Objective To observe the cardiac function in acute brain injury patients(ABI)and the relationship between ABI and plasma neuropeptideY(NPY),and to inspect the mechanism and find the evidences for preventing cardiac impairment caused by ABI. Methods 89 patients with acute brain injury within 24 hours after the injury were divided into severe group(n =47)and mild group(n = 42)according to Glasgow Coma Scale(GCS),and 35 normal healthy adults were selected as control group.In 24 hours and 72 hours after the brain injury,all patients were examined with echocardiography to observe cardiac structure,Doppler blood flow velocity and cardiac function,and in the same time the plasma NPY were determined by radioimmunoassay.Then the results were compared with controls. Results The parameters of cardiac function such as EF、 SV.AV、CO、CI had statistical change in 24 hours and 72hours after the brain injury between severe ABI group and mild ABI group,and it also had statistical change between severe ABI group and control group(all P <0.05),but no statistical change between mild ABI group and control group(all P ＜0.05).The level of plasma NPY in ABI patients was significantly higher than that before injury,there was statistically different change between severe ABI group and mild ABI group,and it also had statistical change between severe ABI group and control group(all P＜0.05).The parameters of cardiac function was negatively correlated with the rise of plasma NPY by pearson correlation analysis(EF:r =- 0.79,P <0.01; SV:r =- 0.71,P <0.01;AV:r=-0.67,P ＜0.01 ;E/A:r =-0.63,all P ＜0.01)and(CO:r =- 0.32,P ＜0.05;CI:r =-0.35,all P ＜0.05). Conclusion The parameters of cardiac function were significantly decreased in the patients with acute brain injury,and it was closely related with the level of plasma NPY.

Objective To evaluate the value of glycogen phosphorylase isoenzyme BB (GPBB) in the diagnosis of early acute myocardial infarction (AMI). Methods The plasma levels of GPBB were mea-sured by sandwich ELISA in 115 patients with suspected AMI at admission within 6 hours after onset of chest pain and 55 normal healthy subjects. The plasma concent of cardiac troponin-Ⅰ (cTnI), creatine kinase-MB (CK-MB) and myoglobin (MYO) was assayed at the same time by using corpuscle chemiluminescence. The patients were classified retrospectively into AMI group (n = 45) , unstable angina pectoris (UAP) group (n =40) , stable angina pectoris (SAP) group (n = 13) and non-cardiac chest pain (NCCP) group (n =17).The diagnostic validity was evaluated in terms of sensitivity and specificity. Results The diagnostic sensitivity of GPBB for AMI was 64.29 % within 3 hours and 88.89 % within 6 hours after onset of chest pain,which is significantly higher than that of cTnI (28.57 %, 60.00 %) and CK-MB (21.43 %, 64.44 % ). There was no significant difference in specificity among the four markers. The diagnostic accuracy of GPBB within 3hours and 6 hours (80.77 %, 89.57% ) was significantly higher than that of cTnI (61.54%, 81.74% ),CK-MB (50.00%, 75.65%) and MYO (73.08% ,73.91%). Conclusions GPBB seems to be a sensitive and specific biochemical cardiac marker for AMI in the early stage. Its diagnostic accuracy is higher than that of cTnI, CK-MB, MYO.

Objective To compare the changes of plasma lipid indexes and coronary artery atherosclerotic plaque in TaqI B genotypes in CHD patients with impaired glucose tolerance (IGT) before and after statin therapy. Methods A total of 196 CHD with IGT and 160 controls were included. The changes of plasma lipid indexes and coronary artery atherosclerotic plaque in TaqI B genotypes were analyzed before and after Rosovastatin therapy. Sequenom Mass ARRAY platform was used to detect the CETP TaqI B SNPs. Results The genotype frequency of the B1B1, B1B2 and B2B2 in CHD with IGT group was 35.7%, 48.0% and 16.3% respectively, while in control group was 31.3%, 53.1% and 15.6% respectively. HDL-C, PA and MLA levels increased after Rosuvastatin therapy, while LDL-C, TG, TCH, Lpa, PA, EEMA and PB levels decreased. Conclusions CETP gene polymorphisms TaqI B would have association with the effects of Rosuvastatin therapy in the CHD with IGT.

Objective To investigate the anti-oxidative effects of alprostadil on contrast-induced nephropathy(CIN)after percuteous coronary intervention (PCI)in patients with chronic kidney disease(CKD).Methods A total of 200 patients with CKD were enrolled in our hospital.According to the random number table was divided into alprostadil 100 cases,100 cases of conventional treatment group.The levels of serum creatinine (Scr),creatinine clearance (eGFR),serum cystatin C (ScysC)and 8-hydroxy-deoxyguanine (8-OHdG)were observed before and after operation at 72 h and 7 d after operation.Results The incidence of CIN in the alprostadil group was significantly lower than that in the conventional treatment group (6% vs 12%,P<0.05).There was no significant difference in the level of Scr,eGFR,ScysC and 8-OHdG between the alprostadil group and the conventional treatment group (P>0.05).The level of Scr in the alprostadil group was significantly lower than that in the conventional treatment group at 72 h and 7 d after operation.The level of eGFR was significantly higher than that of the conventional treatment group (P<0.05).The levels of ScysC and 8-OHdG in the two groups were significantly higher than those before operation at 72 h and 7 d(P>0.05).The levels of ScysC and 8-OHdG in the alprostadil group were significantly lower than those in the conventional treatment group at 72 h and 7 d after PCI(P<0.05).Conclusion Alprostadil may improve the oxidative stress in patients with CKD and provide a preventive effect on CIN.