Objective To compare the clinical efficacy and safety of early endovascular treatment(EVT)for the stroke patients caused by large vessel occlusion(LVO)due to intracranial atherosclerosis(ICAS)or due to cardioembolism(CE).Methods The clinical data of 488 patients with acute anterior circulation LVO stroke,who received early endovascular treatment at the Yijishan Hospital of Wannan Medical College of China from October 2015 to December 2023,were retrospectively analyzed.According to the cause of disease,the patients were divided into ICAS group(n=108)and CE group(n=380).The clinical data,mainly including the proportion of patients having a good prognosis at 90 days after operation(modified Rankin Scale score ≤2 points),the incidence of symptomatic intracranial cerebral hemorrhage(sICH),and the mortality of patients at 90 days after operation.Multivariate logistic regression analysis was used to analyze the factors influencing patient's prognosis.Results Of the 488 patients,29(5.9％)developed postoperative sICH,242(49.6％)achieved a good prognosis at 90 days after the operation,and 91(18.6％)died.The above outcomes in the ICAS group were one,66,and 11 patients respectively,which in the CE group were 28,176,and 80 respectively,and the differences between the two groups were statistically significant(all P＜0.05).Multivariate logistic regression analysis indicated that good prognosis at 90 days after the operation(OR=0.962,95％CI:0.404-2.288,P=0.930)and the postoperative 90-day mortality(OR=1.379,95％CI:0.436-4.362,P=0.584)were not the factors influencing prognosis,while the postoperative sICH(OR=19.132,95％CI:1.332-274.791,P=0.030)was the factor influencing prognosis.Conclusion In CE group,the incidence of sICH and the postoperative 90-day mortality are higher,while in ICAS group,the postoperative 90-day good prognosis rate is higher.The postoperative sICH is the factor influencing prognosis.

Objective To evaluate the role of c?Jun N?terminal kinase ( JNK) and p38 mitogen?ac?tivated protein kinase ( p38MAPK) signaling pathways in attenuation of myocardial ischemia?reperfusion ( I∕R) injury by morphine postconditioning. Methods Healthy adult male Sprague?Dawley rats, weighing 180-240 g, were used in the study. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with Krebs?Ringer ( K?R) buffer saturated with 95% O2?5% O2 at 37℃. After 15 min of equili?bration, 52 isolated hearts were divided into 4 groups ( n=13 each) using a random number table: control group (group C), I∕R group, morphine postconditioning group (group MP), and morphine postcondition?ing plus anisomycin group ( group MP+A) . The hearts were continuously perfused with K?R buffer for 105 min in group C. In group I∕R, the hearts were subjected to 45 min of global ischemia by stopping perfusion with K?R buffer, followed by 60 min of reperfusion by restoration of perfusion with K?R buffer. In group MP, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and then by 50 min of reperfusion with K?R buffer. In group MP+A, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and 1?0 μmol∕L anisomycin ( an activator of JNK and p38MAPK) and then by 50 min of reperfusion with K?R buffer. At 60 min of reperfusion, 8 hearts in each group were selected for measurement of the myocardial infarction and amount of creatine kinase?MB ( CK?MB) released from the myocardium, and the myocardial infarct size was calculated. At 20 min of reperfusion, 5 hearts in each group were selected to detect the expression of phosphorylated JNK ( p?JNK ) , phosphorylated p38MAPK ( p?p38MAPK) and cytochrome c ( Cyt c) in myocardial tissues ( by Western blot) and content of nicotinamide adenine dinucleotide ( NAD+) in myocardial tissues ( by spectrophotometry ) . Results Compared to group C, the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regulated, and the content of NAD+ was significantly decreased in I∕R, MP and MP+A groups ( P<0?05) . Compared to group I∕R, the myocardial infarct size and amount of CK?MB released from the myocardium were signifi?cantly decreased in MP and MP+A groups, and the expression of p?JNK, p?p38MAPK and Cyt c was sig?nificantly down?regulated, and the content of NAD+ was significantly increased in group MP (P<0?05). Compared to group MP , the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regula?ted, and the content of NAD+ was significantly decreased in group MP+A (P<0?05). Conclusion The mechanism by which morphine postconditioning attenuates myocardial I∕R injury is related to inhibition of activation of JNK and p38MAPK signaling pathways in rats.

ObjectiveTo investigate the effects of sleep deprivation on expressions of Mir-132,mir-134 in the different regions of rat brain.MethodsAll the male SD rats were divided into control group ( normal sleep group),sleep deprivation (SD).The modified multiple platform method (MMPM) was used to establish sleep deprivation model.Mir-132,mir-134 level was detected by real time PCR.ResultsMir-132 were significantly increased in SD groups in hippocampus compared with the control groups ( 51.87 ± 8.13 vs 67.25 ± 7.59 ) (P ＜0.01 ).Mir-134 were significantly decreased in SD groups compared with the control groups( 1.82 ±0.15 vs 1.45± 0.12 )(P ＜ 0.01 ).There were no statistically significant differences in cortex and thalamus (P ＞ 0.05 ).Cortex mir-132 level in SD group and control group was 1.57 ±0.10,1.48 ±0.11 respectively,and it was 1.37 ±0.09,1.36 ±0.11 in thalamus;Cortex mir-134 level in SD group and control group was 98.26 ± 5.17,100.80 ±4.15respectively,and it was 97.56 ± 6.28,91.01 ± 4.07 in thalamus.ConclusionThe upregulation of mir-132 and downregulation of mir-134 implies that two miRNAs did opposite actions in the processes of sleep deprivation.This findings indicate that hippocampus mir-132,mir-134 levels in the SD rat may reflect associated depressive patho-physiological processes.

To summarize the experiences of optimization of emergency medical care in Nanjing General Hospital.The principles and methods of optimizing emergency medical care were analyzed and summarized.The following methods were used to improve the emergency medical care: Applying modern conceptions of emergency medicine and establishing professional physician teams;Reinforcing the duty of each position and improving the quality of medical care;Modifying the mode and improving the working efficiency;Establishing clinical pathways for disasters and other accidents.The roles of emergency medicine are changed and modernized. Optimization of emergency care and popularization of emergency care skills may improve the quality and efficiency of emergency medical care.