Objective:To explore the effectiveness and safety of simvastatin combined ezetimibe in patients with acute coronary syndrome (ACS).Methods:A total of 124 ACS patients complicated low density lipoprotein cholesterol (LDL-C)>100 mg/dl were selected from our hospital from May 2012 to May 2013. They were randomly and equal-ly divided into rosuvastatin group (received rosuvastatin 20mg/d)and combined treatment group (received simvasta-tin 40mg/d plus ezetimibe 10mg/d),both groups were treated for one month.Blood lipid levels and incidence rates of adverse reactions were observed in two groups.Results:Compared with before treatment,after one-month treat-ment there were significant reductions in levels of LDL-C,total cholesterol (TC)and triglyceride (TG)and signifi-cant rise in levels of high density lipoprotein cholesterol (HDL-C)in both groups (P <0.01 all),and there were no significant difference in all above blood lipid levels between two groups (P >0.05).Incidence rate of myalgia in combined treatment group was significantly lower than that of rosuvastatin group (4.8% vs.17.7%,P =0.023), but there were no significant difference in incidence rates of other adverse reactions between two groups (P >0.05 all).Conclusion:It′s effective and safe to use simvastatin combined ezetimibe in patients with acute coronary syn-drome,which is worthy extending.

Objective By exploring echocardiographic ch aracters and pathologic examination of noncompacted ventricular myocardium(NVM), to prevent life-threatening arrhythmias and embolism. Methods Echocardiographic examinations included four-chamber view, two-chamber view and short axis view of left ventricle, with an emphasis on observing left ventricular myocardium and endocardium approach to one-third of apex of heart. Results All 24 patients showed obvious echocardiographic findings characterized by prominent and excessive myocardial trabeculations and deep intratrabecular recesses in the affected ventricular cavity. Three cases complicated with other congenital heart malformations, 20 cases with congestive heart failure and only 2 cases were asymptomatic. Coronary arteriography was performed in 13 cases and revealed normal findings. Two cases eventually underwent heart transplantation because of severe congestive heart failure. Gross and histological findings demonstrated prominent muscular trabeculations, with deep intratrabecular recesses into lesion heart. Serial section from the base of the ventricle toward the apex revealed gradually weaker myocardium. Noncompaction of ventricular myocardium showed a thin, compacted epicardial and an extremely thickened endocardium by fibrous tissue. Conclusions Noncompaction of ventricular myocardium has characteristic echocardiographic manifestations and specific pathologic changes, which are different from those of primary enlarged type of cardiomyopathy.

Objective To study effects of 1 800 MHz electromagnetic field exposure in pregnancy on the ultrastructure of the hippocampus of offspring rats. Methods Ninety Wistar rats(female and male was 2:1) were mated,and the pregnant rats were exposed to 1 800 MHz microwave field with power density of 0.5 mW/cm2 or 1.0 mW /cm2,12 h/d,for 21 consecutive days,the rats in the control group received dummy exposure. Three rats aged 3 days and 72 days were selected from groups for ultrastructure observation of hippocampus. Results No significant pathological changes were observed in nerve cells and capillary vessels in the hippocampus. Conclusion The results of the present paper indicate that pregnancy exposure to 1 800 MHz electromagnetic field,may not lead to abnormal ultrastructure changes in hippocampus of offspring rats

The current complex medical environment has a negative influence on doctors and also hinders the further development of healthcare industry in China.By analyzing the problems of medical social workers in doctors' social support system,this paper proposes the roles medical social workers should play in constructing a new social support system of doctors.

Objective To investigate the effects of nitric oxide(NO) and its donor(L-arginine) on focal cerebral ischemic injury in rats. Methods Forty-two healthy male SD rats weighing 250-300g were used. The animals were anesthetized with 20% urethane 1g? kg-1. Common carotid artery (CAA), external carotid artery(ECA) and internal carotid artery were(ICA) exposed through a median incision in the neck. Middle cerebral artery occlusion (MCAO) was produced by insertion of a 40 mm long nylon thread (0.3 mm in diameter) into ICA through ECA. The tip of the nylon thread was made into a ball of 0.5 mm in diameter with heat and the length of insertion was (18.5?0.5)mm on average. The animals were randomly divided into four groups: group 1: sham operation; group 2: ischemia group; group 3: low dose L-arginine(300mg?kg-1 intraperitoneal injection) and group 4: high dose L-arginine(500mg?kg-1 IP). Group 3 and 4 were further divided into 3 subgroups: subgroup A: L-arginine was given 1h after MCAO and the animals were killed 2h after medication (1h + 2h); subgroup B: L-arginine was given 3h after MCAO and the animals were killed 3h after medication(3h + 3h) and subgroup C: L-arginine was given 6h after MCAO and the animals were killed 3h after medication(6h + 3h) . The brain was removed immediately. The volume of cerebral infarct/volume of whole brain was calculated(%) . The NO, MDA content and NOS, SOD activity in the brain tissue of ischemic hemisphere were measured. Results L-arginine significantly decreased cerebral infarct volume and ameliorated focal cerebral ischemia. The effects in high dose group were better than in low dose group. L-arginine significantly increased NO content, decreased MDA content and enhanced the SOD activity in the focal ischemic cerebral tissue. Conclusions It may be concluded that L-arginine has beneficial effect on brain injury in acute ischemic stage and high dose provides better effects.

Objective To compare the clinical pharmacodynamics of domestic and imported propofol by target-controlled infusion. Methods This was a prospective,randomized,double-blind,cross-over study. Eighteen ASA Ⅰ or Ⅱ patients aged 45-55 yr undergoing substitute valve operation for severe deep venous were randomly divided into sequential Ⅰ and Ⅱ , in sequence Ⅰ , the imported propofol was applied in the first stage of surgery and then domestic propofol in the second stage surgery, while in sequence Ⅱ the order was reversed. The target plasma concentration of propofol was initially set at 0.5 μg/ml, followed by increments of 0.5 μg/ml when the effect-site concentration and plasma concentrations was balanced, until the predicted effect-site concentrations reached 3.5 μg/ml. BIS value, RR, SpO2 and hemodynamics were recorded at 0,0.5, 1.0,1.5,2.0,2.5,3.0 and 3.5 μg/ml effect-site concentration level, the predicted effect-site concentrations and the BIS value at loss of consciousness in 5%, 50% and 95% of the patients were calculated. Adverse reactions were recorded during the trial period.Results Under the same effect-site concentration,there was no significant difference in BIS value,RR, SpO2 and hemodynamic monitoring indicators between the two drugs( P ＞ 0.05). There was no significant difference in predicted effect-site concentrations of propofol, the BIS value at loss of consciousness in 5%, 50% and 95% of the patients and the incidence of adverse reaction between the two drugs ( P ＞ 0.05). Conclusion The domestic propofol and imported propofol have clinical bioequivalence.

Objective: To investigate the beneficial effect of NG-nitro-L-arginine(L-NA) on cerebral ischemic injury and the possible mechanism by evaluating the effect of nitric oxide synthase(NOS) inhibitor,L-NA,on the contents of aspartate,glutamate,glycine and?-aminobutyric acid(GABA),respectively,in striatum,hippocampus and cortex of rat brain following cerebral ischemia. Methods:The model of focal cerebral ischemia in rat was prepared.Rats were divided into sham-operated group,ischemic group and L-NA group.Each group was further divided into 3 subgroup(n=6 for each): the middle cerebral artery occlusion(MCAO) was maintained for 2,6 and 12h,respectively.L-NA(20 mg/kg,ip) was administrated after MCAO,two times a day,for 3 consecutive days.The changes of infarcted volume and the contents of amino acids were assayed. Results:The infarcted volume(IV%) was not significantly different among the ischemic groups with or without L-NA administrated 2 or 6 h after MCAO;and was markedly decreased in the ischemic group with L-NA administrated 12 h after MCAO(P

Aim To examine the effect of selective inducile nitro oxide synthase inhibitor, aminoguanidine(AG), on mitochondria injury in focal cerebral ischemia rats. Methods Rats were randomly devided into sham, ischemia and AG treatment groups. The model of focal cerebral ischemia in rats was prepared with thread embolism. AG was administered respectively at 2,6,12 h after MCAO. Rats were killed and mitochondria of cerebral tissue were isolated with differential centrifugation 3 d after AG treatment. Activities of ATPase, SOD and GSH-Px and contents of NO and MDA in mitochondria were measured. Ultrastructure changes of neuronal mitochondria were examined with electronic microscope after the ischemia and AG treatment. Results The contents of mitochondria NO and MDA markedly increased. The activities of mitochondria ATPase,SOD and GSH-Px markedly decreased in MCAO rats. Compared with ischemia group, the activities of ATPase, SOD and GSH-Px in mitochondria enhanced and the contents of NO and MDA in mitochondria decreased in ischemia 2,6,12 h group administered with AG. The study showed that the neuronal cytoplasm and the mitochondria swelled, the cristae were disrupted, dissolved or disappeared in MCAO rats. AG ameliorated these injuries induced by cerebral ischemia in rats. Conclusion AG can inhibit the production of NO, beneficially improve mitochondria energy pump and ameliorate oxidative injury after cerebra ischemia, and thus effectively protect brain damage induced by focal cerebral ischemia.

Aim To investigate the effect of L-NA on cerebral ischemic injury and the possible mechanism by evaluating the effect of N~G-nitro-L-arginine(L-NA) on neuronal apopotosis induced by transient focal cerebral ischemia in rats.Methods Male SD rats weighing 250～300 g were randomly divided into 3 groups: sham operation group(SH),ischemic group(IS) and LNA group(L-NA).IS and L-NA group were further divided into 3 subgroups according to the duration of ischemia 2 h,6 or 12 h(n=6).In L-NA group,L-NA(20 mg?kg~(-1),ip) was administrated,2 times per day,for 3 consecutive days.Saline was administrated in IS group.The focal cerebral ischemic model(MCAO) was made by thread embolism of left middle cerebral artery.In sham operation group,the external carotid artery was surgically prepared for insertion of the filament,but the filament was not inserted.Rats were killed at the scheduled time.Apoposis was detected with FCM.The expression of caspase-3 protein was observed using Western blot analysis and immunohistochemistry.The expression of bcl-2 and Bax protein was measured using immunohistochemistry and FCM.Results After MCAO significant DNA fragmentation was detected.The percentage of apoptotic cells and the expression of caspase-3 and Bax protein were increased.The ratio of bcl-2/Bax was decreased.The difference of bcl-2 protein between IS group and L-NA group was not statistically significant.In L-NA 12 h group,the percentage of apoptotic cells and the expression of caspase-3 and Bax protein were decreased.The expression of bcl-2 and the ratio of bcl-2/Bax were increased.There was no significant difference in the percentage of apoptotic cells and the expression of caspase-3,Bax,bcl-2 protein and bcl-2 /Bax between L-NA 2,6 h group and IS group.Conclusion L-NA has beneficial effect on late stage ischemic brain of rats.The protective mechanism is that administration of L-NA could reduce the expression of caspase-3,increase the expression of bcl-2 protein,and regulate the balance between bcl-2 and Bax protein.

AIM: To evaluate the effect of aminoguanidine (AG) on inflammatory factors and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury. METHODS: Thirty male SD rats (weighing 250 g-280 g) were randomly divided into three groups: (1) sham operated group (SH group, n=10), (2) ischemic groups (IS group, n=10), (3) AG group (n=10). In AG group, AG at dose of 100 mg?kg-1 was given intraperitoneally twice a day for 3 consecutive days. In IS group, normal saline was given instead of AG. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group, the carotid artery was exposed but no thread was inserted. The expression of tumor necrosis factor-?(TNF-?) was determined by immunochemistry and the content of interleulin-1?(IL-1?) was measured by radioimmunoassay. The expressions of Bcl-2 and Bax protein were detected by flow cytometry. RESULTS: The expression of TNF-? and the content of IL-1? were markedly increased after MCAO. Significantly increased DNA fragmentation, the indication of apoptosis, was detected after MCAO. The expression of TNF-? and the content of IL-1? were significantly lower in AG group than those in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in AG group than those in IS group but still significantly higher than those in SH group. The expression of Bcl-2 protein was markedly higher in AG group than that in IS group. No significant difference in the expression of Bcl-2 protein between IS and SH group was observed. CONCLUSION: AG inhibits the increase in the expression of TNF-? and the content of IL-1?, and protects neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.