<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>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>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><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><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><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: </b>Liver cancer poses a significant health challenge worldwide, but its burden in low Socio-Demographic Index (SDI) countries remains understudied. These countries face unique obstacles, including limited healthcare resources, inadequate screening programs, and a higher prevalence of risk factors like hepatitis B and C. Liver cancer has become a pressing public health issue, impacting individuals, communities, and healthcare systems in low SDI countries.

<div><p><b>Background:</p> </b><p><strong> </strong>Infections with multidrug-resistant organisms (MDR) are a common cause of organ failures and increased fatality in patients with cirrhosis. Sepsis is associated with increased oxidative stress with widespread endothelial, cellular injury and acute deficiency of vitamin C. Polymyxins used for <span>MDR infections have increased incidence of nephrotoxicity.

<div><p><b>Background:<span> </b>Chronic hepatitis B (CHB) suppressive therapy with tenofovir disoproxil (TDF) or entecavir (ETV) has been shown to reduce the risk of hepatocellular carcinoma (HCC) and mortality. However, controversy exists regarding if one treatment is better than the other.</span></p>

<div><p><b>Background: </b>Detecting patients with undiagnosed chronic liver disease is a public health challenge. Patients with advanced fibrosis or compensated cirrhosis have much better outcomes than those with decompensated disease and may be eligible for interventions to prevent disease progression</p>