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Hu, Ben, Zeng, Lei-Ping, Yang, Xing-Lou, Ge, Xing-Yi, Zhang, Wei, Li, Bei, Shen, Xu-Rui, Zhang, Yun-Zhi, Wang, Ning, Luo, Dong-Sheng, Zheng, Xiao- Shuang, Wang, Mei-Niang, Daszak, Peter, Wang, Lin-Fa, Cui, Jie, Shi, Zheng- Li (2017): Discovery of a rich gene pool of bat SARSrelated coronaviruses provides new insights into the origin of SARS coronavirus. PLoS Pathogens 13 (11), No. 1006698: 1-27, DOI: 10.1371/journal.ppat.1006698

Geographical map of Jianchuan country and the sampling areas. Figure S2. Alignment and predicted domains and cleavage sites of AcCoV-JC34 spike protein. NTD, N-terminal domain; RBD, receptor-binding domain; HR, heptad repeat; TM, transmembrane anchor. The signal peptide corresponds to residues 1 to 19. The cleavage sites were indicated by arrows. (PDF 223Â kb)

Multidrug resistance has became the major obstacle to cancer chemotherapy. Recent studies suggest that quercetin could enhance the response of tumors to chemotherapy although the mechanism by which quercetin enhances the sensitivity of tumor cells to chemical drugs remains elusive. Therefore, in this study, we examined the effects of quercetin on doxorubicin cytotoxicity in human breast cancer cells and investigated the underlying mechanisms. MCF-7 and MCF-7/ dox cells were exposed to doxorubicin, quercetin, or combination of both agents for 36 hours. Cell proliferation, cell invasion, intracellular doxorubicin concentration and expression of hypoxia-inducible factor-1 alpha (HIF-1α) and P-glycoprotein (P-gp) were then assessed. Quercetin had little effect on cell proliferation at concentrations less than 0.7 μM. Compared to treatment with doxorubicin alone, combined treatment with doxorubicin and quercetin (0.7 μM) significantly inhibited cell proliferation and invasion and suppressed the expression of HIF-1α and P-gp. Quercetin (0.7 μM) increased the intracellular doxorubicin concentration and enhanced doxorubicin cytotoxicity as 1.49-fold in MCF-7 cells and 1.98-fold in MCF-7/dox cells. These data suggest that quercetin can increase the chemosensitivity of breast cancer cells to doxorubicin.

During 11-18 September 2014, the size-resolved aerosol Cloud Condensation Nuclei (CCN) activity and mixing state were measured using Cloud Condensation Nuclei Counter (CCNC), Aerosol Particle Mass (APM) and Scanning Mobility Particle Sizer (SMPS). The results showed that aerosols mainly existed as an internal mixture. For 76, 111, 138 and 181 nm particles, black carbon (BC) accounted for 5.4%, 10%, l0.7% and 6.7% of the particle mass, but as high as 51%, 57%, 70% and 59% of the particle number concentrations, respectively, suggesting that BC was a type of important condensation nuclei in the atmosphere and made significant contributions to particle numbers. The occasionally observed external mixtures were mainly present in 111 and 138 nm particles. The critical supersaturation was 0.25%, 0.13%, 0.06% and 0.015% for 76, 111, 138 and 181 nm particles, respectively. Precipitation and haze had significant effects on the particle CCN activity. The hygroscopicity parameter K was 0.37, 0.29 and 0.39 in rainy, clear and hazy days, respectively. Particle density and CCN activity were impacted by chemical compositions. Compared with clear days, higher contents of inorganic salts and lower contents of organics were found on hazy days, accompanied by lower particle density and higher CCN activity.

Predicted genes of WIV19 and comparison to those of known adenoviruses. (DOCX 20Â kb)

Our previous study indicated that nontoxic doses of quercetin (Que) could increase the chemosensitivity of breast cancer cells to doxorubicin (Dox) although the mechanism still remains elusive. Therefore, in this study, we aimed to investigate the underlying mechanisms. MCF-7 cells and MCF-7/dox cells were exposed to PTEN inhibitor bpV (HOpic), Dox, or combination of Dox and Que with or without bpV (HOpic) intervention for 24 hours. Cell proliferation, cell apoptosis, cell invasion and expression of PTEN and phospho-Akt (p-Akt) were then assessed. bpV (HOpic) had little effect on cell proliferation at concentrations less than 1 μM. Compared to treatment with Dox alone, combined treatment with Dox and Que significantly inhibited cell proliferation and invasion, increased cell apoptosis, up-regulated the expression of PTEN and down-regulated the expression of p-Akt. However, co-treatment with PTEN inhibitor bpV (HOpic) could revert the effects of Que on Dox. These data indicate that Que can increase the sensitivity of breast cancer cells to Dox through down regulation of p-Akt expression arising from increased expression of PTEN.

To summarize the clinical characteristics, diagnosis and treatment of gastric neurogenic tumors.Clinical data of 11 patients with gastric neurogenic tumors confirmed by pathology, operation and immunohistochemistry were analysed retrospectively.There were 7 males and 4 females with a median age of 55.5 years. The main manifestations were gastrointestinal hemorrhage, abdominal pain, upper abdominal discomfort and anaemia. Nine patients underwent gastroscopy and only one case was confirmed by the examination. Two patients were diagnosed during operation. Eight patients were submitted to subtotal gastrectomy, three were partial gastrectomy. All patients were followed up, and perioperative death occurred in one patient because of respiratory failure, recurrence occurred in two patients. Other patients with long- term follow- up had a good prognosis.Gastric neurogenic tumors have no specific clinical characteristics preoperatively, and the misdiagnosis rate is high. Once the diagnosis of gastric neurogenic tumors is made, an operation should be performed as early as possible.