AIM To analyze the effects of glycyrrhetic acid (GA) on c-fos expression and cell proliferation in rat vascular smooth muscle cell (VSMC), and to figure out the mechanisms of binding GA to angiotensin Ⅱ(AⅡ) receptor. METHODS Primary cell culture of rat VSMC, Northern blot, TdR incorporation DNA assay and MTT assay were used in this study. RESULTS ① GA at both low (1?10 -9 mol?L -1) and high concentration (1?10 -5 mol?L -1) quickly induced c-fos expression in VSMC. Sar-AⅡ(1?10 -5 mol?L -1)inhibited both GA induced and AⅡ (1?10 -5 mol?L -1) induced c-fos expression. GA enhanced AⅡ induced c-fos expression at both low and high concentration in VSMC. ② Low level of GA stimulated the proliferation of VSMC. This stimulatory effect decreased with increasing GA concentration, and changed to be inhibitory at high concentration of GA. Not only did Sar-AⅡ eliminate the stimulatory effect of low concentration of GA on cell proliferation, it also eliminated the inhibitory effect of high concentration of GA. Low concentration of GA enhanced the stimulation of AⅡon cell proliferation, while the inhibitory effect of high concentration of GA on cell proliferation was relieved by adding 1?10 -7 mol?L -1 AⅡ. CONCLUSION This study suggests that GA activates transcription factor c-fos and promotes the proliferation of VSMC. GA may exert its effects on cells through AT 1 receptor since it induces similar changes as AⅡ and its effects can be inhibited by AT 1 receptor antagonist.

Objective In this paper,major issues for all those who have been selected in China national treatment program for patients with chronic Keshan disease (CNTP-CKD) were uncovered through evaluation of the annually reported data from participating provinces,in order to improve the performance quality of the program.Methods The datasets 2005-2012 were merged after cleaning them,and the composition of the treated patients was statistically analyzed,including gender and age distribution,diagnosis evidence for chronic Keshan disease (ECG,cardiothoracic ratio by X-ray,heart function grade of NYHA),and proportion of cases who had received treatment more than once.Results ①A total of 2 649 patients participated in the treatment,of them 1 115 patients were males accounting for 42.1％ (1 115/2 649),1 534 patients were females accounting for 57.9％ (1 534/2 649).Age of the patients were mainly distributed in 41 to 70 years old,and 24 CKD patients under 10 years accounting for 0.9％ (24/2 649).②2 313 cases of the involved patients were diagnosed with sufficient evidence,accounting for 81.9％ (2 313/2 823) and 121 cases with full misdiagnosis,accounting for 18.1％ (121/2 823).③There were 881 patients been treated for more than once,accounting for 38.3％ (881/2 301) of the number of treatment.Conclusions ① Diagnosis for CKD remains a key problem,suggesting that medical record for each patient diagnosed by province-level doctors' needs to be built up as early as possible.The rate of patient treatment for more than once is low which is not beneficial to the patients.② Treatment period for CKD patients is highly recommended to expand to at least one year,and the disease should be enrolled in the free cost list of the new rural cooperative medical system (NCMS).

Objective:To optimize the formulation of HA-CA liposomes and to study the anti-tumor effect of HA-CA liposomes on uterine cervical carcinoma mice.Methods:The methods of preparing HA-CA liposomes were screened,and the optimal fomulation was selected by the orthogonal design experiment with the the phospholipids/cholesterol ratio,the drug/lipids ratio and the pH value of PBS buffer was 7.4 as entrapment enfficiency was the index.The release of HA-CA liposomes was studyed by dialysis bag method.Uterine cervical carcinoma cells were inoculated subcutaneously into right axillary ofBal b/c mice,after continuous treatment of 14 d,we weighed the tumor and calculated the rate of tumor growth inhibition.Results:HA-CA liposomes were prepared by thin film hydration methods.The optimal parameters were as follows:the phospholipids/cholesterol ratio was 4∶1,the drug/lipids ratio was 1∶ 30,the pH value of PBS buffer was 7.4.The release curve of HA-CA liposome and CA liposome was basically the same,both of which a sustained-release efficacy.The cumulative release of HA-CA liposomes and CA liposomes were 78.39％ and 83.01％ at 48h.The inhibition rate of HA-CA liposomes on U14 cervical cancer mice was 60.39％ and significantly higher than that of positive control group,which was higher than that of CA and CA liposomes.Conclusions:HA-CA liposomes can significantly inhibit the effect of U14 cervical cancer nude mice higher than that of CA and CA liposomes owe to the modification of the active target ligand HA.

Objective To investigate the role of interferon regulatory factor-1 (IRF-1) in liver ischemia/reperfusion (IR) injury and its underlying mechanism,and identify effective managements in alleviating liver IR injury.Methods Three groups of mice models with liver IR injury were well established,including control group (S),warm liver IR injury group (IR) and recombinant IRF-1 group (IRF-1).The levels of mRNA and protein,liver function and pathological changes of liver tissue were detected in group S and group IR.Additionally,the marker of IRF-1,p-Stat1,p-P38,PARP1 and Caspase-3 were measured and PCNA expression was determined in group IR and group IRF-1 mice with 6-hour liver IR injury.Results IRF-1 mRNA and protein and the levels expression of proteins were significantly elevated with peak occurred after 6-hour IR injury,which was statistic difference compare to the group S (t2h =-3.512,t6h =-4.247,t12h =-4.088,t24h =-3.851;P ＜ 0.05).Serum ALT and AST of mice detected in group IR were higher than group S at all endpoints (tALT =4.931,4.592,4.277,4.809;tAST =4.980,4.617,4.336,4.915;P ＜ 0.05).Furthermore,pathological damage change was more distinct compared with group S.The elevated levels of IRF-1,p-Statl,p-P38,PARP1 and Caspase-3 and decreased PCNA expression were determined in mice models with recombinant IRF-1 intervention.Conclusion IRF-1 expression could be closely correlated with liver IR injury,and its underlying mechanism may be attributed to activation of JNK MAPK protein and inhibition of PCNA expression.

Objective:To explore the role CD4+CD45RO+memory T cells in the pathogenesis of Hashimoto's thyroiditis (HT) by detecting the percentages of CD4+CD45RO+ memory T cells in peripheral blood mononuclear cells in peripheral blood of newly diagnosed HT patients. Methods:53HT patients and 43 matched healthy controls (HC) were included in this study. According to the thyroid functions,HT patients were divided into euthyroid subset(HT-A,n =15) ,subclinical hypothyroidism(HT-B,n=14) and overt hypothyroidism subset (HT-C,n=24). The percentages of CD4+CD45RO+memory T cells in PBMCs,as well as the level of serum IFN-γ and IL-17,and thyroid functions,and the titers of thyroid-specific autoantibodies (TPOAb,TgAb) were respectively detected by flow cytometry,ELISA,and ECLIA. Results:The percentages of CD4+CD45RO+ memory T cells in PBMCs,as well as the level of serum IFN-γ and IL-17,the titers of TPOAb,TgAb were all significantly higher than that in HC(P<0. 01). Bivariate correlation revealed that the percentages of CD4+CD45RO+ memory T cells positively correlated with the level of serum IFN-γ,TPOAb and TgAb(P<0. 01,P=0. 015,P<0. 01) in HT patients. Conclusion:The significant increase of CD4+CD45RO+memory T cells in peripheral blood of patients with HT suggested a role of CD4+CD45RO+ memory T cells in the pathogenesis of this disease.

Objective To evaluate the effects of celecoxib on tumor growth,COX-2 and survivin expressions and angiogenesis in nude mice. Methods Xenograft animal model was established by injecting human colon cancer HT-29 cells into the BALB/c nude mice subcutaneously. Fifty mice were randomly divided into 4 groups 16 d after injection:control group,celecoxib group(receiving 25,50,75,100 mg?kg-1?d-1 for 35 d). Tumor volumes were measured every week. The expression level of COX-2,survivin and the microvessel density (MVD) of the xenograft tumor tissues were measured by immunohistochemistry,and mRNA level of VEGF by RT-PCR. Results Celecoxib at dose of 25,50,75 and 100 mg?kg-1?d-1 inhibited the tumor volume by 34.94%,39.20%,53.50%,59.20% respectively,and showed more effective in suppressing the tumor growth than the control group(P

Objective To study blood type B antigen elimination with α-galactosidase in human liver tissue,and discuss the feasibility of blood type conversion in human liver.Methods The liver specimens from patients with blood type B in liver transplantation were collected,and an in vitro liver perfusion model was established.The in vitro livers were perfused with UW solution +/-α-galactosidase.The effect of enzyme in B antigen of human liver were analyzed by immunofluorescence.Results With UW solution containing α-galactosidase to perfuse the in vitro livers,immunohistochemistry showed the level of blood type B antigen in liver was significantly reduced after hypothermic perfusion and preservation.The B antigen level in 1 h perfusion was reduced to approximate 58％ of this figure prior to perfusion,in 2 h was 10％,and in 4 h was 4％.Among the different intervals,the blood group antigen levels showed significant differences (P ＜ 0.05).In the control group,the blood group antigen levels showed no obvious change on statistical analysis.Conclusions α-galactosidase was effective to clear blood type B antigen in isolated liver tissue.In the experimental group,Although the B antigen did not fall to a undetectable level,liver blood type conversion from B→O remains a promising potential which has been meaningful for related researches on blood type conversion of human organs.

In China medical university 8 weeks early exposing to scientific research have been arranged for the students on seven-year program of clinical medicine. The purpose is to let the students understand scientific research procedures based on the tutor's research project. The students gain great achievements. The result of questionnaire shows that the attitudes of the students are positive and 81% of them are satisfied in general. The paper also summarizes the experiences of the practice.

Vascular calcification is a complex pathological process involving multiple factors.The latest research has confirmed that mitochondria plays an important role in the process of vascular calcification. Inorganic phosphate treatment, oxidative stress, autophagy, apoptosis, power related protein, mitochondrial DNA damage can affect the process of changing the calcification of the arterial by affecting mitochondrial function. So we will review the role of mitochondria in vascular calcification, further study the molecular mechanism of vascular calcification, and provide a theoretical basis for the formulation of new treatment strategies.

Objective To research the combined prognostic utility of NT-proBNP and hs-CTNI in NSTE-ACS risk stratification and early intervention therapy .Methods A total of 245 NSTE-ACS patients were divided to 4 groups(Aa ,Ab ,Ba ,Bb groups) ac-cording to immediate admission NT-proBNP and hs-CTNI .Patients were accepted percutaneous coronary intervention (PCI) ,coro-nary artery bypass grafting and conservative treatment were taken 6 months follow-up .Results The heart failure incidence of Aa group was significantly higher than Ba group(P<0 .05) .6 patients happened left main lesion or multivessel lesion in Aa group were obviously higher than other groups .The incidence of Bb group accepted PCI was obviously higher than Aa group (P<0 .05) .Bb group patients were accepted PCI earlier than other groups ,there was no significance(P>0 .05) .In 6 months follow-up ,5 patients died and 10 patients accepted revascularization again because of severe angina and AMI .Conclusion In NSTE-ACS patient ,NT-proBNP and hs-CTNI elevation was closely related with severe coronary lesions and worse prediction ,which could undergo early in-tervention therapy .