Objective To evaluate the influence of tirofiban on myocardial perfusion through percutaneous coronary intervention (PCI) and platelet activation in patients with acute myocardial infarction (AMI). Methods Eighty patients with acute myocardial infarction who underwent emergency PCI within 12 hours were randomly divided into 2 groups due to the random number table method: tirofiban group (40 patients) and control group (40 patients). The control group received conventional anticoagulant therapy (aspirin + low molecular weight heparin + clopidogrel). The tirofiban group additionally received intracoronary tirofiban hydrochloride injection of 10 μg/kg PCI during PCI, intravenous maintenance dose of 0. 15 after PCI 15 mins, the changes of platelet activation before and after treatment 7 days,the bleeding complications and major adverse cardiac events (MACE) within 30 days after PCI. Results The TMPG 3 perfusion percentage of tirofiban group (97.5% ,39/40) after PCI 15 minutes was significantly higher than that (80. 0%,32/40) of the control group( x2 = 4. 507,P ＜ 0. 05 ) ;The expression positive rate of platelet activation CD62P,CD63, MPA of the tirofiban group after treatment of 7 days were ( 1.7 ± 0. 7 ) %, ( 1.5 ± 0. 7 ) % and ( 11.7 ±3.8)% ,respectively,which were significantly lower than those of before treatment ([7.2 ± 2. 5]%, [6. 9 ±1.8]% and [22. 0 ± 7. 8] %, respectivley) and those of the control group after treatment of 7 days ( [2. 9 ±1.2]% ,[3.9 ±0.6]% and [16.2 ±4.2]% ,respectivley)(t =5.463,16. 468 and 5.025, Ps ＜0.01 );The incidence of cardiovascular events of the tirofiban group (0) was significantly lower than that of the control group ( 15.0%, 12/40 ) after treatment of 30 days ( x2 = 4. 504, P ＜ 0. 05 ); The incidence of bleeding complications was not significant between the 2 groups ( x2 = 0. 180, P ＞ 0. 05 ). Conclusion The application of tirofiban hydrochloride in intervention in acute myocardial infarction can improve myocardial perfusion, and further inhibiting platelet activation and reduce the incidence of major adverse cardiac events after PCI while does not increase the incidence of severe bleeding.

Objective To investigate the induction of L-forms of Yersinia pestis by enrofloxacin,in order to know more about the formation conditions and biological characteristics of L-form Yersinia pestis.Methods Yersinia pestisEV were cultured in Hiss agar media containing 0,0. 5,5,10,50,100,500 and 1 000 ng/mL enrofloxacin respectively. The cultures containing 50 ng/mL enrofloxacin was subcultured in Hiss agar media without enrofloxacin for reversion. The colonial morphology of each sample was observed. The bacterial morphology was observed by Gram staining and cell wall staining,while the cell wall integrity by transmission electron microscope. Yersinia pestis EV and L-form Yersinia pestis were identified by 16S rDNA,analyzed for the homology and the phylogenetic tree were constructed.Results Enrofloxacin 0. 5 ng/mL contained in Hiss agar media caused morphological changes of Yersinia pestis,from typical short-rod to long-rod shape. When the concentration of enrofloxacin was 50 ng/mL,the cell wall of Yersinia pestis was deficient,and the bacteria could not divide and proliferate normally,but showed long-rod shape and coiled into a mass,with the colonial morphology like fried eggs. Enrofloxacin-induced L-form Yersinia pestis reversed in normal Hiss agar media,and displayed a typical Yersinia pestis short-rod shape. 16S rDNA identification showed that the homology between the induced strain and the parent EV strain before induction was 100%.Conclusion Enrofloxacin can induce the L-forms of Yersinia pestis.

Objective:To investigate the inhibitory effect and mechanism of different doses of Xiao Chai Hu Tang on C6 glioma cells cultured in vitro. Methods:C6 glioma cells were inoculated in 96 holes,24 holes and 6 holes,each culture plate was divided into 4 groups:control group, low dose group, middle dose group and high dose group, when the cells covered the bottom of culture plate 80%-90%,began adding,cultured for 24 hours after the ter mination of training. Cell proliferation activity,cell viability,protein content and protein positive expression intensity of VEGF and ESM-1,cell apoptosis in early and late stage were detected by CCK-8,in vivo staining,ELISA, immunocytochemistry and flow cytometry. Results: CCK-8 assay showed that the growth of C6 glioma cells was inhibited by low,medium and high dose group;ELISA and immunocytochemistry showed that the expression of VEGF and ESM-1 was lower in the lower, middle and high dose groups, and the levels of protein expression and protein levels were decreased. The flow cytometry showed that the low dose of small radix,middle and high dose group could promote the cell apoptosis. Inverted microscope ob-servation showed that with the increase of dose,the number of cells increased gradually,and the number of dead cells increased,and all kinds of detection methods showed that the inhibition effect increased with dose and dose dependence. The difference between the two groups was statistically significant(P<0. 01). Conclusion:The growth of C6 glioma cells was significantly inhibited by Xiao Chai Hu Tang. It may play a role in inhibiting tumor growth by down regulating ESM-1 and VEGF protein level and promoting cell apoptosis.

The Longhua Zhang's internal medicine,the famous clinical inheritance of Chinese medical schools in Shanghai,was well-known by their expert skills and high medical ethics during 370 years.This paper introduces the family origin and its academic characteristic.By studying the Shanghai local chronicles and the Longhua Zhang's genealogy,we learn how they innovating and improving the school.

Objective:To explore the relationship among clinical manifestations ,SⅠ QⅢ TⅢ feature of ECG ,plasma level of D‐dimer (DD) and diagnosis of pulmonary embolism (PE) .Methods :Clinical data of 212 inpatients ,who received pulmonary CT angiography (CTA) in our hospital from Jun 2012 to May 2014 ,were retrospectively ana‐lyzed .According to pulmonary CTA results ,patients were divided into PE group (n=56) and non‐PE group (n=156) .Basic hospitalization data ,including clinical manifestations ,ECG features and plasma DD level ,were collect‐ed and compared between two groups .Results:Compared with non‐PE group ,there were significant rise in percent‐ages of dyspnea (44.87% vs .75% ) and prolonged bedridden time (3.85% vs .14.29% ) ,significant reduction in percentage of no clinical manifestations (38.46% vs .3.57% ) in PE group , P<0.01 all .Percentage of ECG SⅠQⅢTⅢ feature in PE group was significantly higher than that of non‐PE group (50% vs .23.08% ) , P<0.01. Compared with non‐PE group ,percentage of plasma DD>10μg/ml significantly rose (19.23% vs .32.14% ) in PE group ,P<0.05 .Conclusion:Patients with dyspnea and/or prolonged bedridden time ,that cannot be explained by other car‐diopulmonary diseases ,and SⅠ QⅢ TⅢ feature of ECG ;plasma DD level significant rising (> 10 μg/ml) should be considered to be PE .

Objective To assess the predictive value of neutrophil gelatinase associated protein lipocalin (uNGAL) in urine for detection of acute kidney injury(AKI) in patients with severe traumatic brain injury. Methods Patients with severe traumatic brain injury from the ICU were collected from Jan. 2011 to May. 2013 in our hospital. 43 cases that met the RIFLE criteria for diagnosis of AKI in the ICU within 7 days were selected as AKI group. Another 43 cases that were matched for age ,gender ,illness severity , surgery method with AKI cases ,selected as non‐AKI group. The levels of uNGAL and Scr were measured when the patients admit‐ted in the ICU with 15 min ,at 24 h ,48 h ,72 h. the sensitivity and specificity of uNGAL and Scr for diagnosis for AKI were evalua‐ted by ROC curve. Results The incidence of severe traumatic brain injury AKI was 42. 16% (43/102). The uNGAL levels in the AKI group were higher when the patient stayed in the ICU longer and no obvious in the non AKI group. When admitted to the ICU 24 h ,the level of uNGAL(720. 32 ± 684. 25)ng/mL in AKI group was significantly higher than that (421. 92 ± 351. 20)ng/mL in non AKI group. The difference was statistically significant (P< 0. 05). The levels of Scr between two groups were not statistically significant. The area under ROC curve of uNGAL and Scr were 0. 879 (95% CI :0. 807 - 0. 949) and 0. 612 (95% CI :0. 493 -0. 731). When the cutoff value of uNGAL was 180 ng/mL ,the sensitivity and specificity were 0. 890 and 0. 823 respectively. The sensitivity was superior to Scr. Conclusion uNGALis superior to Scr for early diagnosis of AKI in patients with severe traumatic brain injury and it could be used as a biomarker for early diagnosis of AKI.

Objective To estimate the effect of berberine on the proliferation of and expressions of apoptosisrelated factors Bax and Bcl-2 in a human skin squamous cell carcinoma cell line A431.Methods A431 cells were cultured in vitro,and classified into various groups to be treated with berberine at different concentrations (12.5,25,5,100 mg/L) or cisplatin at 250 mg/L (positive control group) for different durations (12,24,48 and 72 hours).The A431 cells remaining untreated served as the negative control group.Subsequently,methyl thiazolyl tetrazolium (MTT) assay was performed to evaluate cell growth,and inverted microscopy to observe cell morphology.Real time quantitative reverse transcription-PCR and an immunofluorescence assay were conducted to measure the mRNA and protein expressions of Bax and Bcl-2 respectively.Statistical analysis was done by multi-way analysis of variance (ANOVA) using the software SPSS 13.0.Results MTr assay showed that berberine inhibited the growth of A431 cells,and the inhibitory effect increased with the increase in concentration (F =1118.312,P ＜ 0.001) and treatment duration (F =510.927,P ＜ 0.001) of berberine.Moreover,there was a significant interaction between the concentration and treatment duration of berberine (F =70.239,P ＜ 0.001).Inverted microscopy revealed that when the concentration of berberine increased,cell density was reduced,and cell morphology changed from polygonal to round with cell body shrinkage.The ratio of bax to Bcl-2 mRNA was elevated with the increase in treatment duration and concentration of berberine,and there were significant differences in the mRNA ratio among cells treated with berberine for different time durations at same concentrations (F =226.231,1300.636,4325.139 for berberine at 25,50 and 100 mg/L respectively,all P＜ 0.001).Immunofluorescence staining indicated that the fluorescence intensity of Bax was enhanced,while that of Bcl-2 was weakened after berberine treatment.Conclusions Berberine inhibits the growth of A431 cells in a dose-and timedependent manner,and may induce the apoptosis of A431 cells via regulating the expressions of Bax and Bcl-2.

Objective To prevent and treat of ceramic membrane purification of membrane fouling process of TCM extracts; To explore new methods of forecasting membrane fouling degree.Methods BP neural network model was improved. Methods to fast determine the optimal number of neurons in the hidden layer and fast algorithm for optimizing the weight and threshold of BP neural network were studied. Data of 207 groups of TCM extracts were under network training and prediction.ResultsCompared with the models of multiple regression analysis, basic BP neural network and RBF neural network, the error of the improved BP neural network model was less than that of the BP neural network model, and the mean square error was only 0.0057. In addition, the improved BP neural network model performance was more stable. In the 20 random running experiments, the goal of the success rate achieved up to 95%.Conclusion The improved model has a good network performance, the fitting effect and prediction ability, and can forecast the fouling degree of membrane stably and accurately.

Aim Toresearchthemolecularmecha-nisms of adriamycin-induced cardiomyocyte apoptosis based on β-adrenoceptor signaling pathway during de-velopmentofheartfailure.Methods SeventymaleSD rats were assigned randomly into two groups:the con-trol group(CON,n=30)and the ADR-induced cardio-toxicity group (ADR,n =40 ).ADR was administered intraperitoneally in five equal injections (each contai-ning 3 mg·kg-1 )over a period of two weeks,with a total cumulative dose of 15 mg · kg-1 body weight. Age-matched rats injected with saline were used as controls.The general condition of all rats was observed, and transthoracic echocardiography was performed im-mediately following the final ADR injection,and then every other week.Serum and myocardial tissue were harvested at W2,W4 and W6 separately.The serum contents of brain natriuretic peptide(BNP)and cardiac troponin-T(cTn-T)were analyzed by euzymelinked im-munosorbent assay (ELISA ).The pathological change and apoptosis were determined by HE,Masson and ter-minal deoxyribonucleotide transferase-mediated dUTP nick end labeling (TUNEL).The protein expressions ofβ1-AR,β2-AR,PKA and CaMK Ⅱ were detectedbyWesternblot.Results FollowingthefinalADRin-jection,cardiac systolic function and SV declined, which was accompanied by marked atrophy of the heart,low levels of cardiomyocyte fibrosis and apopto-sis,significantly increased serum BNP and cTn-T and decreased β1-AR,PKA and CaMK Ⅱ protein expres-sion.However,cardiac systolic function was improved with the extension of time but remained depressed as compared to CON group.The serum BNP and cTn-T concentration kept on rising.The gradual aggravation apoptosis and concomitant fibrosis in the ADR group heart were observed following ADR withdrawal.β1-AR protein expression was continuously down-regulated,β2-AR protein expression unchanged.Expression of PKA and CaMKⅡ proteins in hearts from ADR-injec-ted rats gradually increased.Conclusion β-AR/PKA/CaMKⅡ signaling pathway mediates cardiomyo-cyte apoptosis during the progress of ADR-induced car-diac dysfunction and pathological remodeling and apop-tosis.

BACKGROUND:Compared with mesenchymal stem cells from bone marrow and fat, human umbilical cord-derived mesenchymal stem cells, as one of the most potential cellsources to repair the central nervous system, are easy-based, more primitive, and not limited by ethical and legal.
OBJECTIVE:To explore differentiation of human umbilical cord-derived mesenchymal stem cells into neural stem cells induced by the recombinant human basic fibroblast growth factor and recombinant human epidermal growth factor.
METHODS:The human umbilical cord-derived mesenchymal stem cells were induced by basic fibroblast growth factor and epidermal growth factor in vitro. The cellmorphology was observed by invert microscope. The differentiation status was detected by immunofluorescence. The Nestin expression in mRNA level before and after induction was detected by real-time PCR.
RESULTS AND CONCLUSION:The neural stem cellbal s were observed after induction. And the Nestin was detected by immunofluorescence and real-time PCR. Nestin could further differentiate to the neuronal markproteins neuron-specific enolase, microtubule-associated protein 2 protein and glial fibril ary acidic protein. Results from this study show that basic fibroblast growth factor and epidermal growth factor can induce human umbilical cord-derived mesenchymal stem cells to differentiate to neural stem cells, neurons and glial cells.