Institution
Institute of Chartered Accountants of Nigeria
About: Institute of Chartered Accountants of Nigeria is a based out in . It is known for research contribution in the topics: Population & Adipose tissue. The organization has 528 authors who have published 579 publications receiving 18688 citations.
Topics: Population, Adipose tissue, Insulin resistance, Genome-wide association study, Extracorporeal membrane oxygenation
Papers published on a yearly basis
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TL;DR: Obesity triggers T-cell-mediated inflammation and enterocyte insulin resistance in the jejunum with potential broader systemic implications, and statistical links between T cell densities and BMI, NAFLD, or lipid metabolism suggest tissue crosstalk.
129 citations
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Imperial College London1, St George's, University of London2, University of the Witwatersrand3, University of São Paulo4, University of Manchester5, University of Western Australia6, Saint Joseph's University7, Sultan Qaboos University8, Medical University of Łódź9, Instituto Nacional de Saúde Dr. Ricardo Jorge10, Institute of Chartered Accountants of Nigeria11, Nanyang Technological University12, Innsbruck Medical University13, Hebrew University of Jerusalem14, Masaryk University15, University of Lisbon16, McGill University17, Ege University18, National University of Singapore19, University of Latvia20, Saarland University21, University of Ioannina22, Linköping University23, Copenhagen University Hospital24, Mashhad University of Medical Sciences25, Technische Universität München26, United Arab Emirates University27, National Taiwan University28, University of Helsinki29, University of Milan30
TL;DR: Although early detection and treatment with statins and other LDL-C lowering therapies can improve survival, FH remains widely underdiagnosed and undertreated, thereby representing a major global public health challenge.
123 citations
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University of California, San Diego1, Broad Institute2, Boston Children's Hospital3, University of Helsinki4, University of Virginia5, University College Dublin6, University of Utah7, University of Pennsylvania8, Joslin Diabetes Center9, University of Edinburgh10, University of Oxford11, Lund University12, Steno Diabetes Center13, University of Michigan14, Boehringer Ingelheim15, National Institutes of Health16, University of Wisconsin-Madison17, George Washington University18, University of Minnesota19, University of Washington20, University of Pittsburgh21, University of Paris22, Institute of Chartered Accountants of Nigeria23, University of Colorado Denver24, Stanford University25, Lunenfeld-Tanenbaum Research Institute26, McMaster University27, University of Dundee28, Paracelsus Private Medical University of Salzburg29, University of Latvia30, Latvian Biomedical Research and Study centre31, Lithuanian University of Health Sciences32, Carol Davila University of Medicine and Pharmacy33, China Pharmaceutical University34, Umeå University35, Karolinska Institutet36, Karolinska University Hospital37, University of Copenhagen38, French Institute of Health and Medical Research39, Queen's University Belfast40
TL;DR: In this paper, a large collection of type 1 diabetes cohorts with harmonized diabetic kidney disease phenotypes were assembled through collaboration with the Diabetes Nephropathy Collaborative Research Initiative, and 16 genome-wide significant risk loci were identified.
Abstract: Background Although diabetic kidney disease demonstrates both familial clustering and single nucleotide polymorphism heritability, the specific genetic factors influencing risk remain largely unknown. Methods To identify genetic variants predisposing to diabetic kidney disease, we performed genome-wide association study (GWAS) analyses. Through collaboration with the Diabetes Nephropathy Collaborative Research Initiative, we assembled a large collection of type 1 diabetes cohorts with harmonized diabetic kidney disease phenotypes. We used a spectrum of ten diabetic kidney disease definitions based on albuminuria and renal function. Results Our GWAS meta-analysis included association results for up to 19,406 individuals of European descent with type 1 diabetes. We identified 16 genome-wide significant risk loci. The variant with the strongest association (rs55703767) is a common missense mutation in the collagen type IV alpha 3 chain (COL4A3) gene, which encodes a major structural component of the glomerular basement membrane (GBM). Mutations in COL4A3 are implicated in heritable nephropathies, including the progressive inherited nephropathy Alport syndrome. The rs55703767 minor allele (Asp326Tyr) is protective against several definitions of diabetic kidney disease, including albuminuria and ESKD, and demonstrated a significant association with GBM width; protective allele carriers had thinner GBM before any signs of kidney disease, and its effect was dependent on glycemia. Three other loci are in or near genes with known or suggestive involvement in this condition (BMP7) or renal biology (COLEC11 and DDR1). Conclusions The 16 diabetic kidney disease-associated loci may provide novel insights into the pathogenesis of this condition and help identify potential biologic targets for prevention and treatment.
122 citations
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University of California, San Francisco1, University of Southern California2, Mayo Clinic3, Brigham and Women's Hospital4, Harvard University5, University of Manchester6, Manchester Academic Health Science Centre7, Federal University of Amazonas8, Hamad Medical Corporation9, Karolinska Institutet10, University of Lyon11, university of lille12, University of Paris13, Université Paris-Saclay14, University of Giessen15, Ludwig Maximilian University of Munich16, Universidade Federal de Juiz de Fora17, University of Brasília18, University of Cambridge19, King's College London20, University of Washington21, Scientific University of the South22, University of Michigan23, Royal Hallamshire Hospital24, University of Queensland25, Institute of Chartered Accountants of Nigeria26, University of Otago27, Boston University28, McMaster University29, HealthPartners30, Royal Brisbane and Women's Hospital31
TL;DR: In this article, the authors investigated baseline use of biologic or targeted synthetic (b/ts) disease-modifying antirheumatic drugs (DMARDs) and COVID-19 outcomes in rheumatoid arthritis (RA).
Abstract: Objective To investigate baseline use of biologic or targeted synthetic (b/ts) disease-modifying antirheumatic drugs (DMARDs) and COVID-19 outcomes in rheumatoid arthritis (RA). Methods We analysed the COVID-19 Global Rheumatology Alliance physician registry (from 24 March 2020 to 12 April 2021). We investigated b/tsDMARD use for RA at the clinical onset of COVID-19 (baseline): abatacept (ABA), rituximab (RTX), Janus kinase inhibitors (JAKi), interleukin 6 inhibitors (IL-6i) or tumour necrosis factor inhibitors (TNFi, reference group). The ordinal COVID-19 severity outcome was (1) no hospitalisation, (2) hospitalisation without oxygen, (3) hospitalisation with oxygen/ventilation or (4) death. We used ordinal logistic regression to estimate the OR (odds of being one level higher on the ordinal outcome) for each drug class compared with TNFi, adjusting for potential baseline confounders. Results Of 2869 people with RA (mean age 56.7 years, 80.8% female) on b/tsDMARD at the onset of COVID-19, there were 237 on ABA, 364 on RTX, 317 on IL-6i, 563 on JAKi and 1388 on TNFi. Overall, 613 (21%) were hospitalised and 157 (5.5%) died. RTX (OR 4.15, 95% CI 3.16 to 5.44) and JAKi (OR 2.06, 95% CI 1.60 to 2.65) were each associated with worse COVID-19 severity compared with TNFi. There were no associations between ABA or IL6i and COVID-19 severity. Conclusions People with RA treated with RTX or JAKi had worse COVID-19 severity than those on TNFi. The strong association of RTX and JAKi use with poor COVID-19 outcomes highlights prioritisation of risk mitigation strategies for these people.
121 citations
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TL;DR: It is indicated that the intestinal microbiota determines the circulating cholesterol level and may thus represent a novel therapeutic target in the management of dyslipidemia and cardiovascular diseases.
Abstract: Management of blood cholesterol is a major focus of efforts to prevent cardiovascular diseases. The objective of this study was to investigate how the gut microbiota affects host cholesterol homeostasis at the organism scale. We depleted the intestinal microbiota of hypercholesterolemic female Apoe−/− mice using broad-spectrum antibiotics. Measurement of plasma cholesterol levels as well as cholesterol synthesis and fluxes by complementary approaches showed that the intestinal microbiota strongly regulates plasma cholesterol level, hepatic cholesterol synthesis, and enterohepatic circulation. Moreover, transplant of the microbiota from humans harboring elevated plasma cholesterol levels to recipient mice induced a phenotype of high plasma cholesterol levels in association with a low hepatic cholesterol synthesis and high intestinal absorption pattern. Recipient mice phenotypes correlated with several specific bacterial phylotypes affiliated to Betaproteobacteria, Alistipes, Bacteroides, and Barnesiella taxa. These results indicate that the intestinal microbiota determines the circulating cholesterol level and may thus represent a novel therapeutic target in the management of dyslipidemia and cardiovascular diseases.
116 citations
Authors
Showing all 528 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald M. Evans | 199 | 708 | 166722 |
Thierry Poynard | 119 | 668 | 64548 |
Heikki Joensuu | 108 | 571 | 50300 |
Gilles Montalescot | 100 | 641 | 58644 |
François Cambien | 92 | 251 | 36260 |
Antoine Danchin | 80 | 483 | 30219 |
Laurence Tiret | 79 | 194 | 25231 |
Karine Clément | 78 | 275 | 32185 |
Karine Clément | 73 | 228 | 14710 |
Pascal Ferré | 69 | 241 | 23969 |
Michael T. Osterholm | 68 | 260 | 22624 |
Vincent Jarlier | 67 | 278 | 17060 |
Florent Soubrier | 67 | 226 | 24486 |
Stephen H. Caldwell | 66 | 308 | 18527 |
Christian Funck-Brentano | 64 | 267 | 70432 |