<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.

<div><p><b>Background: </b>The relative prevalence of health care barriers for patients with CLD vs. those with non-CLD chronic diseases and the cumulative effect of these barriers on recurrent acute care use remains unknown. We aimed to assess the number of health care barriers and their association with acute care use by CLD vs. chronic obstructive pulmonary disease (COPD) and/or cardiovascular disease (CVD).</p>

<div><p><b>Background:</p> </b><p>The homeostasis of gut microbiota is pivotal to maintaining the physiological liver-gut axis. In cholestatic diseases, impaired bile flow changes the composition of gut bacteria and subsequently dysregulates the bile acids metabolisms. Beneficial roles of vancomycin (VCM) in treating patients with sclerosing cholangitis have been reported; yet the mechanism is not clear. The therapeutic values of the intestinal microbiome restoration in cholestatic disease are less explored.</p>

<div><p><b>Background: </b>Metabolic dysfunction-associated steatohepatitis (MASH) is the fastest-growing etiology of liver disease for patients with hepatocellular carcinoma (HCC) added to the liver transplantation (LT) waitlist in the US. Patients with MASH-HCC are disproportionately of Hispanic ethnicity, who have historically had poorer access to LT than non-Hispanic (NH) whites. However, it is unclear whether racial and ethnic minorities are waitlisted and transplanted for MASH-HCC at lower-than-expected rates.</p>

<div><p><b>Background: </b>Macrophage (MF) are recruited to the liver during MASH progression, including fibrogenic TREM2+ hepatic lipid associated MF (LAMs). However, the TREM2 receptor itself is anti-fibrotic, in that <em>Trem2^-/-</em> mice have more severe MASH than WT mice. Despite these recent studies, little is known about mechanisms that regulate MF function during MASH regression.