Tetrabromobisphenol S (TBBPS) exposure causes gastric cell senescence and inflammation by inducing iron overload.

Tetrabromobisphenol S (TBBPS) is a brominated flame retardants (BFRs). TBBPS is widely used as a new type of BFR to replace TBBPA. Here, we used gastric cells as a model for evaluating the effect of TBBPS on the toxicology of gastric cells.

Gradient inflammation in the pancreatic stump after pancreaticoduodenectomy: Two case reports and review of literature.

Background: Postoperative pancreatic fistula (POPF) contributes significantly to morbidity and mortality after pancreaticoduodenectomy (PD). However, the underlying mechanisms remain unclear. This study explored this pathology in the pancreatic stumps and elucidated the mechanisms of POPF following PD.

A novel HCP (heparin-binding protein-C reactive protein-procalcitonin) inflammatory composite model can predict severe acute pancreatitis.

Severe acute pancreatitis (SAP) presents with an aggressive clinical presentation and high lethality rate. Early prediction of the severity of acute pancreatitis will help physicians to further precise treatment and improve intervention. This study aims to construct a composite model that can predict SAP using inflammatory markers.

Effect of laparoscopic pancreaticoduodenectomy on the incidence of surgical-site wound infection: A meta-analysis.

A meta-analysis was conducted to assess the impact of robotic and laparoscopic pancreaticoduodenectomies on postoperative surgical site wound infections. A comprehensive computerised search of databases, such as PubMed, EMBASE, Cochrane Library, Web of Science, China National Knowledge Infrastructure, Chinese Biomedical Literature Database, and Wanfang Data, was performed to identify studies comparing robotic pancreaticoduodenectomy (PD) with laparoscopicPD. Relevant studies were searched from the inception of the database construction until April 2023.

Identification of the prognostic, diagnostic, and biological significance of the miR-148a-3p/cathepsin A axis in hepatocellular carcinoma.

A comprehensive analysis of the prognostic, diagnostic, and biological significance of miR-148a-3p and cathepsin A (CTSA) in hepatocellular carcinoma (HCC) was performed using bioinformatics algorithms with The Cancer Genome Atlas (TCGA) data. miR-148a-3p and CTSA gene expression in HCC tissues and nontumor specimens was analyzed using TCGA database with R software. CTSA staining analysis was validated using the Human Protein Atlas database.

FXYD6 overexpression in HBV-related hepatocellular carcinoma with cirrhosis.

Objective: The aim of this study was to investigate the expression of FXYD domain-containing ion transport regulator 6 (FXYD6) mRNA and protein in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) tissues with cirrhosis, the corresponding paracancerous tissues and the normal liver tissues, and to explore the clinical significance of FXYD6 expression in HBV-related HCC with cirrhosis.

Methods: The FXYD6 mRNA and protein were examined by semi-quantitative reverse transcription polymerase chain reaction and immunohistochemistry, respectively.

Results: The FXYD6 mRNA in HBV-related HCC tissues was significantly higher than that in the cirrhosis tissues or that in the normal liver tissues.

Knockdown of interferon-induced transmembrane protein 1 inhibited proliferation, induced cell cycle arrest and apoptosis, and suppressed MAPK signaling pathway in pancreatic cancer cells.

Pancreatic cancer (PC), highly malignant, is one of the most lethal cancers. Interferon-induced transmembrane protein 1 (IFITM1) has recently been regarded as a new molecular marker in human cancers. However, the role of IFITM1 in PC remains unclear.

Revealing gene clusters associated with the development of cholangiocarcinoma, based on a time series analysis.

Cholangiocarcinoma (CC) is a rapidly lethal malignancy and currently is considered to be incurable. Biomarkers related to the development of CC remain unclear. The present study aimed to identify differentially expressed genes (DEGs) between normal tissue and intrahepatic CC, as well as specific gene expression patterns that changed together with the development of CC.