In the development cohort, LSV, ICG-R15 and ALBI scores were significantly different between patients with and without PHLF, while no significant difference of APRI and FIB-4 scores was found. LSV had higher AUC (the area under the receiver operating characteristic curve) (AUC = 0.795) for PHLF prediction than ICG-R15 (AUC = 0.619) and ALBI scores (AUC = 0.686) (p < 0.05 for all comparisons). In the validation cohort, the cutoff value ofLSVobtained from thedevelopment cohort, 10.35 kPa, revealed higherspecificity (76.3%) for PHLF prediction than ICG-R15 (specificity 66.1%) and ALBI scores (specificity 69.5%) (p < 0.0001). Compared with ICG-R15, ALBI scores, APRI and FIB-4, LSV measured by 2D-SWE may demonstrate better efficacy for preoperative PHLF prediction in patients with HCC.Compared with ICG-R15, ALBI scores, APRI and FIB-4, LSV measured by 2D-SWE may demonstrate better efficacy for preoperative PHLF prediction in patients with HCC. Nutritional status has been considered as a key factor in preventing the development of the frailty syndrome. However, sex-specific dietary consumption transition over time and how it impacts of frailty status are unclear. We assessed 113,039 adults (aged 50 years and over) from the 45 and Up Study who had completed both baseline (2006-2009) and follow-up (2012-2015) surveys. Dietary consumption was assessed by a short food frequency questionnaire. Frailty was identified by the FRAIL scale. Multinomial regression models were used to examine the association between a long-term dietary consumption and frailty, stratified by sex. Of a total of 113,039 participants, females had a higher percentage of pre-frailty and frailty than males (pre-frailty 35.5% for female and 30.1% for male; frailty 4.86% for female and 3.56% for male). As age increased, males had significant decreases in overall dietary risk scores, while females had significant increases in overall dietary risk scores. Selleck (L)-Dehydroascorbic Males and females with a loon of frailty needs to be further developed. Acute coronary syndrome (ACS) remains the leading cause of cardiovascular disease mortality and morbidity worldwide. While the management quality measures and clinical outcomes of patients with ACS have been evaluated widely in developed countries, inadequate data are available from sub-Saharan Africa countries. So, this study aimed to assess the clinical profiles, management quality indicators, and in-hospital outcomes of patients with ACS in Ethiopia. AProspective observational study was conducted at two tertiary hospitals in Ethiopia from March 2018 to November 2018.The primary outcome of the study was in-hospital mortality. Data wereanalyzed using SPSS version 23.0. Multivariable cox-regression was conducted to identify predictors of time to in-hospital mortality. Variable with p -value < 0.05 was considered statistically significant. Among 181 ACS patients enrolled, about (61%) were presented with ST-elevation myocardial infarction (STEMI). The mean age of the study participant was 55.8 ± 11.9 yes to reduce pre-hospital delay.In the present study, the use of guideline-directed in-hospital medications was sub-optimal. The overall in-hospital mortality rate was unacceptably high and highlights the urgent need for national quality-improvement focusing on timely initiation of evidence-based medications, reperfusion therapy, and strategies to reduce pre-hospital delay. Ferroptosis is an iron-dependent cell death that is distinct from apoptosis. Based on excessive amounts of iron and reactive oxygen species in varicocele (VCL) rats, we hypothesize that ferroptosis might be involved in VCL. In addition, since alpha-lipoic acid (ALA) was shown to have both antioxidant and anti-ferroptotic activity we assessed in the present work the status of ferroptosis in our varicocele model and the protective effect of ALA. To this end, 70 male Wistar rats were divided into 7 groups control, sham and varicocele groups which were initially sacrificed 2 months after the operation to verify the induction of varicocele. A second batch of the same 3 groups were sacrificed 4 months after varicocele induction to evaluate the effect of ALA supplementation. The parameters measured were chromatin integrity (aniline blue and acridine orange staining), lipid peroxidation (BODIPY staining), testicular morphometry and iron content. In addition, redox (GSH and NADPH) and ferroptosis (Nrf2, Slc7a11, P53 involvement of ferroptosis. This could be explained by the mosaic nature of the varicocele affecting some seminiferous tubules and not others which could mask variations in molecular markers. In parallel, our study confirms that ALA stimulates the NRF2 pathway. Vascular endothelial cells (ECs) are subject to continuous shear stress due to blood circulation. Mechanical stress due to high shear flow can also cause arteriovenous malformation (AVM) when ECs respond hyper-sensitively to shear flow. This study was conducted to test the hypothesis that angiogenesis could be promoted in response to mechanical stress via regulation of pro-angiogenic factors in AVM cells. ECs were extracted from the tissue samples from six AVM patients and six normal patients. Shear stress at 7 dynes/cm2 were applied for 24h. Before and after application of shear stress to each group, RT-PCR was performed to access the expression levels of angiopoietin2(AGP2), aquaporin1(AQP1) and TGFβR1. Immunofluorescences was also performed to evaluate the level of protein expressions. In both normal and AVM tissues, AGP2 and TGFβR1 under the shear stress showed increased expression in the ECs compared to the non-sheared samples. When AVMs and normal arterial vasculature were compared, the expression levels of both AGP2 and TGFβR1 in AVMs were higher when compared to normal arterial vasculature with or without shear stress. Immunofluorescence-based protein analysis also confirmed shear-induced AGP2 and TGFβR1 in both samples of normal and AVM patients. AVMs exhibited higher sensitivity to shear stress by producing higher expressions of some marked genes and proteins that regulate the endothelial functions upon exposure to shear stress. While the physiological mechanism for AVMs remain elusive, our study shows the plausibility of physical stress imposed by the shearing flow can cause the occurrence of AVMs.AVMs exhibited higher sensitivity to shear stress by producing higher expressions of some marked genes and proteins that regulate the endothelial functions upon exposure to shear stress. While the physiological mechanism for AVMs remain elusive, our study shows the plausibility of physical stress imposed by the shearing flow can cause the occurrence of AVMs.