Objective To study the clinical features and diagnostic analysis of 30 cases with refractory myco-plasma pneumonia.Methods 60 patients with mycoplasma pneumonia treated in our hospital during 2012.03 to 2014.03 were selected, and 30 cases were diagnosed as normal mycoplasma pneumonia and the others as refractory mycoplasma pneumonia.The clinical manifestations, percentage of neutrophils, peripheral blood leukocytes , C -re-active protein (CRP) level, and chest radiographic were retrospectively analyzed , and the clinical judging indicators of refractory mycoplasma pneumonia were obtained by multivariate logistic regression analysis .Results Considering the time of fever, the difference between two groups was statistically significant (χ2 =12.27, p <0.01).The differ-ence of percentage of neutrophils , peripheral blood leukocytes and CRP between the two groups were all significant (p <0.05); Logistic regression analysis showed that time of fever >10 d, CRP >40 mg /L, appearance of large high -density lung opacities were the judging indicators of mycoplasma pneumonia refractory .Conclusion Time of fever, CRP level and imaging Findings are the judging indicators of mycoplasma pneumonia refractory .

Objective To observe the expression of survivin and Aurora B in human pancreatic cancer BXPC3 cells after the treatment of sulindac and to explore the potential mechanism. Methods MTr assay was used to determine the effect of sulindac on the proliferation of the BXPC3 cells. RT-PCR was used to detect the expression of mRNA level of survivin and Aurora B, western blot was used to detect protein expression of survivin and Aurora B Thr-232. Cell cycle and apoptosis were detected by flow eytometry (FCM). Results The BXPC3 cells were inhibited by sulindac in a dose and time-dependent manner; the expression of mRNA of survivin and Aurora B were both significantly decreased from 1.5644 and 0.6554 to 0. 4372 and 0.1132 (P< 0.01), the expression of survivin protein and the phosphorylation of Aurora B Thr-232 were also decreased from 1.2735 and 0.4680 to 0.2126 and 0.2546 (P<0.01); the proportion of cells in the G0/G1 phase was increased from (56.65±1.93)% to (70.58±3.21)% (P<0.01). Conclusions Sulindac had inhibitory effects on the growth of BXPC3 cells, the possible mechanism was via decreasing the expression of survivin which depressed the activity of Aurora B, then the CPC was influenced. The most of the cells were blocked in the G0/G1 phase, and the cells' mitosis was inhibited.

Objective To investigate the effect of genistein on Notch-1, SHH and HHIP gene expression and on the cell cycle and proliferation of of BxPC3 cells. Methods Human pancreatic cancer cell line BxPC3 was cultured. The BxPC3 cells were treated with genistein and then the total RNA and protein were extracted. RT-PCR was used to detect the expression of Notch-1 mRNA, SHH mRNA and HHIP mRNA. Noteh-1 and SHH protein was determined by western blotting. MTT assay was used to detect proliferation of BxPC3 cells. The cell cycle of BxPC3 cells was measured by Propidium iodide (PI) and flow cytometry. Results The inhibiting rate was 67.17%±2.32% when BxPC3 cell lines were treated by 20μg/ml genistein for 48 hours. Notch-1 mRNA was down-regulated from 2.454±0.068 to 1.304±O.169 ; SHH mRNA was down-regulated from 0.959±0.023 to O.472±0.077 ; HHIP mRNA was up-regulated from 0.625±O.158 to 1.761±0.121. Notch-1 protein expression was down-regulated from 1.361±0.109 to 0.760±0.114; SHH protein expression was down-regulated from 0.265±0.018 to 0.129±0.013. (52.77±9.47)% cells were hindered in G2/M stage. Conclusions Genistein could down-regulate Notch-1 expression and inactivate Hedgehog signaling pathway and inhibit the proliferation of pancreatic cancer cells.

Objective To investigate the perioperative complications of stenting with symptomatic intracra-nial artery stenosis and study the mechanism and prevention of complications. Methods 63 patients were collect-ed from Stroke Center of Guangxi. They were proved intracranial artery stenosis and performed intracranial stents. Patients′ age,with hypertension,diabetes and hyperlipidemia or not,smoking or not,types and occurrence time of complications were registered. Results 63 patients were registered and 2 patients terminated operation due to blood vessels circuity or serious vessel spasm. Operation success rate reached 96.83％. 5 patients had complications among 63 cases,with complication incidence of 8.20％. 3 patients experienced cerebral hemorrhage and two cere-bral infarction in peri-operation period. 2 patients died of complications and mortality rate was 3.28％. Conclu-sions The incidence rate of complications of intracranial stenting with symptomatic intracranial artery stenosis is relatively high and it can be reduced by preoperative sufficient assessment and prudent selection ,careful operation and strict management after operation.

Objective To investigate the effect of miR-218-1-3p on the proliferation,cycle,and apoptosis of A549 cells in non-small-cell lung cancer.Methods miR-218-1-3p was transfected into non-small cell lung cancer A549 cells by LipofectamineTM 2000 Reagent,and the expression of miR-218-3p was detected by real-time PC R.Invasion and migration were assayed using the Transwell method.The effect of miR-218-1-3p on the proliferation of A549 cells was assayed by the MTS method.Changes in the cell cycle and apoptosis of A549 cells transfected with miR-218-1-3p was detected by flow cytometry.Changes in indicators related to cell proliferation,cycle,and apoptosis were detected by fluorescence quantitative PCR.Results Compared to the control group,the cell proliferation of A549 cells was significantly inhibited (P ＜ 0.05) and the proportion of cells in the S and G2-M phases was significantly decreased when miR-218-1-3p was up-regulated.In addition,compared with the control group,the early apoptotic rate was significantly increased by up-regulating miR-218-1-3p.We further detected indicators related to cell proliferation,cycle,and apoptosis and found that CYCLIN-D1 and BCL-2 were significantly downregulated.Conclusion miR-218-1-3p may inhibit proliferation,induce cell cycle arrest,and promote cell apoptosis of non-small cell lung cancer A549 cells by regulating CYCLIN-D 1 and BCL-2.