Aim To explore the effect of survivin in PC12 cells against injuries induced by cobalt chloride(CoCl_2).Methods PC12 cells were exposed to CoCl_2 at different doses in different time to set up the chemical hypoxia induced PC12 cells injuries model.Cell viability was tested by using cell counter kit-8.Dose-effect(200～1 000 μmol·L~(-1))and time-effect(0～48 h)relationship between hypoxia induced by CoCl_2 and the expression of survivin was evaluated by western blot.Results PC12 cells viability was inhibited significantly by CoCl_2 in a dose and time dependent manners;At the concentrations from 200 to 600 μmol·L~(-1) CoCl_2 for 24 h,survivin expression was upregulated in a dose dependent manner,peaking at 600 μmol·L~(-1) CoCl_2 treatment,exceeding this concentration of CoCl_2,with dose increasing,survivin expression decreased.At the dose of CoCl_2 up to 1 000 μmol·L~(-1),survivin did not express basically;Treatment with 600 μmol·L~(-1) CoCl_2 in different time,within the range of 0～36 h,the expression of survivin enhanced in time dependent manner.But with the extension of time,survivin expression was declining; 17-allylamino-17-demethoxygeldanamycin (2 μmol·L~(-1)),an inhibitor of Hsp90,not only decreased survivin overexpression but also obviously enhanced the injuries of PC12 cells induced by CoCl_2,which didn't damage PC12 cells alone.Conclusion Upregulation of survivin expression may be one of the endogenous defense mechanisms for PC12 cells against chemical hypoxia.

Objective: To analysis the risk factors of postoperative bleeding of endoscopic submucosal dissection (ESD) for early gastrointestinal cancer. Methods: A retrospective study was performed on the data of 430 patients (449 lesions) with early gastrointestinal cancer undergoing ESD in Fujian Provincial Hospital Digestive Endoscopic Center from June 2008 to February 2015 and in Fujian Provincial Hospital South Branch Digestive Endoscopic Center from May 2015 to April 2018. Patients with postoperative bleeding were compared with those without postoperative bleeding on the basis of general conditions, endoscopic performance, postoperative pathology and so on to analysis the risk factors for postoperative bleeding of ESD. Results: Among the 430 cases (449 lesions)of early gastrointestinal cancer undergoing ESD, 16 cases (3.7%) had postoperative bleeding. According to whether the occurrence of postoperative hemorrhage, patients were divided into bleeding group (n=16) and not bleeding group (n=433). Univariate analysis suggested that whether had hypertension was statistically significant between the two groups (χ²=4.793, P=0.029), while patients age (t=0.465, P=0.642), gender (χ²=0.035, P=0.642), whether to have diabetes (χ²=0.647, P=0.421), whether to have coronary heart disease (P=1.000), lesion size (t=1.598, P=0.111), whether two or more lesions (P=1.000), lesion site (χ²=6.183, P=0.289), operation time (t=1.335, P=0.201), pathological grading (χ²=0.687, P=0.709), and lesion infiltration depth (χ²=0.134, P=0.714) were not statistically significant between the two groups. Logistic regression analysis showed that hypertension (OR=3.358, 95%CI: 1.227-9.186, P=0.018) was an independent risk factor of bleeding after ESD for early gastrointestinal cancer. Conclusion Hypertension is closely related to postoperative bleeding following ESD for early gastrointestinal cancer.Patients with hypertension are at a greater risk of bleeding after ESD.