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Prevalence of heat resistant bacteria in beef poses a potential problem as thermal interventions are routinely used in beef processing to control contamination. Despite extreme heat resistant (XHR) E. coli having been isolated from a ground beef processing plant, there has not been a study to assess the prevalence of XHR E. coli amongst cattle. Therefore, this study utilized a screening assay for XHR gram negative bacteria and its molecular determinant, the Locus of Heat Resistance (LHR), on feces collected from United States (US) cattle. Fecal samples were collected from fed (n=538), cull dairy (n=425), and cull beef (n=475) cattle at nine regional beef processing plants located across the US. Among the 1,438 cattle sampled from northern (n=288), southern (n=288), eastern (n=287), western (n=287), and central (n=288) regions of the US, 91 (6.3%) showed presence of XHR bacteria, as evident by growth in MacConkey broth following heat treatment of 80°C for 15 min, in their feces. Heat resistant bacteria (n=140) were isolated from the 91 fecal samples. Prevalence of XHR bacteria was highest (11%) in cattle from the northern region. Ninety percent of the XHR isolates were identified as E. coli.  Multiplex PCR of all 1438 fecal samples showed that the LHR was entirely absent in 40.7% samples while intact in 18.7% samples. Despite the higher prevalence of intact LHR from PCR analysis, only 11 samples (0.8%) were confirmed to contain bacteria with an intact LHR. The LHR was entirely absent in 91% of XHR bacteria and only 7.9% of XHR bacteria had intact LHR, suggesting a novel mechanism of heat resistance. By developing and utilizing the screening assays, this study established the prevalence of XHR bacteria (6.3%) and LHR+ bacteria (0.8%) in US beef cattle.Reactivation of fetal hemoglobin remains a critical goal in the treatment of patients with sickle cell disease and β-thalassemia. Previously, we discovered that silencing of the fetal γ-globin gene requires the erythroid-specific eIF2α kinase HRI, suggesting that HRI might present a pharmacologic target for raising fetal hemoglobin levels. Here, via a CRISPR-Cas9 guided loss-of-function screen in human erythroblasts we identify transcription factor ATF4, a known HRI-regulated protein, as a novel γ-globin regulator. ATF4 directly stimulates transcription of BCL11A, a repressor of γ-globin transcription, by binding to its enhancer and fostering enhancer-promoter contacts. Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable. Our studies uncover a linear signaling pathway from HRI to ATF4 to BCL11A to γ-globin and illustrate potential limits of murine models of globin gene regulation. Copyright © 2020 American Society of Hematology.OBJECTIVE The study aimed to assess and compare the prevalence of caesarean birth and associated factors among women gave birth at public and private health facilities in Bahir Dar city, Amhara region, Ethiopia. METHODS An institution-based comparative cross-sectional study design was conducted from March1-April 15, 2019 at health facility provide emergency obstetrics service in Bahir Dar city. Study participants 724(362 for each public and private facility) were recruited using a systematic random sampling technique. Structured interview administered questionnaires and chart review checklist were used to collect data. The data were entered into Epi info version 7.2 and analyzed using SPSS version 23.0 software. read more A binary logistic regression model was fitted and an adjusted odds ration with 95% CI was used to determine the presence and strength of association between independent variables and cesarean birth. RESULTS The response rate was 98.3% and 97.2% for public and private health facilities respectively. Thof caesarean birth in public and private health facilities.BACKGROUND Genetic predispositions in cases suffering sudden unexpected infant death have been a research focus worldwide during the past decade. Despite large efforts, there is still uncertainty concerning the molecular pathogenesis of these deaths. With genetic technology in constant development, the possibility of an alternative approach into this research field has become available, like mRNA expression studies. METHODS In this study, we investigated mRNA gene expression in 14 cases who died suddenly and unexpectedly from infection without a history of severe illness prior to death. The control group included eight accidents, two cases of natural death, one undetermined, one case of medical malpractice, and two homicides. The study included tissue from liver, heart, and brain using Illumina whole-genome gene expression assay. RESULTS From the array, 19 genes showed altered expression in the infectious deaths compared to controls. Tissue from the heart showed 15 genes with altered mRNA expression compared to the control group. CONCLUSIONS Downregulation of KCNE5 in heart tissue from cases of infectious death was of particular interest. Variants of KCNE5 are associated with Brugada syndrome and sudden death and could be responsible for the fatal outcome in the group of infectious death. IMPACT KCNE5 is downregulated in tissue from the heart in cases of infectious death in infancy.This study provides knowledge about the gene expression profile in cases of infectious death.Variants of a gene known to give increased risk of cardiac arrhythmia is downregulated in cases of infectious death in infancy.The results could give us better knowledge as to why some infants do not survive an infection.This study provides a candidate gene for future studies.INTRODUCTION Kisspeptin (KP) neurons in the rostral periventricular area (RP3V) of female rodents mediate positive estrogen feedback to gonadotropin-releasing hormone neurons and thus, play fundamental role in the mid-cycle luteinizing hormone (LH) surge. The RP3V is sexually dimorphic and male rodents with lower KP cell numbers are unable to mount estrogen-induced LH surges. OBJECTIVE To find and characterize the homologous KP neurons in the human brain, we studied formalin-fixed post mortem hypothalami. METHODS Immunohistochemical techniques were used. RESULTS Distribution of KP neurons in the rostral hypothalamus overlapped with different subdivision of the paraventricular nucleus. Cell numbers decreased after menopause, indicating that estrogens positively regulate KP gene expression in the rostral hypothalamus in humans, similarly to several other species. Young adult women and men had similar cell numbers, as opposed to rodents having more KP neurons in the RP3V of females. Human KP neurons differed neurochemically as well from the homologous rodent cells in that they were devoid of enkephalins, galanin and tyrosine hydroxylase.

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