目的联合应用抗血小板聚集(拜阿司匹林片)、和(或)抗凝(法安明)、和(或)降脂(辛伐他汀)和(或)溶栓(rt-PA)治疗急性脑梗死,同时观察血清死亡蛋白激酶1(death-associated protein kinase1,DAPK1)含量的变化,进一步探讨NMDA受体和死亡蛋白...目的联合应用抗血小板聚集(拜阿司匹林片)、和(或)抗凝(法安明)、和(或)降脂(辛伐他汀)和(或)溶栓(rt-PA)治疗急性脑梗死,同时观察血清死亡蛋白激酶1(death-associated protein kinase1,DAPK1)含量的变化,进一步探讨NMDA受体和死亡蛋白激酶(DAPK1)在脑梗死的相互作用,为缺血性脑血管疾病的防治提供临床依据。方法选择发病在72h以内住院急性脑梗死患者,分为溶栓组11例、常规治疗组56例,并选择我科因后循环缺血住院患者46例做为对照组。溶栓组除了给予rt-PA溶栓外,与常规治疗组均联合应用抗血小板聚集(阿司匹林肠溶片100mgqd)、和(或)抗凝(低分子肝素5000u皮下注射,每日2次)、和(或)降脂(辛伐他汀片20mgqN)及活血化瘀(奥扎格雷钠40mgqd)、清除自由基(依达拉奉30mg bid)等治疗,对照组仅给予常规的活血化瘀、营养神经等治疗,观察治疗前和治疗10d后患者的血清死亡蛋白激酶1(DAPK1)含量的变化,以及肝功能、血小板、凝血机制及临床神经功能缺损评分进行评定,进一步探讨NMDA受体和死亡蛋白激酶1(DAPK1)在缺血性脑血管疾病的相互作用机制。结果溶栓组及常规治疗组患者的死亡蛋白激酶1(DAPK1)含量均高于对照组,治疗10天后溶栓组及常规治疗组患者的死亡蛋白激酶1(DAPK1)含量均降低,常规治疗组更明显(P<0.05),溶栓组的神经功能缺损评分(NIHSS)明显降低(P<0.05),临床疗效明显优于常规治疗组(P<0.05),肝功能、血小板、凝血功能、血脂的指标均在正常范围内。结论死亡蛋白激酶1(DAPK1)通过与NMDA受体的NR2B亚型结合激活神经细胞死亡通路,激发神经细胞死亡,形成卒中[2],为缺血性脑血管病的防治提供临床依据。展开更多
p53 mutations have been linked with shortened survival rates in non-small cell lung cancer (NSCLC). Hypermethylation of RASSF1 and DAPK1 genes, which are downstream targets of p53, has also been linked to a poor progn...p53 mutations have been linked with shortened survival rates in non-small cell lung cancer (NSCLC). Hypermethylation of RASSF1 and DAPK1 genes, which are downstream targets of p53, has also been linked to a poor prognosis in lung cancer patients. We investigated whether p53 mutations, assessed as p53 stabilization by immunohistochemistry (IHC), were independent of DAPK1 and RASSF1 promoter hypermethylation. We examined 103 resected NSCLC tumors for which we had p53 IHC and RASSF1 and DAPK1 methylation data. p53 protein expression was determined by IHC and graded using a semi-quantitative scoring method. DAPK1 and RASSF1 methylations were determined on tumor blocks by MethyLight real-time PCR assays represented as the percent of methylated reference DNA (PMR). Our primary results found no evidence for an association between the p53 IHC score and RASSF1 and DAPK1 PMR values, P = 0.46 and P = 0.68, respectively.展开更多
文摘目的联合应用抗血小板聚集(拜阿司匹林片)、和(或)抗凝(法安明)、和(或)降脂(辛伐他汀)和(或)溶栓(rt-PA)治疗急性脑梗死,同时观察血清死亡蛋白激酶1(death-associated protein kinase1,DAPK1)含量的变化,进一步探讨NMDA受体和死亡蛋白激酶(DAPK1)在脑梗死的相互作用,为缺血性脑血管疾病的防治提供临床依据。方法选择发病在72h以内住院急性脑梗死患者,分为溶栓组11例、常规治疗组56例,并选择我科因后循环缺血住院患者46例做为对照组。溶栓组除了给予rt-PA溶栓外,与常规治疗组均联合应用抗血小板聚集(阿司匹林肠溶片100mgqd)、和(或)抗凝(低分子肝素5000u皮下注射,每日2次)、和(或)降脂(辛伐他汀片20mgqN)及活血化瘀(奥扎格雷钠40mgqd)、清除自由基(依达拉奉30mg bid)等治疗,对照组仅给予常规的活血化瘀、营养神经等治疗,观察治疗前和治疗10d后患者的血清死亡蛋白激酶1(DAPK1)含量的变化,以及肝功能、血小板、凝血机制及临床神经功能缺损评分进行评定,进一步探讨NMDA受体和死亡蛋白激酶1(DAPK1)在缺血性脑血管疾病的相互作用机制。结果溶栓组及常规治疗组患者的死亡蛋白激酶1(DAPK1)含量均高于对照组,治疗10天后溶栓组及常规治疗组患者的死亡蛋白激酶1(DAPK1)含量均降低,常规治疗组更明显(P<0.05),溶栓组的神经功能缺损评分(NIHSS)明显降低(P<0.05),临床疗效明显优于常规治疗组(P<0.05),肝功能、血小板、凝血功能、血脂的指标均在正常范围内。结论死亡蛋白激酶1(DAPK1)通过与NMDA受体的NR2B亚型结合激活神经细胞死亡通路,激发神经细胞死亡,形成卒中[2],为缺血性脑血管病的防治提供临床依据。
文摘p53 mutations have been linked with shortened survival rates in non-small cell lung cancer (NSCLC). Hypermethylation of RASSF1 and DAPK1 genes, which are downstream targets of p53, has also been linked to a poor prognosis in lung cancer patients. We investigated whether p53 mutations, assessed as p53 stabilization by immunohistochemistry (IHC), were independent of DAPK1 and RASSF1 promoter hypermethylation. We examined 103 resected NSCLC tumors for which we had p53 IHC and RASSF1 and DAPK1 methylation data. p53 protein expression was determined by IHC and graded using a semi-quantitative scoring method. DAPK1 and RASSF1 methylations were determined on tumor blocks by MethyLight real-time PCR assays represented as the percent of methylated reference DNA (PMR). Our primary results found no evidence for an association between the p53 IHC score and RASSF1 and DAPK1 PMR values, P = 0.46 and P = 0.68, respectively.
