Spatial patterns and effects of air pollution and meteorological factors on hospitalization for chronic lung diseases in Beijing,China

Chronic obstructive pulmonary disease(COPD), lung cancer(LC) and tuberculosis(TB) are common chronic lung diseases that generate a large disease burden and significant health care resource use in China. The aim of this study was to quantify spatial patterns and effects of air pollution and meteorological factors on hospitalization of COPD, LC and TB in Beijing. Daily counts of hospitalization for 2010 were obtained from the Beijing Urban Employees Basic Medical Insurance(UEBMI) system.Bayesian hierarchical Poisson regression models were applied to identify spatial patterns of hospitalization for COPD, LC and TB at the district level and explore associations with inhalable particulate matter(aerodynamic diameter 10 μm, PM_(10)), sulfur dioxide(SO_2), nitrogen dioxide(NO_2), mean temperature and relative humidity. There were 18,882, 14,295 and 2,940 counts of hospitalizations for COPD, LC and TB respectively, in Beijing in 2010. Clusters of high relative risk were in different locations for the three diseases. The effect of relative humidity on COPD hospitalization was most significant with a relative risk(RR) of 1.070(95%CI: 1.054, 1.086) per one percent increase. For lung cancer hospitalization, exposure to ambient SO_2 was associated with a RR of 1.034(95%CI: 1.011, 1.058) per μg m~(–3) increase. For tuberculosis, the effect of mean temperature was significant with a RR of 1.107(95%CI: 1.038, 1.180) per °C increase. Risk factors and spatial patterns were different for hospitalization of non-infectious and infectious chronic lung disease in Beijing. Even over a short time period(one year), associations were apparent with air pollution and meteorological factors.     

Nicorandil alleviates apoptosis in diabetic cardiomyopathy through PI3K/Akt pathway

Nicorandil exerts myocardial protection through its antihypoxia and antioxidant effects. Here, we investigated whether it plays an anti‐apoptotic role in diabetic cardiomyopathy. Sprague‐Dawley rats were fed with high‐fat diet; then single intraperitoneal injection of streptozotocin was performed. Rats with fasting blood glucose (FBG) higher than 11.1 mmol/L were selected as models. Eight weeks after the models were built, rats were treated with nicorandil (7.5 mg/kg day and 15 mg/kg day respectively) for 4 weeks. H9c2 cardiomyocytes were treated with nicorandil and then stimulated with high glucose (33.3 mmol/L). TUNEL assay and level of bcl‐2, bax and caspase‐3 were measured. 5‐HD was used to inhibit nicorandil. Also, PI3K inhibitor (Miltefosine) and mTOR inhibitor (rapamycin) were used to inhibit PI3K/Akt pathway. The results revealed that nicorandil (both 7.5 mg/kg day and 15mg/kg day) treatment can increase the level of NO in the serum and eNOS in the heart of diabetic rats compared with the untreated diabetic group. Nicorandil can also improve relieve cardiac dysfunction and reduce the level of apoptosis. In vitro experiments, nicorandil (100 µmol) can attenuate the level of apoptosis stimulated by high glucose significantly in H9C2 cardiomyocyte compared with the untreated group. The effect of nicorandil on apoptosis was blocked by 5‐HD, and it was accompanied with inhibition of the phosphorylation of PI3K, Akt, eNOS, and mTOR. After inhibition of PI3K/Akt pathway, the protective effect of nicorandil is restrained. These results verified that as a NO donor, nicorandil can also inhibit apoptosis in diabetic cardiomyopathy which is mediated by PI3K/Akt pathway.     

Soluble CXCL16 promotes TNF‐α‐induced apoptosis in DLBCL via the AMAD10‐NF‐κB regulatory feedback loop

We had previously identified that the co‐expression of transmembrane CXCL16 (TM‐CXCL16) and its receptor CXCR6 is an independent risk factor for poor survival in patients with diffuse large B‐cell lymphoma (DLBCL). However, the impact of the soluble form of CXCL16 (sCXCL16) on the pathogenesis of DLBCL remains unknown. In the present study, the synergistic effect of sCXCL16 and tumor necrosis factor α (TNF‐α) on apoptosis in DLBCL cell lines (OCI‐LY8 and OCI‐LY10) was investigated in vitro. sCXCL16 reinforced TNF‐α‐mediated inhibition of DLBCL cell proliferation, as determined by the cell counting kit‐8 assay. The results of annexin V staining showed that sCXCL16 enhanced TNF‐α‐induced apoptosis in OCI‐LY8 and OCI‐LY10 cells through a death receptor‐caspase signaling pathway. The results of gene microarray suggested a significant upregulation of differentially expressed genes in the TNF signaling pathway. sCXCL16 increased the concentration of extracellular TNF‐α by binding to CXCR6 to activate the nuclear factor‐κB (NF‐κB) signaling pathway. TNF‐α also induced the secretion of sCXCL16 by increasing the expression of ADAM10, which is known to cleave TM‐CXCL16 to yield sCXCL16. Moreover, bioinformatics analysis revealed that elevated TNF‐α and ADAM10 expression levels in tumor tissues predicted better survival in patients with DLBCL. Thus, our study suggests that sCXCL16 enhances TNF‐α‐induced apoptosis of DLBCL cells, which may involve a positive feedback loop consisting of TNF‐α, ADAM10, sCXCL16, and members of the NF‐κB pathway. sCXCL16 and TNF‐α may be used as prognostic markers in the clinic, and their combinational use is a promising approach in the context of DLBCL therapy.     

Resolving Cell Fate Decisions during Somatic Cell Reprogramming by Single-Cell RNA-Seq

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SubCellBarCode: Proteome-wide Mapping of Protein Localization and Relocalization

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Understanding high ε-poly-l-lysine production by Streptomyces albulus using pH shock strategy in the level of transcriptomics

Journal of Industrial Microbiology & Biotechnology - ε-Poly-l-lysine (ε-PL) is a natural food preservative, which exhibits antimicrobial activity against a wide spectra of...