Objective To investigate the effect of heme oxygenase-1 (HO-1) on hypoxia-reoxygenation (H/R) injury in cultured neonatal rat cardiomyocytes. Methods Primary cultured neonatal rat cardiomyocytes were randomly divided into4 groups: Ⅰ control group (group C), Ⅱ H/R group, Ⅲ hemin group and Ⅳ hemin+zinc protoporphyrin (ZnPP) group. In group H/R, the cardiomyocytes were exposed to 2 h of hypoxia followed by 6 h of reoxygenation. Hemin was added to the culture medium with a final concentration of 20 μmol/L 24 h before hypoxia and immediately before hypoxia in group hemin. Hemin and ZnPP were added to the culture medium with final concentrations of 20 μmol/L 24 h before hypoxia and immediately before hypoxia in group Henin + ZnPP. The cells were incubated in 35 mm culture dishes (2 ml in each dish) and 50 ml culture flasks (3 ml in each flask)(45 dishes and 3 flasks in each group). The HO-1 expression, cell survival rate, LDH activity, malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were detected after the end of reoxygenation. Results Compared with group C, the LDH activity, MDA level and HO-1 expression were significantly increased, while the cell survival rate and SOD activity decreased in the other three groups ( P ＜ 0.05). Compared with group H/R,the LDH activity and MDA level were significantly decreased, while the HO-1 expression, cell survival rate and SOD activity increased in group hemin ( P ＜ 0.05 ), but no significant change was found in group hemin + ZnPP (P ＞0.05). H/R injury was obvious in group H/R and hemin + ZnPP, but was significantly attenuated in group hemin. Conclusion HO-1 can protect cardiomyocytes against H/R injury in neonatal rats.

Objective　To study β-AR density relativity between porcine myocardial tissue and circulating lymphocytes and clinical significance ．Methods　 48 porcines(seven months old），were　taken a few of myocardial tissue and peripheral blood．Assay　β-AR density with radioactive isotope to study the　relativity．Results　Scatter plot of β-AR　density　 circulating lymphocytes and myocardial tissue showed　 linear　Correlation（r＝0.845，P＜0.001　Y＝0.002527X＋0.726）．Conclusion　There　was　obvious　 correlation on β-AR　density in circulating lymphocytes and myocardial membrane　of pigs．Determination of β-AR　density　in　circulating lymphocytes can reflect alteration of that in myocardial tissue．Therefore，we can use it to monitor and investigate　self-induced and drug-induced β-AR changes．

Tumor invasion model is an important tool to study the mechanisms of tumor mvasion and to evaluate prevention and treatment of cancer.Compared to the in vitro model,in vivo model can simulate the tumor microenvironment and tumor mvasion biological behaviour better.Morphological observation and invasion-related protein detection can be used to evaluate the animal invasion model,which are widely used in basic and clinical research now.

Objective To analyze the application of bar code mode in LIS and help select a fit bar code mode for the hospital. Methods The mode of print bar code was chosen on the base of LIS that was programmed with ORACLE database and PowerBuider9.0 so as to manage laboratory information. Results The bar code management in LIS was realized and no- paper thoroughly in hospital. Conclusion The print bar code mode is more suitable for information-based hospital.

Objective To study the expression of EI-1 in myocardium during cerebral ischemia and reper-fusion, and to investigate the mechanism of cerebral cardiac syndrome. Method Two hundred and eight SD rats weighting 220～250 gram, were divided into three groups: sham control group (n=48), cerebral ischemia group (n=80), cerebral ischemia/reperfusion group (n=80). The area of cerebral ischemia, and the concentration of sennn ET-1 and CK-MB, and the content of myocardial ET-1 were determined in 0,6, 12,24,48,72 h after cerebral ischemia and reperfusion, and were analyzed by t-test or F-test. Results Cerebral necrosis area was ob-served at 6 h after cerebral ischemia in cerebral ischemia group, and peaked at 12 h (P>0.05). The concentra-tion of CK-MB increased gradually after cerebral ischmia, peaked at 12 h (P<0.05), and then gradually de-creased. The serum concentration of ET-1 peaked at 6 h and then gradually decreased. The content of ET-1 in my-ocardium began to increase at 6 h after cerebral ischemia, and peaked at 12 h (P<0.05). In cerebral ischemia/reperfusion group, all of cerebral necrosis size, CK-MB concentration and myocardial ET-1 concent paelced at 12 h and then gradually decreased (P<0.05). Change of ET-1 concentration in blood was similar to that in cerebral ischemia group. Compared with cerebral ischemia group, the size of cerebral necrosis reduced obviously at 24 h,48 h,72 h in cerebral ischemia/reperfusion group (P<0.05). The concentration of CK-MB in cerebral ischemia/ reperfusion group was higher than that in cerebral isehemia group (P<0.05). The peak time of myocardial ET-1 was shatened in cerebral ischemia/reperfusion group. The change of serum ET-1 was not different between two groups. Conclusions Large area of cerebral ischemia, might cause myocardial injury. ET-1 is involved in the course of myocardial injury following cerebral ischemia. Though cerebral reperfusion can protect brain,but it make myocardial injury more serious,and ET-1 might participate in this course.

Objective To study the cardioprotection effects of heme oxygenase-1(HO-1)on cardiopulmonary resuscitation(CPR).Method Male Sprague-Dawley rats were asphyxiated for 9 minutes and resuscitated.Rats wefe randomly divided into 4 groups,namely,sham asphysiation group,CPR group,Hemin group and Heroin +ZnPP group(zinc protoporyphyrin IX).Resuscitated groups were further divided into two subgroups according to various intervals:6 hours and 24 hours after resuscitation.Hemodynamic was observed.Serum creatine phosphokinase-MB(CPK-MB)and lactate dehydrogenase were determined.HO-1 in heart tissue homogenates was assayed.Ultrastructure of rats hearts was examined.Statical evaluation was performed with analysis of variance.Results The mean blood pressure(MBP)in resuscitated groups was significantly reduced after resuscitation,hadn't any difference between supgroups.The scores of dp/dt 40 and-dp/dt were significantly decreased in CPR group and Hemin+ZnPP group after resuscitation(all P＜0.05),but dP/dt40 in Heroin group did nol differ significantly after resuscitation.and-dp/dt decreased only 0.5 hours and one hour after resuscitation and returned to baseline values two hours after resuscitation.The scores of dp/dt 40and-dp/dt in Heroin group at different intervals after resuscitation were significantly higher than those in CPR group and Hemin+ZnPP group(all P＜0.05).Serum CPK-MB and LDH in CPR group and Hemin+ZnPP group at 6 hours and 24 hours after resuscitation were significantly higher than those in Hemin group(all P＜0.05).The cardiac tissue ultrastructure of rats in Hemin group was more intact than that of CPB group and Hemin+ZnPP goup.HO-1 levels in heart tissue homogenates of Hemin group at 6 hours and 24 hours after resuscitation were significantly higher than those in CPR group and Heroin+ZnPP group(all P＜0.05).Conclusions HO-1 expression induced by Heroin can effectively improve post-resuscitation myocardial dysfunction,alleviate cardiac injury,keep the ultrassructure integrity of cardiac myocytes.It may be a new approach to treat myocardial dysfunction after resuscitation.

Objective To explore the changes of matrix metalloproteinase-9 and blood brain barrier in cardiopulmonary resuscitation rats and effects of MMP-9 inhibitor on them.Method One hundred and twenty Sprague-Dawley(SD) rats were randomly divided into 3 groups:the sham-operated group,the resuscitation with treatment group and the resuseimfion without treatment group as control.The experiment was made in the animal experiment center of Sun Yat-sen University in Gtlangzhou.The rat eardiopulmonary resuscitation model was made by clipping trachea until asphyxia,and the restoration of spontaneous circulation(ROSC)Was defined by restoration of superventricular rhythm and mean artery pressure (MAP)≥60 mmHg for more than 5 min utes.The rats of sham-operated group were anesahetized only and endotracheal intubation WaS performed.In the resuscitation with treaUnent group ss-3cr(25,ng/ks body weight)Was given intraperitoneally after ROSC.The rats were sacrificed and samples of the brain tissue were taken inmaediately and 3 h,9 h,24 h and 48 h later.After that,the expression of MMP-9 and MMP-9 mRNA in brain tissue were detected.Water oontent and Evans blue in brain tissue Were observed.The uhmmicrostructure of brain tissue was observed under electron microscope.Analysis ofvariance wilE, done with Spssll.0 software.Results 11le expressions of MMP.9 and MMP-9m RNA ofbraintissueiUthe shanloperated group didn't show significant changees in all specimens taken at different intervals and neither the water content and tvans blue did.The Pvalue were 1.0000,0.6831,0.7124 and 0.99r75,respectively.There was no u1.tramicrostruclure change in the sham-operated group.The expressions of MMP_9 and MMP-9 mRNA in the resuscitation control group obviously increased after eardiopulmonary resuscitation,80 did the water content and Evans blue content.Compared with sham-operated group,the P value were 0.0264,0.0163,0.0000 and 0.0412,respee.tively.111e elge of ultmmicrostmeture in the resuscitation control group at different intervals were obvious.The changes of obove biomarkers in the resuscitation treatment group Was siroilar to but less in magnitude than those in the resuscitation control group.The P valHe were 0.0392,0.0373,0.O004 and 0.0180,respectively.Conclusions The expressions of MMP-9 and MMP.9 mRNA obviously increases in the cerebral ischemia model of rats with CPR,and reaches peak at 24 h.Water content and Evans blue content in brain risque obviously increases in the cerebral ischemia model of rats with CPR.BBB iS destroyed.and the peak time iS at 24 h.The injury of ultrami.crostructure of brain tissue under electron microscope iS obvious,and the peak time is at 24 h.The SB-3CT.specif-iC inhibitor of MMP-9 could decrease the expression of MMP-9 and decrease cerebral edema in the cerebral is.chemia modeJ of rats with CPR,and the protection from cerebral isehemia/reperfusion injury after CPR is obvious.

Objective To investigate the effects of mitochondrial division inhibitor 1 (mdivi-1) in rats after cardiopulmonary resuscitation (CPR) and its mechanism.Methods Fifty Sprague-Dawley (SD) rats were randomly (random number table) divided into sham group (n =8),cardiac arrest (CA) model group (n =14),dimethyl sulfoxide post-treatment control group (DMSO group,n =14),and mdivi-1 post-treatment group (mdivi-1 group,n =14).Asphyxial CA was reproduced in animals,and they were resuscitated by CPR.In the mdivi-1 group or DMSO group,the animals were given mdivi-1 (1.2 mg/kg) or DMSO (0.1％) intravenously after restoration of spontaneous circulation (ROSC).The neurological functions were assessed using neurological deficit score (NDS) determined at 24,48 and 72 hours after CPR.The brain tissues were harvested at 72 hours after CPR.The histopathologic changes were assessed by hematoxylin and eosin (HE) staining,and the normal neuron was counted.The neuronal apoptosis was assessed with terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining,and the expressions of cytochrome C (Cyt-C) protein in mitochondria and cytoplasm from hippocampus were determined by Western Blot.Results NDS in all experiment groups was gradually increased after CPR,and they were significantly lower than thoseo.f the sham group at 24,48,and 72 hours (51.5±3.7 vs.80.0±0.0,59.3±3.6 vs.80.0±0.0,66.7±2.6 vs.80.0±0.0,all P ＜ 0.05).The number of normal pyramidal neurons in the hippocampal CA1 region was markedly reduced (cells/HP:4.4± 1.1 vs.23.1 ± 4.0,P ＜ 0,05),the apoptotic index was significantly increased [(86.9 ± 6.9)％ vs.(3.4 ± 0.8)％,P ＜ 0.05],the expressions of Cyt-C in mitochondria were significantly decreased (A value:0.46±0.18 vs.1.00±0.00,P ＜ 0.05),and the expressions of Cyt-C in cytoplasm were significantly up-regulated (A value:6.65±0.21 vs.1.00±0.00,P ＜ 0.05).Compared with the CA group,NDS at 24 hours and 48 hours in mdivi-1 group was slightly increased (55.2 ± 3.3 vs.51.5 ± 3.7,64.7 ± 2.4 vs.59.3 ± 3.6,both P ＞ 0.05),and it was significantly increased at 72 hours (74.5±2.3 vs.66.7 ± 2.6,P ＜ 0.05),the number of normal pyramidal neurons in the hippocampal CA1 region was markedly increased (cells/HP:16.2±2.4 vs.4.4± 1.1,P ＜ 0.05),the apoptotic index was dramatically reduced [(42.3 ± 3.9)％ vs.(86.9 ± 6.9)％,P ＜ 0.05],the expressions of Cyt-C in mitochondria were significantly increased (A value:0.83 ± 0.22 vs.0.46 ± 0.18,P ＜ 0.05),and the expressions of Cyt-C in cytoplasm were significantly decreased (A value:3.84±0.47 vs.6.65±0.21,P ＜ 0.05).There was no statistically significant difference in above indexes between CA group and DMSO group.Conclusion By inhibiting mitochondrial Cyt-C apoptotic pathway to reduce neuronal apoptosis in rats after CA-CPR,mdivi-1 can improve brain function after CPR.

OBJECTIVE:To observe the clinical efficacy and safety of flunarizine combined with salvianolate in the treatment of acute migraine. METHODS:A total of 72 patients with acute migraine were randomly divided into control group(36 cases)and observation group (36 cases). Based on routine treatment,control group was given Flunarizine hydrochloride capsules orally,10 mg for 65 year-old and below once a day,5 mg for more than 65 year-old once a day. Observation group was additionally given Flunarizine hydrochloride for injection 200 mg intravenously,once a day,on the basis of control group. Both groups were treated contineously till cured or for 2 weeks. Clinical efficacy,onset time,recovery time,VAS score,frequency and duration of head-ache attack,ADR were observed in 2 groups. RESULTS:In the course of treatment,the two groups did not terminate and fall off, and all of them completed the treatment. The total response rate(97.22%)of observation group was significantly higher than that (86.11%)of control group;onset time and recovery time of observation group were both shorter than those of control group,with statistical significance (P<0.05). Before treatment,there was no statistical significance in VAS score,frequency or duration of headache attack between 2 groups (P>0.05). After treatment,VAS score,frequency and duration of headache attack in 2 groups were all significantly lower than before,and the observation group was significantly lower than the control group,with statistical significance (P<0.05). There was no statistical significance in the incidence of ADR between 2 groups (P>0.05). CONCLU-SIONS:Based on routine treatment,flunarizine hydrochloride capsules combined with Salvianolate injection show significant effica-cy for acute migraine with good safety.

Objective To investigate the expression of Fascin in early-stage NSCLC, evaluate the relevance between Fascin expression level and prognosis.Methods The immunohistochemistry method was used to assess the expression of Fas-cin in 111 lung cancer FFPE tissues with stage Ⅰ and Ⅱ NSCLC.The relationship between Fascin expression and the clinico-pathological characteristics was analyzed.The prognostic significance of Fascin expression was evaluated with Kaplan-Meier sur-vival analysis.Results In the early-stage of NSCLC, the positive rate of Fascin expression was 64.8%, no expression in the paracarcinoma tissue.The positive rate of squamous cell carcinoma was 78.7% and was significantly higher than that in adeno-carcinoma 48.0%(P<0.01).Whether in squamous cell carcinoma or adenocarcinoma group, the expression of Fascin was correlated significantly with lymph node metastasis tumor stages and DFS(P<0.05).And the positive expression of Fascin was an independent risk factor of poor prognosis for patient with NSCLC .Conclusion Fascin is expected to be a biomarker for the prognosis of patients with early-stage NSCLC.