<div><p><b>Background: </b>Tumor microenvironment(TME) reflects the intertwined crosstalk between cancer cells and tumor-infiltrating immune cells, affecting the efficiency of immunotherapy. Metabolic reprogramming, one of the major hallmarks of hepatocellular carcinoma(HCC), is unclear in the aspect of reshaping TME. In this study, we report the vital role of SLC1A5, the major glutamine transporter of tumor cells, in HCC progression and the formation of immunosuppressive TME.</p>

<div><p><b>Background:</p> </b><p>Accurate alcohol assessments after liver transplants (LT) are crucial for understanding alcohol use and guiding treatment, particularly among LT recipients with prior alcohol-related liver disease (ALD). Biomarkers offer objective measures of alcohol exposure, but LT centers have not universally implemented routine biomarker use. Phosphatidylethanol (PEth) is a blood biomarker capable of detecting alcohol use during the prior 3-4 weeks.

<div><p><b>Background: </b>An assessment of varices is required prior to systemic therapy in patients with HCC. However, current non-invasive criteria, including the Baveno criteria, have not been validated in patients with HCC, and performing an EGD can delay HCC treatment initiation. We aimed to develop a noninvasive algorithm for assessing varices in patients with unresectable HCC.</p>

<div><p><b>Background:<span> </b>Patients with Alpha-1-antitrypsin Pi*ZZ homozygotes are at risk for developing liver cirrhosis and hepatocellular carcinoma. However, there is a high degree of variability in the clinical manifestations of patients with A1AT Pi*ZZ suggesting that genetic and environmental disease modifiers play an important role in the disease process. The prevalence of nonalcoholic fatty liver disease (NAFLD) has been rising worldwide.

<div><p><b>Background: </b>Metabolic dysfunction associated steatohepatitis (MASH) involves immune mechanisms and the contribution of adaptive immunity to disease progression has been increasingly recognized. B cells, with their ability to modulate inflammation, are key players in inflammatory diseases. However, their precise role and underlying mechanisms in MASH pathogenesis remain unclear. Therefore, our research aims to investigate the mechanisms driving B cell activation and their pro-inflammatory activity in MASH.</p>

<div><p><b>Background:<span data-contrast="auto" xml:lang="EN-GB" lang="EN-GB" class="TextRun SCXW196881610 BCX0"> </b><span class="NormalTextRun SCXW196881610 BCX0">Following</span><span class="NormalTextRun SCXW196881610 BCX0"> </span><span class="NormalTextRun SCXW196881610 BCX0">reductions in </span><span class="NormalTextRun SCXW196881610 BCX0">steatosis and </span><span class="NormalTextRun SCXW196881610 BCX0">bod

<div><p><strong><b>Background:</strong> </b>NCC and UCE are recommended for treatment monitoring in Wilson Disease (WD)(1). NCC is assumed to reflect the bioavailable copper (Cu) in plasma and is in equilibrium with the pool of stored Cu. UCE reflects body stores of Cu and is also influenced by the cupriuretic effect of therapy. Current methods to estimate NCC are flawed.

<div><p><b>Background: </b>Human pluripotent stem cell (PSC) derived hepatocyte-like cells and primary human hepatocytes applications for clinical or research uses is dependent on the ability to generate phenotypically and functionally relevant hepatocytes or hepatocyte-containing constructs.

<div><p><b>Background:</p> </b><p>The mechanisms contributing to the progression to NASH in patients with NAFLD are unclear. Our central hypothesis is that the inability of hepatic mitochondria to enhance nutrient oxidation in the setting of nutrient oversupply plays a key role in the progression of liver disease in NAFLD. The aim of this study was to explore the relationship between adipose tissue insulin resistance (IR), liver fat, and <em>in vivo</em> hepatic mitochondrial function.</p>

<div><p><b>Background:</p> </b><div><p><span lang="EN-US">Current guidelines for the diagnosis of HRS-AKI require the use of albumin as volume expander to exclude pre-renal azotemia. The treatment of HRS-AKI (hepatorenal syndrome) also recommends the use of terlipressin with albumin at a dose of 20-40g per day. However, the optimal dose of albumin to be given in the pre- and during treatment remains unclear.