<div><p><b>Background: </b>Nonalcoholic fatty liver disease (NAFLD)-related fibrosis is heritable, but it is unclear how family history may be used to identify first-degree relatives with advanced fibrosis. We aimed to develop and validate a simple risk score to identify first-degree relatives of probands who have undergone assessment of liver fibrosis who are at higher risk of NAFLD with advanced fibrosis.</p>

<div><p><b>Background: </b>AASLD and EASL guidelines recommend all people with cirrhosis undergo twice yearly screening for hepatocellular carcinoma (HCC) with hepatic imaging. However, patient, provider, and system level barriers impede ongoing surveillance efforts. This stepped-wedge hybrid effectiveness-implementation trial assessed the impacts of using a quality improvement playbook called Getting to Implementation (GTI) to support VA facilities to select, implement, and evaluate data-driven strategies to improve HCC surveillance.</p>

<div><p><b>Background: </b>Environmental pollutants cause liver damage and telomere shortening. Effects may vary by race/ethnicity. This study examined interactions among liver-related outcomes, telomere length, and environmental pollutants by race/ethnicity.</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.

<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:</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>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:<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><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><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.