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
Papers
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Beth Israel Deaconess Medical Center1, Boston Children's Hospital2, HealthPartners3, Boston University4, University College London5, Harvard University6, Institute of Chartered Accountants of Nigeria7, University of Queensland8, University of California, San Francisco9, University of Otago10, McMaster University11
TL;DR: The COVID-19 pandemic has disrupted the way that clinical care is delivered and research is conducted and there has never been such an urgent need to understand, prevent, and find effective treatments for a disease.
Abstract: Introduction The COVID-19 pandemic has disrupted the way that clinical care is delivered and research is conducted. Clinical encounters have been postponed or transitioned to telehealth, research laboratories throughout the world have shut down, and many clinical research studies have been suspended. At the same time, there has never been such an urgent need to understand, prevent, and find effective treatments for a disease. At the time of this writing, SARS-CoV-2, the virus that causes COVID-19, has infected more than seven million people around the world and caused the deaths of almost half a million people, less than six months after it was first identified (1).
8 citations
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TL;DR: A novel association of PAH and a channelopathy due to mutation in ATP1A2 (encoding the α2-subunit of the Na+/K+-ATPase), a mutation known to cause familial hemiplegic migraine (FHM), a rare autosomal dominant disease is described.
Abstract: To the Editor:
Pulmonary arterial hypertension (PAH) has been the focus of major research in recent years [1]. Involvement of mutations in genes encoding for members of the transforming growth factor-β signalling pathway ( BMPR2 , ACVRL1 , ENG and SMAD8 ) has been demonstrated in the development of heritable PAH, allowing novel experimental and clinical approaches [2–4]. However, ∼30% of familial forms of PAH remain without any identification of genetic mutations. Recently, mutations of the KCNK3 gene (encoding K+ channel subfamily K member 3) have been reported in patients with familial and sporadic PAH [5]. KCNK3 belongs to a family of mammalian K+ channels, and are involved in the regulation of resting membrane potential, pulmonary vascular tone and in vascular remodelling. This result paves the way to the involvement of novel signalling pathways in the development of heritable PAH. Herein, we describe a novel association of PAH and a channelopathy due to mutation in ATP1A2 (encoding the α2-subunit of the Na+/K+-ATPase), a mutation known to cause familial hemiplegic migraine (FHM), a rare autosomal dominant disease [6].
A 24-year-old male was referred with a 1-year history of progressive exertional dyspnoea. Since the age of 8 years, he has reported recurrent episodes of hemiplegic migraine associated with muscle weakness and pain. The proband’s mother (II4) (fig. 1) and two of his brothers (III6 and III7) had recurrent hemiplegic migraine with aura. There was no familial history of PAH. On admission, the patient was in New York Heart Association (NYHA) functional class III. His 6-min …
8 citations
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TL;DR: In this article, the authors performed 3'RNA sequencing with 44 leiomyoma and 5 myometrium FFPE samples, revealing that the samples clustered according to the mutation status of MED12, HMGA2, and FH.
Abstract: Uterine leiomyomas are benign smooth muscle tumors occurring in 70% of women of reproductive age. The majority of leiomyomas harbor one of three well-established genetic changes: a hotspot mutation in MED12, overexpression of HMGA2, or biallelic loss of FH. The majority of studies have classified leiomyomas by complex and costly methods, such as whole-genome sequencing, or by combining multiple traditional methods, such as immunohistochemistry and Sanger sequencing. The type of specimens and the amount of resources available often determine the choice. A more universal, cost-effective, and scalable method for classifying leiomyomas is needed. The aim of this study was to evaluate whether RNA sequencing can accurately classify formalin-fixed paraffin-embedded (FFPE) leiomyomas. We performed 3'RNA sequencing with 44 leiomyoma and 5 myometrium FFPE samples, revealing that the samples clustered according to the mutation status of MED12, HMGA2, and FH. Furthermore, we confirmed each subtype in a publicly available fresh frozen dataset. These results indicate that a targeted 3'RNA sequencing panel could serve as a cost-effective and robust tool for stratifying both fresh frozen and FFPE leiomyomas. This study also highlights 3'RNA sequencing as a promising method for studying the abundance of unexploited tissue material that is routinely stored in hospital archives.
8 citations
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TL;DR: Three distinct TIL subtypes are characterized and their proportions in association with patient demographics and survival inesticular diffuse large B‐cell lymphoma.
Abstract: Objectives Testicular diffuse large B-cell lymphoma (T-DLBCL) is a rare and aggressive extranodal lymphoma. We have previously shown that high content of tumor-infiltrating lymphocytes (TILs) and PD-1 expressing TILs associate with better survival in T-DLBCL. In this study, we have further characterized distinct TIL subtypes and their proportions in association with patient demographics and survival. Methods We used multiplex immunohistochemistry to characterize TIL phenotypes, including cytotoxic T-cells (CTLs; CD8+ , OX40+ , Granzyme B+ , Ki-67+ , LAG-3+ , TIM-3+ , PD-1+ ), CD4+ T-cells (CD3+ , CD4+ , TIM-3+ , LAG-3+ ), regulatory T-cells (Tregs; CD3+ , CD4+ , FoxP3+ ), and T helper 1 cells (Th1; CD3+ , CD4+ , T-bet+ ) in 79 T-DLBCLs, and correlated the findings with patient demographics and outcome. Results We observed a substantial variation in TIL phenotypes between the patients. The most prominent CD8+ TILs were Ki-67+ and TIM-3+ CTLs, whereas the most prominent CD4+ TILs were FoxP3+ Tregs. Despite the overall favorable prognostic impact of high TIL content, we found a subpopulation of T-bet+ FoxP3+ Tregs that had a significant adverse impact on survival. Lower content of CTLs with activated or exhausted phenotypes correlated with aggressive clinical features. Conclusions Our results demonstrate significant variation in TIL phenotypes and emphasize the adverse prognostic impact of Tregs in T-DLBCL.
8 citations
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TL;DR: It is shown that GG/GT patients for rs4522461 and AA/AC patients forrs4790694 have a lower response to AD than other genotype groups, providing additional evidence that ARRB2 is a regulator of intracellular signal transduction processes involved in AD treatment.
Abstract: The study of genetic polymorphisms involved in antidepressants (AD) response is essential to provide a personalized medicine approach in the field of depression. β-arrestin 2 (ARRB2) is a candidate gene in the pharmacogenetics of AD as it is involved in the signaling cascade downstream of numerous neurotransmitter receptors. We investigated the association between five ARRB2 single nucleotide polymorphisms (SNPs): rs1045280, rs2036657, rs4790694, rs3786047 and rs452246, and response to AD treatment in a sample of 569 patients with a major depressive episode treated for 6months. We show that GG/GT patients for rs4522461 (n=534) and AA/AC patients for rs4790694 (n=244) have a lower response to AD than other genotype groups (HDRS score of 10.9 vs 8.0 after 6months, multivariate analysis: p=0.03; 12.2 vs 9.6, p=0.02, respectively). These data provide additional evidence that β-arrestin 2 is a regulator of intracellular signal transduction processes involved in AD treatment.
8 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 |