OBJECTIVE:To provide references for the improvement of civil relief system for adverse drug reactions.METHODS:The approaches for Japan in handling the "quinoform" drug injury event were compared with the way of China in dealing with drug injury events.RESULTS & CONCLUSION:The approaches for Japan in handling the"quinoform" drug injury event give some hints for China,i.e.the defective drugs should be comprehensively judged by judges,the causal relations should be determined by using the probability theory and the time point of producers' exemption should be revised.

Aim To study the protective effects of Ganoderma lucidum polysaccharides peptide(GLPP)on ECV304 from oxidative injury.Methods Cultured ECV304 were injured by oxygen free radicals derived from tBOOH.Various concentrations of GLPP(12.5,25,50,100 mg?L-1)were added into culture medium.The survival rate of cells was measured by MTT assay.The morphological change of cells and injury of mitochondria were examined under the light and electron microscopes.The percentage of apoptosis of ECV304,labeled with AnnexinV/PI,was measured by flow cytometry.Results GLPP(12.5,25,50,100 mg?L-1)could reduce oxidative injury induced by tBOOH in ECV304 cells.The survival rate of cells treated with GLPP increased.The light microscopic examination showed that the injured cells decreased in GLPP-treated groups.Under the electron microscope it was found that GLPP(50 mg?L-1,incubated for 24 h)could protect the organelle such as mitochondria from oxidative injury and cells from apoptosis by tBOOH.The result of flow cytometry showed that the total percentage of apoptosis in control,GLPP and injury treated group was 2.24%?0.43%,24?6.4%(P

Aim To study the effects of Ganoderma polysaccharide peptide (GLPP) on the production of nitric oxide (NO) in mice peritoneal macrophages induced by LPS and its mechanism. Methods The effects of GLPP on the NO releasing from mice peritoneal macrophages induced by LPS were detected by using Griess reagent and the expression of iNOS by GLPP in mice peritoneal macrophages was detected by immunohistochemical method.Result The production of NO was increased by GLPP.(25～200 mg?kg -1) ig for five days or by GLPP(3.125～200 mg?L -1) in vitro but the effects of LPS on the production of NO was not influenced significantly. The expression of iNOS was increased by GLPP(25～200 mg?kg -1) ig for five days or GLPP(3.125～200 mg?L -1) in vitro.Conclusion GPP in vivo or in vitro could increase the production of NO in mice peritoneal macrophages. It might take effects by enhancing the synthesis of iNOS.

AIM: To investigate the free radical scavenging activity of Ganoderma lucidum polysaccharides peptide (GLPP) on peritoneal macrophages in mice. METHODS: Alloxan and tert butylhydroperoxide (tBOOH) were used as an oxidant to injury peritoneal macrophages in vivo in mice or in vitro, respectively. 2', 7' dichlorodihydrofluorescein diacetate (DCHF DA) was used as fluorescent probe. The fluorescence from cells was observed under the laser confocal microscope. Time series scan of conforcal microscope was used to observe the changes of fluorescence by GLPP in mice peritoneal macrophages over time. RESULTS: The results of confocal microscopy showed that GLPP (100 mg?kg -1 , ig for 5 d ) lowed fluorescence in the mice macrophages injured by alloxan (75 mg?kg -1 iv). GLPP (10 mg?L -1 ) also lowed fluorescence in the mice macrophages injured by tBOOH ( 7.76 ?10 -5 mol?L -1 ) in vitro as well. Time series scan showed that GLPP (10 mg?L -1 ) lowed fluorescence in the mice macrophages at rest state or during the respiratory burst induced by PMA (50 nmol?L -1 ). CONCLUSION: GLPP shows antioxidant effects and might have free radical scavenging effects on peritoneal macrophages in mice.

Objective To observe the therapeutic effect of Jingganquzhi decoction(JQ,净肝祛脂汤) in treating non-alcoholic fatty liver.Methods Eighty patients with non-alcoholic fatty liver were randomly divided into treatment group to receive JQ and control group to receive Dongbaogantai(DG,东宝肝泰) orally for 3 months.The changes of liver function,blood lipids,B ultrasonic examination were observed.Results After the treatment,the liver function criteria: alanine aminotransferase(ALT),aspartate aminotransferase(AST),alkaline phosphatase(ALP),?-glutamyltransferase(?-GGT) and blood lipids of triglycerides(TG),total cholesterol(TC) were lower than those before the treatment,while the high-density lipoprotein cholesterol(HDL-C) was higher than that before the treatment in both groups(all P

Hypertension is one of the high prevalence diseases in Xinjiang,which severely affect the body-mind heath of the people.In Northwest area,particularly in xinjiang,dryness syndrome is prevailed owing to environmental factor.Therefore,dryness syndrome of climacteric hypertension in xinjiang is more prevalent than that in other areas.Discussion on the effect of environmental factors on climacteric hypertension is a main aspect of Northwest dryness syndrome study.It may provide reliable and helpful basis of prevention and treatment of climacteric hypertension in xinjiang.

Aim To study the protective effects of Ganoderma lucidum polysaccharides peptide(GLPP)on the human umbilical vein endothelial cells(HUVECs)injured by reactive oxygen species(ROS),derived from tert-butylhydroperoxide(t-BOOH).Methods Vascular endothelial cells were obtained from infant umbilical cord for primary cultivation,identified by endothelial cell adhesion molecule-1(CD31)by fluorescence microscope.HUVECs were injured by ROS,derived from t-BOOH.The survival rate of cells was measured by Cell Counting Kit-8 assay.Hoechst 33258 nucleus staining was used to observe the early apoptosis injury by ROS.And the activation of Caspase-3 was detected by spectrophotometry.Electron microscopy was used to show the morphological changes in HUVECs.Results GLPP(6.125,12.5,25,50,100 mg?L-1)could inhibit the apoptosis of HUVECs by ROS.The survival rate of HUVECs was increased by GLPP and the percentage of cell apoptosis was decreased by it too.GLPP decreased the activation of Caspase-3 of HUVECs up-regulated by ROS.Electron microscope showed that the organelle such as mitochondria injury by ROS could be relieved by GLPP.Conclusion GLPP can prevent human umbilical vein endothelial cells from oxidative injury.

Objective To explore the effect of evidence-based medicine combined withcase based learning(CBL) in pediatric residency training.Methods Totally 52 residents were equally divided into two groups:experiment group and control group.Method of CBL combined with the evidencebased medicine (Taking two residents as one group,firstly teacher posed the questions and then residents searched for references when off duty and made evidence-based case presentation at fixed time when doing teaching ward around,after wards all personnel in the department made case discussion,finally teacher made the summary) was used in experimental group while traditional teaching method (teacher guided the residents to analyze the case by clinical experiences,residents took notes and sometimes asked questions,teacher directly gave the answers)was used in control group.The teaching effect is evaluated by questionnaire,theory test and clinical skills assessment.Statistical analysis was carried out on appraisal results with SPSS 16.0 software,test results and appraisal results were expressed as ((x-) ±s) and t test was performed,P ＜ 0.05 was taken as statistically significant.Results Residents in experimental group had more advantages in self-study ability,literature retrieval ability,physician teamwork spirit,clinical thinking,PowerPoint making and language expression after receiving CBL combined with evidence-based medicine.Theory examination showed that average score of experimental group was better than that of control group (75.46 ± 6.646) vs.(71.38 ±4.758),with statistically significantly differences (P =0.014),especially in subjective items.Clinical skills assessment showed that experimental group was better than control group in writing medical records and doing clinical thinking.Conclusions Teaching method of evidence-based medicine combined with CBL is significantly better than traditional indoctrination teaching in improving the abilities of self-study,cultivating clinical thinking,literature retrieval,language performance and other skills.This teaching method is more suitable for pediatric residency training.

AIM: To investigate the effect of 17?-estradiol(E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism.METHODS: Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17?-estradiol on myocardial hypertrophy were observed.The role of ERK1/2 in the effects of 17?-estradiol was also detected.RESULTS: Compared with control group,ET-1 increased cell protein content,cell surface area and -Leucine(-Leu) incorporation.Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and -Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2.The ability of ET-1 to stimulate -Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of -Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION: E2 can inhibit cardiomyocyte hypertrophy induced by ET-1.This effect is mediated by estrogen receptor.ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1.

[Objective] The aim of the present study was to investigate the role of membrane estrogen receptor (mER) mediated pathway in the proliferation and apoptosis of endothelial progenitor cells (EPCs). [Methods] Bone marrow (BM)-derived EPCs were cultured. The cells were divided into different groups, plus or not plus estrogen receptor blocker (ICI 182,780), PI3K inhibitors (LY294002), and NOS inhibitor (L-NAME) to show the effect of E_2-BSA on EPCs. The proliferation of EPCs was determined by MTT and nitric oxide (NO) release was measured by chromatometry. Apoptotic cell death was determined using the Hochest 33258 staining. The expression of phosphorylated eNOS (p-eNOS) were detected by Western blot. [Results] E_2-BSA could increase EPCs proliferation, and this effect was inhibited by estrogen receptor blocker ICI 182,780, thus indicated that mER-initiated membrane signaling pathways were involved in the action of estrogen on EPCs. E_2-BSA increased nitric oxide production and inhibited apoptosis induced by serum withdrawal, and this effect also inhibited by PI3K inhibitor (LY294002), NOS inhibitor (L-NAME)and estrogen receptor blocker(ICI 182,780), thus indicated that PI3K/Akt/NO pathway was involved the effect of estrogen on EPCs apoptosis. Moreover, E_2-BSA treatment increased phosphorylation of eNOS (p-eNOS). PI3K inhibitors (LY294002) also blocked these effects. [Conclusions] The results of present study suggested that mER mediated EPCs proliferation and apoptosis were related to the PI3K/Akt/eNOS pathway.