<div><p><b>Background: </b>Cross-sectional studies have identified individuals from sub-Saharan Africa with (SSA) chronic hepatitis B (CHB) as a potential risk group for hepatocellular carcinoma (HCC) and advocate enrolment in an HCC surveillance program even in the absence of cirrhosis. However, the incidence of HCC and performance of HCC risk scores in this population are unknown.</p>

<div><p><b>Background: </b>The rising prevalence of alcohol-associated liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) has led to increases in the need for liver transplantation (LT). The purpose of our study was to investigate disparities in access to LT, and whether those disparities were consistent across etiology of liver disease.</p>

<div><p><b>Background: </b>Food insecurity can increase the risk for NAFLD. We assessed the association between food insecurity and NAFLD among adolescents in the United States.</p>

<div><p><strong><b>Background:<span> </b></span></strong>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death, with high morbidity and mortality among vulnerable populations. We hypothesized the social determinants of health (SDOH), downstream social risks, and health behaviors impact access to curative therapies.</p>

<div><p><b>Background: </b>The non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. We aim to develop a novel non-invasive model for predicting CSPH in patients with compensated advanced chronic liver disease, and investigate whether carvedilol could prevent hepatic decompensation in high-risk CSPH patients stratified by the novel model.</p>

<div><p><b>Background:</p> </b><p>Long term reduction and alcohol abstinence have been known to reduce both short and long term mortality in patients with Alcohol associated Liver diseases (AaLD). Naltrexone, despite being known efficacy in Alcohol dependence, has not been tested in liver disease patients. We aimed to evaluate six and twelve month abstinence rates (and new onset decompensation events over 12 months) after 12 weeks of Naltrexone (50 mg) compared with placebo in patients with underlying AaLD.</p>

<div><p><strong><b>Background:</strong> </b>Alcoholic associated liver disease (AALD) is a poorly characterized pathology characterized by <span> </span>steatosis, inflammation and fibrosis. The lack of an animal model which recapitulates key features of AALD has been a major limitation in understanding its etiology and in the development of effective therapies.

<div><p><strong><b>Background:</strong> </b>Oxygen and inflammation levels in the gut have emerged as important factors in liver disease progression. Intestinal hypoxia, caused by altered blood flow and impaired oxygen delivery, triggers inflammation, and disrupts the intestinal barrier, leading to bacterial translocation and could encourage dysbiosis with facultative anaerobes. Bacterial translocation and their products reach the liver, promoting inflammation, oxidative stress, and liver damage.

<div><p><strong>Background</strong>: Wilson’s disease (WD) is an autosomal recessive disorder caused by inactivating mutations in the copper (Cu⁺⁺) transporting P-type ATPase. Loss of Atp7b function prevents translocation of Cu⁺⁺ into the trans-Golgi network and excretion into bile. Cu⁺⁺ exposure results in oxidative stress, inflammation, and mitochondrial dysfunction and fibrosis, cirrhosis, and liver failure.

<div><p><b>Background:<span> </b>Biliary atresia (BA) is the most common reason for liver transplantation in infants, but its etiopathology is still not completely understood. A nationwide genomic study identified mutations in <i>PKD1L1</i> as a BA candidate gene. Liver-specific deletion of <i>Pkd1l1 </i>in<i> </i>mice results in liver pathology analogous to changes seen in BA, but how <i>Pkd1l1</i>-deficient cholangiocytes differ from wild type cells is unknown.