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 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

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.

AIM To investigate the beneficial effects of aminoguanidine(AG), a selective inducible nitric oxide synthase (iNOS) inhibitor, on cerebral ischemic injury of rats and the possible mechanism. METHODS The middle cerebral artery occlusion model was prepared with thread embolism. AG 100 mg·kg-1 was injected ip first at 2, 6 and 12 h, respectively, after ischemia, then 2 times a day for 3 consecutive days. The infarct volume of brain tissue was determined with tetrazolium chloride staining. The mitochondria in brain tissue were isolated for measuring integrity of electron transport chain (ETC), mitochondrial swelling, NO and malondialdehyde (MDA) contents, ATPase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. In addition, the neuronal cells of newborn rats were cultured in glucose-free medium with sodium hydrosulfite for cell viability, lactate dehydrogenease (LDH) and NO analysis. RESULTS AG significantly reduced infarct volume, ameliorated neuronal ultramicrostructural damages induced by ischemia. And the swelling of mitochondria, the lesions of ETC, the contents of MDA and NO in mitochondria were markedly decreased, the activities of ATPase, SOD and GSH-Px in mitochondria were increased. In vitro, compared with the ischemic group, AG(10, 20 and 100 μmol·L-1)increased the cell viability and reduced the contents of LDH and NO in culture medium. CONCLUSION AG has protective effects on cerebral ischemic injury through inhibiting the production of oxygen free radical, increasing antioxidation, ameliorating energy metabolism, and beneficially improving the integrity of structure and function of mitochondria in brain tissue.

AIM To investigate the beneficial effect of aminoguanide (AG) on cerebral ischemic injury and the possible mechanism. METHODS The model of focal cerebral ischemia in rat was prepared. Rats were divided into sham-operated group, ischemic group and AG group. Each group was further divided into 3 subgroups (n=6 for each): drugs were administrated at 2, 6 and 12 h after the middle cerebral artery occlusion (MCAO), respectively. AG (100 mg·kg-1, ip) was administrated, 2 times a day, for 3 consecutive days. The changes in infarcted volume and the contents of amino acids were assayed. RESULTS The infarcted volume (15.1±3.4, 18.4±5.1, 25.7±3.5) was much decreased compared with that of ischemic group (23.2±2.9, 28.0±3.9, 37.2±2.9) when AG was administrated at 2, 6 and 12 h after MCAO respectively (%, P<0.05, n=6). The contents of aspartate, glutamate, glycine and GABA in striatum, hippocampus and cortex in ischemic group were significantly increased compared with sham-operated group(P<0.05 or P<0.01, n=6). The contents of glutamate in striatum, hippocampus and cortex were markedly decreased when AG was given at 2, 6 and 12 h after ischemia respectively(P<0.05 or P<0.01, n=6). The contents of aspartate in striatum, hippocampus and cortex were markedly decreased when AG was given at 2 and 6 h, and the contents of aspartate in hippocampus and cortex were decreased when AG was given at 12 h after ischemia (P<0.05 or P<0.01, n=6). The contents of GABA in hippocampus and cortex were increased when AG was given at 2 and 6 h, and the contents of GABA in striatum and cortex were increased when AG was given at 12 h after ischemia(P<0.05 or P<0.01, n=6). Thecontents of glycine were increased in striatum, hippocampus and cortex when AG was given at 2 h, the contents of glycine were increased in cortex when AG was given at 6 h, and the contents of glycine in hippocampus and cortex when AG was given at 12 h after ischemia respectively(P<0.05 or P<0.01, n=6). CONCLUSION AG has beneficial effect on ischemic cerebral injury. The possible mechanism is that AG can decrease the contents of aspartate and glutamate, increase the contents of glycine and GABA.

Ob jectiev Oxidized low-density lipoprotein ( ox-LDL) induces vascular endothelial cell injury , which is one of the factors initiating atherosclerosis .This study aimed to investigate the protective effect of Tongxinluo ( TXL ) on vascular endothelial cells with ox-LDL-induced injury . Methods Human umbilical vein endothelial cells ( HUVEC ) were cultured in vitro and divided into five groups:normal control, oxidative stress injury (OSI) model, and high, medium and low dose TXL.The HUVECs were incubated with ox-LDL at the concentration of 30 mg/L for 24 hours to induce oxidative stress injury and then treated with TXL at 50, 100 and 150 mg/L for 4 hours, followed by 24 hour incubation with 30 mg/L ox-LDL added to the culture medium .The viability of the cells was detected by MTS assay, the nitric oxide (NO) content, superoxide dismutase (SOD) activity and mitochondrial membrane poten-tial ( MMP) in the cell culture supernatant were measured with respective kits , and the expressions of iNOS , MMP9, and NF-κBp65 proteins were determined by Western blot . Results The HUVECs of the OSI model group showed a significant decrease in cell via-bility compared with the normal control , ([73 .89 ±0.67] vs [100.00 ±2.23]%, P<0.01) but a remarkably increase after treated with medium and high dose TXL ([92.15 ±0.76]%and [ 97.19 ±1.45]%, P<0.01).The MMP, NO content, and SOD activity were markedly reduced in the model group (P<0.01) but elevated in the low, medium, and high dose TXL groups (P<0 .01).The expressions of the iNOS, MMP9, and NF-κBp65proteins were significantly up -regulated in the model group (P<0.01) but down reg-ulated in the low, medium, and high dose TXL groups (P<0.05).C on clusion TXL has the effects of anti-oxidation and anti-in-flammation and can protect vascular endothelial cells against ox-LDL-induced injury .

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