08T09:04:16Z","timestamp":1744103056000},"source":"Crossref","is-referenced-by-count":3,"title":["Examining the relationship between anthropometric and body composition measures with coronary heart disease events: the multi-ethnic study of atherosclerosis"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3341-1071","authenticated-orcid":false,"given":"Amier","family":"Haidar","sequence":"first","affiliation":[{"name":"Division of Cardiology, David Geffen School of Medicine at UCLA , 10833 LeConte Ave CHS A2- 237, Los Angeles, CA 90095 ,","place":["USA"]}]},{"given":"Richard","family":"Kronmal","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington , Seattle, WA ,","place":["USA"]}]},{"given":"Matthew","family":"Allison","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California at San Diego , San Diego, CA ,","place":["USA"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3658-6165","authenticated-orcid":false,"given":"Karol","family":"Watson","sequence":"additional","affiliation":[{"name":"Division of Cardiology, David Geffen School of Medicine at UCLA , 10833 LeConte Ave CHS A2- 237, Los Angeles, CA 90095 ,","place":["USA"]}]},{"given":"Preethi","family":"Srikanthan","sequence":"additional","affiliation":[{"name":"Division of Cardiology, David Geffen School of Medicine at UCLA , 10833 LeConte Ave CHS A2- 237, Los Angeles, CA 90095 ,","place":["USA"]}]},{"given":"Tamara","family":"Horwich","sequence":"additional","affiliation":[{"name":"Division of Cardiology, David Geffen School of Medicine at UCLA , 10833 LeConte Ave CHS A2- 237, Los Angeles, CA 90095 ,","place":["USA"]}]}],"member":"286","published-online":{"date-parts":[[2025,4,8]]},"reference":[{"key":"2025042311211347200_zwaf212-B1","doi-asserted-by":"crossref","first-page":"e23855","DOI":"10.1002\/ajhb.23855","article-title":"Trends in obesity and severe obesity prevalence in the United States from 1999 to 2018","volume":"35","author":"Fan","year":"2023","journal-title":"Am J Hum Biol"},{"key":"2025042311211347200_zwaf212-B2","doi-asserted-by":"crossref","first-page":"810","DOI":"10.1093\/ije\/dyz273","article-title":"Has the prevalence of overweight, obesity and central obesity levelled off in the United States? 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All rights reserved.","name":"copyright","label":"Copyright"}]},{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T22:12:34Z","timestamp":1772748754166,"version":"3.50.1"},"reference-count":54,"publisher":"Public Library of Science (PLoS)","issue":"6","license":[{"start":{"date-parts":[[2025,6,13]],"date-time":"2025-06-13T00:00:00Z","timestamp":1749772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92022D00001"],"award-info":[{"award-number":["75N92022D00001"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92022D00002"],"award-info":[{"award-number":["75N92022D00002"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92022D00003"],"award-info":[{"award-number":["75N92022D00003"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92022D00004"],"award-info":[{"award-number":["75N92022D00004"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["75N92022D00005"],"award-info":[{"award-number":["75N92022D00005"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800013I"],"award-info":[{"award-number":["HHSN268201800013I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800014I"],"award-info":[{"award-number":["HHSN268201800014I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800015I"],"award-info":[{"award-number":["HHSN268201800015I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800010I"],"award-info":[{"award-number":["HHSN268201800010I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800011I"],"award-info":[{"award-number":["HHSN268201800011I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HHSN268201800012I"],"award-info":[{"award-number":["HHSN268201800012I"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["T32-HL007055"],"award-info":[{"award-number":["T32-HL007055"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:sec>\n<jats:title>Introduction<\/jats:title>\n<jats:p>Social isolation and low social support are associated with low self-rated health (SRH) cross-sectionally, but few studies have assessed longitudinal associations.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Aims<\/jats:title>\n<jats:p>Assess the associations of isolation, support, and different types of support with SRH trajectories over 28 years. Examine 10-year changes in isolation and support and their associations with 18-year SRH trajectories.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>The Atherosclerosis Risk in Communities (ARIC) Study and the Jackson Heart Study (JHS) are population-based prospective cohort studies with some shared participants. We included 10,855 ARIC participants (56% women, 24% Black, mean age 57 (standard deviation: 6) years) with one measure of isolation and support in ARIC (1990\u20131992), and a subset of 911 ARIC\/JHS shared cohort participants with these measures again in JHS (2000\u20132004). Isolation was measured using the 10-item Lubben Social Network Scale in ARIC, and with 3 questions from the Berkman Social Network Index in JHS. Support was measured using the 16-item Interpersonal Support Evaluation List in both studies. SRH was measured annually and scored from 0\u2013100. We used linear mixed effects models adjusted for confounders to assess these associations.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Results<\/jats:title>\n<jats:p>In ARIC, high isolation was associated with lower SRH both at baseline and over follow-up, with SRH decreasing at a slightly greater rate for those with high isolation compared to low. High support was associated with greater SRH over 28 years compared to those with low support, but the rate of decline in SRH was similar. On average, over 10 years, support was stable and isolation increased in ARIC\/JHS. Although confidence intervals were wide, 10-year maintenance of high\/moderate support and increases in support were associated with greater SRH over time compared to decreases in support and stable low support.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Conclusion<\/jats:title>\n<jats:p>Low isolation and high support at baseline and over 10 years may be positively associated with longitudinal SRH.<\/jats:p>\n<\/jats:sec>","DOI":"10.1371\/journal.pone.0326196","type":"journal-article","created":{"date-parts":[[2025,6,13]],"date-time":"2025-06-13T17:40:15Z","timestamp":1749836415000},"page":"e0326196","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["Longitudinal, prospective cohort study of social relationships and self-rated health in the Atherosclerosis Risk in Communities (ARIC) Study cohort and ARIC\/Jackson Heart Study (JHS) shared cohort"],"prefix":"10.1371","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7085-7072","authenticated-orcid":true,"given":"Kennedy M.","family":"Peter-Marske","sequence":"first","affiliation":[]},{"given":"Annie Green","family":"Howard","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3720-5830","authenticated-orcid":true,"given":"Kelly R.","family":"Evenson","sequence":"additional","affiliation":[]},{"given":"Sara Jones","family":"Berkeley","sequence":"additional","affiliation":[]},{"given":"Joanna","family":"Maselko","sequence":"additional","affiliation":[]},{"given":"Mario","family":"Sims","sequence":"additional","affiliation":[]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9864-467X","authenticated-orcid":true,"given":"Anna","family":"Kucharska-Newton","sequence":"additional","affiliation":[]},{"given":"Kevin J.","family":"Sullivan","sequence":"additional","affiliation":[]},{"given":"Wayne D.","family":"Rosamond","sequence":"additional","affiliation":[]}],"member":"340","published-online":{"date-parts":[[2025,6,13]]},"reference":[{"key":"pone.0326196.ref001","doi-asserted-by":"crossref","DOI":"10.1093\/med\/9780195377903.003.0007","volume-title":"Social Network Epidemiology","author":"LF Berkman","year":"2014"},{"issue":"5","key":"pone.0326196.ref002","doi-asserted-by":"crossref","first-page":"471","DOI":"10.1097\/PSY.0000000000000809","article-title":"Review of the association between number of social roles and cardiovascular disease: graded or threshold effect?","volume":"82","author":"B Chin","year":"2020","journal-title":"Psychosom Med"},{"key":"pone.0326196.ref003","doi-asserted-by":"crossref","first-page":"469","DOI":"10.1146\/annurev.publhealth.26.021304.144542","article-title":"Psychosocial factors and cardiovascular diseases","volume":"26","author":"SA Everson-Rose","year":"2005","journal-title":"Annu Rev Public Health"},{"issue":"6","key":"pone.0326196.ref004","doi-asserted-by":"crossref","first-page":"869","DOI":"10.1097\/01.psy.0000188393.73571.0a","article-title":"Social support and coronary heart disease: epidemiologic evidence and implications for treatment","volume":"67","author":"HS Lett","year":"2005","journal-title":"Psychosom Med"},{"issue":"7196","key":"pone.0326196.ref005","doi-asserted-by":"crossref","first-page":"1460","DOI":"10.1136\/bmj.318.7196.1460","article-title":"Evidence based cardiology: psychosocial factors in the aetiology and prognosis of coronary heart disease. 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All participants were monitored for incident atherosclerotic cardiovascular disease (ASCVD) events. TAC is defined as calcification in the ascending aorta, aortic arch and descending aorta on chest CT. The quantification of TAC was measured using the Agatston method. Time-dependent receiver-operating characteristic (ROC) curves were used to compare the prognostic value of TAC and CAC scores.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Participants were 69\u00b19 years of age and 47% were male. The Spearman correlation between TAC and CAC scores was 0.46 (p&lt;0.001). During the median follow-up period of 8.8 years, 234 participants (9.7%) experienced ASCVD events. In multivariable Cox regression analysis, TAC score was independently associated with increased risk of ASCVD events (HR 1.31, 95% CI 1.09 to 1.58) as well as CAC score (HR 1.82, 95% CI 1.53 to 2.17). However, the area under the time-dependent ROC curve for CAC score was greater than that for TAC score in all participants (0.698 and 0.641, p=0.031). This was particularly pronounced in participants with borderline\/intermediate and high 10-year ASCVD risk scores.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Our study demonstrated a significant association between TAC and CAC scores but a superior prognostic value of CAC score for ASCVD events. These findings suggest TAC on chest CT provides supplementary data to estimate ASCVD risk but does not replace CAC on ECG-gated cardiac CT.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/heartjnl-2023-323838","type":"journal-article","created":{"date-parts":[[2024,4,16]],"date-time":"2024-04-16T13:25:18Z","timestamp":1713273918000},"page":"947-953","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":7,"title":["Thoracic versus coronary calcification for atherosclerotic cardiovascular disease events prediction"],"prefix":"10.1136","volume":"110","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0657-514X","authenticated-orcid":false,"given":"Keishi","family":"Ichikawa","sequence":"first","affiliation":[{"name":"The Lundquist Institute, Torrance, California, USA"}]},{"given":"Rui","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington, Seattle, Washington, 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<jats:p>Idiopathic pulmonary fibrosis (IPF) causes progressive lung scarring and high mortality. Reliable and accurate prognostic biomarkers are urgently needed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To identify and validate circulating protein biomarkers of IPF survival.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>High-throughput proteomic data were generated using prospectively collected plasma samples from patients with IPF from the Pulmonary Fibrosis Foundation Patient Registry (discovery cohort) and the Universities of California, Davis; Chicago; and Virginia (validation cohort). Proteins associated with three-year transplant-free survival (TFS) were identified using multivariable Cox proportional hazards regression. Those associated with TFS after adjustment for false discovery in the discovery cohort were advanced for testing in the validation cohort, with proteins maintaining TFS association with consistent effect direction considered validated. After combining cohorts, functional analyses were performed, and machine learning was used to derive a proteomic signature of TFS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Of 2,921 proteins tested in the discovery cohort (n\u2009=\u2009871), 231 were associated with differential TFS. Of these, 140 maintained TFS association with consistent effect direction in the validation cohort (n\u2009=\u2009355). After cohorts were combined, the validated proteins with the strongest TFS association were latent-transforming growth factor \u03b2-binding protein 2 (hazard ratio [HR], 2.43; 95% confidence interval [CI]\u2009=\u20092.09\u20132.82), collagen \u03b1-1(XXIV) chain (HR, 2.21; 95% CI\u2009=\u20091.86\u20132.39), and keratin 19 (HR, 1.60; 95% CI\u2009=\u20091.47\u20131.74). In decision curve analysis, a proteomic signature of TFS outperformed a similarly derived clinical prediction model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In the largest proteomic investigation of IPF outcomes performed to date, we identified and validated 140 protein biomarkers of TFS. These results shed important light on potential drivers of IPF progression.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202301-0117oc","type":"journal-article","created":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T13:29:20Z","timestamp":1697549360000},"page":"1111-1120","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":52,"title":["Proteomic Biomarkers of Survival in Idiopathic Pulmonary Fibrosis"],"prefix":"10.1093","volume":"209","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4957-8869","authenticated-orcid":false,"given":"Justin M.","family":"Oldham","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"},{"name":"Department of Epidemiology, and"}]},{"given":"Yong","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia"}]},{"given":"Swaraj","family":"Bose","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Michigan, Ann Arbor, Michigan"}]},{"given":"Shwu-Fan","family":"Ma","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia"}]},{"given":"John S.","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia"}]},{"given":"Alexandra","family":"Schwab","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia"}]},{"given":"Christopher","family":"Ting","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"}]},{"given":"Kaniz","family":"Mou","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"}]},{"given":"Cathryn T.","family":"Lee","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois"}]},{"given":"Ayodeji","family":"Adegunsoye","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois"}]},{"given":"Sahand","family":"Ghodrati","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Davis, Davis, California"}]},{"given":"Janelle Vu","family":"Pugashetti","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"}]},{"given":"Nazanin","family":"Nazemi","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"}]},{"given":"Mary E.","family":"Strek","sequence":"additional","affiliation":[{"name":"Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois"}]},{"given":"Angela L.","family":"Linderholm","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Davis, Davis, California"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4211-9988","authenticated-orcid":false,"given":"Ching-Hsien","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Davis, Davis, California"}]},{"given":"Susan","family":"Murray","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Michigan, Ann Arbor, Michigan"}]},{"given":"Rachel L.","family":"Zemans","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"}]},{"given":"Kevin R.","family":"Flaherty","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine"},{"name":"Pulmonary Fibrosis Foundation, Chicago, Illinois; and"}]},{"given":"Fernando J.","family":"Martinez","sequence":"additional","affiliation":[{"name":"Weill Cornell Medical Center, New York, New York"}]},{"given":"Imre","family":"Noth","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia"}]}],"member":"286","published-online":{"date-parts":[[2024,5,1]]},"reference":[{"key":"2026012204263418600_bib1","doi-asserted-by":"crossref","first-page":"e44","DOI":"10.1164\/rccm.201807-1255ST","article-title":"Diagnosis of Idiopathic Pulmonary Fibrosis. 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We investigated the associations between brachial\u2013ankle pulse wave velocity (baPWV), a measure of arterial stiffness, and each of office brachial systolic BP (SBP) with and without an observer present (attended or unattended office brachial SBP), attended or unattended office central SBP, and home brachial SBPs (specifically, the means of morning, evening, or morning\u2013evening home brachial SBP) in patients being treated for hypertension. Measurements were performed among 70 adults (mean age, 67.0 \u00b1 9.4 years; women, 51.4%) with a mean attended office brachial SBP of 127.6 \u00b1 14.5 mmHg and mean baPWV of 16.3 \u00b1 2.8 m\/s. Univariate analysis showed that higher attended office brachial SBP, morning home brachial SBP, and morning\u2013evening home brachial SBP were each statistically significantly associated with higher baPWV (<jats:italic toggle=\"yes\">r<\/jats:italic> = 0.25, <jats:italic toggle=\"yes\">P<\/jats:italic> = 0.04; <jats:italic toggle=\"yes\">r<\/jats:italic> = 0.37, <jats:italic toggle=\"yes\">P<\/jats:italic> = 0.002; and <jats:italic toggle=\"yes\">r<\/jats:italic> = 0.32, <jats:italic toggle=\"yes\">P<\/jats:italic> = 0.006, respectively). Multiple linear regression analysis with adjustments for traditional cardiovascular risk factors showed that only morning home brachial SBP was statistically significantly associated with baPWV [<jats:italic toggle=\"yes\">\u03b2<\/jats:italic> = 0.06, 95% confidence interval (0.01\u20130.11), <jats:italic toggle=\"yes\">P<\/jats:italic> = 0.02). 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implicated in the development of hypertension. However, epidemiologic studies have yet to compare multiple corresponding biomarkers in relation to risk of hypertension, particularly in multiethnic populations.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>We identified 800 individuals with incident hypertension and 800 matched controls, each group with equal numbers of white and black women, in a nested case-control study within the Women's Health Initiative Observational Study. We measured markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, IL-1\u03b2, tumor necrosis factor receptor 2 (TNF-r2)] and endothelial activation [soluble intercellular adhesion molecule-1 (sICAM-1)] in baseline blood samples.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>Before adjustment for measures of adiposity, higher hsCRP and IL-6 concentrations were associated with increased risk of hypertension in both white and black women, higher TNF-r2 was associated with increased risk of hypertension in black women only, and IL-1\u03b2 and sICAM-1 were not associated with risk of hypertension. All the positive associations were attenuated after adjustment for body mass index. The resulting multivariable-adjusted relative risks (95% CI) of hypertension comparing the highest vs lowest quartile were 1.52 (0.94\u20132.48) and 1.23 (0.76\u20131.97) for hsCRP and IL-6 in white women and 1.30 (0.81\u20132.07), 1.58 (0.96\u20132.59), and 1.49 (0.94\u20132.36) for hsCRP, IL-6, and TNF-r2 in black women. The results after adjustment for waist circumference were similar.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>After adjustment for measures of adiposity, there was no significant association of hsCRP, IL-6, IL-1\u03b2, TNF-r2, or sICAM-1 with incident hypertension in either white or black women. The interrelationships between inflammation and adiposity in development of hypertension need further investigation.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1373\/clinchem.2010.156794","type":"journal-article","created":{"date-parts":[[2011,3,14]],"date-time":"2011-03-14T00:01:21Z","timestamp":1300060881000},"page":"729-736","source":"Crossref","is-referenced-by-count":28,"title":["Circulating Inflammatory and Endothelial Markers and Risk of Hypertension in White and Black Postmenopausal Women"],"prefix":"10.1093","volume":"57","author":[{"given":"Lu","family":"Wang","sequence":"first","affiliation":[{"name":"Division of Preventive Medicine"}]},{"given":"JoAnn E","family":"Manson","sequence":"first","affiliation":[{"name":"Division of Preventive Medicine"},{"name":"Department of Epidemiology, Harvard School of Public Health, Boston, MA"}]},{"given":"J Michael","family":"Gaziano","sequence":"first","affiliation":[{"name":"Division of Preventive Medicine"},{"name":"Division of 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Ltd.","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int J Blood Transfus Immunohematol"],"abstract":"<jats:p>Four main blood types routinely identified today are A, B, AB, and O. Universal donors have type \"O\" blood, and have no \"A\" or \"B\" antigens. In turn, no blood reactions will occur in recipients. Conversely, universal recipients having type \"AB\" blood will have no antibodies to the \"A\" or \"B\" antigens. Bombay phenotype has no \"A\" or \"B\" antigens, classifying it as \"O\" blood type. Furthermore, Bombay phenotype lacks expression of the H antigen, which is present on every blood cell. When mixed with any type of blood other than Bombay blood, hemolytic reactions occur. A 55-year-old male had his blood typed and screened after trauma activation for an eye injury. On forward grouping, the patient was identified as blood type \"O\". On reverse grouping, agglutination occurred. Laboratory procedures were evaluated and an expanded antigen panel was performed which confirmed this agglutination, which led to the suspicion of a rare blood type. The patient did not require blood transfusion and was further evaluated by New York Blood Center where the diagnosis of Bombay Phenotype was confirmed. This case emphasizes the importance of proper laboratory investigations for rare blood types, preventative strategies, as well as management of Bombay blood type.<\/jats:p>","DOI":"10.5348\/ijbti-2016-23-cr-3","type":"journal-article","created":{"date-parts":[[2020,7,18]],"date-time":"2020-07-18T11:23:10Z","timestamp":1595071390000},"page":"1-4","source":"Crossref","is-referenced-by-count":3,"title":["Bombay blood phenotype: Laboratory detection and transfusions recommendations"],"prefix":"10.5348","volume":"6","author":[{"given":"Nicholas","family":"Suraci","sequence":"first","affiliation":[{"name":"Pathology, jamaica Hospital Medical Center, Queens, NY, US."}]},{"given":"Maximo","family":"Mora","sequence":"first","affiliation":[{"name":"Pathology, jamaica Hospital Medical Center, Queens, NY, US."}]}],"member":"3299","published-online":{"date-parts":[[2016,3,29]]},"reference":[{"key":"ref=1","doi-asserted-by":"crossref","unstructured":"Das S, Kumar HRA. Bombay Blood A Rare Entity. Journal of Clinical Biomedical Science 2011;1(3):122\u20135 \u00a0\u00a0\u00a0","DOI":"10.58739\/jcbs\/v01i3.1"},{"key":"ref=2","unstructured":"Dipta TF, Hossain AZ. The Bombay blood group: are we out of risk? Mymensingh Med J 2011 Jul;20(3):536\u201340. \u00a0\u00a0 \u00a0\u00a0\u00a0"},{"key":"ref=3","doi-asserted-by":"crossref","unstructured":"Dipta TFA, Hossain KN, Khatun A, et al. Bombay Phenotype: Report of 2 Cases. Journal of Bangladesh College of Physicians and Surgeons 2011;29(4):241\u20133. \u00a0\u00a0\u00a0","DOI":"10.3329\/jbcps.v29i4.11347"},{"key":"ref=4","doi-asserted-by":"crossref","unstructured":"Balgir RS. Identification of a rare blood group, \"Bombay (Oh) phenotype,\" in Bhuyan tribe of Northwestern Orissa, India. Indian J Hum Genet 2007 Sep;13(3):109\u201313. \u00a0\u00a0 \u00a0\u00a0 \u00a0\u00a0\u00a0","DOI":"10.4103\/0971-6866.38985"},{"key":"ref=5","doi-asserted-by":"crossref","unstructured":"Malhotra S, Dhawan HK, Jain A, Sachdev S, Marwaha N. Acute Hemolytic Transfusion Reaction in a Patient with Bombay Phenotype: Implications for ABO Grouping. Indian J Hematol Blood Transfus 2014 Sep;30(Suppl 1):108\u201310. \u00a0\u00a0 \u00a0\u00a0 \u00a0\u00a0\u00a0","DOI":"10.1007\/s12288-013-0277-9"},{"key":"ref=6","unstructured":"Khan M. Bombay Blood Group: A Case Report. The Pacific Journal of Science and Technology 2009 May;10(1):333\u20137. \u00a0\u00a0\u00a0"},{"key":"ref=7","doi-asserted-by":"crossref","unstructured":"O'Donnell JS, McKinnon TA, Crawley JT, Lane DA, Laffan MA. Bombay phenotype is associated with reduced plasma-VWF levels and an increased susceptibility to ADAMTS13 proteolysis. Blood 2005 Sep 15;106(6):1988\u201391. \u00a0\u00a0 \u00a0\u00a0 \u00a0\u00a0\u00a0","DOI":"10.1182\/blood-2005-02-0792"},{"key":"ref=8","doi-asserted-by":"crossref","unstructured":"Shrivastava M, Navaid S, Peethambarakshan A, Agrawal K, Khan A. Detection of rare blood group, Bombay (Oh) phenotype patients and management by acute normovolemic hemodilution. Asian J Transfus Sci 2015 Jan-Jun;9(1):74\u20137. \u00a0\u00a0 \u00a0\u00a0 \u00a0\u00a0\u00a0","DOI":"10.4103\/0973-6247.150957"},{"key":"ref=9","unstructured":"Avidan M, Silvergleid A. Surgical blood conservation: Intraoperative hemodilution. In: Kleinman S, Hines R eds. UpToDate, Waltham, MA. [Available at: http:\/\/www.uptodate.com\/contents\/surgical-blood-conservation-intraoperative-hemodilution] \u00a0\u00a0\u00a0"},{"key":"ref=10","doi-asserted-by":"crossref","unstructured":"Seifinejad A, Taei A, Totonchi M, et al. Generation of human induced pluripotent stem cells from a Bombay individual: moving towards \"universal-donor\" red blood cells. Biochem Biophys Res Commun 2010 Jan 1;391(1):329\u201334. \u00a0\u00a0 \u00a0\u00a0\u00a0","DOI":"10.1016\/j.bbrc.2009.11.058"}],"container-title":["International Journal of Blood Transfusion and Immunohematology"],"original-title":["Bombay blood phenotype: Laboratory detection and transfusions 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         <jats:title>Background<\/jats:title>\n                    <jats:p>Sepsis is a life-threatening complication of infection with high mortality. A high-throughput analysis of circulating blood proteins may provide mechanistic insight and potent therapeutic targets for the prevention of sepsis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used multivariable Cox regression analysis to examine the association of 4955 plasma proteins, measured by SomaScan, with the risk of incident sepsis among 11 065 participants of the Atherosclerosis Risk in Communities (ARIC) Study (visit 3 in 1993 to 1995; mean age, 60.1 years, 54.4% female, 21.0% Black). Proteins (false discovery rate [FDR] of P &amp;lt; 0.05) discovered at visit 3 were replicated using data at visit 5 (n = 4869 in 2011 to 2013: mean age, 75.5 years) and in the Cardiovascular Health Study (CHS) (n = 3512 in 1992 to 1993; mean age, 74.5 years). Canonical pathways were identified by enrichment analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>At ARIC visit three, 669 proteins were associated with the risk of sepsis; 175 were replicated at visit 5. Of these, 90 were validated in the CHS. The top 20 proteins ranked by P value were relevant to acute inflammatory signaling in innate immunity. Pathway analyses implicated activation of pro-inflammatory pathways (e.g., cytokine storm signaling) as well as inhibition of anti-inflammatory pathways (e.g., liver X receptor\/retinoid X receptor [LXR\/RXR] activation), which also play relevant roles in lipid metabolism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In this analysis, levels of acute inflammatory proteins measured during routine visits were associated with the subsequent incidence of sepsis. An increased risk of sepsis associated with the inhibition of anti-inflammatory pathways, such as LXR\/RXR warrants further mechanistic investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/jalm\/jfaf179","type":"journal-article","created":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T13:12:04Z","timestamp":1764162724000},"page":"281-294","source":"Crossref","is-referenced-by-count":0,"title":["Proteomics Analysis of Plasma for Risk of Sepsis: Findings from the Atherosclerosis Risk in Communities Study"],"prefix":"10.1093","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6396-3723","authenticated-orcid":false,"given":"Junichi","family":"Ishigami","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health , Baltimore, MD ,","place":["United States"]},{"name":"Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University , Baltimore, MD ,","place":["United 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College of Medicine , Houston, TX ,","place":["United States"]}]},{"given":"Morgan E","family":"Grams","sequence":"additional","affiliation":[{"name":"Department of Population Health and Medicine, New York University Langone , New York, NY ,","place":["United States"]}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4598-0669","authenticated-orcid":false,"given":"Josef","family":"Coresh","sequence":"additional","affiliation":[{"name":"Department of Population Health and Medicine, New York University Langone , New York, NY ,","place":["United States"]}]},{"given":"James S","family":"Floyd","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, University of Washington , Seattle, WA ,","place":["United States"]},{"name":"Cardiovascular Health Research Unit, Department of Medicine, University of Washington , Seattle, WA ,","place":["United 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Institute","doi-asserted-by":"publisher","award":["N01HC85086"],"award-info":[{"award-number":["N01HC85086"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U01HL080295"],"award-info":[{"award-number":["U01HL080295"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["U01HL130114"],"award-info":[{"award-number":["U01HL130114"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["agsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J American Geriatrics Society"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND\/OBJECTIVES<\/jats:title>\n                    <jats:p>Non\u2010esterified fatty acids (NEFAs) play central roles in the relationship between adiposity and glucose metabolism, and they have been implicated in the pathogenesis of cardiovascular disease, but few studies have assessed their effects on complex geriatric syndromes like frailty that cross multiple organ systems. We sought to determine the relationships between NEFAs and incident frailty, disability, and mobility limitation in a population\u2010based cohort of older persons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>We analyzed 4,710 Cardiovascular Health Study (CHS) participants who underwent measurement of circulating total fasting NEFAs in 1992\u20131993 and were assessed for frailty in 1996\u20131997 and for disability and mobility limitation annually. We used ordinal logistic regression to model incident frailty, linear regression to model components of frailty, and Cox regression to model disability and mobility limitation in relation to baseline NEFAs. To ensure proportional hazards, we truncated follow\u2010up at 9\u2009years for disability and 6.5\u2009years for mobility limitation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>A total of 42 participants became frail and 510 became pre\u2010frail over a 4\u2010year period, and we documented 1,720 cases of disability and 1,225 cases of mobility limitation during follow\u2010up. NEFAs were positively associated in a dose\u2010dependent manner with higher risks of incident frailty, disability, and mobility limitation. The adjusted odds ratios for frailty were 1.37 (95% confidence interval [CI] = 1.01\u20131.86; P = .04) across extreme tertiles and 1.17 (95% CI = 1.03\u20131.33; P = .01) per standard deviation increment. The corresponding hazard ratios for incident disability were 1.14 (95% CI = 1.01\u20131.30; P = .04) and 1.11 (95% CI = 1.06\u20131.17; P\u2009&lt;\u2009.0001); those for incident mobility limitation were 1.23 (95% CI = 1.06\u20131.43; P = .006) and 1.15 (95% CI = 1.08\u20131.22; P\u2009&lt;\u2009.0001). Results were largely consistent among both men and women. Among individual components of frailty, NEFAs were significantly associated with self\u2010reported exhaustion (\u03b2 = .07; standard error = .03; P = .02).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSION<\/jats:title>\n                    <jats:p>Circulating NEFAs are significantly associated with frailty, disability, and mobility limitation among older adults. These results highlight the broad spectrum of adverse health issues associated with NEFA in older adults.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jgs.16793","type":"journal-article","created":{"date-parts":[[2020,9,23]],"date-time":"2020-09-23T01:35:34Z","timestamp":1600824934000},"page":"2890-2897","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["<scp>Non\u2010Esterified<\/scp>\n                    Fatty Acids and Risks of Frailty, Disability, and Mobility Limitation in Older Adults: The Cardiovascular Health Study"],"prefix":"10.1111","volume":"68","author":[{"given":"Peter","family":"Ahiawodzi","sequence":"first","affiliation":[{"name":"Department of Public Health Campbell University College of Pharmacy and Health Sciences  Buies Creek North Carolina USA"}]},{"given":"Luc","family":"Djousse","sequence":"additional","affiliation":[{"name":"Division of Aging, Department of Medicine Brigham and Women\u02bcs Hospital and Harvard Medical School  Boston Massachusetts USA"}]},{"given":"Joachim H.","family":"Ix","sequence":"additional","affiliation":[{"name":"Divisions of Nephrology and Preventive Medicine University of California, San Diego  San Diego California USA"}]},{"given":"Jorge R.","family":"Kizer","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Veterans Affairs Medical Center University of California  San Francisco California USA"}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biochemistry University of Vermont College of Medicine  Burlington Vermont USA"}]},{"given":"Alice","family":"Arnold","sequence":"additional","affiliation":[{"name":"Department of a Biostatistics University of Washington  Seattle Washington USA"}]},{"given":"Anne","family":"Newman","sequence":"additional","affiliation":[{"name":"Departments of Epidemiology and Medicine University of Pittsburgh  Pittsburgh Pennsylvania USA"}]},{"given":"Kenneth J.","family":"Mukamal","sequence":"additional","affiliation":[{"name":"Division of General Medicine Beth Israel Deaconess Medical Center and Harvard Medical School  Boston Massachusetts USA"}]}],"member":"311","published-online":{"date-parts":[[2020,9,22]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1079\/PNS19970076"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2261-14-159"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-004-1443-2"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1992.263.6.E1063"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119636"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1210\/en.2009-1122"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2012.05.017"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2018.07.034"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117252"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20811"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.2337\/diab.45.4.446"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-005-0051-0"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.chembiol.2006.09.010"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1093\/gerona\/56.3.M146"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1111\/jgs.15205"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCHEARTFAILURE.113.000521"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2012.03.010"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/1047-2797(91)90005-W"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.115.018610"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/1047-2797(94)00093-9"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/1047-2797(93)90105-D"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1093\/clinchem\/41.2.264"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1093\/aje\/kwf156"},{"key":"e_1_2_6_25_1","unstructured":"RuifengLi EllenHertzmark MaryLouie LinlinChen andDonnaSpiegelman. 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About 0.4 ml dextran-saline solution was used as nondiffusible indicator and injected into the feline cerebral circulation for each measurement. The subsequent cerebrocortical transit of the hemodiluted bolus was detected as a temporary change in the tissue optical density [OD( t)] and interpreted as indicator dilution, C( t). This gave the data necessary to calculate the microregional blood volume (mrCBV), mean transit time of the bolus (mrMTT), and the microregional blood flow (mrCBF = mrCBV\/mrMTT). A two-dimensional record of the OD( t) function was made on Kodak SO 115 film by 16-mm cinematography, as a reflectometric tool, over an exposed area of the brain cortex during the bolus perfusion. Later, the microregional OD( t) functions were retrieved for analysis in a square array from the developed film by computer-controlled, frame-by-frame scanning densitometry. Maps of mrCBF, mrCBV, and mrMTT were presented as square arrays of gray-scaled pixels. The maximal spatial and temporal resolution of the method was 0.015 mm<jats:sup>2<\/jats:sup> (mrCBF), 0.004 mm<jats:sup>2<\/jats:sup> (mrCBV), 6 maps\/min (mrCBF), and 600 maps\/min (mrCBV). <\/jats:p>","DOI":"10.1038\/jcbfm.1982.5","type":"journal-article","created":{"date-parts":[[2011,4,7]],"date-time":"2011-04-07T17:10:50Z","timestamp":1302196250000},"page":"41-53","source":"Crossref","is-referenced-by-count":15,"title":["Reflectometric Mapping of Microregional Blood Flow and Blood Volume in the Brain Cortex"],"prefix":"10.1177","volume":"2","author":[{"given":"Andras","family":"Eke","sequence":"first","affiliation":[{"name":"Department of Neurology, University of Alabama in Birmingham, Birmingham, Alabama 35294, U.S.A."}]}],"member":"179","published-online":{"date-parts":[[1982,3,1]]},"reference":[{"key":"bibr1-jcbfm.1982.5","first-page":"289","volume-title":"Prostacyclin","author":"Branan R.C.","year":"1979"},{"key":"bibr2-jcbfm.1982.5","first-page":"H759","volume":"236","author":"Eke A.","year":"1979","journal-title":"Am J Physiol"},{"volume-title":"Brain Work: The Coupling of Function, Metabolism and Blood Flow in the Brain","year":"1975","author":"Ingvar D.H.","key":"bibr3-jcbfm.1982.5"},{"key":"bibr4-jcbfm.1982.5","doi-asserted-by":"publisher","DOI":"10.1016\/0026-2862(80)90019-9"},{"key":"bibr5-jcbfm.1982.5","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1954.6.12.731"}],"container-title":["Journal of Cerebral Blood Flow &amp; Metabolism"],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1038\/jcbfm.1982.5","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1038\/jcbfm.1982.5","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,3,10]],"date-time":"2025-03-10T22:12:57Z","timestamp":1741644777000},"score":8.487857,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1038\/jcbfm.1982.5"}},"issued":{"date-parts":[[1982,3]]},"references-count":5,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1982,3]]}},"alternative-id":["10.1038\/jcbfm.1982.5"],"URL":"https:\/\/doi.org\/10.1038\/jcbfm.1982.5","ISSN":["0271-678X","1559-7016"],"issn-type":[{"type":"print","value":"0271-678X"},{"type":"electronic","value":"1559-7016"}],"published":{"date-parts":[[1982,3]]}},{"indexed":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:26:20Z","timestamp":1745468780142,"version":"3.40.4"},"reference-count":18,"publisher":"S. Karger AG","issue":"6","license":[{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"},{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/karger.com\/pages\/terms-and-conditions"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Blood Purif"],"published-print":{"date-parts":[[2024]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Introduction:&lt;\/i&gt;&lt;\/b&gt; Continuous monitoring of relative blood volume (percentage BV) in hemodialysis (HD) is critical for determining dry weight and preventing intradialytic hypotension. However, the cause of the BV variation remains unknown. This research aimed to examine factors that influence the percentage BV. &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; We devised a formula based on coefficients (\u201ca,\u201d \u201c\u03c4,\u201d and \u201cb\u201d) to predict changes in percentage BV. \u201ca\u201d denotes a significant decrease in percentage BV in the early stages of HD. \u201c\u03c4\u201d represents the transition from early to late phase of HD. \u201cb\u201d denotes the slope of the decrease in percentage BV in the late phase of HD. We measured the percentage BV in 18 patients with end-stage renal disease. The coefficients were estimated by fitting experimental data from patients using a least squares optimization algorithm. A correlation analysis of these parameters and patient predialysis data was performed. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; Ultrafiltration rate (UFR) was found to be negatively correlated with \u201cb\u201d (&lt;i&gt;r&lt;\/i&gt; = \u22120.851, &lt;i&gt;p&lt;\/i&gt; &amp;lt; 0.01). However, UFR was not significantly related to \u201ca.\u201d Predialysis serum total protein level was negatively correlated with \u201ca\u201d (&lt;i&gt;r&lt;\/i&gt; = \u22120.531, &lt;i&gt;p&lt;\/i&gt; = 0.042). Predialysis serum albumin and predialysis sodium were not significantly correlated with \u201ca\u201d and \u201c\u03c4.\u201d Plasma osmolarity did not have a significant relationship with \u201ca\u201d and \u201c\u03c4.\u201d &lt;b&gt;&lt;i&gt;Discussion\/Conclusion:&lt;\/i&gt;&lt;\/b&gt; UFR influenced the decrease in percentage BV in the late phase but did not influence the decrease of percentage BV in the early phase. \u201ca\u201d was associated with predialysis serum total protein level but not with plasma osmolality or predialysis sodium. This implies that colloid oncotic pressure is important for plasma refilling immediately after dialysis begins. During the change of percentage BV, the decrease in the early phase of dialysis was not related to UFR, but related to other parameters, especially predialysis total protein level. A decrease in the late phase of dialysis is related to UFR. <\/jats:p>","DOI":"10.1159\/000536073","type":"journal-article","created":{"date-parts":[[2024,2,5]],"date-time":"2024-02-05T22:02:15Z","timestamp":1707170535000},"page":"505-510","source":"Crossref","is-referenced-by-count":0,"title":["The Changes in Relative Blood Volume during Dialysis Are Characterized by Ultrafiltration Rate and Predialysis Blood Test 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Since lung fibrosis is associated with downregulation of DAF, we hypothesize that overexpression of DAF in fibrosed lungs will limit fibrotic injury by restraining complement dysregulation. Normal primary human alveolar type II epithelial cells (AECs) exposed to exogenous complement 3a or 5a, and primary AECs purified from IPF lungs demonstrated decreased membrane-bound DAF expression with concurrent increase in the endoplasmic reticulum (ER) stress protein, ATF6. Increased loss of extracellular cleaved DAF fragments was detected in normal human AECs exposed to complement 3a or 5a, and in lungs of IPF patients. C3a-induced ATF6 expression and DAF loss was inhibited using pertussis toxin (an enzymatic inactivator of G-protein coupled receptors), in murine AECs. Treatment with soluble DAF abrogated tunicamycin-induced C3a secretion and ER stress (ATF6 and BiP expression) and restored epithelial cadherin. Bleomycin-injured fibrotic mice subjected to lentiviral overexpression of DAF demonstrated diminished levels of local collagen deposition and complement activation. Further analyses showed diminished release of DAF fragments, as well as reduction in apoptosis (TUNEL and caspase 3\/7 activity), and ER stress-related transcripts. Loss-of-function studies using Daf1 siRNA demonstrated worsened lung fibrosis detected by higher mRNA levels of Col1a1 and epithelial injury-related Muc1 and Snai1, with exacerbated local deposition of C5b-9. Our studies provide a rationale for rescuing fibrotic lungs via DAF induction that will restrain complement dysregulation and lung injury.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0463oc","type":"journal-article","created":{"date-parts":[[2022,7,27]],"date-time":"2022-07-27T13:26:30Z","timestamp":1658928390000},"page":"459-470","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":15,"title":["Overexpression of Decay Accelerating Factor Mitigates Fibrotic Responses to Lung Injury"],"prefix":"10.1093","volume":"67","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4520-9663","authenticated-orcid":false,"given":"Ragini","family":"Vittal","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care, Department of Internal Medicine and"}]},{"given":"Amanda J.","family":"Fisher","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care, Department of Medicine and"}]},{"given":"Eric 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potentiates lung injury via complement sensitisation","volume":"21","author":"Lin","year":"2019","journal-title":"Cell Microbiol"}],"container-title":["American Journal of Respiratory Cell and Molecular 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Benoit et al. (1957). C. R. Ac. Sc. 244: 2320.","journal-title":"C. R. Ac. 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When the physician seeks to enlist during World War II, his request for a commission is rejected when his old college records reveal his Negro blood. Before this revelation, in a dramatic scene in the film, a nurse holds a bottle of blood. When someone mentions \u201cNegro blood,\u201d she drops the bottle, it crashes to the floor and the blood splashes over the white hospital tiles. Lost Boundaries was based on a \u201ctrue story.\u201d<\/jats:p>","DOI":"10.1093\/oso\/9780195161502.003.0004","type":"book-chapter","created":{"date-parts":[[2023,11,1]],"date-time":"2023-11-01T01:36:16Z","timestamp":1698802576000},"page":"107-142","source":"Crossref","is-referenced-by-count":1,"title":["Lost Boundaries: Race, Blood, and Bodies"],"prefix":"10.1093","author":[{"given":"Susan E","family":"Lederer","sequence":"first","affiliation":[]}],"member":"286","container-title":["Flesh and 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Institute","doi-asserted-by":"publisher","award":["N01-HC-95168"],"award-info":[{"award-number":["N01-HC-95168"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["N01-HC-95169"],"award-info":[{"award-number":["N01-HC-95169"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2019,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Purpose<\/jats:title>\n                  <jats:p>Based on the 2018 American College of Cardiology\/American Heart Association cholesterol guidelines, the number of individuals eligible for statin therapy to reduce atherosclerotic cardiovascular disease risk has greatly expanded. Statins inhibit cholesterol biosynthesis, which can impair gonadal steroidogenesis. We evaluated the effect of statins on endogenous sex hormones in a large epidemiological study.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>A total of 6814 Multi-Ethnic Study of Atherosclerosis (MESA) participants underwent the baseline examination. Of these, 6171 had measurements of serum sex hormones available: dehydroepiandrosterone (DHEA), SHBG, estradiol, and total and bioavailable testosterone. Multivariable linear regression models were used to assess the relationship of statin use with each sex hormone.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>A total of 345 women (17.4%) and 464 men (14.7%) were statin users (mean age, 67 years; 41% white, 29% black, 11% Chinese, and 19% Hispanic). Among the users vs nonusers of statins, the mean SHBG was 3.54 nmol\/L (P &lt; 0.01) lower in women and 3.37 nmol\/L (P &lt; 0.001) lower in men; the mean DHEA was 1.06 nmol\/L (P &lt; 0.05) lower in women and 0.70 nmol\/L (P &lt; 0.01) lower in men, after adjustment for potential confounders. With further propensity score adjustment, the mean DHEA and SHBG levels were 0.67 nmol\/L (P &lt; 0.05) and 3.49 nmol\/L (P &lt; 0.001) lower, respectively, for statin users vs nonusers. No statistically significant association was noted between estradiol, total testosterone, and bioavailable testosterone and statin use.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Statin users have lower levels of SHBG and DHEA. This is especially relevant owing to the increasing use of statin therapy.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jc.2019-00530","type":"journal-article","created":{"date-parts":[[2019,6,3]],"date-time":"2019-06-03T09:05:37Z","timestamp":1559552737000},"page":"4600-4606","source":"Crossref","is-referenced-by-count":28,"title":["Association Between Statin Use and Sex Hormone in the Multi-Ethnic Study of Atherosclerosis Cohort"],"prefix":"10.1210","volume":"104","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0944-4591","authenticated-orcid":false,"given":"Oludamilola W","family":"Oluleye","sequence":"first","affiliation":[{"name":"Essentia Health-Fargo Heart and Vascular Center, Fargo, North Dakota"}]},{"given":"Richard A","family":"Kronmal","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Washington, Seattle, Washington"}]},{"given":"Aaron R","family":"Folsom","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota"}]},{"given":"Dhananjay M","family":"Vaidya","sequence":"additional","affiliation":[{"name":"Johns Hopkins University School of Medicine, Baltimore, Maryland"}]},{"given":"Pamela","family":"Ouyang","sequence":"additional","affiliation":[{"name":"Johns Hopkins University School of Medicine, Baltimore, Maryland"}]},{"given":"Daniel A","family":"Duprez","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota"}]},{"given":"Adrian S","family":"Dobs","sequence":"additional","affiliation":[{"name":"Johns Hopkins University School of Medicine, Baltimore, Maryland"}]},{"given":"Hirad","family":"Yarmohammadi","sequence":"additional","affiliation":[{"name":"Columbia University, New York, New York"}]},{"given":"Suma H","family":"Konety","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, Department of 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Possible pathways could involve an association of liver fat with cardiac structural or functional abnormalities even after accounting for body size.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We analysed N\u00a0=\u00a02356 Framingham Heart Study participants (age 52\u00a0\u00b1\u00a012\u00a0years, 52% women) who underwent echocardiography and standardized computed tomography measures of liver fat.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In cross\u2010sectional multivariable regression models adjusted for age, gender, cohort and cardiovascular risk factors, liver fat was positively associated with left ventricular (LV) mass (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a01.45; 95% confidence interval (CI): 0.01, 2.88), LV wall thickness (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.01; 95% CI: 0.00, 0.02), mass volume ratio (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.02; 95% CI 0.01, 0.03), mitral peak velocity (E) (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.83; 95% CI 0.31, 1.36) and LV filling pressure (E\/e\u2032 ratio) (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.16; 95% CI 0.09, 0.23); and inversely associated with global systolic longitudinal strain (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.20, 95% CI 0.07, 0.33), diastolic annular velocity (e\u2032) (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a0\u22120.12; 95% CI\u00a0\u2212\u00a00.22, \u22120.03), and E\/A ratio (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a0\u22120.01; 95% CI\u00a0\u2212\u00a00.02, \u22120.00). After additional adjustment for body mass index (BMI), statistical significance was attenuated for all associations except for that of greater liver fat with increased LV filling pressure, a possible precursor to HF (<jats:italic>\u03b2<\/jats:italic>\u00a0=\u00a00.11; 95% CI 0.03, 0.18).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Increased liver fat was associated with multiple subclinical cardiac dysfunction measures, with most of associations mediated by obesity. Interestingly, the association of liver fat and LV filling pressure was only partially mediated by BMI, suggesting a possible direct effect of liver fat on LV filling pressure. Further confirmatory studies are needed.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.14600","type":"journal-article","created":{"date-parts":[[2020,7,12]],"date-time":"2020-07-12T06:32:12Z","timestamp":1594535532000},"page":"2445-2454","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["The association of non\u2010alcoholic fatty liver disease and cardiac structure and function\u2014Framingham Heart Study"],"prefix":"10.1111","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0840-3704","authenticated-orcid":false,"given":"Laura S.","family":"Chiu","sequence":"first","affiliation":[{"name":"Section of Gastroenterology Boston Medical Center Boston University School of Medicine Boston MA USA"}]},{"given":"Alison","family":"Pedley","sequence":"additional","affiliation":[{"name":"Merck Research Labs Kenilworth NJ USA"}]},{"given":"Joseph M.","family":"Massaro","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute\u2019s and Boston University\u2019s Framingham Heart Study Framingham MA USA"},{"name":"Department of Mathematics and Statistics Boston University Boston MA USA"}]},{"given":"Emelia J.","family":"Benjamin","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute\u2019s and Boston University\u2019s Framingham Heart Study Framingham MA USA"},{"name":"Section of Cardiovascular Medicine Boston Medical Center Boston University School of Medicine Boston MA USA"},{"name":"Department of Epidemiology Boston University School of Public Health Boston MA USA"}]},{"given":"Gary F.","family":"Mitchell","sequence":"additional","affiliation":[{"name":"Cardiovascular Engineering, Inc Norwood MA USA"}]},{"given":"David D.","family":"McManus","sequence":"additional","affiliation":[{"name":"Cardiology Division Department of Medicine and the Department of Quantitative Health Sciences University of Massachusetts Medical School Worchester MA USA"}]},{"given":"Jayashri","family":"Aragam","sequence":"additional","affiliation":[{"name":"Cardiovascular Division VA Boston Healthcare System Boston MA USA"},{"name":"Division of Cardiovascular Medicine Brigham and Women's Hospital Boston MA USA"},{"name":"Harvard Medical School Boston MA USA"}]},{"given":"Ramachandran S.","family":"Vasan","sequence":"additional","affiliation":[{"name":"National Heart, Lung, and Blood Institute\u2019s and Boston University\u2019s Framingham Heart Study Framingham MA USA"},{"name":"Section of Cardiovascular Medicine Boston Medical Center Boston University School of Medicine Boston MA USA"},{"name":"Department of Epidemiology Boston University School of Public Health Boston MA USA"},{"name":"Section of Preventive Medicine and Epidemiology Department of Medicine Boston Medical Center Boston MA 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and coalitions are promising approaches for childhood obesity prevention, yet there is little empirical evidence about<jats:italic>how<\/jats:italic>they affect change. We hypothesized that changes in knowledge of, and engagement with, childhood obesity prevention among coalition members can diffuse through social networks to influence policies, systems, and environments.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We studied a community coalition (<jats:italic>N<\/jats:italic>\u2009=\u200916, Shape Up Under 5 \u201cSUU5 Committee\u201d) focused on early childhood obesity prevention in Somerville, MA from 2015\u201317. Knowledge, engagement, and social network data were collected from Committee members and their network contacts (<jats:italic>n<\/jats:italic>\u2009=\u2009193) at five timepoints over two years. Policy, systems, and environment data were collected from the SUU5 Committee. Data were collected via the validated COMPACT Stakeholder-driven Community Diffusion survey and analyzed using regression models and social network analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Over 2\u00a0years, knowledge of (<jats:italic>p<\/jats:italic>\u2009=\u20090.0002), and engagement with (<jats:italic>p<\/jats:italic>\u2009=\u20090.03), childhood obesity prevention increased significantly among the SUU5 Committee. Knowledge increased among the Committee\u2019s social network (<jats:italic>p<\/jats:italic>\u2009=\u20090.001). Significant changes in policies, systems, and environments that support childhood obesity prevention were seen from baseline to 24\u00a0months (<jats:italic>p<\/jats:italic>\u2009=\u20090.003).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>SUU5 had positive effects on \u201cupstream\u201d drivers of early childhood obesity by increasing knowledge and engagement. 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We evaluated the association of higher urinary zinc level with new diagnosis of incident type 2 diabetes mellitus (T2DM) in adult populations with a high burden of T2DM from AZ, OK, and ND and SD. We also assessed the cross-sectional association of urinary zinc levels with prevalent prediabetes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                    <jats:p>We included 1,339 adults free of T2DM at baseline (1989\u20131991) followed through 1998\u20131999 in the Strong Heart Study (SHS) and 1,905 family members of SHS participants followed as part of the Strong Heart Family Study (SHFS) through 2006\u20132009.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>T2DM incidence was 14.7% (mean follow-up 6.6 years) in the SHS and 13.5% (mean follow-up 5.6 years) in the SHFS. After adjustment for sex, site, education, smoking status, BMI, and estimated glomerular filtration rate, the hazard ratio of T2DM in comparing 75th vs. 25th percentiles of urinary zinc distribution was 1.21 (95% CI 1.08, 1.36) in the SHS and 1.12 (0.96, 1.31) in the SHFS. These associations were attenuated but significant in the SHS after adjustment for HOMA of insulin resistance (HOMA-IR) score. With exclusion of participants with prediabetes at baseline, urinary zinc remained significantly associated with T2DM in the SHS. In cross-sectional analyses, prediabetes was associated with higher urinary zinc levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>Urinary zinc levels were associated with T2DM incidence and prediabetes prevalence even after adjustment for HOMA-IR in populations with a high burden of T2DM. These results highlight the importance of zinc metabolism in diabetes development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/dc22-1152","type":"journal-article","created":{"date-parts":[[2022,9,22]],"date-time":"2022-09-22T08:09:49Z","timestamp":1663834189000},"page":"2561-2569","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":33,"title":["Urinary Zinc and Incident Type 2 Diabetes: Prospective Evidence From the Strong Heart Study"],"prefix":"10.2337","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1996-7425","authenticated-orcid":false,"given":"Marta","family":"Galvez-Fernandez","sequence":"first","affiliation":[{"name":"1Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY"},{"name":"2Department of Preventive Medicine, Hospital Universitario Severo Ochoa, Madrid, Spain"}]},{"given":"Martha","family":"Powers","sequence":"additional","affiliation":[{"name":"3Department of Sociology and Anthropology, Northeastern University, Boston, MA"}]},{"given":"Maria","family":"Grau-Perez","sequence":"additional","affiliation":[{"name":"4Biomedical Research Institute of Valencia (INCLIVA), Valencia, Spain"}]},{"given":"Arce","family":"Domingo-Relloso","sequence":"additional","affiliation":[{"name":"1Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY"}]},{"given":"Nancy","family":"Lolacono","sequence":"additional","affiliation":[{"name":"1Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY"}]},{"given":"Walter","family":"Goessler","sequence":"additional","affiliation":[{"name":"5Institute of Chemistry, University of Graz, Graz, Austria"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[{"name":"6Department of 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Sciences","doi-asserted-by":"publisher","award":["UL1-TR-000040"],"award-info":[{"award-number":["UL1-TR-000040"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1-TR-001079"],"award-info":[{"award-number":["UL1-TR-001079"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006108","name":"National Center for Advancing Translational Sciences","doi-asserted-by":"publisher","award":["UL1-TR-001420"],"award-info":[{"award-number":["UL1-TR-001420"]}],"id":[{"id":"10.13039\/100006108","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[2024,6,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Elevated small dense LDL cholesterol (sd-LDL-C) increases atherosclerotic cardiovascular disease (CVD) risk. Although coronary artery calcification (CAC) is widely used for predicting CVD events, few studies have examined the relationship between sd-LDL-C and CAC.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>This study included 4672 individuals with directly measured baseline sd-LDL-C and CAC from the Multi-Ethnic Study of Atherosclerosis [mean (standard deviation) age: 61.9 (10.4) years; 52.5% women; 47.3% with baseline CAC (mean score &amp;gt;0)]. We used multi-variable general linear models and restricted cubic splines with the goodness of fit testing to evaluate the association of sd-LDL-C with the presence of CAC. Odds ratios [OR (95% confidence interval)] were adjusted for demographics and cardiovascular risk factors, including estimated total LDL-C. Higher quartiles of sd-LDL-C were associated with the presence of CAC, even after accounting for total LDL-C. Compared with the lowest quartile of sd-LDL-C, participants in Quartiles 2, 3, and 4 had higher odds for the presence of baseline CAC [Quartile 2 OR: 1.24 (1.00, 1.53); Quartile 3 OR: 1.51 (1.19, 1.93); and Quartile 4 OR 1.59 (1.17, 2.16)]. Splines suggested a quadratic curvilinear relationship of continuous sd-LDL-C with CAC after adjustment for demographics and CVD risk factors (quadratic vs. first-order sd-LDL-C terms likelihood ratio test: P = 0.015), but not after accounting for total LDL-C (quadratic vs. first-order terms: P = 0.156).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>In a large, multi-ethnic sample without known CVD, higher sd-LDL-C was associated with the presence of CAC, above and beyond total LDL-C. Whether selective direct measurement of sd-LDL-C is indicated to refine cardiovascular risk assessment in primary prevention warrants further investigation.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/eurjpc\/zwae049","type":"journal-article","created":{"date-parts":[[2024,2,7]],"date-time":"2024-02-07T11:43:06Z","timestamp":1707306186000},"page":"1048-1054","source":"Crossref","is-referenced-by-count":10,"title":["Small dense low-density lipoprotein cholesterol and coronary artery calcification in the Multi-Ethnic Study of Atherosclerosis"],"prefix":"10.1093","volume":"31","author":[{"given":"Rishi","family":"Rikhi","sequence":"first","affiliation":[{"name":"Centre for Prevention of Cardiovascular Disease, Section on Cardiovascular Medicine, Department of Internal Medicine, Wake Forest University School of Medicine , 1 Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5302-0828","authenticated-orcid":false,"given":"Christopher L","family":"Schaich","sequence":"additional","affiliation":[{"name":"Department of Surgery, Hypertension and Vascular Research Centre, Wake Forest University School of Medicine , 575 N Patterson Ave, Suite 120, Winston-Salem, NC 27101 , USA"}]},{"given":"George W","family":"Hafzalla","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Loma Linda University Health , 11234 Anderson St, Loma Linda, CA 92354 , USA"}]},{"given":"Nisha A","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Wake Forest University School of Medicine , 1 Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]},{"given":"Jordan E","family":"Tannenbaum","sequence":"additional","affiliation":[{"name":"Centre for Prevention of Cardiovascular Disease, Section on Cardiovascular Medicine, Department of Internal Medicine, Wake Forest University School of Medicine , 1 Medical Center Blvd, Winston-Salem, NC 27157 , USA"}]},{"given":"Charles A","family":"German","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Cardiology, University of Chicago , 5841 S Maryland Ave, Chicago, IL 60637 , USA"}]},{"given":"Tamar","family":"Polonsky","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Cardiology, University of Chicago , 5841 S Maryland Ave, Chicago, IL 60637 , USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7553-3408","authenticated-orcid":false,"given":"Michael Y","family":"Tsai","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota , 420 Delaware St SE, Minneapolis, MN 55455 , USA"}]},{"given":"Muhammad Imtiaz","family":"Ahmad","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section on Hospital Medicine, Medical College of Wisconsin , 8701 W Watertown Plank Rd, Milwaukee, WI 53226 , 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We hypothesized that an integrative multi\u2010omics approach might improve identification of subgroups of individuals with obesity who have distinct cardiometabolic disease patterns.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed machine learning\u2010based, integrative unsupervised clustering to identify proteomics\u2010 and metabolomics\u2010defined subpopulations of individuals living with obesity (BMI\u2009\u2265\u200930\u2009kg\/m<jats:sup>2<\/jats:sup>), leveraging data from 243 individuals in the Multi\u2010Ethnic Study of Atherosclerosis (MESA) cohort. Omics that contributed to the observed clusters were functionally characterized. We performed multivariate regression to assess whether the individuals in each cluster demonstrated differential patterns of cardiometabolic traits.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We identified two distinct clusters (iCluster1 and 2). iCluster2 had significantly higher average BMI values, fasting blood glucose, and inflammation. iCluster1 was associated with higher levels of total cholesterol and high\u2010density lipoprotein cholesterol. Pathways mediating cell growth, lipogenesis, and energy expenditures were positively associated with iCluster1. Inflammatory response and insulin resistance pathways were positively associated with iCluster2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Although the two identified clusters may represent progressive obesity\u2010related pathologic processes measured at different stages, other mechanisms in combination could also underpin the identified clusters given no significant age difference between the comparative groups. For instance, clusters may reflect differences in dietary\/behavioral patterns or differential rates of metabolic damage.<\/jats:p><\/jats:sec>","DOI":"10.1002\/oby.24137","type":"journal-article","created":{"date-parts":[[2024,11,5]],"date-time":"2024-11-05T08:52:45Z","timestamp":1730796765000},"page":"2024-2034","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Machine learning\u2010based clustering identifies obesity subgroups with differential multi\u2010omics profiles and metabolic patterns"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2349-8214","authenticated-orcid":false,"given":"Mohammad Y.","family":"Anwar","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Gillings School of Global Public Health University of North Carolina at Chapel Hill  Chapel Hill North Carolina 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D.","family":"Taylor","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics The Lundquist Institute for Biomedical Innovation at Harbor\u2010UCLA Medical Center  Torrance California USA"}]},{"given":"Russell P.","family":"Tracy","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Larner College of Medicine University of Vermont  Burlington Vermont USA"}]},{"given":"Peter","family":"Durda","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Larner College of Medicine University of Vermont  Burlington Vermont USA"}]},{"given":"Yongmei","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine Duke University Medical Center  Durham North Carolina USA"}]},{"given":"Craig W.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Biostatistics University of Washington  Seattle Washington USA"}]},{"given":"Francois","family":"Aguet","sequence":"additional","affiliation":[{"name":"Program of Medical and Population Genetics Broad Institute of MIT and Harvard  Cambridge Massachusetts USA"}]},{"given":"Kristin G.","family":"Ardlie","sequence":"additional","affiliation":[{"name":"Program of Medical and Population Genetics Broad Institute of MIT and Harvard  Cambridge Massachusetts USA"}]},{"given":"Robert E.","family":"Gerszten","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center, Massachusetts General Hospital Harvard Medical School  Boston Massachusetts USA"}]},{"given":"Clary B.","family":"Clish","sequence":"additional","affiliation":[{"name":"Metabolite Profiling Platform Broad Institute of MIT and Harvard  Cambridge Massachusetts USA"}]},{"given":"Leslie A.","family":"Lange","sequence":"additional","affiliation":[{"name":"Department of Epidemiology University of Colorado Anschutz Medical Campus  Aurora Colorado USA"}]},{"given":"Jingzhong","family":"Ding","sequence":"additional","affiliation":[{"name":"Section of Gerontology and Geriatric Medicine, Department of Internal Medicine Wake Forest University School of Medicine  Winston\u2010Salem North Carolina USA"}]},{"given":"Mark O.","family":"Goodarzi","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes, and Metabolism, Cedars\u2010Sinai Medical Center  Los Angeles California USA"}]},{"given":"Yii\u2010Der Ida","family":"Chen","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics The Lundquist Institute for Biomedical Innovation at Harbor\u2010UCLA Medical Center  Torrance California USA"}]},{"given":"Gina M.","family":"Peloso","sequence":"additional","affiliation":[{"name":"Department of Biostatistics Boston University School of Public Health, Boston University  Boston Massachusetts USA"}]},{"given":"Xiuqing","family":"Guo","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics The Lundquist Institute for Biomedical Innovation at Harbor\u2010UCLA Medical Center  Torrance California USA"}]},{"given":"Maggie A.","family":"Stanislawski","sequence":"additional","affiliation":[{"name":"Department of Biomedical Informatics University of Colorado Anschutz Medical Campus  Aurora Colorado USA"}]},{"given":"Jerome I.","family":"Rotter","sequence":"additional","affiliation":[{"name":"The Institute for Translational Genomics and Population Sciences, Department of Pediatrics The Lundquist Institute for Biomedical Innovation at Harbor\u2010UCLA Medical Center  Torrance California USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3872-7793","authenticated-orcid":false,"given":"Stephen S.","family":"Rich","sequence":"additional","affiliation":[{"name":"Center for Public Health Genomics University of Virginia  Charlottesville Virginia USA"}]},{"given":"Anne E.","family":"Justice","sequence":"additional","affiliation":[{"name":"Department of Population Health Sciences Geisinger Health System  Danville Pennsylvania USA"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0703-0742","authenticated-orcid":false,"given":"Ching\u2010ti","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Biostatistics Boston University School of Public Health, Boston University  Boston Massachusetts USA"}]},{"given":"Kari","family":"North","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Gillings School of Global Public Health University of North Carolina at Chapel Hill  Chapel Hill North Carolina 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All other rights reserved.","name":"copyright","label":"Copyright"}],"article-number":"100079"},{"indexed":{"date-parts":[[2025,11,16]],"date-time":"2025-11-16T18:54:35Z","timestamp":1763319275024,"version":"3.45.0"},"reference-count":0,"publisher":"Oxford University PressNew York, NY","isbn-type":[{"type":"print","value":"9780195129298"},{"type":"electronic","value":"9780197737453"}],"content-domain":{"domain":[],"crossmark-restriction":false},"published-print":{"date-parts":[[1999,3,18]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>On a warm afternoon in the autumn of 1996, a limousine pulled up at the gates of the Bayer AG plant in Berkeley, California1. A handful of young men piled out of the car, megaphones to the ready. \u201cWe are here to take your name away!\u201d they shouted. \u201cI.G. Farben, I.G. Farben, Zyklon B, Zyklon B\u201d\u2014an unsubtle reference to the lethal gas manufactured by the German pharmaceutical house and used to devastating effect in the Holocaust\u2014\u201d4000 dead, 4000 dead, 4000 dead.\u201d A cameraman recorded the scene, hoping to persuade local 1V stations to air this \u201cgreat source tape.\u201d \u201cDemo by limo,\u201d these demonstrators\u2014\u201dthe wrecking crew ... the Northern California boys in the band,\u201d as they called themselves\u2014exulted in their Internet posting2. \u201cHow much more newsworthy can a story be?\u201d Abruptly, however, the tone of the posting shifted and the demonstrators stood revealed as desperately sick, if still defiant, young men. \u201cWe might not be able to walk, but we can still demo!\u201d During the late 1980s and early 1990s, AIDS activists launched similar \u201czaps\u201d against drug companies. Those demonstrators were mainly gay men, members of ACT UP, expert practitioners in dramaturgical activism 3. The object of their animus was the alleged profiteering by pharmaceutical companies that put AZT and other drugs in the HIV arsenal out of the reach of many people with AIDS. 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