<div><p><b>Background: </b>Recent data have indicated that decompensated cirrhosis is characterized by an imbalance in the innate immune system, leading to low-grade systemic inflammation. In particular, inflammatory cytokines secreted by monocytes and macrophages have been implicated in the pathogenesis of portal hypertension and its complications. Additionally, MerTK-expressing monocytes participate in the determination of severity of acute liver failure.

<div><p><b>Background:</p> </b><div><p><span lang="EN-US">Liver cells paracrinally affect neighboring cells through the release of extracellular vesicles (EVs), which may contain microRNAs (miRNAs). Our aim was to investigate the role of miRNAs enclosed in hepatocyte-derived EVs as modulators of endothelial dedifferentiation in chronic liver disease (CLD).</span></p></div>

<div><p><strong>Background</strong>: Corticosteroids are the standard of care for SAH in the absence of contraindications. Survival benefits conferred by steroids are often gained at the expense of increased infection risk. We investigated the co-incidental impact of infection mitigation measures during the COVID pandemic on mortality in SAH patients treated with corticosteroids.</p>

<div><p><strong><b>Background:</strong> </b>Treating portal vein thrombosis in patients with cirrhosis becomes increasingly challenging when there is also significant thrombocytopenia (&lt;50*10³/uL). As suggested by various international medical societies, a 50% reduction in the standard anticoagulation dosage has been recommended for individuals with significant thrombocytopenia.

<div><p><b>Background: </b>Conventional therapy for late T cell mediated acute cellular rejection (ACR) in liver transplant includes corticosteroids and anti-thymocyte globulin, has remained unchanged for six decades, and is not infrequently met with treatment failure. Here, we used single cell RNAseq with TCR V(D)J profiling to identify expanded (ie, alloreactive) T cell clones and their gene expression profiles in response to anti-rejection treatment.</p>

<div><p><strong><b>Background:</strong> </b>Metabolic dysfunction-associated steatotic liver disease (MASLD), represent the most common cause of chronic liver disease in Western countries. MASLD patients are at increased risk for developing clinically meaningful cardiovascular diseases (CVD), including stroke and coronary artery disease and its fatal and nonfatal ischemic complications.

<div><p><b>Background: </b>Albumin reduces mortality in spontaneous bacterial peritonitis (SBP) and is recommended by national guidelines. However, gaps and potential disparities in standard of care are not well-studied in large cohorts. We investigated temporal trends, center-level variation, and racial disparities in guideline-recommended albumin use for patients hospitalized with SBP in a large national cohort of Veterans with cirrhosis (VOCAL).</p>

<div><p><b>Background: </b>Emerging evidence demonstrates microbial metabolites play pivotal roles in onset and progression of liver fibrosis and imidazole propionate (ImP) as a microbially produced histidine-derived metabolite was significantly increased in patients with chronic hepatitis B/cirrhosis compared to healthy controls. However, whether ImP is involved in hepatic fibrosis remains unclear. The present study aimed to explore the effects of ImP on hepatic fibrosis and its potential mechanisms.</p>

<div><p><b>Background:</p> </b><p>The emergence of direct-acting anti-HCV agents has led to a significant increase of patients who achieve sustained virologic response (SVR) but remain at risk of HCC development over a decade. HCC risk stratification post SVR is urgently needed.</p>

<div><p><b>Background:</p> </b><p style="font-weight: 400;">Active HCV infection has decreased with the introduction of direct-acting antivirals (DAAs). However, a subset of patients remains at risk for HCC development even after achieving a sustained virologic response (SVR). Chemopreventive measures post SVR are urgently needed to reduce incident HCC.</p>