Objective To observe the effect of Chinese medicine of Gukang(GK) on bone mineral density(BMD) in osteoporosis rats.Methods Seventy-two female SD rats were randomized into 6 groups: pseudo-operation group,model group,nilestriol group(in the dose of 1mg/kg),and high-,middle-and low-dose GK groups(9.6,4.8 and 2.4 g?kg-1?d-1 respectively).Rat models of osteoporosis were induced by removal of bilateral ovaries.Three months after operation,the rats were given the corresponding medicine according the experimental design.After treatment for 3 months,in-vivo BMD as well as the in-vitro BMD in the isolated left femur and tibia was detected with dual energy X-ray bone densitometer.Results The in-vivo general BMD and lumbar BMD of the model group were decreased(P

Objective To study the effect of integrated tradition and western medicine on unstable angina.Methods Sixty-six patients with unstable angina were randomized into two groups:control group treated only with routine therapy(n=33) and experiment group treated with routine and jia jian luang gan jian therapy(n=33).The difference of EKG,symptoms and clinic comprehensive evaluation between before treatment and after-3-week-treatment were compared.Results The rate of symptoms and ECG improvement was higher in experiment group than control group(94% vs 73%;73% vs 45%).The difference of clinic comprehensive score between before treatment and after 3 weeks treatment was significantly higher in experiment group.Conclusion The treatment of integrated tradition and western medicine on patients with unstable angina is more effective.

BACKGROUND:Transgenosis of basic fibroblast growth factor (bFGF) gene has been successfully performed into the muscle satellite cells of rat extraocular muscles in the previous study of the research group, proving that bFGF could express in the myoblasts of extraocular muscles, also promote cell proliferation and differentiation.OBJECTIVE: To further investigate the methods for regulating the expression of the bFGF in myoblasts following transfection. METHODS: Target gene bFGF was connected with inducing expression vector pcDNA4/T0/myc-His?A, followed by masculine clone sequencing identified by colony PCR and enzyme digestion, EcoR I and Hind III restriction enzyme digestion, as well as Xho I single enzyme verification. C2C12 myoblasts antibiotics sensitivity was screened and finally defined. By use of lipofection transfection technology, cell lines where C2C12 stably expressed pcDNA6/TR were estabolishd and then identified by Western blot. The pcDNA4/TO/myc-His?A-bFGF was transfected into pcDNA6/TR- C2C12 cells. The bFGF expression and secretion in C2C12 cells following tetracycline-induced pcDNA4/TO/myc-His?A-bFGF transfection were determined by immunofluorescence and Western blot, the controls were established.RESULTS AND CONCLUSION: ① The conjunction between the bFGF and inducing expression vector pcDNA4/TO/myc-His?A was proved successfully by sequencing comparison, double digestion and single digestion. ②The minimal lethal concentration of blasticidin to C2C12 cells was 10 mg/L, while that of zeocin was 750 mg/L. ③ The pcDNA6/TR-C2C12 cell lines were established correctly. ④ The myoblasts treated by tetracycline and transfected with pcDNA4/TO/myc-His?A-bFGF were positive for gene expression, those untreated exhibited a negativity; bFGF protein could be produced in myoblasts treated by tetracycline and transfected with pcDNA4/TO/myc-His?A-bFGF, the production reached a peak at 24 hours, while those untreated can not produce bFGF protein. Results suggest that the bFGF expression in the myoblasts can be controlled by tetracycline inhibition and regulatory systems.

AIM　To improve the treatment efficacy of anti-tumor drug mitoxantrone, the conjugation of mitoxantrone-loaded nanospheres and anti-C-erbB-2 monoclonal antibodies were prepared. METHODS Mitoxantrone-loaded nanospheres were prepared with emulsion-heating solidification technique. A heterobifunctional reagent, N-succinimidyl 3-(2-pyridyldithio) propionate (SPDP), was used as the crosslinker of mitoxantrone-loaded nanospheres and anti-C-erbB-2 monoclonal antibodies; pharmaceutical properties of immunonanocapsuls were studied; the conjugates of nanospheres and monoclonal antibodies was confirmed with immunological methods such as slide agglutination test, fluorescent immunossay and rosset formation test, fluorescent staining and scanning electron microscope. RESULTS　Mitoxantrone-loaded nanospheres were spherical, with smooth surface and median diameter of 0.665 micron. When stored at 3-5, 20-25 and 37℃, RH 75% for three months, the appearance, morphology, size distribution, drug loading and in vitro release characteristics showed no significant change and the stability was satisfactory. The size analysis demonstrated that there was no obvious increase in the particle size of nanoparticles after conjugation. Immunological tests indicate highly selective binding of antibody-targeted nanospheres to C-erbB-2-overexpressing cells SK-BR-3. CONCLUSION　The conjugation of mitoxantrone-loaded nanospheres and anti-C-erbB-2 monoclonal antibodies can keep the activity of anti-C-erbB-2 and increase the therapeutic efficacy of anti-mammary cancer drugs.

Objective To compare the difference of serum heme oxygenase-1 (HO-1) and carbon monoxide(CO) levels between the patients with coronary heart disease(CHD) caused chronic heart failure(CHF) and CHD patients with normal cardiac function,and further to explore the protective mechanism of HO-1/CO system during the pathogenesis process of CHF.Methods Ninety-one patients with CHF were selected as the observation group and 72 CHD cases with normal cardiac function were taken as the control group.The concentration of HO-1 was determined by ELISA arid the Chalmer S method was used to detect serum CO concentration.The general clinical data of the two groups were recorded by the using the heart failure questionnaire.And the liver and kidney functions,blood lipids,NT-proBNP,BNP and cardiac echocardiography examination were performed.Results The serum HO-1 level in the observation group was (8.13±0.27)ng/mL,which was higher than (2.80±0.52)ng/mL in the control group;the CO level in the observation group was (0.35±0.06)mg/L,which was lower than(0.59±0.07)mg/L in the control group,the difference was statistically significant(P＜0.01);the HO-1 level in the observation group was gradually increased with the increase of cardiac function grade (P＜0.01);while the CO level was decreased with the increase of cardiac function grade (P＜0.01).Conclusion The serum HO-11evel in the patients with CHF is highly expressed with the heart failure aggravation;endogenous CO is gradually decreased due to consumption after cardiac failure aggravation.

Objective:To explore the effect of remote ischemic post-conditioning (RIPoC) on oxidation/reduction response, energy metabolism and inlfammatory reaction of ischemic myocardial tissue in rats with ischemic reperfusion (IR) injury.
Methods:IR model was established by 30 min left anterior descending (LAD) artery occlusion followed by 120 min reperfusion, conditioning was defined as 3 cycles of 30 seconds ischemia followed by 30 seconds reperfusion in adult rats. The rats were divided into 5 groups:①ischemic pre-conditioning (IPC) group, the rats received the conditioning prior to IR treatment,②ischemic post-conditioning (IPoC) group, the rats received 30 min LAD occlusion followed by conditioning at the beginning of 120 min reperfusion, ③ remote ischemic post-conditioning(RIPoC) group, the rats received 30 min LAD occlusion, followed by femoral artery conditioning at the beginning of 120 min reperfusion, ④ IR group, ⑤ Sham group. n=8 in each group.Ischemic myocardial tissue was collected at the end of experiment, superoxide dismutase (SOD) activity was assayed by xanthine oxidase method,malondialdehyde (MDA) content was examined by thiobarbituric acid method, myeloperoxidase (MPO) activity was determined by chemistry colorimetric method, adenosine triphosphate(ATP)amount was measured by bioluminescence method;expressions of myocardial stromal cell derived factor-1 (SDF-1) and vascular endothelial growth factor (VEGF), mitochondrial function related genes Ndufa2, Ndufa4, Cox4il and Cox7a2 were evaluated by real time quantitative PCR.
Results:In IPC, IPoC and RIPoC groups, the ischemic myocardial tissue had increased SOD activity and ATP amount, decreased MDA content and MPO activity; induced expressions of SDF-1, VEGF, mitochondrial function related genes Ndufa2, Ndufa4, Cox4il and Cox7a2.
Conclusion:RIPoC may increase anti-oxidation/reduction response, protect energy metabolism and reduce inlfammatory reaction in ischemic myocardial tissue, the effect was similar to pre-conditioning and post-conditioningin rats with IR injury.

AIM: This study was designed to investigate the inhibition of tanshinone ⅡA on C6 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation of C6 cultured with tanshinone ⅡA at different concentrations. The effects of tanshinone ⅡA on cell cycle of C6 were observed by FCM. The change of DNA was observed by Sepharose electrophoresis. The expression of proto-oncogenes c-myc was measured by RT-PCR. RESULTS: The proliferation of C6 was obviously inhibited by tanshinone ⅡA in a dose-dependent manner. The outcome of FCM showed that the apoptotic cell rate was 7.7%, when cultured with tanshinone ⅡA at 1.0 mg/L for 3 days. The apoptotic cell rate was 21.6%, when cultured with tanshinone ⅡA at 2.0 mg/L in 3 days. CONCLUSION: Tanshinone ⅡA inhibits the proliferation of C6 cells, induces apoptosis and inhibits the expression of proto-oncogene c-myc.

OBJECTIVE:To analyze the utilization of drugs in children with ventricular septal defect(VSD) undergoing operation.METHODS:The medical orders of 120 VSD children patients in our hospital in 2005 were analyzed retrospectively.RESULTS:The per capita drug cost was(3 067.20? 325.04) yuan,accounting for 9.52% of the total medical cost.Circulatory system drugs and antibiotics were the chief categories.Leading the first 3 places in terms of DDDs were cefuroxime,vecuronium bromide and furosemide,respectively.CONCUSION:The drug cost for VSD children patients was relatively low and reasonable.

OBJECTIVE:To investigate the preparation technic and method of quality control of Xinyoukexing tincture(XYKX) METHODS:To determine the content of Valaciclovir by spectrophotography,and podophyllotoxin by dual-wavelength spectrophotography RESULTS:In the range of 14 88～34 72?g/ml,the Valaciclovir concentration in XYKX was in direct proportion to the absorption at 310 4nm,C=44 5 905A+1 7 556,r=0 9 998 In the range of 17 50～50 12?g/ml,the podophyllotoxin concentration in XYKX was in direct proportion to the absorption at 292nm,C=97 7 981Ap292+1 3 614,r=0 9 999,AP292=As292-As325 CONCLUSION:The preparation technic of XYKX is simple and the method of quality control is feasible

Objective To investigate the expression of poly (ADP-ribose) polymerase-1 (PARP-1 ), cytokeratins (CK) 7/20, and p53 in patients with Barrett's esophagus and esophageal adenocareinoma,and to evaluate their significance. Methods Expression of PARP-1, CK7/20 and p53 were determined by immunohistochemistry in 108 patients (including 40 Barrett's esophagus, 28 esophageal adenocarcinoma and 40 cardiac mucosa). Results The expression of PARP-1 was found in Barrett's esophagus, esophageal ade-nocarcinoma and cardiac epithelium with a significantly higher level in esophageal adenocarcinoma than the other two groups (P <0. 01 ). CK7/20 was expressed in much of intestinal metaplasia, part of cardiac epi-thelium and adenocarcinoma cells. The positive expression of p53 was observed in all three groups, and it was significantly higher in adenocarcinoma group than in other two groups (P < 0. 05 ). PARP-1 expression is highly correlated with that of p53 in Barrett's esophagus ( r= 0.49, P < 0.01 ). Conclusion CK7/20 is a sensitive but less specific indicator for intestinal metaplasia. Both PARP-1 and p53 are involved in the patho-genesis of esophageal adenocarcinoma and might help to determine the risk of Barrett's esophagus developing into esophageal adenocarcinoma.