Effect of Xylopia aethiopica, Fiscus mucuso and Anthocleista vogelli extracts on some Biochemical Parameters following ethanol-Induced Toxicity.

A total of forty rats were divided into eight groups (n= 5). Group A were control rats; Group B 27 were administered with absolute ethanol; Group C were ethanol administered rats treated with 28 Xylopia aethiopica; Groups D were ethanol administered rats treated with Fiscus mucuso, Group 29 E were ethanol administered rats treated with Anthocleista vogelli; Group F were normal rats 30 administered orally with Xylopia aethiopica; Group G were normal rats administered orally with 31 Fiscus mucuso; Group H were normal rats administered orally with Anthocleista vogelli. At the 32 end of the experimental period, the animals were sacrificed and serum was obtained for total 33 protein, uric acid, creatinin, urea, Aspartate aminotrasferase (AST) and Alanine aminotransferase 34 (ALT) analysis using respective research kits. 35 The result showed that Xylopia aethiopica had protective effect on the kidney as compared with 36 Fiscus mucuso and Anthocleista vogelli treated rats. Also, The AST and ALT was lowered with 37 the start of Xylopia aethiopia treatment. The total protein, creatinin and urea were slightly 38 (p> 0.05) affected with ethanol, an effect which was normalized with the start of extract 39 treatment. 4

Novel functional insights into ischemic stroke biology provided by the first genome-wide association study of stroke in indigenous Africans

\ua9 The Author(s) 2024. Background: African ancestry populations have the highest burden of stroke worldwide, yet the genetic basis of stroke in these populations is obscure. The Stroke Investigative Research and Educational Network (SIREN) is a multicenter study involving 16 sites in West Africa. We conducted the first-ever genome-wide association study (GWAS) of stroke in indigenous Africans. Methods: Cases were consecutively recruited consenting adults (aged > 18 years) with neuroimaging-confirmed ischemic stroke. Stroke-free controls were ascertained using a locally validated Questionnaire for Verifying Stroke-Free Status. DNA genotyping with the H3Africa array was performed, and following initial quality control, GWAS datasets were imputed into the NIH Trans-Omics for Precision Medicine (TOPMed) release2 from BioData Catalyst. Furthermore, we performed fine-mapping, trans-ethnic meta-analysis, and in silico functional characterization to identify likely causal variants with a functional interpretation. Results: We observed genome-wide significant (P-value < 5.0E−8) SNPs associations near AADACL2 and miRNA (MIR5186) genes in chromosome 3 after adjusting for hypertension, diabetes, dyslipidemia, and cardiac status in the base model as covariates. SNPs near the miRNA (MIR4458) gene in chromosome 5 were also associated with stroke (P-value < 1.0E−6). The putative genes near AADACL2, MIR5186, and MIR4458 genes were protective and novel. SNPs associations with stroke in chromosome 2 were more than 77 kb from the closest gene LINC01854 and SNPs in chromosome 7 were more than 116 kb to the closest gene LINC01446 (P-value < 1.0E−6). In addition, we observed SNPs in genes STXBP5-AS1 (chromosome 6), GALTN9 (chromosome 12), FANCA (chromosome 16), and DLGAP1 (chromosome 18) (P-value < 1.0E−6). Both genomic regions near genes AADACL2 and MIR4458 remained significant following fine mapping. Conclusions: Our findings identify potential roles of regulatory miRNA, intergenic non-coding DNA, and intronic non-coding RNA in the biology of ischemic stroke. These findings reveal new molecular targets that promise to help close the current gaps in accurate African ancestry-based genetic stroke’s risk prediction and development of new targeted interventions to prevent or treat stroke

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries

Fakunle,et al,Paste Production Paste Production From Synodontis Membranaceus Using Different Percentages of Ginger (Zingiber officinale)

Abstract: Synodontis membranaceus was subjected to fermentation (34 +-3 o C) for a period of 4-weeks (one month) with varying concentrations of ginger (5%, 10%, 15%, 20%) and 20% salt as spices to produce paste. The samples were analyzed for proximate composition, pH, microbial load and organoleptic properties at the beginning and end of the fermentation. Results showed steady increase in nutrients such as crude fat, ash, and NFE (nitrogen free extract) but decrease in crude fibre. There were fluctuations in the crude protein of the fermented fish samples. There was an increase in the microbial load of the fermented fish and a slight decrease in the moisture content. The organoleptic test showed preference for taste, aroma, and overall acceptability for fish fermented with 20% ginger

The structure of euphorianin, an ingol diterpenoid from <i>Euphorbia poisonii</i>

The residual uncertainty in the structure of euphorianin, an ingol diterpenoid from the latex of Euphorbia poisonii, has been resolved by nuclear Overhauser enhancement difference experiments which revealed the configuration at C-19 to be S. The 1H and 13C NMR spectroscopic properties of euphorianin and its transformation products are described

Evaluation of in-vitro antioxidant activities of methanol extracts of Persea americana and Cnidosculus aconitifolius

The present study was undertaken to investigate the antioxidant activities of Persea americana and Cnidosculous aconitifolius. The in-vitro antioxidant activity of the methanol extracts of the leaves of Persea americana and Cnidosculous aconitifolius was evaluated using various experimental methods such as 1,1-diphenyl-2-picryl-hydrazyl (DPPH), nitric oxide and reducing power radical-scavenging activity assay. Phytochemical screening as well as the amounts of total phenol and flavonoids were also determined. The present study revealed that both the methanol extracts of the leaves of Persea americana and Cnidosculous aconitifolius possess significant antioxidant activities. However, Persea americana was found to have higher radical scavenging activity than Cnidosculous aconitifolius but the phenol content of Cnidosculous aconitifolius was higher than that of Persea americana whereas Persea americana was observed to possess more flavonoids than Cnidosculous aconitifolius

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Glucose-6-phosphate dehydrogenase deficiency in blood donors and jaundiced neonates in Osogbo