NEGATIVE IMPACT OF PNPLA3 rs738409 C>G IS SIGNIFICANTLY MODIFIED BY DIETARY FACTORS, CAFFEINE AND NON-HEAVY ALCOHOL CONSUMPTION IN THE US POPULATION

<div><p><b>Background:</p> </b><p><em>PNPLA3</em> rs738409 C&gt;G is strongly associated with NAFLD and its severity. <em>PNPLA3</em> expression is highly regulated by changes in energy balance; however, little is known about the interplay between <em>PNPLA3</em>, dietary factors, alcohol intake, and risk of liver-related death (LRD).

HIGH DOSES OF ALBUMIN INCREASES MORTALITY AND COMPLICATIONS IN TERLIPRESSIN TREATED PATIENTS WITH CIRRHOSIS: INSIGHTS FROM THE ATTIRE TRIAL

<div><p><strong>Background</strong>: The CONFIRM trial revealed potential harm with terlipressin in a subset of patients, who developed respiratory failure. It remains unclear to what degree concomitant albumin contributes to the undesirable outcomes of terlipressin treatment. Using ATTIRE trial data, we compared safety of serum targeted albumin infusions to standard-of-care in patients with cirrhosis receiving terlipressin.</p>

AN OPEN-LABEL ROLLOVER STUDY FOLLOWING A RANDOMIZED TRIAL FOR CHRONIC HEPATITIS B WITH HIGH SERUM VIRAL LOAD BUT MILD ELEVATED AMINOTRANSFERASE

<div><p><b>Background: </b>This study extends the follow-up of participants who completed a randomized placebo-controlled trial evaluating the safety and efficacy of tenofovir disoproxil fumarate (TDF) in reducing the risk of histological progression in patients with chronic hepatitis B (CHB) characterized by high viral load and minimally raised serum alanine aminotransferase (ALT) levels. We report herein the outcomes of patients who received three years of open-label TDF treatment after completing a randomized trial</p>

HEAR-MHE: POINT-OF-CARE ANALYSIS OF RECORDED SPEECH AS A NOVEL METHOD TO DETECT HEPATIC ENCEPHALOPATHY

<div><p><strong>Background</strong>: Variation in speech may be an early sign of minimal hepatic encephalopathy (MHE) or future overt HE (OHE). Though a battery of tests is available for MHE assessment, these are cumbersome and rarely used in clinical practice. In a prospective study, we evaluated the ability of speech recorded at home or in the office to correlate with validated HE assessments in patients of diverse backgrounds.</p>

HEPATIC LOBULAR INFLAMMATION IS THE MOST IMPACTED PROGNOSTIC FACTOR RATHER THAN FIBROSIS IN PATIENTS WITH BIOPSY-PROVEN MASLD: MULTI-CENTER STUDY

<div><p><b>Background: </b>Metabolic dysfunction-associated steatotic liver disease (MASLD) captures patients at high risk of hepatic fibrosis and cardiovascular disease. However, limited information is available on the prognosis of MASLD. This study aimed to investigate the prognosis of patients with biopsy-proven MASLD and validate a group of fatty liver patients excluded from MASLD because of no metabolic abnormalities by a multi-center longitudinal cohort.

PSMP INHIBITS HCC PROGRESSION BY REGULATING THE POLARIZATION OF TUMOR-ASSOCIATED MACROPHAGES THROUGH THE PI3K/AKT PATHWAY

<div><p><b>Background:</p> </b><p>Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver and represents a major global health-care challenge. PC3 secreted microprotein (PSMP) is a novel chemotactic cytokine that can recruit peripheral blood monocytes and lymphocytes through its chemokine receptor CCR2. Our previous study found that PSMP is significantly highly expressed in human and mouse liver fibrosis/cirrhosis.

CHRONIC ETHANOL INSULT INCREASES HSD17beta13 ON HEPATOCELLULAR LIPID DROPLETS VIA A LOSS OF AN ASSOCIATED SEGREGASE p97/VCP TO PROMOTE HEPATIC STEATOSIS

<div><p><b>Background: </b>Chronic EtOH insult is known to lead to an accumulation of lipid droplets (LDs) in hepatocytes resulting in hepatic steatosis. Our previous study reported that EtOH resulted in a 10-fold reduction of the LD-associated segregase VCP/p97, a protein implicated in LD protein clearance. Concomitant with this decrease was a 6-fold increase in the association of the hydroxysteroid enzyme HSD17β13 known to play an important role in hepatic steatosis.

ESTABLISHMENT OF PFIC 3 MOUSE MODEL CARRYING HUMAN-LIKE BILE ACID COMPOSITION BY IN VIVO LIVER-SPECIFIC GENE DELETION USING ADENO-ASSOCIATED VIRUS AND CRISPR/Cas9 SYSTEM

<div><p><strong><span><b>Background:</span> </b></strong><span>Progressive familial intrahepatic cholestasis (PFIC) 3 is a life-threatening hereditary disease caused by adenosine triphosphate-binding cassette subfamily B member 4 (ABCB4) gene mutations. The murine bile acid composition is different from that of humans. Mice are less likely to develop cholestasis due to the predominance of hydrophilic bile acids such as muricholic acids, which are synthesized by enzymes including Cyp2c70.

MOLECULAR SIGNATURE OF PERIPHERAL CIRCULATING TUMOR CELLS IN CANCER PROGRESSION OF HEPATOCELLULAR CARCINOMA PATIENTS TREATED BY ATEZOLIZUMAB PLUS BEVACIZUMAB

<div><p><b>Background:</p> </b><p>The mechanisms leading to cancer progression of hepatocellular carcinoma (HCC) such as acquired resistance to immunotherapies and metastatic progression are not clear. Circulating tumor cells (CTCs) have been defined as cancer cells released into the blood circulation from primary tumor. CTCs have notable advantages in that they are noninvasive and real-time biomarker that provide information about metastatic process.

HEPATOCYTE-SPECIFIC HIF-1α DELETION ACCELERATES NON-ALCOHOLIC STEATOHEPATITIS PROGRESSION TO LIVER FIBROSIS

<div><p><b>Background:</p> </b><p>Non-alcoholic steatohepatitis (NASH) is prevalent, yet lacks for effective treatments to hinder rapid fibrosis progression, which is the main factor that limits patient prognosis. The role of Hypoxia-inducible factor 1α (HIF-1α) in NASH progression remains unclear. This study investigates the impact and mechanism of hepatocyte-specific HIF-1α deletion on NASH fibrosis, aiming to uncover a novel therapeutic target.</p>

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