LOSS OF TAZ AFTER YAP DELETION SEVERELY IMPAIRS FOREGUT DEVELOPMENT AND WORSENS CHOLESTATIC HEPATOCELLULAR INJURY

<div><p><b>Background:</p> </b><p>We previously showed that loss of Yes-associated protein 1 (YAP) in early liver development (YAP<sup>KO</sup>) leads to an Alagille syndrome-like phenotype, with failure of intrahepatic bile duct development, severe cholestasis, and chronic hepatocyte adaptations to reduce liver injury. TAZ, a paralog of YAP, was significantly upregulated in YAP<sup>KO</sup> hepatocytes and interacted with TEAD transcription factors, suggesting possible compensatory activity.</p>

MODELLING PROGRESSIVE FAMILIAL INTRAHEPATIC CHOLESTASIS TYPE 1 USING PATIENT-SPECIFIC INDUCED PLURIPOTENT STEM CELLS

<div><p><b>Background:<span> </b>Progressive familial intrahepatic cholestasis (PFIC) are a group of recessive disorders linked by the inability to appropriately excrete bile salts (BS) from hepatocytes. PFIC1 results from mutations in <em>ATP8B1 </em>encoding FIC1, an apical membrane aminophospholipid translocase.

ALCOHOL-RELATED CIRRHOSIS EXPERIENCES LOWER 6-WEEK MORTALITY AFTER ACUTE VARICEAL BLEEDING COMPARED TO OTHER ETIOLOGIES USING A LARGE PROPENSITY SCORE MATCHED INTERNATIONAL COHORT

<div><p><b>Background:</p> </b><p>Acute variceal bleeding (AVB) is a cause of serious morbidity and mortality in cirrhosis. While more severe disease (e.g. higher Child-Turcotte-Pugh [CTP] score) has been shown to correlate with worse outcomes after AVB, it is unclear if this correlation remains universal across all cirrhosis etiologies.

RIVET TRIAL: PHASE 2 RCT OF RIFAMYCIN SV MMX, A NOVEL RIFAMPIN ANALOGUE, ON GUT-BRAIN AXIS CHANGES IN CIRRHOSIS AND MINIMAL HEPATIC ENCEPHALOPATHY

<div><p><strong>Background</strong>: Minimal hepatic encephalopathy (MHE) is associated with poor outcomes but treatment strategies are limited. Rifamycin SV MMX (RiVM) is a novel rifampin derivative which a non-absorbable antibiotic with maximal impact in the colon. <u>Aim</u>: Evaluate impact of RiVM on microbiome, safety &amp; gut-brain axis in an RCT.</p>

GLOBAL PREVALENCE OF INFECTIONS AND IMPACT OF REGIONAL VARIATIONS ON OUTCOMES: MULTI-NATIONAL CONSORTIUM OF CIRRHOSIS STUDY

<div><p><strong>Background</strong>: Regional differences in environment, health-care system, microbiology lab capabilities, countermeasures of drug resistance may greatly impact the occurrence and evolution of infection in cirrhosis. We aimed to assess the prevalence, characteristics, clinical impact, and variations in infection on admission (AdI) across a global population of cirrhosis inpatients.</p>

THE RISK OF LIVER FIBROSIS IS GREATEST IN AREAS OF HIGHER SOCIOECONOMIC DEPRIVATION: A RISK-FACTOR BASED POPULATION SCREENING STUDY.

<div><p><b>Background:</p> </b><p>Early detection of liver disease has been identified as a public health priority in the UK. Symptoms are rare before advanced stages and case finding using risk factors improves identification. In financially constrained health systems, case finding in areas with greater disease burden is prudent. Socio-economic deprivation is associated with advanced liver disease. We assessed the incidence of liver disease by population deprivation using a community case finding pathway.</p>

ROLE OF AUTOPHAGY IN HEPATIC ACETYLOME REGULATION

<div><p><b>Background: </b>Liver acetylome is a set of protein acetylation’s whose level reflects cellular metabolic health and is directly linked to intracellular pathways. However, to date, little is known about the cellular pathways that maintain the hepatic acetylome levels. Here, we show that macroautophagy hereafter referred to as autophagy, an intracellular lysosomal degradative pathway, regulates the hepatic acetylome.</p>

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