{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T10:57:42Z","timestamp":1766401062346},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,6,30]],"date-time":"2015-06-30T00:00:00Z","timestamp":1435622400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"ecoNugenics, Inc."}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Clinical Apheresis"],"published-print":{"date-parts":[[2016,8]]},"abstract":"<jats:sec><jats:title>Background:<\/jats:title><jats:p>Plasma galectin\u20103 (Gal\u20103) is elevated in, and drives, diverse systemic inflammatory disorders, including cancer, cardiovascular diseases, and diabetes. Circulating Gal\u20103 promotes tumorigenesis and metastasis, as well as fibrotic remodeling, and is a promising therapeutic target. Apheresis has proven utility in reducing circulating disease\u2010promoting substances, exemplified by the success of lipoprotein apheresis (LA) in abrogating cardiovascular disease progression in drug\u2010refractory hypercholesterolemia patients. We compared the clinical utility of two FDA\u2010approved LA systems in reducing plasma Gal\u20103 in humans.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>Plasma Gal\u20103 levels were assessed by ELISA in blinded samples drawn pre\u2010 and post\u2010apheresis from hypercholesterolemia patients (<jats:italic>n<\/jats:italic>\u2009=\u200910\/group) undergoing therapeutic LA using either a <jats:styled-content>h<\/jats:styled-content>eparin\u2010induced <jats:styled-content>e<\/jats:styled-content>xtracorporeal <jats:styled-content>L<\/jats:styled-content>DL <jats:styled-content>p<\/jats:styled-content>recipitation (HELP) or <jats:styled-content>d<\/jats:styled-content>extran <jats:styled-content>s<\/jats:styled-content>ulfate\u2010<jats:styled-content>a<\/jats:styled-content>dsorption (DSA) system.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>Mean baseline plasma Gal\u20103 concentrations (\u00b1SD) were 14.3\u2009\u00b1\u20095.1 (range 6.6\u201322.8) and 14.5\u2009\u00b1\u20092.8 (range 10.6\u201319.8) ng\/mL in the HELP and DSA groups, respectively. Post\u2010apheresis Gal\u20103 levels were respectively reduced by 19.4% and 22.7% in the HELP (<jats:italic>P<\/jats:italic>\u2009=\u20090.0094) and DSA (<jats:italic>P<\/jats:italic>\u2009=\u20090.0027) systems (paired <jats:italic>t<\/jats:italic>\u2010tests); the difference between devices was insignificant (<jats:italic>P<\/jats:italic>\u2009=\u20090.5288; Mann\u2013Whitney). Post\u2010treatment Gal\u20103 levels were 11.3\u2009\u00b1\u20093.7 (HELP; range 4.5\u201316.3) and 11.3\u2009\u00b1\u20093.8 (DSA; range 7.5\u201320.7) ng\/mL.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>Circulating Gal\u20103 levels showed a statistically significant decrease in humans undergoing therapeutic LA. Although absolute Gal\u20103 reduction was \u224819\u201323%, this effect, combined with reducing atherogenic LDL and other inflammation mediators (e.g., CRP, fibrinogen, Lp\u2010PLA<jats:sub>2<\/jats:sub>), may enhance apheresis clinical benefits. Applying new Gal\u20103\u2010specific extraction technologies to apheresis may be advantageous in treating diverse pathologies that are promoted by elevated plasma Gal\u20103. J. Clin. Apheresis 31:388\u2013392, 2016. \u00a9 2015 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jca.21413","type":"journal-article","created":{"date-parts":[[2015,6,30]],"date-time":"2015-06-30T08:03:36Z","timestamp":1435651416000},"page":"388-392","source":"Crossref","is-referenced-by-count":11,"title":["Lipoprotein apheresis reduces circulating galectin\u20103 in humans"],"prefix":"10.1002","volume":"31","author":[{"given":"Isaac","family":"Eliaz","sequence":"first","affiliation":[{"name":"Amitabha Medical Clinic and Healing Center Santa Rosa California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elaine","family":"Weil","sequence":"additional","affiliation":[{"name":"Amitabha Medical Clinic and Healing Center Santa Rosa California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie\u2010Ann","family":"Dutton","sequence":"additional","affiliation":[{"name":"University of Kansas Medical Center, Atherosclerosis and Lipid\u2010Apheresis Center Kansas City Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Audrey E.","family":"McCalley","sequence":"additional","affiliation":[{"name":"University of Kansas Medical Center, Atherosclerosis and Lipid\u2010Apheresis Center Kansas City Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbie","family":"Nolte","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Kansas Medical Center Kansas City Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrick M.","family":"Moriarty","sequence":"additional","affiliation":[{"name":"University of Kansas Medical Center, Atherosclerosis and Lipid\u2010Apheresis Center Kansas City Kansas"},{"name":"Department of Internal Medicine University of Kansas Medical Center Kansas City Kansas"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,6,30]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2009.00794.x"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2012.04.053"},{"key":"e_1_2_6_4_1","first-page":"88.","article-title":"Galectins in cancer: carcinogenesis, diagnosis and therapy","volume":"2","author":"Ebrahim AH","year":"2014","journal-title":"Ann Transl Med"},{"key":"e_1_2_6_5_1","doi-asserted-by":"crossref","first-page":"20807","DOI":"10.1016\/S0021-9258(17)31891-4","article-title":". 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