A case of collagenous gastritis and literature review: A case report.

RATIONAL: Collagenous gastritis (CG) is rarely encountered in clinical practice. Here, we reported a case of CG with iron-deficiency anemia as the main symptom. PATIENT CONCERNS: The patient was a 26-year-old woman who sought medical advice with a chief complaint of recurrent upper abdominal distention and anemia since the last 3 years. DIAGNOSES: Gastroscopy at admission showed diffuse nodular mucosa. The pathology showed the formation of a belt hyperplasia of collagen in the superficial mucosa along with the infiltration of inflammatory cells. The subepithelial collagen band was 17.68 to 35.73-µm thick and tested positive for Masson staining, thereby confirming the diagnosis of CG. INTERVENTIONS: A polysaccharide iron complex capsule was given in a dosage of 0.3 t.i.d., p.o. in combination with an omeprazole capsule (20 mg q.d. p.o). OUTCOMES: The symptoms (upper abdominal distention and anemia) were ameliorated after 8-week treatment. Blood routine showed that the hemoglobin level rose to 91 g/L. LESSONS: It is difficult to diagnose CG. Hence, a comprehensive examination based on clinical manifestations, endoscopic findings, and pathological features is required.

Key Regulatory Effect of Activated HIF-1α/VEGFA Signaling Pathway in Systemic Capillary Leak Syndrome Confirmed by Bioinformatics Analysis.

Systemic capillary leak syndrome (SCLS) is a rare disorder characterized by capillary leakage of plasma fluids throughout the endothelium. The mechanism of SCLS is still unknown. Vascular endothelial growth factor (VEGF), an inducer or barrier disruption, is markedly upregulated in SCLS. This study was to investigate the molecular mechanisms involving SCLS-related inflammation and neuron damage in SCLS remain unclear. Data files of GSE97287 dataset were extracted and processed for identification of differentially expressed genes (DEGs), including upregulated adrenomedullin (ADM) gene, hypoxia-inducible factor-1α (HIF-1α) and VEGFA; and downregulated aldehyde dehydrogenase 1A1 (ALDH1A1) gene and interleukin (IL)-2 receptor ß (IL-2RB) gene. Weighted gene coexpression network analysis (WGCNA) was performed for DEGs and four significant modules were identified and were enriched Gene Ontology (GO) biological processes and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways related to immune response, angiogenesis, neuroblast proliferation, HIF-1 signaling pathway, and Parkinson's disease. The activated HIF-1α/VEGFA signaling in SCLS patients might well be responsible for the impaired inflammatory, nervous, and immune systems.

The miR-15a-5p-XIST-CUL3 regulatory axis is important for sepsis-induced acute kidney injury.

Background: Acute kidney injury (AKI) refers to a sudden loss of renal function. This study was performed to identify the key RNAs acting in the mechanism of sepsis-induced AKI. Methods: Microarray dataset GSE94717 (including six sepsis-induced AKI samples and three control samples) was downloaded from Gene Expression Omnibus database. Differentially expressed miRNAs (DE-miRNAs) were identified. The miRNA targets were predicted and enrichment analysis was performed. Protein-protein interaction (PPI) and competing endogenous RNA (ceRNA) regulatory networks were constructed. Mouse podocytes were treated with lipopolysaccharide (LPS), following by cell viability and PCR analysis. Cellular apoptosis and the ceRNA network were validated. Results: Thirty-one common DE-miRNAs (two up-regulated and 29 down-regulated) by AKI versus control and male AKI versus control were identified. We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway. RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network. The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR. The miR-15a-5p-XIST-CUL3 regulatory axis was identified and was validated. We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3. Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics. Conclusion: The miR-15a-5p-XIST-CUL3 regulatory axis was related to the pathogenesis of sepsis-induced AKI. Highlights Totally, 31 miRNAs were dysregulated between disease and control groups. MiR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway. MiR-16-5p and miR-29b-3p were implicated in PI3K-Akt signaling pathway. The miR-15a-5p-XIST-CUL3 axis was critical for sepsis-induced AKI.

The regulatory role of microRNA-mRNA co-expression in hepatitis B virus-associated acute liver failure.

INTRODUCTION AND OBJECTIVES: Acute liver failure (ALF) is a dramatic disorder requiring intensive care. MicroRNAs (miRNAs) have been identified to play important roles in ALF. This study was performed to identify miRNA-mRNA co-expression network after ALF to investigate the molecule mechanism underlying the pathogenesis of ALF. MATERIALS AND METHODS: The microarray dataset GSE62030 and GSE62029 were downloaded from Gene Expression Omnibus database. Overlapping differentially expressed miRNAs (DEmiRNAs) and genes (DEGs) were identified in liver tissues from patients with hepatitis B virus (HBV)-associated ALF in comparison with normal tissues from donors. Gene enrichment analysis was performed. Key pathways associated with the DEGs were identified. The miRNA-mRNA regulatory network was constructed. RESULTS: Total 42 DEmiRNAs and 523 DEGs were identified in liver tissues from patients with HBV-associated ALF. Gene ontology and pathways enrichment analysis showed upregulated DEGs were related to immune responses, inflammation, and infection, and downregulated DEGs were associated with amino acids, secondary metabolites and xenobiotics metabolism. In miRNA-mRNA co-expression network, DEGs were regulated by at least one DEmiRNA and transcription factor. Further analysis showed DEmiRNAs, including has-miR-55-5p, has-miR-193b-5p, has-miR-200b-3p, and has-miR-3175 were associated with amino acid metabolism, drug metabolism and detoxication, and signaling pathways including mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/AKT, Ras, and Rap1. CONCLUSIONS: These miRNA-mRNA pairs and changed profiles were associated with and might be responsible for the impairment of detoxification and metabolism induced by HBV-associated ALF.

Serum soluble fibrinogen-like protein 2 concentration predicts delirium after acute pancreatitis.

OBJECTIVE: Inflammation can cause delirium. Soluble fibrinogen-like protein 2 (sFGL2) is a modulator of the immune response and more recently found to be a biomarker for brain injury. This study was designed to discover the predictive capability of serum sFGL2 concentrations for delirium after acute pancreatitis (AP). MATERIALS AND METHODS: In this prospective, observational study, serum sFGL2 concentrations were quantified in 184 healthy controls and in 184 AP patients. Disease severity was assessed by Acute Physiology and Chronic Health Care Evaluation II score, Ranson score, multiple organ dysfunction score, and sequential organ failure assessment score. Delirium was recorded during hospital stay. Predictors of delirium were identified using multivariate analysis. RESULTS: Serum sFGL2 concentrations were substantially higher in AP patients than in controls. Serum sFGL2 concentrations were intimately correlated with the preceding severity parameters. Serum sFGL2 and the aforementioned severity parameters were independent predictors for delirium. Under receiver operating characteristic curve, the discriminatory ability of serum sFGL2 was equivalent to those of the above-mentioned severity parameters. Moreover, serum sFGL2 dramatically improved the predictive value of the aforementioned severity parameters. CONCLUSIONS: Elevation of serum sFGL2 concentrations is strongly associated with the AP severity and has the potential to distinguish delirium after AP.

Anticancer activity of genistein on implanted tumor of human SG7901 cells in nude mice.

AIM: To investigate genistein-induced apoptosis of implanted tumors of SG7901 cells in nude mice, and the relationship between this apoptosis and expression of Bcl-2 and Bax. METHODS: Establishing a transplanted tumor model by injecting human SG7901 cells into subcutaneous tissue of nude mice. Genistein (0.5, 1 and 1.5 mg/kg) was directly injected adjacent to the tumor, six times at 2-d intervals. Then, changes in tumor volume were measured continuously and tumor inhibition rate of each group was calculated. We observed the morphological alterations by transmission electron microscopy (TEM), measured the apoptotic rate by the TUNEL staining method, and detected the expression of apoptosis-regulated gene Bcl-2 and bax by immunohistochemical staining and RT-PCR. RESULTS: Genistein 0.5, 1 and 1.5 mg/kg significantly inhibited carcinoma growth when it was injected near the tumor by 10.8%, 29.9% and 39.6%, respectively. Genistein induced implanted tumor cells to undergo apoptosis, with apoptotic characteristics seen by TEM. The apoptosis index was increased progressively with increasing genistein dose (28.9%+/-1.2%, 33.8%+/-1.6% and 37.7%+/-1.2%). The positive rate of Bcl-2 protein was decreased progressively (11.9%+/-0.9%, 5.9%+/-0.7% and 4.2%+/-0.6%), and the positive rate of bax protein was increased progressively (0.9%+/-1.7%, 24.9%+/-0.8% and 29.6%+/-1.7%) by immunohistochemical staining, with increasing dose of genistein. The density of Bcl-2 mRNA decreased progressively and the density of bax mRNA increased progressively with elongation of time by RT-PCR. CONCLUSION: Genistein was able to induce apoptosis of transplanted tumor cells. This apoptosis may be mediated by down-regulation of the apoptosis-regulated gene Bcl-2 and up-regulation of apoptosis-regulated gene bax.