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Background The poor prognosis of patients with ovarian cancer is mainly due to cancer progression. γ-Synuclein (SNCG) has reported as a critical player in cancer metastasis. However, its biological roles and mechanism are yet incompletely understood in ovarian cancer, especially in high-grade serous ovarian cancer (HGSOC). Methods This is a retrospective study of 312 patients with ovarian cancer at a single center between 2006 and 2016. Ovarian cancer tissues were stained by immunohistochemistry to analyze the relationship between SNCG expression and clinicopathologic factors. The clinical outcomes versus SNCG expression level were evaluated by Kaplan–Meier method and multiple Cox regression analysis. Next, systematical functional experiments were given to examine the proliferation and metastatic abilities of SNCG both in vitro and in vivo using loss- and gain- of function approaches. Furthermore, the mechanisms of SNCG overexpression were examined by human phospho-kinase array kit and western blot analysis. Results Clinically, the expression of SNCG was significantly upregulated in ovarian cancer compared with the borderline and benign tumor, normal ovary, and fallopian tube. Notably, the high level of SNCG correlated with high-risk clinicopathologic features and showed poor survival for patients with HGSOC, indicating an independent prognostic factor for these patients. Functionally, we observed that overexpression of SNCG promoted cell proliferation, tumor formation, migration, and invasion both in vitro and in vivo. Mechanistically, we identified that SNCG promoted cancer cell metastasis through activating the PI3K/AKT signaling pathway. Conclusions Our results reveal SNCG up-regulation contributes to the poor clinical outcome of patients with HGSOC and highlight the metastasis-promoting function of SNCG via activating the PI3K/Akt signaling pathway in HGSOC.

Hepatitis B virus covalently closed circular DNA in the serum of patients with hepatitis B, peripheral mononuclear cells (PBMC) and liver tissue distribution.Serum HBV DNA10(5) copies/ml 50 cases of hepatitis B patients, serum HBV DNA10(5) copies/ml 30 cases of hepatitis B patients, patients with fatty liver (hepatitis B) 20 cases, using real-time quantitative polymerase chain reaction for detection of serum, and liver tissue in PBMC HBVcccDNA the existence.Of 50 serum HBV DNA10(5) copies/ml cccDNA the serum specimens were 28 cases, 56% detection rate, 29 cases were PBMC HBVcccDNA, 58% detection rate, liver tissue HBVcccDNA were 44 cases, 88% detection rate, serum, the PBMC were detected in liver tissue were significant differences in P0.005, compared serum PBMC were no significant differences in P0.005. 30 serum HBV DNA10(5) copies/ml the serum specimens, PBMC cccDNA detected two cases were 6.67% detection rate, liver tissue cccDNA were six cases 20% detection rate, serum, PBMC, were among the liver tissue was not significantly different P0.005. 20 in the serum of patients with fatty liver, liver tissue in PBMCwere not detected HBVcccDNA.HBVcccDNA mainly in the liver of patients with hepatitis B, hepatitis B patients and also cccDNA PBMC in the presence of liver tissue but a few of many.

The change in the UV-absorption spectrum and fluorescence spectrum of acridine orange(AO) due to the addition of surfactant dodecyi benzene sulfonic acid sodium sait (SDBS) and bovine serum albumin(BSA) was studied. Meanwhile, the effects of the in situ formed AOAO dimer in SDBS as a fluorescence probe and BSA were discussed. A new method for the determination of BSA using fluorescence is presented. The results indicate that the method is sensitive and rapid. The linear range of determination is 0-4. 17 x 10(-7) mol x L(-1). The relative standard deviation is 1.9%, and the detection limit is 8.73 x 10(-10) mol x L(-1).