AIM　To observe the protective effects of TGP on local cerebral ischemia. METHODS　The local cerebral ischemia in rat was made by middle cerebral artery occlusion(MCAO). The infraction weight was determined by NBT stain. SOD, MDA and apoptosis were determined with different method respectively. RESULTS　TGP 20 mg*kg-1 ip markedly improved the abnormal nervous symptoms, increased the SOD activity and reduced contentes of MDA in MCAO rat. TGP 20 mg*kg-1 ip significantly decreased the numbers of apoptotic cells in ischemic cortex. CONCLUSION　TGP has protective effects against cerebral infarction, and its mechanism may be related to anti-apoptosis and free radical.

Objective To investigate the diagnostic value of serum tumor markers carcinoembryonic antigen (CEA) ,neuron spe-cific enolase(NSE) ,cytokeratin-19 fragments(CYFRA21-1) ,squamous cell carcinoma antigen(SCCA)in the lung cancer .Methods By using electro chemiluminescence immunoassay ,the concentrations of CEA ,NSE ,CYFRA21-1 and SCCA were determined in 98 cases of lung cancer and 30 cases of healthy control group ,and the positive rate ,sensitivity ,specificity ,accuracy were calculated .Re-sults In different lung cancer pathological groups ,the concentrations of the 4 serum tumor markers were significantly higher than the control group(P<0 .05) .CEA had the highest diagnostic sensitivity for detecting adeno carcinoma ,NSE had the highest diag-nostic sensitivity for detecting small cell lung cancers ,CYFRA21-1 had the highest diagnostic sensitivity for detecting squamous carcinoma .The combined tests of four serum tumor markers had higher diagnostic sensitivity and accuracy than single test for lung cancers .Conclusion The four serum tumor markers are valuable in the pathological classification ,diagnosis and differential diagno-sis of lung cancer .The diagnostic sensitivity and the accuracy are obviously higher in combined tests .

In this paper, we studied the effect of total flavones of Hippophae rhamnoides L (TFH) on beating and transmembrane potential of cultured sucking rat cardiac cell. The results indicated that cellular beating rate and beating amplitude were significantly reduced, the action potential duration of 50% and 90% repolarization was sbortened, the slope of phase 4 depolarization was decreased, and other parameters of the action potential showed no significant change. In addition, we also observed that TFH could make the spontaneous abnormal beating of cell change into regular beating. These findings suggested that the mechanism of TFH on cultured cardiac cell might have some relation to antagonizing inward flow of Ca~(2+) and aocelerating the move of k' outward.

Objective To express P38 of Schistosoma japonicum in Escherichia coli BL21 and develop the monoclonal antibodies (McAb) against rSjP38. Methods The recombinant plasmid pET32(a)-P38 was transformed into E.coli BL21(DE3). 1 mmol/L IPTG (isopropyl-beta D-thiogalactopyranoside) was used to induce the expression of the recombinant rSjP38. The rSjP38 was soluble in supernatant after sonication and further purified by His-Ni chromatography. BALB/c mice were immunized with the purified rSjP38 and hybridomas were generated with traditional technique. McAbs were screened by ELISA with limited dilution. The subtype and specificity of McAb were identified by kit and Western blot respectively. Results Eight hybridoma cell lines secreting monoclonal antibodies to rSjP38 were obtained. The subtype of all the 8 McAbs are IgG1. Western blotting showed that the 8 McAbs reacted strongly and specifically with native antigen (P38) of Schistosoma japonicum. Conclusions Eight hybridoma cell lines secreting highly specific McAbs against P38 have been established.

Objective:To study the prevalence of mild cognitive impairment (MCI) among elderly people and associated factors to it.Method:A sample of 1865 elderly people aged 60 or above living in Beijing metropolitan area was investigated by a two-stage survey.In the first stage, a door-to-door visit to the subjects was performed by a trained interviewer to conduct general questionnaire including activity daily living assessment, memory and cognitive test.On the second stage, neurologists examined all screened subjects to collect family history and to finish general and neurological examination as well as neuropsychological testing.MCI was diagnosed by the consensus of 2 neurologists.Result:Among the 1865 subjects visited, 217 (11.6%) were defined to have MCI.After adjusted for age and gender the standardized prevalence reaches 8%.Within the people with MCI 22.6% was classified as vascular MCI.The prevalence of MCI was higher in people living in rural area, in people with lower educational attainment, and in people who were labor workers.The prevalence increased with age advancing.Conclusion:Similar to dementia, people with advance aged, with low education and living in rural area are those at high risk of developing MCI.

[Objective]Giant cell tumor of bone is notorious for its local aggressive behavior and its tendency to recur after operative treatment.Bisphosphonates is the drug of anti-osteoporosis.It is found also have anti-cancer effect recently.We conducted experiment examing the effect of bisphosphonates alendronate on the growth and survival of the cells.To study if bisphosphonates are capable of inducing cells death and significantly inhibiting their growth in vitro.[Method]Cells viability was detected by MTT Assay after the tumor cells were cured with different concentration and different time.Tumor cells apoptosis with in situ TUNEL assay and flow cytometry was detected.The active Caspase-3 was also detected.[Result]After exposure to alendronate,the cells exhibited the characteristic features of cell shrinkage,rounding and partial detachment,and demonstrated the lobulated appearance of apoptotic cells.It was much more prominent while the treating time prolonged or the concentration increased.Alendronate((5 200) M) treatment for 24 h,resulted in 2.79%~31.17% decrease in cell viability,and 11.13%~49.94% for 72 h,respectively.A significant dose-dependent and time-dependent decrease in the number of viable cells was observed in the GCT cells.After Alendronate treat for 24 h,the mean cell population in apoptosis was 14.32% at concentration 5 mmol/l,and 40.24% at 200 mmol/l.It was up to 18.41% and 42.22% respectively after 48 h.In Alendronate-treated GCT cells,Caspase-3 activation was observed.The cell response varied with doses of Alendronate showing the levels of Caspase-3 expression with a dose dependent response.[Conclusion]In conclusion,we demonstrated that bisphosphonate alendronate could inhibit GCT cells in the present study.This response was time-dependent and dose-dependent.Alendronate inducing apoptosis in GCT cells is mediated by the activation of Caspase-3.

Objective To compare the application of three diagnostic criteria for metabolic syndrome(MS) among the elderly in community. Methods 773 elderly people in the community were diagnosed for MS by the Chinese Medical Association Diabetes Society (CDS),International Diabetes Federation (IDF) and revised National Cholesterol Education Prongram-Adult Treatment Panel(ATP Ⅲ* ) criteria,respectively.The diagnosis accordance rates were compared among the different diagnostic criteria. Results The MS prevalence rates in the elderly were 32.5％ (251/773),53.4％ (413/773) and 47.2％ (365/773) according to CDS,IDF and ATP Ⅲ* criteria,respectively and there were significant difference among the criteria (Q=173.10,P＜0.01 ).The MS prevalence was higher in women than in men especially by IDF [57.3％ (284/487)vs.45.1％ (129/286),x2=12.64,P＜0.01]and ATPⅢ* criteria [53.0％(258/487)vs. 37.4％ (107/286),x2=17.52,P＜0.01].The coincidences in the diagnosis of MS were 88.6％ (Kappa=0.773,P＜0.01)using IDF and ATPⅢ * definitions,75.7％ using CDS and ATPⅢ *,and 73.7％ using CDS and IDF.Conclusions The agreement in the diagnosis of MS using IDF and ATPⅢ* definitions is higher than using CDS and IDF or ATPⅢ * definitions.

With a comparison between the Non-paper Test model and the traditional one in pharmacology test, an objective analysis was made about the strengths and weaknesses of two test models. This practice shows that the paperless examination can promote teaching and help to improve the teaching quality, but need to be further improved.

Objective To investigate the effect of an anti-HER-2 engineered antibody,chA21,on the expression of MMP-2 and TIMP-2 in human ovarian cancer SKOV3 cells that highly express HER-2.Methods After exposure to chA21 at concentrations of 6 mg/L and 12 mg/L for 36 hours,respectively,the expression of MMP-2 and TIMP-2 proteins was detected by immunocyctochemistry.SKOV3 cells were inoculated into nude mice to establish animal models.The mice were respectively administered with normal saline and chA21(30 mg/kg) via injection twice a week for 6 consecutive weeks,and then were killed after 44 days' administration of the drugs.Immnohistochemical staining of MMP-2 and TIMP-2 was observed on tissue microarray sections.Results After exposed to chA21,TIMP-2 protein was increased(P

Background and purpose:Many studies indicate that nonsteroidal anti-inflammatory drugs(NSAIDs) may inhibit cancer growth.However,the molecular mechanisms may involve different pathway and still remain unclear.The aim of this experiment was to investigate the influence of aspisol against breast cancer lines,including MDA-MB-231(estrogen receptor-negative),MCF-7(estrogen receptor-positive),and reveal the potential signaling pathway mechanism of aspisol effect on breast cancer lines.Methods:MDA-MB-231 and MCF-7 human breast cancer cell lines were treated with aspisol in vitro.Cell proliferation was evaluated by MTT assay and rate of apoptosis were determined by flow cytometry.Extracellular signal regulated kinase(ERK),phosphor-ERK(P-ERK) protein expressed in breast cancer cell lines were analyzed by Western blot.Results:①The results of MTT assay demonstrated that the growth of MDA-MB-231,MCF-7 cells were inhibited by aspisol in a time-and dose-dependent fashion(P0.05).Conclusions:aspisol inhibits proliferation and induces apoptosis not only in ER-positive but also in ER-negative breast cancer cells.The mechanism may relate to ERK signal pathway.