20 research outputs found

    Thirty-five years (1986–2021) of HIV/AIDS in Nigeria: bibliometric and scoping analysis

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    Background Acquired immunodeficiency syndrome (AIDS) is an acquired defect of the cellular immunity associated with the infection by the human immunodeficiency virus (HIV). The disease has reached pandemic proportion and has been considered a public health concern. This study is aimed at analyzing the trend of HIV/AIDS research in Nigeria. Method We used the PUBMED database to a conduct bibliometric analysis of HIV/AIDS-related research in Nigeria from 1986 to 2021 employing “HIV”, “AIDS”, “acquired immunodeficiency syndrome”, “Human immunodeficiency virus”, and “Nigeria” as search description. The most common bibliometric indicators were applied for the selected publications. Result The number of scientific research articles retrieved for HIV/AIDS-related research in Nigeria was 2796. Original research was the predominant article type. Articles authored by 4 authors consisted majority of the papers. The University of Ibadan was found to be the most productive institution. Institutions in the United States dominated external production with the University of Maryland at the top. The most utilized journal was PLoS ONE. While Iliyasu Z. was the most productive principal author, Crowel TA. was the overall most productive author with the highest collaborative strength. The keyword analysis using overlay visualization showed a gradual shift from disease characteristics to diagnosis, treatment and prevention. Trend in HIV/AIDS research in Nigeria is increasing yet evolving. Four articles were retracted while two had an expression of concern. Conclusion The growth of scientific literature in HIV/AIDS-related research in Nigeria was found to be high and increasing. However, the hotspot analysis still shows more unexplored grey areas in future

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Haematological, Biochemical and Antioxidant Changes in Wistar Rats Exposed to Dichlorvos Based Insecticide Formulation Used in Southeast Nigeria

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    The indiscriminate use of pesticide is a treat to non-target organisms. This study evaluates the haematological and biochemical changes induced by inhalation of local Nigerian dichlorvos insecticide on rats. The rats were randomly assigned to a control group which received only food and water and a test group which, in addition to food and water, was exposed to the pesticide for a period of 4 h daily for 28 days, after which exposure was discontinued for seven days. Five animals were sacrificed from each group on days 1, 7, 14, 21, 28 and 35, and blood was collected by cardiac puncture for haematological, biochemical and antioxidant analysis. Results obtained showed lowered values of red blood cell count (RBC), packed cell volume (PCV), haemoglobin, mean cell haemoglobin (MCH) and mean cell haemoglobin concentration (MCHC) (p < 0.05) with increased white blood cell count (WBC) and platelet counts after day 14 when compared to the control group. Liver enzymes aspartate amino transaminase (AST) and alanine amino transaminase (ALT) were higher in the exposed rats compared to the control group (p < 0.05). Urea and creatinine concentrations increased significantly after day 1 and at day 28, while superoxide dismutase (SOD), gluthathione (GSH) and catalase (CAT) activity increased significantly compared to the control after day 1, day 14 and day 21, respectively. The RBC, PCV and haemoglobin values of all exposed rats were restored to normal following withdrawal of the pesticide, though AST, ALT, urea, creatinine and, glutathione values remained significantly high compared to the control. Inhalation of the local insecticide is toxic to the blood, liver and kidney of laboratory rats and may be deleterious to human health following long-term exposure

    A second update on mapping the human genetic architecture of COVID-19

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    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Positional distributions of fatty acids in glycerolipids

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    Molecular species of triacylglycerols, diacylglycerols derived from complex lipids, and related lipids

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    Isolation of fatty acids and identification by spectroscopic and related techniques

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    Chromatographic analysis of molecular species of intact phospholipids and glycolipids

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