Specialized medical Predictors associated with COVID19 Severity and Death A new Viewpoint

OBJECTIVE Policies of insurance carriers have used truncal vein size as a criteria for coverage. The objective of this study was to compare the effect of great saphenous vein (GSV) size > 5 mm versus 5 mm have similar improvement in their symptomatology but sustain an increased complication rate. Patients with smaller vein size should not be denied intervention or coverage based on size criteria. OBJECTIVE The quality of available evidence regarding new minimally invasive techniques to abolish great saphenous vein reflux is moderate. This study aimed to assess whether radiofrequency ablation (RFA) was noninferior to each of the stripping (HL/S) and CHIVA methods on clinical and ultrasound recurrence at 2 years in patients with primary varicose veins (VV) due to great saphenous vein (GSV) insufficiency. METHODS A randomized, single-centre, open-label, controlled, noninferiority trial comparing RFA with two surgical techniques for the treatment of primary VV due to GSV insufficiency. The noninferiority margin was set at 15% for absolute differences. Patients aged over 18 years with primary VV and GSV incompetence, with or without clinical symptoms, C2 - C6 clinical class of CEAP and GSV diameter >4 mm were randomized with a 111 ratio to RFA, HL/S or CHIVA. Rate of clinical recurrence at 24 months was the primary endpoint and was analyzed using a delta noninferiority margin of 15%. Ultrasound recurrence,rence to HL/S and CHIVA in the treatment of VV due to the insufficiency of GSV. On November 15, 2019, the 24th annual Alcohol and Immunology Research Interest Group (AIRIG) meeting was held as a satellite conference during the annual Society for Leukocyte Biology meeting in Boston, MA. The 2019 meeting focused on alcohol, immunity and organ damage and included two plenary sessions. Breviscapin The first session highlighted new research exploring the mechanisms of alcohol-induced inflammation and liver disease including effects on lipidomics and lipophagy, regulatory T cells, epigenetics, epithelial cells and age-related changes in the gut. The second session covered alcohol-induced injury of other organs, encompassing diverse areas of research ranging from neurodegeneration, to lung barrier function, to colon carcinogenesis, to effects on viral infection. The discussions also highlighted current laboratory and clinical research used to identify biomarkers of alcohol use and disease. The present study investigates the potential neuroprotective effect of Argan Oil (AO), a natural vegetable oil, commonly used in folk Moroccan medicines, on adolescent intermittent ethanol intoxications (IEI) induced voluntary ethanol consumption and withdrawal syndrome in rats. Animals were treated with ethanol (ip. 3g/kg bw) in intermittent doses (2 days on; 2days off, from postnatal day 30 to 43) with/without orally AO pre-treatment (10 ml/Kg/day bw, from postnatal day 21 to 121). A 2-bottle free access test was performed over 10 weeks to assess 10% ethanol consumption. Behavioral signs of withdrawal were observed after 2, 6, 24, 48 and 72-h ethanol removal. Anxiety-like behaviors in the elevated plus maze and the light/dark box tests were also performed at 72-h of withdrawal. We found that AO pre-treatment decreased significantly the voluntary ethanol consumption induced by adolescent IEI. Also, by establishing a low ethanol consumption, AO pre-treatment counteracts negative effects of ethanol withdrawal and anxiety-like behaviors in ethanol treated rats after 72-h of abstinence. Following behavioral assays, oxidative stress markers and histologic analysis of neurodegeneration was also performed. The results showed that the low ethanol drinking in the AO supplemented rats was associated with inhibition of oxidative stress and neurodegeneration in the rat's brain. These findings provide evidence for the promising neuroprotective effect of AO dietary in voluntary ethanol consumption and withdrawal syndrome at least in part through counteracting oxidative stress markers and neurodegeneration. Hepatocyte nuclear factor 4 alpha (HNF4α) regulates the expression of essential genes involved in very-low-density lipoprotein (VLDL) homeostasis and gluconeogenesis.　18β-glycyrrhetinic acid (GA) is an active ingredient of Glycyrrhiza uralensis an herbal medicine used for treating liver aliments. In this study, we established that GA functions as a partial antagonist of HNF4α through HNF4α-driven reporter luciferase assay and co-immunoprecipitation experiments with co-activator PGC1α. By virtual docking and site-directed mutagenesis analysis, we confirmed that serine 190 and arginine 235 of HNF4α are both essential for GA to exert its antagonistic action on HNF4α. Importantly, GA suppressed the expression of HNF4α target genes such as apolipoprotein B (ApoB), microsomal triglyceride transfer protein (MTP) and phospholipase A2 G12B (PLA2G12B) modulating hepatic VLDL secretion in mice fed on a high fat diet. In addition, GA also suppressed gluconeogenesis and ameliorated glucose intolerance via down-regulating the expression of HNF4α target genes glucose-6-phosphatase (G6pc) and phosphoenolpyruvate carboxykinase (Pepck). Furthermore, GA significantly lowered blood glucose and improved insulin resistance in db/db mice. In all, we established that GA acts as a partial HNF4α antagonist modulating lipid and carbohydrate metabolism. Cardiac injury is followed by fibrosis, characterized by myofibroblast activation. Excessive deposition of extracellular matrix (ECM) impairs the plasticity of myocardium and results in myocardial systolic and diastolic dysfunction. Mangiferin is a xanthonoid derivative rich in plants mangoes and iris unguicularis, exhibiting the ability to ameliorate metabolic disorders. This study aims to investigate whether mangiferin attenuates cardiac fibrosis via redox regulation. The transverse aortic constriction (TAC) in mice induced cardiac fibrosis with impaired heart function. Oral administration of mangiferin (50 mg/kg, 4 weeks) inhibited myofibroblast activation with reduced formation of ECM. The impaired left ventricular contractive function was also improved by mangiferin. TGF-β1 stimulation increased glutaminolysis to fuel intracellular glutamate pool for the increased demands of nutrients to support cardiac myofibroblast activation. Mangiferin degraded Keap1 to promote Nrf2 protein accumulation by improving its stability, leading to Nrf2 activation.