Bioinformatics analysis to reveal the key genes related to obstructive sleep apnea.

PURPOSE: Obstructive sleep apnea (OSA) is induced by obstruction of the upper airway, which can raise multiple health risks. This study is designed to reveal the key genes involved in OSA. METHODS: GSE38792 was extracted from Gene Expression Omnibus database, including ten visceral adipose tissues from OSA patients and eight visceral adipose tissues from normal controls. Differential expression analysis was conducted using limma package, and then the functions of the differentially expressed genes (DEGs) were analyzed using DAVID database, followed by protein-protein interaction (PPI) network, and integrated regulatory network analysis was performed using Cytoscape software. RESULTS: A total of 368 DEGs (176 upregulated and 192 downregulated) were identified in OSA samples. Epstein-Barr virus infection (involving IL10RB, MAPK9, and MAPK10) and olfactory transduction were the main pathways separately enriched for the upregulated genes and the downregulated genes. After the PPI network was built, the top ten network nodes (such as TXN) were selected according to node degrees. Two significant PPI network modules were identified. Moreover, the integrated regulatory network was constructed. CONCLUSION: IL10RB, MAPK9, MAPK10, and TXN might function in the pathogenesis of OSA.

The correlation between obstructive sleep apnea and diabetic neuropathy: A meta-analysis.

BACKGROUND: The aim of this study was to explore the correlation between obstructive sleep apnea (OSA) and diabetic neuropathy. MATERIALS AND METHODS: After working out searching strategy, literatures were screened from the electronic databases: PubMed, Embase, and the Cochrane library. R 3.12 was utilized to perform meta-analysis, and odds ratio (OR) and its 95% confidence interval (CI) were used to present effect size. Heterogeneity was assessed by χ2-based Q test and I2 statistics. Publication bias was estimated by Egger's test and sensitivity was evaluated by leave one out methods. RESULTS: According to the criteria, a total of 11 studies with 1842 patients were enrolled in this study. With a significant heterogeneity (Q=31.83, I2=68.60%), the random effects model was utilized to assess the effect size of pooled data. A remarkable correlation was identified OSA and diabetic neuropathy (OR=1.84, 95% CI: 1.18-2.87) without publication bias (t=1.68, P=0.13). Meanwhile, the result of leave one out performed a well sensitivity. Moreover, the subgroup analyses presented that OSA was significantly correlated with type 1 diabetic neuropathy (OR=1.97, 95% CI: 1.19-3.25), but no remarkable correlation was identified between OSA and type 1 (OR=1.84, 95% CI: 0.86-3.93) or 1+2 (OR=1.30, 95% CI: 0.43-3.92) diabetic neuropathy. CONCLUSION: OSA was significantly correlated with neuropathy in type 1 diabetes, but not in type 2 and type 1+2 diabetes.

Cefoperazone/Sulbactam-Induced Abdominal Wall Hematoma and Upper Gastrointestinal Bleeding: A Case Report and Review of the Literature.

An 87-year-old woman developed abdominal wall hematoma and upper gastrointestinal bleeding during treatment with cefoperazone/sulbactam for pneumonia. The woman received cefoperazone/sulbactam at 4.5 g twice daily for intravenous infusion. After 7 days, she developed sudden onset of left lower abdominal pain, associated with subcutaneous mass, and vomited a coffee-colored liquid. Investigations revealed a coagulation index abnormality and activated partial thromboplastin time and prothrombin time increased obviously. She was diagnosed with cefoperazone-induced hemorrhage. Cefoperazone/sulbactam was discontinued and the patient received vitamin K1. The blood coagulation function improved and hematoma disappeared after 3 days. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's coagulation function disorder and her use of the suspect drug.

A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression.

BACKGROUND: "Phosphatase and tensin homolog deleted on chromosome 10" (PTEN) is mostly considered to be a cancer-related gene, and has been suggested to be a new pathway of pathogenesis of asthma. The purpose of this study was to investigate the effects of the glucocorticoid, dexamethasone, on PTEN regulation. METHODS: OVA-challenged mice were used as an asthma model to investigate the effect of dexamethasone on PTEN regulation. Immunohistochemistry was used to detect expression levels of PTEN protein in lung tissues. The human A549 cell line was used to explore the possible mechanism of action of dexamethasone on human PTEN regulation in vitro. A luciferase reporter construct under the control of PTEN promoter was used to confirm transcriptional regulation in response to dexamethasone. RESULTS: PTEN protein was found to be expressed at low levels in lung tissues in asthmatic mice; but the expression was restored after treatment with dexamethasone. In A549 cells, human PTEN was up-regulated by dexamethasone treatment. The promoter-reporter construct confirmed that dexamethasone could regulate human PTEN transcription. Treatment with the histone deacetylase inhibitor, TSA, could increase PTEN expression in A549 cells, while inhibition of histone acetylase (HAT) by anacardic acid attenuated dexamethasone-induced PTEN expression. CONCLUSIONS: Based on the data a new mechanism is proposed where glucocorticoids treat asthma partly through up-regulation of PTEN expression. The in vitro studies also suggest that the PTEN pathway may be involved in human asthma.