Objective To discuss the effect of interferon ?-2a on the radiosensitivity and cell cycle for nasopharyngeal carcinoma cell line CNE-I. Methods Interferon ?-2a was given by different concentration. Then the cells were radiated with X-ray (6?MV) and the cell survival rate was calculated. The change of cell cycle dynamics was measured with flow cytometry. Results The cell survival fraction was 0.62, 0.43 and 0.20 respectively after the interferon ?-2a was given by different concentration(0.5?106, 1.0?106 and 1.5?106?IU/L). The radiosensitization ratio was 1.16, 1.57 and 1.93 respectively. Compared with the control group, increasing cell percentage in G_1 and G_2+M phage and decreasing cell percentage in S phage were observed on 24 h after the interferon ?-2a(1?106?IU/L) was given(P

Differentiation strategy includes self examination on ability,location and intention,strengthening self rarity according to its own characteristics,and improving core competitive power.This article reviewed several related issues in R&D fields,and suggested to set up new evaluation systems which focus on discipline construction,scientific research output,classified evaluation and representative work.

The main purposes of translational Medicine is to break the barrier among the basic medicine,clinical medicine and drug R&D in order to establish direct and close connection and cooperation between them.However,so far almost in the world wide,translational medicine is still at the exploration stage and far away from the real transformation.This article reviewed the difficult position of translational medicine cooperation from the three aspects of cooperative resources,sponsor and domestic culture,and then suggested to promote clinical medicine research,set up new assessment systems which focus on classified evaluation and representative work,as well as create the culture of cooperation.

This paper analyzed the type and the discipline distributions of the research projects funded by NSFC between 2003~2007 in our university,the age group distribution,academic and professional title structure of the researchers in charge of these projects,finally discussed the insufficiencies of the scientific staff and put forward relevant countermeasures.

Objective To evaluate the role of pl20-catenin protein (p120) in mechanical stretchinduced transferring of E-cadherin to cytoplasm in mouse alveolar epithelial cells.Methods Experiment Ⅰ Mouse alveolar epithelial cells (MLE-12 cells) were seeded in 6-well cell stretch plates at a density of (1.0-1.5) ×106 cells/well and divided into 3 groups (n=12 each) using a random number table:control group (group C),cyclic stretch for 2 h group (group CS2) and cyclic stretch for 4 h group (group CS4).The cells underwent 20％ cyclic stretch at 0.5 Hz (stretch:intermittence =1 ∶ 1) for 2 and 4 h in CS2 and CS4 groups,respectively.The cells underwent no cyclic stretch in group C.The expression of p120,E-cadherin and phosphorylated Src kinase (p-Src) and expression of E-cadherin in cytomembrane and cytoplasma were detected by Western blot.Experiment Ⅱ MLE-12 cells were seeded in 6-well cell stretch plates at a density of (1.0-1.5)× 106 cells/well and divided into 4 groups (n =6 each) using a random number table:control group (group C),cyclic stretch group (group CS),p120 small interfering RNA (siRNA) transfection group (group p120 siRNA),and p120 siRNA transfection plus cyclic stretch group (group p120 siRNA+CS).The cells were transfected with scramble siRNA in C and CS groups,and 24 h later the cells underwent 20％ cyclic stretch for 2 h at 0.5 Hz (stretch:intermittence =1 ∶ 1) in group CS.The cells were transfected with p120 siRNA in p120 siRNA and p120 siRNA+CS groups,and 24 h later the cells underwent 20％ cyclic stretch for 2 h at 0.5 Hz (stretch ∶ intermittence =1 ∶ 1) in group p120 siRNA+CS.The expression of E-cadherin in cytomembrane and cytoplasm was detected by Western blot after the end of treatment in each group.Results Experiment Ⅰ Compared with group C,the expression of p120 and E-cadherin was significantly down-regulated,the expression of p-Src was up-regulated,the expression of E-cadherin in cytomembrane was down-regulated,and the expression of E-cadherin in cytoplasm was up-regulated in CS2 and CS4 groups (P ＜ 0.05).Compared with group CS2,the expression of p120 and E-cadherin was significantly down-regulated,the expression of p-Src was up-regulated,the expression of E-cadherin in cytomembrane was down-regulated,and the expression of E-cadherin in cytoplasm was upregulated in group CS4 (P ＜ O.05).Experiment Ⅱ Compared with group C,the expression of E-cadherin in cytomembrane was significantly down-regulated,and the expression of E-cadherin in cytoplasm was up-regulated in CS,p120 siRNA and p120 siRNA+CS groups (P＜ 0.05).Compared with group CS or group p120 siRNA,the expression of E-cadherin in cytomembrane was significantly down-regulated,and the expression of E-cadherin in cytoplasm was up-regulated in group p120 siRNA+CS (P＜0.05).Conclusion The degradation of p120 can promote mechanical stretch-induced transferring of E-cadherin to cytoplasm in mouse alveolar epithelial cells.

Objective To establish the in vivo models of adriamycin(ADR)-induced cardiotoxicity in rabbits, investigate the protective effect of oxymatrine (OMT) on ADR-induced cardiotoxicity, and explore the possible mechanism. Methods Twenty-six rabbits were randomly divided into ADR group (n=8, 2 mg/kg ADR), OMT group (n=5, 10 mg/kg OMT), ADR + OMT group (n=8, 10 mg/kg OMT was injected 30 min before ADR injection) and saline group (n=5, same quantity of normal saline), and rabbits in each group were infused with medicine or normal saline through ear marginal vein once a week for 8 weeks. The apoptosis of myocardial cells was detected by TUNEL methods, and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) was determined. Results After treatment, the body weight of ADR group was significantly lower than that of the other groups(P < 0.05), the activity of SOD and GSH-Px significantly decreased and the apoptosis index (AI) was significantly higher than that of the other groups(P <0.01). There were similar while minor changes in ADR + OMT group. There was no significant adverse effects in OMT group. Conclusion OMT protects heart from adriamycin-induced injury in rabbits, which may relate to the decrease in level of antioxidant and apoptosis of myocardial cells.

AIM:TostudythefunctionofmicroRNA(miR)-19aandmiR-92abyseed-targetinginhibitionin multiple myeloma cells and their signal pathways .METHODS:The experiments were divided into t-antimiR-19a group, t-antimiR-92a group, scramble control group and blank control group .The growth-inhibitory potencies were measured by MTT assay.The ability of cell colony formation was measured by cell colony formation assay .The ability of cell invasion was measured by Transwell experiment .The miR-19a and miR-92a target gene signal pathways were integrated by miRFo-cus software.RESULTS:MTT assay showed that t-antimiR-19a and t-antimiR-92a significantly inhibited the viability of multiple myeloma cells , and the best concentration and time were 0.5μmol/L and 48 h, respectively .The colony number in t-antimiR-19a/92a group was less than that in scramble control group .The transfection with t-antimiR-19a or t-antimiR-92a effectively decreased the cell invasion , as the relative invasion cell number was significantly decreased compared with scramble control group.miR-19a and miR-92a were involved in mTOR signaling, cell cycle and other cancer pathways . CONCLUSION:miR-19a and miR-92a cluster might be a potential target for therapeutic intervention in multiple myelo-ma.

Objecitv e To investigate the effects of a recombinant protein osteoclast inhibitory lectin related protein 2( OCILRP2)-Fc on LPS-induced endotoxemia by blocking OCILRP 2 signaling pathway and to in-vestigate the roles of OCILRP2 during inflammation.Methods Real-time PCR was used to detect OCILRP2 ex-pression at mRNA level in RAW264.7cells before and after in vitro stimulation with LPS.A mouse model of en-dotoxemia was established by intraperitoneal injection of BALB /c mice with a median lethal dose of LPS .Two hours prior to LPS treatment, mice were intraperitoneally injected with OCILRP2-Fc, human IgG or PBS, re-spectively .Several parameters including the survival rate of BALB/c mice with and without LPS treatment , spleen weight for arterial hyperemia analyzing , histopathological changes of lung and liver by HE staining , serum levels of inflammatory cytokines (IL-6, IL-12, TNF-αand IFN-γ)by ELISA , NF-κB activity by Western blot, were analyzed .Results Real-time PCR showed that LPS elevated in vitro OCILRP2 expression at mRNA level in macrophages (P<0.05).Upon the treatment of OCILRP2-Fc, BALB/c mice suffered from endotoxemia showed obviously increased survival rate , decreased spleen hyperemia , attenuated pathological injury of lung and liver, reduced levels of IL-6, IL-12, TNF-αand IFN-γin serum samples (P <0.05) as compared with mice treated with human IgG and PBS .LPS induced NF-κB p65 phosphorylation and IκB degradation were inhibited by OCILRP2-Fc treatment.Conclusion OCILRP2-Fc protects mice from endotoxemia by blocking OCILRP 2 signaling, which suggests that OCILRP2 plays an important role in LPS induced inflammation.

Objective:To investigate the expression and regulation of the platelet-activating factor receptor(PAF-R)in human keratinocytes.Methods:The expression of PAF-R in skin tissues and HaCaT cells was examined by immunohis-tochemistry.The expression of PAF-R in HaCaT cell mRNA level was detected by RT-PCR.The expression and regulation of PAF-R were measured by flow cytometry in HaCaT cells treated with various stimuli.Results:The expression level of PAF- R was very high in human keratinocytes,mainly located on cell membranes and cytoplasma.PAF-R also expressed on HaCaT cells transcription levels,and the tissue-type PAF-R mRNA was more than that of leucocyte-type PAF-R mRNA.PAF-R ex-pressed on both membrane and intracellar part of HaCaT cell,and the intracellular expression was about4.82times that of membrane expression.IFN-?and retinoic acid upregulated the membrane expression of PAF-R in HaCaT cell.Conclusion:Human keratinocytes can highly express PAF-R at cell,protein and transcription levels,and the expression characteristic can be regulated by some inflammatory factors,which indicates the PAF system may play an important role in the skin inflamma-tion. [

Acute Coronary Syndrome ; complications ; drug therapy ; Aged ; Hematoma ; complications ; Heparin, Low-Molecular-Weight ; adverse effects ; therapeutic use ; Humans ; Leg ; Male ; Thrombolytic Therapy ; adverse effects