Background Parquetina nigrescens (Afzel) Bullock is a commonly used medicinal plant in African traditional medicine. The powdered roots and stems of the plant are taken with pap as a memory enhancer among the Yorubas of southwestern Nigeria. The mechanism by which scopolamine induces cognitive deficit mimics the pathogenesis of neurodegeneration in cognitive impairment. This study therefore, aimed at investigating the effect of the methanol stem extract of P. nigrescens on sub-chronically scopolamine-induced cognitive deficit in mice. Method Phytochemical screening was carried out on the extract using standard protocols. The oral median lethal dose (LD50) was estimated according to the Organisation for Economic Cooperation and Development (OECD) 425 limit test guideline. Doses of 250, 500, and 1000 mg/kg of the extract were used for the study. The elevated plus maze (EPM) and novel object recognition tests (NORT) were used to assess cognitive function. The brain tissue was assayed for the level of malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and acetylcholinesterase (AChE) activity. Results The plant extract contains phenolics, carbohydrates, tannins, saponins, and unsaturated sterols.The extract decreased the transfer latencies on days 7 and 8 against the scopolamine group in EPM and increased the discrimination index decreased by scopolamine in NORT. The methanol stem extract of P. nigrescens significantly (p ≤ 0.01) reduced MDA level;  significantly  (p ≤ 0.01) increased SOD activity;  non-significantly increased GSH activity and the activity of AChE apeared not altered. Conclusion The methanol stem extract of P. nigrescens ameliorated sub-chronically scopolamine-induced cognitive deficit via antioxidant mechanism.Background The assessment of measurement uncertainty (MU) in clinical laboratories is essential to the reliable interpretation of results in clinical laboratories. However, despite the introduction of various methods for the expression of uncertainty in measurement, the MUs of coagulation tests have not been extensively studied. The aim of this study was to quantify the MU of various coagulation assays according to international guidelines and to report an expected confidence in the quality of coagulation assays. Methods We selected activated partial thromboplastin time, international normalized ratio (INR), protein C/S, antithrombin, fibrinogen, and Factor V/VIII/X to quantify the MUs of two coagulation testing systems ACL TOP 750 CTS (Instrumentation Laboratory, Bedford, MA, USA) and STA Compact (Diagnostica Stago, Asnières-sur-Seine, France). We used international standards and interlaboratory comparison results in accordance with international guidelines in a top-down approach to the assessment of MU. For INR, MU was estimated in a bottom-up approach using reference thromboplastin and certified plasmas. Results Top-down approaches resulted in MUs between 3.3% and 21.3% for each measurand. In the bottom-up approach, MUs of INR values ranged from 10.9% to 26.4% and showed an upward trend as INR increased. Conclusions In this study, we were successful in quantifying MU of coagulation assays using practical methods. Our results demonstrated that top-down and bottom-up approaches were adequate for coagulation assays. However, some assays showed significant biases against international standards; therefore, standardization would be necessary to ensure more reliable patient results.The long-anticipated ISO/TS 20914, Medical laboratories - Practical guidance for the estimation of measurement uncertainty, became publicly available in July 2019. This ISO document is intended as a guide for the practical application of estimating uncertainty in measurement (measurement uncertainty) in a medical laboratory. In some respects, the guide does indeed meet many of its stated objectives with numerous very detailed examples. Even though it is claimed that this ISO guide is based on the Evaluation of measurement data - Guide to the expression of uncertainty in measurement (GUM), JCGM 1002008, it is with some concern that we believe several important statements and statistical procedures are incorrect, with others potentially misleading. The aim of this report is to highlight the major concerns which we have identified. In particular, we believe the following items require further comment (1) The use of coefficient of variation and its potential for misuse requires clarification, (2) pooled variance and measurement uncertainty across changes in measuring conditions has been oversimplified and is potentially misleading, (3) uncertainty in the results of estimated glomerular filtration rate (eGFR) do not include all known uncertainties, (4) the international normalized ratio (INR) calculation is incorrect, (5) the treatment of bias uncertainty is considered problematic, (6) the rules for evaluating combined uncertainty in functional relationships are incomplete, and (7) specific concerns with some individual statements.Background Growing evidence reports an association between inflammatory markers, obesity and blood pressure (BP). Specifically, the intergenic single nucleotide polymorphism (SNP) rs7556897T > C (MAF = 0.34) located between SLC19A3 and the CCL20 was shown to be associated with chronic inflammatory diseases. In addition, CCL20 expression was found increased in pancreatic islets of obese rodents and human pancreatic β cells under the influence of inflammation. In this study, we hypothesized that SNP rs7556897 could affect BP levels, thus providing a link between inflammation, BP and obesity. Methods BP was measured under supine position with a manual sphygmomanometer; values reported were the means of three readings. We analyzed rs7556897 in 577 normal weight and 689 obese French children.  https://www.selleckchem.com/products/mi-773-sar405838.html  Using real-time polymerase chain reaction (PCR), we quantified CCL20 and SLC19A3 expression in adipose tissue and peripheral blood mononuclear cells (PBMCs) of normal weight and overweight children. Results The rs7556897C alln diastolic BP, possibly via the modulation of CCL20 expression levels.