Association between serum triglyceride level and severity of acute biliary pancreatitis.

Background: Acute biliary pancreatitis (ABP) is the most common type of acute pancreatitis. However, the effect of serum triglyceride (TG) levels on the severity of ABP remains unclear. The aim of this study was to assess the correlation between serum TG levels and the severity of ABP.

Relation between triglycerides and the severity of acute pancreatitis combined with nonalcoholic fatty liver disease: a retrospective study.

Background: Nonalcoholic fatty liver disease (NAFLD) can exacerbate the severity of acute pancreatitis (AP), and this severity is worsened with increased severity of NAFLD. This study aimed to investigate the relation between serum triglyceride (TG) and the severity of AP with NAFLD by collecting clinical data from AP patients with NAFLD.

Methods: AP patients with NAFLD were divided into 2 groups according to TG levels: hypertriglyceridemia (HTG) group and non-hypertriglyceridemia (NHTG) group.

Enhancing chemotherapy sensitivity by targeting PcG via the ATM/p53 pathway.

Histone modification and chromatin remodeling are important events in response to DNA damage, and Polycomb group (PcG) proteins, catalyzing H3K27 methylation, are involved. However, the biological function and mechanism of PcG in DNA damage are not fully understood. Additionally, downstream effectors in hepatocellular carcinoma (HCC) remain unclear.

EZH2 represses target genes through H3K27-dependent and H3K27-independent mechanisms in hepatocellular carcinoma.

Unlabelled: Alterations of polycomb group (PcG) genes directly modulate the trimethylation of histone H3 lysine 27 (H3K27me3) and may thus affect the epigenome of hepatocellular carcinoma (HCC), which is crucial for controlling the HCC cell phenotype. However, the extent of downstream regulation by PcGs in HCC is not well defined. Using cDNA microarray analysis, we found that the target gene network of PcGs contains well-established genes, such as cyclin-dependent kinase inhibitors (CDKN2A), and genes that were previously undescribed for their regulation by PcG, including E2F1, NOTCH2, and TP53.