ANTIMICROBIAL EFFICACY OF TAMARIX DIOCA (L.) LEAVES AND FLOWERS

Tamarix dioca (L.) belongs to family Tamaricaceae is traditionally a vital plant used for treatment of various diseases. Efforts were made to investigate the antimicrobial efficiency of T. dioca.There was three concentrations of crude methanolic extracts of 200µg/ml, 100µg/ml and 50 µg/ml were checked against six pathogenic fungi Aspergillus fumigatus, aspergillus flavus, Fusarium solani, Aspergillus niger, Penicillium digitatum and Penicillium tubesulum and six bacterial strains Bacillus subtilis, Enterobactor aerogenes, Escherichia coli, Kliebsiella pneumoniae, Salmonella typhi and Staphylococcus aureus. It was noted that Percentage inhibition in the growth of fungi and bacteria was dosage dependent. Terbinafine a standard antifungal drug, 10mg/ml and Cefexime 10mg/ml (antibacterial) were used as a positive control. The results were compared with control and most of the results were found significant. Maximum inhibition was showed by T. dioca against fungal strain A. niger (74%) and bacterial strain K. pneumoniae (48%). It can be use as powerful antimicrobial agent in near fture

Substantial and sustained reduction in under-5 mortality, diarrhea, and pneumonia in Oshikhandass, Pakistan : Evidence from two longitudinal cohort studies 15 years apart

Funding Information: Study 1 was funded through the Applied Diarrheal Disease Research Program at Harvard Institute for International Development with a grant from USAID (Project 936–5952, Cooperative Agreement # DPE-5952-A-00-5073-00), and the Aga Khan Health Service, Northern Areas and Chitral, Pakistan. Study 2 was funded by the Pakistan US S&T Cooperative Agreement between the Pakistan Higher Education Commission (HEC) (No.4–421/PAK-US/HEC/2010/955, grant to the Karakoram International University) and US National Academies of Science (Grant Number PGA-P211012 from NAS to the Fogarty International Center). The funding bodies had no role in the design of the study, data collection, analysis, interpretation, or writing of the manuscript. Publisher Copyright: © 2020 The Author(s).Peer reviewedPublisher PD

MRBrainS Challenge: Online Evaluation Framework for Brain Image Segmentation in 3T MRI Scans

Many methods have been proposed for tissue segmentation in brain MRI scans. The multitude of methods proposed complicates the choice of one method above others. We have therefore established the MRBrainS online evaluation framework for evaluating (semi) automatic algorithms that segment gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) on 3T brain MRI scans of elderly subjects (65-80 y). Participants apply their algorithms to the provided data, after which their results are evaluated and ranked. Full manual segmentations of GM, WM, and CSF are available for all scans and used as the reference standard. Five datasets are provided for training and fifteen for testing. The evaluated methods are ranked based on their overall performance to segment GM, WM, and CSF and evaluated using three evaluation metrics (Dice, H95, and AVD) and the results are published on the MRBrainS13 website. We present the results of eleven segmentation algorithms that participated in the MRBrainS13 challenge workshop at MICCAI, where the framework was launched, and three commonly used freeware packages: FreeSurfer, FSL, and SPM. The MRBrainS evaluation framework provides an objective and direct comparison of all evaluated algorithms and can aid in selecting the best performing method for the segmentation goal at hand.This study was financially supported by IMDI Grant 104002002 (Brainbox) from ZonMw, the Netherlands Organisation for Health Research and Development, within kind sponsoring by Philips, the University Medical Center Utrecht, and Eindhoven University of Technology. The authors would like to acknowledge the following members of the Utrecht Vascular Cognitive Impairment Study Group who were not included as coauthors of this paper but were involved in the recruitment of study participants and MRI acquisition at the UMC Utrecht (in alphabetical order by department): E. van den Berg, M. Brundel, S. Heringa, and L. J. Kappelle of the Department of Neurology, P. R. Luijten and W. P. Th. M. Mali of the Department of Radiology, and A. Algra and G. E. H. M. Rutten of the Julius Center for Health Sciences and Primary Care. The research of Geert Jan Biessels and the VCI group was financially supported by VIDI Grant 91711384 from ZonMw and by Grant 2010T073 of the Netherlands Heart Foundation. The research of Jeroen de Bresser is financially supported by a research talent fellowship of the University Medical Center Utrecht (Netherlands). The research of Annegreet van Opbroek and Marleen de Bruijne is financially supported by a research grant from NWO (the Netherlands Organisation for Scientific Research). The authors would like to acknowledge MeVis Medical Solutions AG (Bremen, Germany) for providing MeVisLab. Duygu Sarikaya and Liang Zhao acknowledge their Advisor Professor Jason Corso for his guidance. Duygu Sarikaya is supported by NIH 1 R21CA160825-01 and Liang Zhao is partially supported by the China Scholarship Council (CSC).info:eu-repo/semantics/publishedVersio

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)