Objective To observe the protective effect of GSPB2 for delaying the human endothelial cells apoptosis with H2O2 induced human endothelial cells apoptosis as the model and to investigate its mechanism.Methods The human endothelial cells were pre-treated by 0.5 mmol H2O2,then different concentrations of GSPB2(5.0,10.0,20.0 μmol/L) was added for protecting cells.The cellular apoptosis was detected by TUNEL method;the apoptosis related molecules,such as Caspase-3,Bax,Bcl-2,and influencing apoptosis related molecules such as PI3K,p-Akt and Akt protein expression were detected by Western bl0t;Transwell chamber was used to detect cell migration situation.Results 0.5 mmol H2O2 induced obvious increase of human endothelial cells (P＜0.01).GSPB2 could significantly alleviate the H2O2 induced apoptosis of human endothelial cells(P＜0.05).10 μmol/mL GSPB2 could be close to return to H2O2 untreated control group level.Further found that Caspase-3,Bax protein expression were up-regulaed,Bcl-2 expression was down-regulated and the expression of PI3K,p-Akt and Akt wa sup-regulated.Conclusion The different concentrations of GSPB2 has a protective effect on vascular endothelial cells induced by H2O2,moreover which manifested by the concentration and time dependence.Its mechanism is related with the related molecules PI3K,p-Akt and Akt

Objective To study the influence of hyponatremia on prognosis in hospitalized patients with chronic heart failure . Methods A total of 322 patients with chronic heart failure from Feb .2006 to Aug .2012 were retrospectively reviewed and random-ly divided into hyponatremia group(n=161) and normal serum sodium group(n=161) .The clinical data of the two groups were compared .Results There were significant difference between the two groups in the BNP levels ,length of stay ,hospital mortality and readmission rates(P<0 .05) .Serum sodium concentration in hyponatremia group was decreased with the decrease of cardiac function(P<0 .05) ,BNP levels was elevated with the decrease of blood sodium level (P<0 .05) ,days of hospitalization and hospital mortality were increased with the decrease of cardiac function (P< 0 .05) .Conclusion Patients with heart failure combined hy-ponatremia have poor cardiac function ,higher in-hospital mortality and readmission rates and longer hospital stay .

Objective To investigate the effect of stellate ganglion block ~SGB) on formalin-induced nociceptive behavior of rabbits, the expression of brain-derived neurotrophic factor ~BDNF) of dorsal root ganglia ~DRG) and the concentration of serum interleukin-8 ~IL-8) in rabbits. Methods Twenty-four rabbits were used in this study. Catheters were inserted closely to right stellate ganglia of the animals, which were randomly divided into control group ~A), SGB group ~B) and pain model group ~C). Group B and C were administered with an injection of 0.5ml of 3% formalin into the right front paw subcutaneously, group A 0.5ml saline by the same way. 0.5ml of (0.25)% bupivacaine was administered via the catheter in group B at 10 minutes before injection, while group A and C were given 0.5ml of saline at the same time. Nociceptive behavior was observed for 60 minutes after injection, and assessed by weighted pain score. Serum IL-8 was measured radioimmunologically at 10 minutes ~T_0) before injection, 10 ~T_1), 60 ~T_2) and 120 minutes ~T_3) after injection. The expression of BDNF in the right DRG of cervical 7, 8 and thoracic 1 was investigated immunohistochemically at 120 minutes after injection. Results Formalin-induced nociceptive behavior in phase Ⅱ was relieved following SGB. The concentration of serum IL-8 in groups B and C at T_2 and T_3 was significantly increased than that at T_0 and T_1~P

AIM:To explose the possible existing pathway of intracellular signaling transduction in hypertensive induced by insulin in rat vascular smooth muscle cells proliferation which involved mitogen-activated protein kinase. METHODS:Male spontaneously hypertensive rat (SHR) aorta and WKY(6 weeks old) were isolated and then cultured to make the purified vascular smooth muscle cells.6-8th generation of VSMC were interfered with insulin in vitro . MAPK activity was determined by myelin basic protein method and its volume was measured with Western Blot. And [ 3 H]-TdR was used to measure DNA synthesis in VSMC proliferation. RESULTS: After the interfered with insulin the DNA synthesis was increased obviously in SHR group. MAPK activity and its contains in SHR were increased more than the control group. Protein kinase C inhibitor decreased MAPK activity induced by insulin. CONCLUSION:Proliferation of SHR VSMC in vitro was correlated with increased activity of MAPK. Insulin can affect MAPK induced activity. So an insulin-PKC-MAPK axis may exist in hypertensive VSMC.

Objective To quantitate coronary tortuosity and provide favorable conditions for understanding the hemodynamic effects caused by coronary tortuosity.Methods We obtained all images from 72 patients who received coronary computed tomo-graphy scanning.After image post-processing,we extracted the medial axis of three main coronary vessel and analysed its coordi-nates on three dimensions.Then we calculated the tortuosity coefficient of coronary artery.Results Tortuosity coefficient was 6.66±7.54 in anterior descending,13.43±12.85 in left circumflex,and 1 7.61 ±7.67 in right coronary artery.We had proved its validity by the changes in morphology with simulated shapes.Conclusion We proposed a new method for quantitating coronary tor-tuosity,by computed tomography coronary imaging.The measurement results would not be affected by projection plane,vessel length or other artificial factors.

ObjectiveTo observe the effect on stress response to indwelling gastric tube assisted by bronchofiberoscope and traditional way in patients with severe craniocerebral injury in intensive care unit(ICU). Methods 126 patients admitted in Department of Surgery ICU in Lanzhou University Second Hospital were randomly divided into bronchofiberoscope assisted indwelling gastric tube group(experimental group) and the traditional way of indwelling gastric tube group(control group), 63 cases in each group. In the experimental group, the rod of mirror, Olypus BF-P60, was coated with lidocaine gel, through the nasal cavity it was sent into interior, when arrived at epiglottis, the operator adjusted the mirror head and let it go into the esophagus(about 10 cm), then put a steel wire as a guide into a hole for biopsy, and simultaneously, as the operator pulled out the rod, the wire was continuously pushed slowly further inside; after the bronchofiberoscope was completely withdrawn, valelinum liquidum was used to ensure sufficient lubrication to the external and internal walls of the indwelling gastric tube ready to be sent into the stomach, afterwards the tube was slowly pushed along the guide wire to an appropriate location and then the wire was pulled out, the operator injected air, when he or she heard the gurgling sound as the gas passing water, fixed the tube. In the control group, the traditional way of indwelling gastric tube was applied. Before and after indwelling gastric tube for 1, 3, 5 minutes, the changes of systolic pressure(SBP),diastolic pressure(DBP),heart rate(HR), end-expiratory carbon dioxide partial pressure(PETCO2) and plasma concentrations of norepinephrine(NE), adrenaline, angiotensinⅡ(AngⅡ), glucose(GLU) were examined.Results The plasma levels of SBP, DBP, HR, PETCO2, adrenaline, NE, AngⅡ and blood GLU had no statistical significant differences before operation in comparisons between both groups(allP>0.05). Compared to those before indwelling the tube, the levels of SBP, DBP, HR, PETCO2, NE, adrenaline, AngⅡ and GLU at various time points after the indwelling in experimental group were of no statisticalsignificant differences(allP>0.05), while the levels of SBP, DBP,HR, adrenaline, NE, AngⅡand GLU in control group at various time points after indwelling were higher obviously than those before operation, and the level of PETCO2 was decreased significantly compared with that before operation. The differences in the above indexes were significant between the treatment and control groups at 1 minute after indwelling〔SBP(mmHg, 1 mmHg=0.133 kPa): 125.1±15.4 vs. 135.5±13.6, DBP(mmHg): 85.6±16.1 vs. 91.1±17.2, HR(bpm): 99.4±13.8 vs. 107.9±16.5, PETCO2(mmHg): 32.5±2.8 vs. 29.8±4.1, NE(ng/L): 365.4±29.7 vs. 475.7±49.9, adrenaline(ng/L): 75.4±7.2 vs. 83.6±7.4, AngⅡ(ng/L): 65.3±6.9 vs. 73.3±9.1, GLU(mmol/L): 10.1±1.9 vs. 13.4±3.0, allP<0.05〕; the differences in the above indexes remained significant between the treatment and control groups till 5 minutes after indwelling〔SBP(mmHg): 123.7±14.8 vs. 129.7±15.1, DBP(mmHg): 84.3±14.6 vs. 88.4±14.2, HR(bpm): 97.7±13.6 vs. 31.6±3.9, PETCO2(mmHg): 33.5±3.1 vs. 31.6±3.9, NE(ng/L): 363.9±31.3 vs. 457.7±48.4, adrenaline(ng/L): 74.6±7.8 vs. 83.5±8.5, AngⅡ(ng/L): 64.3±8.4 vs. 71.9±5.9, GLU(mmol/L): 9.6±2.3 vs. 12.7±3.1, allP<0.05〕.ConclusionCompared with traditional way, the indwelling of gastric tube assisted by branchofiberoscopy can induce milder stress response.

AIM: To explore the effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction.METHODS: The mouse model of heart failure was established by ligating the left anterior descending coronary to produce acute myocardial infarction.Thirty-two mice were divided into 4 groups: sham group and groups of post-operation at time points of 2,4 or 6 weeks,respectively.The ventricular dilatation and left ventricular functions were assessed by echocardiography.The expression of GRP78,CHOP,caspase-12,cleaved caspase-12,JNK and phosphorylated-JNK was detected by Western blotting.The cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL).RESULTS: The cardiac expression of endoplasmic reticulum chaperones GRP78 was significantly increased in the hearts with functional failure.The upregulated expression of CHOP,phosphorylated-JNK and cleaved caspase-12 illuminated that the CHOP-JNK-caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis were activated in the heart with functional failure by myocardial infraction.CONCLUSION: These findings suggest that the congestive heart failure induced by myocardial infraction is associated with endoplasmic reticulum stress and activation of CHOP,JNK,caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis.

AIM: To identify proteins involved in insulin stimulation and the molecular mechanism of proliferation and migration in vascular smooth muscle cells (VSMCs). METHODS: A series of methods, including 2-D electrophoresis, PDQuest software analysis of 2-DE gels, peptide mass fingerprinting based on matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) and SWISS-PROT database searching, were used to separate and identify the differentially expressed proteins. The difference of some proteins was proved by Western blotting. Proliferation and migration of VSMCs treated with insulin were also observed. RESULTS: DNA synthesis were increased in VSMCs. ~3H-thymidine incorporation in VSMCs from SHR (14.40?0.85) was higher than that in VSMCs from WKY (9.21?0.93, P

AIM: To investigate the changes of intracellular calcium ion (Ca2+) concentration in mouse H9c2 (2-1) cells transfected with or without FK506 binding protein 12.6(FKBP12.6) gene by ultrasound mediated destruction of microbubbles. METHODS: The pcDNA3.1-FKBP12.6 plasmid, mingled with albumin-coated microbubbles agents, was transfected into H9c2 (2-1) cells by ultrasound-mediated destruction of microbubbles. The H9c2 (2-1) cell growth state was investigated by inverted microscope. The changes of intracellular Ca2+ concentration was determined by laser scanning confocal microscope. The FKBP12.6 protein expression was checked by immunohistochemistry. RESULTS: As compared with control cells, the H9c2 (2-1) cells, transfected with FKBP12.6 gene, grew better, had higher gross intracellular Ca2+ concentration. CONCLUSION: FKBP12.6 gene augments Ca2+ concentration in mouse H9c2 (2-1) cells, enhances the contractibility of the myocardial cell, which may be helpful to improve the myocardial dysfunction.

Objective To evaluate the effects on blood pressure and vascular endothelial-1 function of combined therapy of atrovastin and nifedipine controlled released tablet in essential hypertension.Methods A randomized,double-blind,controlled trial was performed.Eighty-two patients with essential hypertension were randomly divided into two groups,receiving nifedipine controlled released tablet 30 mg once daily,or atrovastin 10 mg once daily and nifedipine controlled released tablet 30 mg once daily for 12 weeks.Another 30 subjects with normal blood pressure served as normal blood pressure control.Antihypertensive efficiency was observed during the whole study period.The concentration of plasma endothelin-1(ET-1) nitric oxide(NO) were measured before and after treatment.Results Blood pressure decreased significantly in both groups,but more significant in combined therapy group.In the combined therapy group,atrovastin resulted in a significant reduction of plasma ET-1 and a rise of nitric oxide(NO)(P