ObjectiveTo explore the molecular mechanism that LRIG1 inhibits signal transduction system of epidermal growth factor receptor(EGFR)by investigating the role of LRIG1 in glioma.MethodsThe plasmid pcDNA3.1-LRIG1 was transfected into primary glioma cells by Lipofectamine.Then,the changes of LRJG1 and EGFR in the transfected glioma cells were measured by RT-PCR and Western blot,and the cell proliferation and apoptosis were analyzed by MTT and flow cytometry.ResultsThe expression levels of LRIG1 mRNA and protein in the glioma cells transfected with pcDNA-LRIG1 were significantly higher than those of control group and pcDNA3.1 transfected glioma cells,while those of EGFR mRNA and protein were significantly lower.The expression of PKC? and Bax was up-regulated,while the expression of bcl-2 was down-regulated.The growth of glioma cells was inhibited and their apoptosis was obviously enhanced.ConclusionBy participating the construction of the negative feedback loop of EGFR,LRIG1 inhibits the occurrence and growth of tumor through several pathways.

Objective To investigate the expression of apoptosis-related proteins in rat cerebral cortex following traumatic brain injuries(TBI)and discuss the role of oxygen free radical-mitochondria signal pathway in Edaravone treating TBI.Methods A total of 180 male adult Sprague-Dawley rats were randomly divided into TBI group,Edaravone treatment group and control group.Each group was divided into six subgroups at 1,3,6,24,48 and 72 hours after TBI.Edaravone treatment group was injected with Edaravone(10 mg/kg)and the other two groups injected with the same volume of 0.9%normal saline.The pathological change in the rat cortex following TBI was observed with HE staining.At different time points,the expressions of Cytc,Bcl-2 and Bax in rat cortex as well as cell apoptosis and MDA change were observed by means of immunohistechemistry,TUNEL and TAB.Results HE staining showed scattered degenerated and necrotic neurous in cerebral cortex six hours after neuron injury,which peaked at 24 hours.Compared with control group,intermediate product MDA of free radical was increased six hours after TBI and peaked at 48 hours in Edaravone treatment group,which was lower than TBI group especially at 24,48 and 72 hours(P＜0.05).Compared with control group,the immunity reaction of Cytc positive cells inereased at six hours and peaked at 24 hours in TBI group,with statistical difference at 3,6,24,48 and 72 hours(P＜0.05).Compared with TBI group,the immunity reaction of Cyte positive cells was decreased obviously at 24,48 and 72 hours in Edaravone treatment group.Hyperexcitability of Bcl-2 after TBI reached peak at 3 hours and decreased gradually.But the expression of Bax was increased gradually after TBI and peaked at 48 hours,when Bax/Bcl-2 reached peak too.Folowing TBI,TUNEL positive cells increased gradually and reached peak at 48 hours,with mainly type Ⅰ TUNEL cells before 24 hours and typeⅡTUNEL cells after 24 hours.Conclusions There exist necrosis and apoptosis of nerve cells in cortex after TBI,especially apoptosis.Oxygen free radical mitochondria is one of the signal transduction pathways of nerve cell apoptosis following TBI.Edaravone exerts certain therapeutic effect on TBI.

Objective:To investigate whether celastrol can increase the cytotoxic activity of γδ T cells against osteosarcoma (OS) cells line HOS through TRAIL way. Methods:The death receptors 4/5 (DR4/5) protein levels in the OS cell lines HOS was in-vestigated by Western blot analysis. Zoledronate ( ZOL) was used to induceγδT cells from PBMCs of healthy volunteers.γδT cell cy-totoxicity against HOS cells was investigated by a standard lactate dehydrogenase release assay ( LDH ) . Results:Celastrol increased DR4/5 protein expression in HOS ( P<0. 05 ) .γδ T cells from PBMCs of healthy volunteers showed cytotoxicity against HOS ( P<0. 05). Following co-culture with HOS pre-treated with celastrol (1 μmol/L) for 24 h,γδ T cells showed significantly higher cytotoxicity against HOS (P<0. 05). The induction of DR4/5 molecules increased lysis of HOS by γδ T cells which was abolished by addition of a blocking TRAIL antibody. Conclusion:Celastrol can enhance γδ T cells'cytotoxic activity against OS cells line HOS through TRAIL way.

Ischemic stroke has the characteristics of high morbidity, high disability rate, and high fatality rate. There is currently no effective rehabilitation treatment method. With the advancement of basic research and preparation technology of stem cells and the extensive development of animal experiments, stem cell transplantation has shown great potential for application in the treatment of ischemic stroke. This article elaborated on the mechanism, types and sources of stem cell transplantation and transplantation methods. By reviewing the research process of stem cells in ischemic stroke model, we can provide reference for clinical research of stem cell transplantation in the treatment of ischemic stroke.

Objective To investigate the risk factors associated with epididymitis after transurethral resection of prostate.Methods A retrospective analysis of 352 patients with benign prostatic hyperplasia (BPH) who underwent transurethral resection of prostate in X'an Aerospace General Hospital from January 2015 to December 2017 was performed.There were 14 cases of epididymitis and 338 cases of nonepididymitis.Measurement data were expressed as ((x) ± s),t test was used for comparison between groups;count data was expressed by rate (％),and chi-square test was used for comparison between groups.Univariate and multivariate logistic regression analyses were used for factors that may lead to post-urethral epididymitis.Results Univariate logistic regression analysis showed that preoperative leukocytic positive,urine glucose positive and prostate volume had significant effects on postoperative epididymitis (P ＜ 0.05).Multivariate logistic regression analysis showed that prostate volume increased (OR =0.182,P =0.005)was an independent risk factor for postoperative epididymitis.Conclusion The enlargement of prostate volume is an independent risk factor for postoperative epididymitis.For large-volume prostate surgery,the purpose of relieving obstruction can be achieved.