0.05),but there were significant differences in liver function and prothrombin activity between the two groups(P

The receptor-interacting protein (RIP) has been identified to play a critical role in necroptosis, which is an inflammatory form of programmed necrosis in trauma, ischemia/reperfusion (I/R), and systemic inflammatory response syndrome (SIRS). Ripoptosome, a newly defined intracellular signaling complex with essential molecule of RIP1, can switch cell death mode between apoptosis and necroptosis. Based on molecular mechanism of RIP-dependent cell death and inflammation, with the understanding of the mechanisms of RIP-dependent apoptosis/necroptosis and its role in inflammation was summed up, and it was found that RIP plays a crucial role in regulating programmed cell death and inflammation. Therefore, further advances in understanding the mechanisms of necroptosis would be important in order to manipulate programmed cell death for therapeutic purposes in I/R injury, trauma, SIRS, and tumor.

Objective To study the effect of TMB 8 on cerebral blood flow(CBF) of focal cerebral ischemia in the rats.Methods CBF in the middle cerebral artery occlusion after the middle cerebral artery occlusion was measured by a Laser Doppler Flowmeter. TMB 8 was administered 30 min before occlusion and 20 min after occlusion respectively.Results CBF was reduced quickly. TMB 8 0.5,1,2 mg/kg was administered 30 min before occlusion of the middle cerebral artery.The dosage inhibited the reduction of CBF,20 min after occlusion, CBF was increased by TMB 8 1 mg/kg significantly.Conclusion TMB 8 could prevent and treat the reduction of CBF in focal cerebral ischemia of MCAO in the rats,and improved the supply of blood in ischemic area.

Objective To measure changes of definitive volume of rebuild CT image in three dimensional conformal radiotherapy (3DCRT) treatment planning system (TPS) under different scanning and observing conditions, which may provide a reference in selecting proper condition of scanning and observing, delineating target volume, and delivering treatment plan. Methods A self-made phantom was scanned under different CT scanning conditions, datas were imported to TPS, CT images were rebuilt in three dimensions under different observing conditions, and then the volumes of large, middle and small simulated tumors on CT images were compared with their real volumes. Results The volume defined by rebuilt CT imags in 3DCRT TPS varied according to different scanning and observing conditions. When scanning axial thickness was set at 10. 000 mm, errors of large, middle and small simulated tumor were - 13.60%, - 17. 68% and - 27. 53%, respectively. When 0. 625 mm was set, errors changed to -0. 50%, -0. 68% and -0. 81% ,respectively. When scanning pitch was set at 0. 562, 0. 938, 1. 375 and 1. 750, the errors were - 1.06%, - 1.09%, 5.52% and 4.75%, respectively. Extreme observing condition, window width and window level markedly increased errors of definitive volume of rebuilt CT images with a maximum of 80. 06%. Conclusions This study may provide clues in selecting scanning and observing condition, delineating target volume, and delivering treatment plan.

Objective:To explore the relationship between tobacco smoking and liver cancer risk.Methods:Cohort studies of cigarette smoking and risk of liver cancer were identified by searching MEDLINE and CBM databases from January 1989 to September 2009. Results from individual studies were combined synthetically by Meta analysis using R software and Meta package. Results:A total of 19 articles were included in our analysis. The cohort totally included 3 023 558 followed-up persons and 9 525 cases of liver cancer patients. The pooled relative risk (RR) of liver cancer was 1.49 (95%CI: 1.17-1.92) for smokers compared with non-smokers. The results showed a statistically moderate association between tobacco smoking and the risk of liver cancer. Subgroup analysis indicated that the pooled RRs for smoking were 1.53(95%CI : 1.29-1.83)for male smokers and 1.70(95%CI :1.17-2.48)for female smokers, respectively.Conclusion:Tobacco smoking is a risk factor for liver cancer in both males and females.

The incidence of candidiasis caused by Candida albicans has increased dramatically in recent years. With the widespread use of antifungal agents, the emergence of drug resistant strains pose a major challenge to drug treatment. The overexpression of membrane proteins functioning as drug efflux pumps is one of the main mechanisms for multidrug resistance of Candida albicans. Membrane transporters associated with drug resistance in Candida albicans are reviewed in this article.

Objective To evaluate recombinant adenovirus microspheres encapsulated with antisense MRP(as-mrp) on reversion of hepatocellular carcinoma.Methods The rats were divided randomly into 5 groups:control group;hepatic arterial injection of normal saline group,microspheres carrying no viruses group,rAdV carrying as-mrp group,and microspheres with encapsulation of as-mrp rAdV(MER) group.The theraputic effect were observed.Results The tumor growth inhibition and the mean life time in MER group were superior to than of other 4 groups(P

Cap1p, encoded by CAP1, is a basic region-leucine zipper (bZip) transcription factor in Candida albicans. It has been proven to play important roles in both drug resistance and oxidative stress. Within the AP-1 family, Cap1p belongs to the same subgroup which also includes Yap1p, Yap2p, and Pap1p. The function of Cap1p is regulated by a nuclear localization mechanism. In recent years, some target genes of Cap1p have been discovered and the differences as well as similarities between Cap1p and Yap1p have been revealed. However, the role of Cap1p in the drug resistance of Candida albicans still needs to be further investigated. Currently drug resistance and oxidative stress are the 2 focuses in the research of fungal pathogens, making Cap1p very important in the future study. The authors have been involved in Cap1p research for a long time and this review introduces the current progress in the area.

Objective To investigate the effects of GGNBP2 on proliferation,migration and invasion of human gli-oma U251 cells and the potential mechanism. Methods U251 glioma cells were transfected with lentiviral vector carrying GGNBP2 to establish a stable overexperssion of GGNBP2 in U251 cell line. After verification of the efficiency of transfec-tion by real-time PCR, Western Blot, PCR and CCK-8 were applied to detect the proliferation of U251 cells. The Tran-swell chamber assay was applied to measure the migration and invasion of human U251 glioma cells. Western blot was applied to measure protein levels of AKT, p-AKT, PCNA and MMP9. Result The stable U251 glioma cell line overex-pressing GGNBP2 was successfully established. Compared with the control group, overexpression of GGNBP2 significant-ly inhibited the proliferation(P<0.05),invasion(57±6 vs. 203±6,205±7,F=512.4,P < 0.05)and migration (74±7 vs. 254±14,248±13,F=242.5,P<0.05) of U251 cells. The protein expression levels of p-AKT (F=45.4, P<0.05), PCNA (F=348.5, P<0.05) and MMP-9 (F=88.7, P<0.05) in GGNBP2 group were markedly decreased compared with the control group. Conclusion GGNBP2 may suppress the proliferation, invasion and migration of glioma though down-regulation of p-AKT, which in turn inhibits PCNA and MMP-9 expression.

Objective:To investigate the effect of rapamycin on cell growth and migration of gallbladder cancer GBC-SD cells, and to discuss its potential in clinical therapy of gallbladder cancer. Methods: Proliferation of GBC-SD cells treated with different concentrations of rapamycin (12.5, 25, and 50 mmol/L) was examined by MTT assay. Cell cycle distribu-tion and apoptosis of GBC-SD cells treated with different concentrations of rapamycin were determined by flow cytometry. Migration ability of GBC-SD cells was assessed by Transwell assay. The expression of mTOR (mammalian target of rapam-ycin) and its phosphorylation in GBC-SD cells were examined by Western blotting assay. Results: Rapamycin significant-ly inhibited the phosphorylation of roTOR, but had no influence on the expression of roTOR in GBC-SD cells. Rapamycin significantly inhibited the growth of GBC-SD cells in a dose-dependent manner (P < 0.01). Raparnycin induced apoptosis of GBC-SD cells and arrested them at the G_1/S phase. Furthermore, rapamycin also significantly suppressed migration of GBC-SD cells as showed by Transwell assay (P < 0.01). Conclusion: Rapamycin can remarkably inhibit the growth and migration of gallbladder cancer cells, probably by inhibition of p-roTOR pathway, induction of apoptosis and cell cycle ar-rest of gallbladder cancer cells.