{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T06:39:29Z","timestamp":1792305569416,"version":"4.4.0"},"reference-count":53,"publisher":"MDPI AG","issue":"18","license":[{"start":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T00:00:00Z","timestamp":1726704000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diagnostics"],"abstract":"<jats:p>Background: Spinal muscular atrophy type 3 (juvenile SMA, Kugelberg\u2013Welander disease) is a genetic disease caused by changes in the survival motor neuron 1 (SMN) gene. However, there is increasing evidence of metabolic abnormalities in SMA patients, such as altered fatty acid metabolism, impaired glucose tolerance, and defects in the functioning of muscle mitochondria. Given that data in the literature are scarce regarding this subject, the purpose of this study was to estimate the prevalence of glucose and lipid metabolism disorders in adult patients with SMA type 3. Methods: We conducted a cross-sectional study of 23 adult patients with SMA type 3 who underwent a comprehensive evaluation, including a physical examination, biochemical analysis, and an oral glucose tolerance test during 2020\u20132023. Results: At least one lipid abnormality was observed in 60.8% of patients. All four lipid parameters were atypical in 4.3% of patients, three lipid parameters were abnormal in 21.7% of patients, and two lipid parameters were altered in 8.7% patients. A total of 91.3% of SMA3 patients met the HOMA-IR criteria for insulin resistance, with 30.43% having impaired glucose tolerance. None of the patients met the criteria for a diagnosis of overt DM2. Conclusions: The prevalence of dyslipidemia and altered glucose metabolism in our study sets apart the adult population with SMA3 from the general population, confirming a significant interplay between muscle, liver, and adipose tissue. Ensuring metabolic care for aging patients with SMA 3 is crucial, as they are vulnerable to metabolic derangements and cardiovascular risks.<\/jats:p>","DOI":"10.3390\/diagnostics14182078","type":"journal-article","created":{"date-parts":[[2024,9,20]],"date-time":"2024-09-20T02:47:07Z","timestamp":1726800427000},"page":"2078","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Glucose and Lipid Metabolism Disorders in Adults with Spinal Muscular Atrophy Type 3"],"prefix":"10.3390","volume":"14","author":[{"given":"Marija","family":"Mileti\u0107","sequence":"first","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia"},{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zorica","family":"Stevi\u0107","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"},{"name":"Clinic of Neurology, University Clinical Center of Serbia, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana","family":"Vujovi\u0107","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia"},{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8365-4840","authenticated-orcid":false,"given":"Jelena","family":"Rako\u010devi\u0107","sequence":"additional","affiliation":[{"name":"Institute of Histology and Embryology \u201cAleksandar \u0110. Kosti\u0107\u201d, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-4212-0182","authenticated-orcid":false,"given":"Ana","family":"Tomi\u0107","sequence":"additional","affiliation":[{"name":"Center for Radiology Imaging-Magnetic Resonance, University Clinical Center of Serbia, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7290-5181","authenticated-orcid":false,"given":"Milina","family":"Tan\u010di\u0107 Gaji\u0107","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia"},{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1935-9094","authenticated-orcid":false,"given":"Milo\u0161","family":"Stojanovi\u0107","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia"},{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4941-1444","authenticated-orcid":false,"given":"Aleksa","family":"Palibrk","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"},{"name":"Clinic of Neurology, University Clinical Center of Serbia, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9977-5970","authenticated-orcid":false,"given":"Milo\u0161","family":"\u017darkovi\u0107","sequence":"additional","affiliation":[{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia"},{"name":"Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,9,19]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"69","DOI":"10.1016\/j.nmd.2008.10.004","article-title":"Ramblings in the history of spinal muscular atrophy","volume":"19","author":"Dubowitz","year":"2009","journal-title":"Neuromuscul. Disord. NMD"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"743","DOI":"10.1016\/j.pcl.2015.03.010","article-title":"Spinal muscular atrophies","volume":"62","author":"Darras","year":"2015","journal-title":"Pediatr. Clin. N. Am."},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"355","DOI":"10.1002\/ana.24864","article-title":"Emerging therapies and challenges in spinal muscular atrophy","volume":"81","author":"Farrar","year":"2017","journal-title":"Ann. Neurol."},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"2120","DOI":"10.1016\/S0140-6736(08)60921-6","article-title":"Spinal muscular atrophy","volume":"371","author":"Lunn","year":"2008","journal-title":"Lancet Lond. Engl."},{"key":"ref_5","doi-asserted-by":"crossref","first-page":"103","DOI":"10.1016\/j.nmd.2017.11.005","article-title":"Diagnosis and management of spinal muscular atrophy: Part 1: Recommendations for diagnosis, rehabilitation, orthopedic and nutritional care","volume":"28","author":"Mercuri","year":"2018","journal-title":"Neuromuscul. Disord."},{"key":"ref_6","doi-asserted-by":"crossref","first-page":"597","DOI":"10.1038\/nrn2670","article-title":"Spinal muscular atrophy: Why do low levels of survival motor neuron protein make motor neurons sick?","volume":"10","author":"Burghes","year":"2009","journal-title":"Nat. Rev. Neurosci."},{"key":"ref_7","doi-asserted-by":"crossref","first-page":"8691","DOI":"10.1523\/JNEUROSCI.0417-15.2015","article-title":"Disease mechanisms and therapeutic approaches in spinal muscular atrophy","volume":"35","author":"Tisdale","year":"2015","journal-title":"J. Neurosci."},{"key":"ref_8","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1146\/annurev-genom-102319-103602","article-title":"Twenty-Five Years of Spinal Muscular Atrophy Research: From Phenotype to Genotype to Therapy, and What Comes Next","volume":"21","author":"Wirth","year":"2020","journal-title":"Annu. Rev. Genomics Hum. Genet."},{"key":"ref_9","doi-asserted-by":"crossref","first-page":"831","DOI":"10.1016\/j.ncl.2015.07.004","article-title":"Spinal Muscular Atrophy","volume":"33","author":"Kolb","year":"2015","journal-title":"Neurol. Clin."},{"key":"ref_10","doi-asserted-by":"crossref","first-page":"518","DOI":"10.1001\/archneur.1995.00540290108025","article-title":"Natural history in proximal spinal muscular atrophy. Clinical analysis of 445 patients and suggestions for a modification of existing classifications","volume":"52","author":"Zerres","year":"1995","journal-title":"Arch. Neurol."},{"key":"ref_11","doi-asserted-by":"crossref","unstructured":"Chen, T.-H. (2020). New and Developing Therapies in Spinal Muscular Atrophy: From Genotype to Phenotype to Treatment and Where Do We Stand?. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21093297"},{"key":"ref_12","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1016\/j.nbd.2017.01.011","article-title":"Spinal muscular atrophy: Factors that modulate motor neurone vulnerability","volume":"102","author":"Tu","year":"2017","journal-title":"Neurobiol. Dis."},{"key":"ref_13","doi-asserted-by":"crossref","first-page":"779","DOI":"10.2174\/1566524016666161128113338","article-title":"Spinal Muscular Atrophy: More than a Disease of Motor Neurons?","volume":"16","author":"Nash","year":"2016","journal-title":"Curr. Mol. Med."},{"key":"ref_14","doi-asserted-by":"crossref","first-page":"1003","DOI":"10.1007\/s00018-015-2106-9","article-title":"Is spinal muscular atrophy a disease of the motor neurons only: Pathogenesis and therapeutic implications?","volume":"73","author":"Simone","year":"2016","journal-title":"Cell. Mol. Life Sci."},{"key":"ref_15","doi-asserted-by":"crossref","first-page":"12","DOI":"10.1016\/j.pediatrneurol.2020.01.003","article-title":"Overturning the Paradigm of Spinal Muscular Atrophy as Just a Motor Neuron Disease","volume":"109","author":"Yeo","year":"2020","journal-title":"Pediatr. Neurol."},{"key":"ref_16","doi-asserted-by":"crossref","first-page":"256","DOI":"10.1002\/ana.23582","article-title":"Glucose metabolism and pancreatic defects in spinal muscular atrophy","volume":"72","author":"Bowerman","year":"2012","journal-title":"Ann. Neurol."},{"key":"ref_17","doi-asserted-by":"crossref","first-page":"1362","DOI":"10.1016\/j.jpeds.2015.09.023","article-title":"Responses to Fasting and Glucose Loading in a Cohort of Well Children with Spinal Muscular Atrophy Type II","volume":"167","author":"Davis","year":"2015","journal-title":"J. Pediatr."},{"key":"ref_18","doi-asserted-by":"crossref","first-page":"80","DOI":"10.1016\/j.pediatrneurol.2015.12.015","article-title":"Nutritional Status and Nutrient Intake Challenges in Children with Spinal Muscular Atrophy","volume":"57","author":"Mehta","year":"2016","journal-title":"Pediatr. Neurol."},{"key":"ref_19","unstructured":"WHO (1995). WHO Expert Committee on Physical Status: The Use and Interpretation of Anthropometry. Physical Status: The Use of and Interpretation of Anthropometry, Report of a WHO Expert Committee, World Health Organization."},{"key":"ref_20","doi-asserted-by":"crossref","first-page":"499","DOI":"10.1093\/clinchem\/18.6.499","article-title":"Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge","volume":"18","author":"Friedewald","year":"1972","journal-title":"Clin. Chem."},{"key":"ref_21","doi-asserted-by":"crossref","unstructured":"American Diabetes Association (2015). 2. Classification and Diagnosis of Diabetes. Diabetes Care, 38, S8\u2013S16.","DOI":"10.2337\/dc15-S005"},{"key":"ref_22","doi-asserted-by":"crossref","first-page":"412","DOI":"10.1007\/BF00280883","article-title":"Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man","volume":"28","author":"Matthews","year":"1985","journal-title":"Diabetologia"},{"key":"ref_23","doi-asserted-by":"crossref","first-page":"512","DOI":"10.1016\/j.nmd.2018.03.009","article-title":"Comprehensive nutritional and metabolic assessment in patients with spinal muscular atrophy: Opportunity for an individualized approach","volume":"28","author":"Martinez","year":"2018","journal-title":"Neuromuscul. Disord."},{"key":"ref_24","doi-asserted-by":"crossref","first-page":"389","DOI":"10.1016\/j.nmd.2008.02.008","article-title":"Feeding problems and malnutrition in spinal muscular atrophy type II","volume":"18","author":"Messina","year":"2008","journal-title":"Neuromuscul. Disord."},{"key":"ref_25","doi-asserted-by":"crossref","first-page":"391","DOI":"10.1016\/j.nmd.2009.03.009","article-title":"Increased fat mass and high incidence of overweight despite low body mass index in patients with spinal muscular atrophy","volume":"19","author":"Sproule","year":"2009","journal-title":"Neuromuscul. Disord."},{"key":"ref_26","doi-asserted-by":"crossref","first-page":"580","DOI":"10.2337\/diab.34.6.580","article-title":"The disposal of an oral glucose load in healthy subjects. A quantitative study","volume":"34","author":"Ferrannini","year":"1985","journal-title":"Diabetes"},{"key":"ref_27","doi-asserted-by":"crossref","first-page":"1130","DOI":"10.2337\/dc05-2179","article-title":"Contributions of beta-cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose","volume":"29","author":"Tripathy","year":"2006","journal-title":"Diabetes Care"},{"key":"ref_28","doi-asserted-by":"crossref","first-page":"281","DOI":"10.2337\/dc08-1264","article-title":"Fasting versus postload plasma glucose concentration and the risk for future type 2 diabetes: Results from the Botnia Study","volume":"32","author":"Lyssenko","year":"2009","journal-title":"Diabetes Care"},{"key":"ref_29","doi-asserted-by":"crossref","first-page":"1650","DOI":"10.2337\/dc08-0225","article-title":"One-hour plasma glucose concentration and the metabolic syndrome identify subjects at high risk for future type 2 diabetes","volume":"31","author":"Ali","year":"2008","journal-title":"Diabetes Care"},{"key":"ref_30","doi-asserted-by":"crossref","first-page":"2090","DOI":"10.2337\/dc09-2261","article-title":"Relationship between Insulin Sensitivity and Cardiovascular Risk (RISC) Consortium. One-hour plasma glucose identifies insulin resistance and beta-cell dysfunction in individuals with normal glucose tolerance: Cross-sectional data from the Relationship between Insulin Sensitivity and Cardiovascular Risk (RISC) study","volume":"33","author":"Manco","year":"2010","journal-title":"Diabetes Care"},{"key":"ref_31","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1001\/archneur.1975.00490450075011","article-title":"Lipid disturbances associated with spiral muscular atrophy. Clinical, electromyographic, histochemical, and lipid studies","volume":"32","author":"Dahl","year":"1975","journal-title":"Arch. Neurol."},{"key":"ref_32","doi-asserted-by":"crossref","first-page":"703","DOI":"10.1038\/ng.381","article-title":"Type 1 Diabetes Genetics Consortium. Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes","volume":"41","author":"Barrett","year":"2009","journal-title":"Nat. Genet."},{"key":"ref_33","doi-asserted-by":"crossref","first-page":"381","DOI":"10.1038\/ng.3245","article-title":"Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers","volume":"47","author":"Chen","year":"2015","journal-title":"Nat. Genet."},{"key":"ref_34","doi-asserted-by":"crossref","first-page":"1433","DOI":"10.2337\/dci17-0014","article-title":"The Promise and Practice of Genetics on Diabetes Care: The Fog Rises to Reveal a Field of Genetic Complexity in HNF1B","volume":"40","author":"Rich","year":"2017","journal-title":"Diabetes Care"},{"key":"ref_35","doi-asserted-by":"crossref","first-page":"215","DOI":"10.1242\/dmm.028225","article-title":"Diabetic polyneuropathy, sensory neurons, nuclear structure and spliceosome alterations: A role for CWC22","volume":"10","author":"Kobayashi","year":"2017","journal-title":"Dis. Model. Mech."},{"key":"ref_36","doi-asserted-by":"crossref","first-page":"291","DOI":"10.1016\/j.nmd.2021.02.002","article-title":"Glucose and lipid metabolism disorders in children and adolescents with spinal muscular atrophy types 2 and 3","volume":"31","author":"Djordjevic","year":"2021","journal-title":"Neuromuscul. Disord."},{"key":"ref_37","doi-asserted-by":"crossref","unstructured":"Fahed, M., Abou Jaoudeh, M.G., Merhi, S., Mosleh, J.M.B., Ghadieh, R., Al Hayek, S., and El Hayek Fares, J.E. (2020). Evaluation of risk factors for insulin resistance: A cross sectional study among employees at a private university in Lebanon. BMC Endocr. Disord., 20.","DOI":"10.1186\/s12902-020-00558-9"},{"key":"ref_38","doi-asserted-by":"crossref","first-page":"888","DOI":"10.1016\/j.nmd.2020.09.025","article-title":"Insulin-like growth factor-1 status is associated with insulin resistance in young patients with spinal muscular atrophy","volume":"30","author":"Brener","year":"2020","journal-title":"Neuromuscul. Disord."},{"key":"ref_39","doi-asserted-by":"crossref","unstructured":"Deguise, M.-O., Chehade, L., and Kothary, R. (2021). Metabolic Dysfunction in Spinal Muscular Atrophy. Int. J. Mol. Sci., 22.","DOI":"10.3390\/ijms22115913"},{"key":"ref_40","doi-asserted-by":"crossref","first-page":"237","DOI":"10.1016\/j.atherosclerosis.2007.03.034","article-title":"Atherogenic lipoprotein phenotype and LDL size and subclasses in patients with peripheral arterial disease","volume":"197","author":"Rizzo","year":"2008","journal-title":"Atherosclerosis"},{"key":"ref_41","doi-asserted-by":"crossref","first-page":"1075","DOI":"10.1016\/j.bbrc.2004.03.151","article-title":"ANGPTL3 is increased in both insulin-deficient and -resistant diabetic states","volume":"317","author":"Inukai","year":"2004","journal-title":"Biochem. Biophys. Res. Commun."},{"key":"ref_42","first-page":"160","article-title":"Non-HDL cholesterol as a metric of good quality of care: Opportunities and challenges","volume":"38","author":"Virani","year":"2011","journal-title":"Tex. Heart Inst. J."},{"key":"ref_43","unstructured":"National Cholesterol Education Program (2001). ATP III guidelines at-a-glance quick desk reference. Natl. Inst. Health, 329, 211."},{"key":"ref_44","doi-asserted-by":"crossref","first-page":"2032","DOI":"10.1194\/jlr.R004739","article-title":"Genetic causes of high and low serum HDL-cholesterol","volume":"51","author":"Pajukanta","year":"2010","journal-title":"J. Lipid Res."},{"key":"ref_45","doi-asserted-by":"crossref","first-page":"1519","DOI":"10.1002\/acn3.50855","article-title":"Abnormal fatty acid metabolism is a core component of spinal muscular atrophy","volume":"6","author":"Deguise","year":"2019","journal-title":"Ann. Clin. Transl. Neurol."},{"key":"ref_46","doi-asserted-by":"crossref","unstructured":"MacDonald, T. (2022). Prevalence of High Cholesterol Among the Adult U.S. Population: NHANES 2013\u20132018. Curr. Dev. Nutr., 6.","DOI":"10.1093\/cdn\/nzac067.045"},{"key":"ref_47","doi-asserted-by":"crossref","first-page":"629","DOI":"10.1016\/0140-6736(90)93426-P","article-title":"Secondary metabolic defects in spinal muscular atrophy type II","volume":"336","author":"Harpey","year":"1990","journal-title":"Lancet Lond. Engl."},{"key":"ref_48","doi-asserted-by":"crossref","first-page":"734","DOI":"10.1002\/ana.410200615","article-title":"Dicarboxylic aciduria in an infant with spinal muscular atrophy","volume":"20","author":"Kelley","year":"1986","journal-title":"Ann. Neurol."},{"key":"ref_49","doi-asserted-by":"crossref","first-page":"337","DOI":"10.1002\/1531-8249(199903)45:3<337::AID-ANA9>3.0.CO;2-U","article-title":"Abnormal fatty acid metabolism in childhood spinal muscular atrophy","volume":"45","author":"Crawford","year":"1999","journal-title":"Ann. Neurol."},{"key":"ref_50","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1016\/0887-8994(94)00100-G","article-title":"Fatty acid oxidation abnormalities in childhood-onset spinal muscular atrophy: Primary or secondary defect(s)?","volume":"12","author":"Tein","year":"1995","journal-title":"Pediatr. Neurol."},{"key":"ref_51","doi-asserted-by":"crossref","first-page":"666","DOI":"10.1001\/jamaneurol.2015.0178","article-title":"Impaired Muscle Mitochondrial Biogenesis and Myogenesis in Spinal Muscular Atrophy","volume":"72","author":"Ripolone","year":"2015","journal-title":"JAMA Neurol."},{"key":"ref_52","doi-asserted-by":"crossref","first-page":"419","DOI":"10.3233\/JND-160171","article-title":"Stress-Induced Ketoacidosis in Spinal Muscular Atrophy: An Under-Recognized Complication","volume":"3","author":"Mulroy","year":"2016","journal-title":"J. Neuromuscul. Dis."},{"key":"ref_53","doi-asserted-by":"crossref","unstructured":"Lipnick, S.L., Agniel, D.M., Aggarwal, R., Makhortova, N.R., Finlayson, S.G., Brocato, A., Palmer, N., Darras, B.T., Kohane, I., and Rubin, L.L. (2019). Systemic nature of spinal muscular atrophy revealed by studying insurance claims. PLoS ONE, 14.","DOI":"10.1371\/journal.pone.0213680"}],"container-title":["Diagnostics"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.mdpi.com\/2075-4418\/14\/18\/2078\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T15:59:59Z","timestamp":1760111999000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.mdpi.com\/2075-4418\/14\/18\/2078"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2024,9,19]]},"references-count":53,"journal-issue":{"issue":"18","published-online":{"date-parts":[[2024,9]]}},"alternative-id":["diagnostics14182078"],"URL":"https:\/\/doi.org\/10.3390\/diagnostics14182078","relation":{},"ISSN":["2075-4418"],"issn-type":[{"value":"2075-4418","type":"electronic"}],"subject":[],"published":{"date-parts":[[2024,9,19]]}}}