Higher serum chromium level may be associated with the presentation of depression in patients with metabolic dysfunction-associated fatty liver disease: evidence from NHANES survey.

Background: Depressive symptoms are frequently observed in patients with Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD), a prevalent metabolic disorder that affects many individuals. It is not yet clear whether there is an association between serum chromium levels and depression. Objective: The purpose of this research was to explore the association between serum chromium level and the manifestation of depression among patients with MAFLD. Methods: The selection of 1837 patients diagnosed with MAFLD was based on data obtained from the 2017-2018 National Health and Nutrition Examination Survey (NHANES) database in this research. The Patient Health Questionnaire-9 (PHQ-9) was employed to evaluate the severity of depression. The researchers utilized logistic regression models that were weighted for multiple variables to investigate the association between depression and serum chromium levels. Results: In our study, we found that 8.98% of US adults with MAFLD were suffering from depression at the time of evaluation. In the logistic regression model, serum chromium levels showed an inverse association with depression (OR=0.82, 95%CI: 0.69-0.96; p=0.016), this relationship remained after adjusting for fully confounding factors (OR=0.83, 95%CI: 0.71-0.97; p=0.021), subgroup analyses showed that the association between serum chromium levels and depression existed in relatively high-prevalence of depression groups. Conclusion: Patients diagnosed with MAFLD have a greater likelihood of experiencing depression, whereas individuals with higher levels of serum chromium are less likely to suffer from depression, and this association persists even after adjusting for other factors. These findings indicate supplementing chromium may be a viable treatment for their depressive symptoms.

Low-dose PPI to prevent bleeding after ESD: A multicenter randomized controlled study.

BACKGROUND: Although proton pump inhibitors (PPIs) are widely used in the prevention of gastric bleeding caused by endoscopic submucosal dissection (ESD), there is no consensus on the optimal regimen for these patients. Therefore, we aim to investigate whether intermittent use of low-dose PPI is sufficient to prevent post-ESD bleeding. METHODS: This multicenter, non-inferiority, randomized controlled trial was conducted at 9 hospitals in China. Consecutive eligible patients with a diagnosis of gastric mucosal lesions after ESD treatment were randomly assigned (1:1) to receive either intermittent low-dose or continuous high-dose PPIs treatment. After three days, all patients administered orally esomeprazole 40 mg once a day for 8 weeks. The primary endpoint was post-ESD bleeding within 7 days. Analysis was done according to the intention-to-treat principle with the non-inferiority margin (Δ) of 5%. RESULTS: 526 consecutive patients were assessed for eligibility from 30 September 2017 to 30 July 2019, of whom 414 were randomly assigned to low-dose (n = 209) or high-dose (n = 205) esomeprazole treatment group without dropouts within7 days. The total post-ESD bleeding is occurred in 13 (6.2 %, 95 % CI 3.3-9.6) of 209 within 7 days in the intermittent low-dose group, and 12 (5.9 %, 95 % CI 2.9-9.3) of 205 in the continuous high-dose group. The absolute risk reduction (ARR) was 0.4 % (-4.2, 4.9). One month after ESD, There are 44 patients (21.1 %, 95 % CI 15.8, 26.8) and 39 patients (19.0 % 95 % CI 13.7, 24.4) in scar stage respectively in low-dose group and high-dose group (P = 0.875).The hospital costs in the low-dose PPI group was lower than high -dose group (P = 0.005). CONCLUSION: The intermittent use of low-dose PPIs is sufficient to prevent post-ESD bleeding. It might be applied in clinical practice to prevent post-ESD bleeding and reduce the costs related to PPIs.

Identification of novel therapeutic target genes and pathway in pancreatic cancer by integrative analysis.

BACKGROUND: Gene alterations are crucial to the molecular pathogenesis of pancreatic cancer. The present study was designed to identify the potential candidate genes in the pancreatic carcinogenesis. METHODS: Gene Expression Omnibus database (GEO) datasets of pancreatic cancer tissue were retrieval and the differentially expressed genes (DEGs) from individual microarray data were merged. Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, protein-protein interaction (PPI) networks, and gene coexpression analysis were performed. RESULTS: Three GEO datasets, including 74 pancreatic cancer samples and 55 controls samples were selected. A total of 2325 DEGs were identified, including 1383 upregulated and 942 downregulated genes. The GO terms for molecular functions, biological processes, and cellular component were protein binding, small molecule metabolic process, and integral to membrane, respectively. The most significant pathway in KEGG analysis was metabolic pathways. PPI network analysis indicated that the significant hub genes including cytochrome P450, family 2, subfamily E, polypeptide 1 (CYP2E1), mitogen-activated protein kinase 3 (MAPK3), and phospholipase C, gamma 1 (PLCG1). Gene coexpression network analysis identified 4 major modules, and the potassium channel tetramerization domain containing 10 (KCTD10), kin of IRRE like (KIRREL), dipeptidyl-peptidase 10 (DPP10), and unc-80 homolog (UNC80) were the hub gene of each modules, respectively. CONCLUSION: Our integrative analysis provides a comprehensive view of gene expression patterns associated with the pancreatic carcinogenesis.