Hepatitis E is an infectious disease of the liver caused by the hepatitis E virus (HEV). Immunocompromised patients present a particular risk group, as chronification of hepatitis E leading to life-threatening cirrhosis occurs when these patients are infected. Therefore, this study aims to estimate and compare the anti-HEV seroprevalence and the rate of HEV RNA positivity in transplant recipients and patients with human immunodeficiency virus (HIV).

This systematic review and meta-analysis involved a literature search (PubMed, Scopus; 1,138 studies) including 120 studies from 1996 to 2019, reporting anti-HEV seroprevalence and/or HEV-RNA positivity. Statistical analysis was performed using a linear mixed-effects meta regression model.

Anti-HEV seroprevalence in 14626 transplant recipients ranged from 6% (95% CI 1.9-17.2) to 29.6% (95% CI 21.6-39.) in different commercially available assays and did not differ significantly compared to 20825 HIV positive patients (range 3.5% (95% CI 0.9-12.8) – 19.4% (95% CI 13.5-26.9). read more In contrast, HEV-RNA positivity rate was significantly higher in transplant recipients than in HIV positive patients (1.2% (95% CI 0.9-1.6) vs 0.39% (95% CI 0.2-0.7); P-value=0.0011).

Anti-HEV seroprevalence did not differ significantly between transplant recipients and HIV positive patients. Interestingly, rates of HEV-RNA positivity, indicating ongoing infection, were significantly higher in transplant recipients. These findings demonstrate that transplant patients have an elevated risk of chronic infection in comparison to HIV patients at comparable risk of HEV-exposure.

Anti-HEV seroprevalence did not differ significantly between transplant recipients and HIV positive patients. Interestingly, rates of HEV-RNA positivity, indicating ongoing infection, were significantly higher in transplant recipients. These findings demonstrate that transplant patients have an elevated risk of chronic infection in comparison to HIV patients at comparable risk of HEV-exposure.

Quantification of myocardial blood flow (MBF) from dynamic contrast-enhanced (DCE) MRI can be performed using a signal intensity model that incorporates T

values of blood and myocardium.

To assess the impact of T

values on pixelwise MBF quantification, specifically to evaluate the influence of 1) study population-averaged vs. subject-specific, 2) diastolic vs. systolic, and 3) regional vs. global myocardial T

values.

Prospective.

Fifteen patients with chronic coronary heart disease.

3T; modified Look-Locker inversion recovery for T

mapping and saturation recovery gradient echo for DCE imaging, both acquired in a mid-ventricular short-axis slice in systole and diastole.

MBF was estimated using Fermi modeling and signal intensity nonlinearity correction with different T

values study population-averaged blood and myocardial, subject-specific systolic and diastolic, and segmental T

values. Myocardial segments with perfusion deficits were identified visually from DCE series.

The relationsantially affect MBF quantification.

3 TECHNICAL EFFICACY STAGE 3.

3 TECHNICAL EFFICACY STAGE 3.Lipid droplets (LDs) are dynamic cytoplasmic organelles present in most eukaryotic cells. The appearance of LDs in neurons is not usually observed under physiological conditions, but is associated with neural diseases. It remains unclear how LD dynamics is regulated in neurons and how the appearance of LDs affects neuronal functions. We discovered that mutations of two key lipolysis genes atgl-1 and lid-1 lead to LD appearance in neurons of Caenorhabditis elegans. This neuronal lipid accumulation protects neurons from hyperactivation-triggered neurodegeneration, with a mild decrease in touch sensation. We also discovered that reduced biosynthesis of polyunsaturated fatty acids (PUFAs) causes similar effects and synergizes with decreased lipolysis. Furthermore, we demonstrated that these changes in lipolysis and PUFA biosynthesis increase PUFA partitioning toward triacylglycerol, and reduced incorporation of PUFAs into phospholipids increases neuronal protection. Together, these results suggest the crucial role of neuronal lipolysis in cell-autonomous regulation of neural functions and neurodegeneration.For most researchers, the time they spend as a postdoc stands out as one of challenge, but also enormous personal and professional growth. This Words of Advice is intended to guide the choice of postdoctoral position to help make the venture a success and to launch the first chapter of a happy and fulfilling professional life.The production of the pyrimidine moiety in thiamine synthesis, 2-methyl-4-amino-5-hydroxymethylpyrimidine phosphate (HMP-P), has been described to proceed through the Thi5-dependent pathway in Saccharomyces cerevisiae and other yeast. Previous work found that ScThi5 functioned poorly in a heterologous context. Here we report a bacterial ortholog to the yeast HMP-P synthase (Thi5) was necessary for HMP synthesis in Legionella pneumophila. Unlike ScThi5, LpThi5 functioned in vivo in Salmonella enterica under multiple growth conditions. The protein LpThi5 is a dimer that binds pyridoxal-5′-phosphate (PLP), apparently without a solvent-exposed Schiff base. A small percentage of LpThi5 protein co-purifies with a bound molecule that can be converted to HMP. Analysis of variant proteins both in vivo and in vitro confirmed that residues in sequence motifs conserved across bacterial and eukaryotic orthologs modulate the function of LpThi5. IMPORTANCE Thiamine is an essential vitamin for the vast majority of organisms. There are multiple strategies to synthesize and salvage this vitamin. The predominant pathway for synthesis of the pyrimidine moiety of thiamine involves the Fe-S cluster protein ThiC. An alternative pathway utilizes Thi5, a novel enzyme that uses PLP as a substrate. The Thi5-dependent pathway is poorly characterized in yeast and has not been characterized in Bacteria. Here we demonstrate that a Thi5-dependent pathway is necessary for thiamine biosynthesis in Legionella pneumophila and provide biochemical data to extend knowledge of the Thi5 enzyme, the corresponding biosynthetic pathway, and the role of metabolic network architecture in optimizing its function.