长沙地区疮疹病毒性脑炎的病原研究

目的：探讨长沙地区病毒性脑炎与疱疹病毒感染的关系。方法：应用间接免疫荧光技术（ＩＥＡ）检测病毒性脑炎患者脑脊液或血清中疱疹病毒特异性ＩｇＧ、ＩｇＭ。结果：９２１例病毒性脑炎患者中有１３３例（１４．４％）诊断为单纯疱疹病毒性脑炎,１０岁以下年龄为发病高峰,９例（０．９８％）诊断为巨细胞病毒性脑炎,１２例（１．３％）为水痘－带状疱疹毒性脑炎。结论：长沙地区疱疹病毒性脑炎病原以单纯疱疹病毒最常见;ＩＦＡ     

铬结合物在铬中毒性肝损害中的作用

目的了解各种铬结合物与肝损害的关系。方法在铬中毒性肝损害的大鼠模型中,采用ＳｅｐｈａｄｅｘＧ５０凝胶层析技术,对肝中铬结合物进行分离和测定。结果铬染毒大鼠肝组织中,除可检出高分子铬结合物（ＨＭＷＣｒ,相对分子质量（ＭＷ）７００００～１２５００）及低分子铬结合物（ＬＭＷＣｒ,ＭＷ１２５００～５００）外,还发现对照组未检出的小分子铬结合物（ＭＭＷＣｒ,ＭＷ＜５００）。随染毒时间延长,肝损害加重,三者肝中分布变化明显：ＨＭＷＣｒ由２２．２％增至３７．０％;ＭＭＷＣｒ由２．２％增至５．０％;ＬＭＷＣｒ则从７５．６％降至５８．０％。结论ＬＭＷＣｒ可能与铬的解毒有关;ＭＭＷＣｒ的出现并增多反映了机体形成ＬＭＷＣｒ能力的紧张;ＭＭＷＣｒ可能是攻击靶器官的主要活性因素。     

金属硫蛋白与镉中毒性肝肾损害的关系

目的观察亚慢性镉中毒性肝肾损害,并初步探讨金属硫蛋白（ＭＴ）与肝肾损害的关系。方法用Ｗｉｓｔａｒ大鼠腹腔注射０．５ｍｇ／ｋｇＣｄ２＋的ＣｄＣｌ２３次／周,共１０周,染毒后不同时期处死大鼠,观察肝肾功能变化。结果染毒６周后,大鼠出现了明显的肝肾损害,相应组织中Ｃｄ∶ＭＴ的摩尔数之比均超过７,且随染毒总剂量的增加,Ｃｄ∶ＭＴ值明显增加,病变程度加重。结论肝肾是亚慢性镉中毒的靶器官,非ＭＴ结合的镉可能是损害肝、肾的主要成分。     

热休克蛋白70抑制大鼠感染性脑水肿炎症因子的研究

为了探讨热休克蛋白７０（ＨＳＰ７０）对大鼠感染性脑水肿的保护作用,该文采用百日咳菌液所致的大鼠感染性脑水肿模型及将大鼠进行热休克处理,观察脑组织中白细胞介素１－β（ＩＬ－１β）、肿瘤坏死因子－α（ＴＮＦ－α）及一氧化氮（ＮＯ）水平的变化,并应用Ｗｅｓｔｅｒｎ印迹分析检测大鼠脑组织的ＨＳＰ７０表达。结果发现感染性脑水肿脑组织ＩＬ－１β、ＴＮＦ－α及ＮＯ浓度均增高,热休克处理可降低以上三者的浓度,Ｗｅ     

膀胱非移行细胞肿瘤

目的 探讨膀胱非移行细胞肿瘤的诊断和治疗,提高该类肿瘤患者的生存率。方法 回顾性总结１９９０年１月￣１９９７年１２月收治的膀胱非移行细胞肿瘤１８例,其中良性非移行细胞肿瘤３例,恶性非移行细胞肿瘤１５例,临床分期Ｔ３以上１１例。比较了该类肿瘤采用膀胱全切、膀胱部分切除和姑息治疗条件下的生存率。结果 ３例良性非移行细胞肿瘤存活至今。随访１４例恶性非移行细胞肿瘤术后１、３及５年生存率分别为８５．７％、６     

潜在健康生命损失天数对脑血管疾病危害综合评价

目的综合评价脑血管疾病对人群健康的危害。方法在长沙市城区运用潜在健康生命损失天数指标从脑血管疾病的发病、病程、伤残、死亡等多方面分析调查资料。结果该城区脑血管疾病的年平均潜在健康生命损失总天数为２６２４．９４天／１０００人口,其中死亡所致寿命损失天数占健康生命损失总天数的百分比为３３．０１％,慢性伤残所致寿命损失天数占健康生命损失总天数的百分比为５３．４４％。结论出血性脑血管疾病的主要危害是死亡,缺血性脑血管疾病的危害主要是慢性伤残。     

Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide

Brief ischaemia or heat stress protects the myocardium against ischaemia-reperfusion injury. Heat stimulus evokes release of sensory nerve transmitters, including calcitonin gene-related peptide (CGRP). Since CGRP has been shown to play an important role in the mediation of ischaemic preconditioning, the present study examined whether early or delayed preconditioning induced by retrograde hyperthermic perfusion in vitro or by whole-body hyperthemia in vivo also involves endogenous CGRP. Isolated rat hearts were perfused in the Langendorff mode and subjected to 30 min global ischaemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure and its first derivatives (±dp/dt) were recorded and the CGRP-like immunoreactivity (CGRP-LI) content and the release of creatine kinase (CK) during reperfusion were measured. Retrograde hyperthermic perfusion (42 °C) for 5 min improved the recovery of cardiac function, decreased the release of CK and elevated the content of CGRP-LI in the coronary effluent. CGRP_8–37 (10^–7 mol/l), a selective CGRP receptor antagonist, abolished the cardioprotection by heat stress. Pretreatment with capsaicin (50 mg/kg s.c.), which specifically depletes sensory nerve transmitter content, abolished both the cardioprotection and the increased release of CGRP-LI. Whole-body hyperthermia (42 °C for 15 min) caused an increase in the plasma concentration of CGRP-LI. Early or delayed protection was shown in the hearts obtained from the animals subjected to whole-body hyperthermia 10 min or 48 h before the experiments. The early or delayed protection by heat stress was also abolished by pretreatment with capsaicin. The present study suggests that, in the rat, the early and delayed cardioprotection induced by heat stress involves endogenous CGRP. Received: 31 December 1998 / Accepted: 6 April 1999     

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Early cardioprotection can be achieved by a brief ischaemia of noncardiac tissues. Our study examined whether a brief ischaemia of the small intestine induces both early and delayed cardioprotection in the rabbit and assessed the possible mechanism involved in the activation of capsaicin-sensitive sensory nerves. The plasma concentration of creatine kinase (CK) and infarct size (necrotic zone/left ventricular zone) after 30 min coronary artery occlusion and 180 min reperfusion were determined in rabbits. Infarct size was 35.5±6.8% in the control non-preconditioned group. Preconditioning induced by a brief period of 10-min small intestine ischaemia significantly reduced infarct size (6.5±1.9%, P<0.01 vs. the control non-preconditioned group) and decreased CK release (3092±236 and 1094±117 U/l for myocardial ischaemia-reperfusion and preconditioning plus myocardial ischemia-reperfusion, respectively, P<0.01), and the protection was partly abolished by pretreatment with capsaicin (50 mg/kg, s.c.) 4 days before the experiments. A brief period of anterior mesenteric artery occlusion caused an increase in the plasma level of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI), an effect which was abolished by pretreatment with capsaicin. Similar protection was shown in the animals subjected to a brief period of anterior mesenteric artery occlusion 24 h before coronary artery occlusion, and this delayed protection was also abolished partly by pretreatment with capsaicin. Capsaicin treatment (50 mg/kg, s.c.) alone also protected the ischa-emic myocardium. The results suggest that brief ischaemia of the small intestine induces both early and delayed protection against reperfusion-induced myocardial injury, and the effects are, at least partly, related to the activation of capsaicin-sensitive sensory nerves. Received: 13 August 1998 / Accepted: 4 January 1999     

腰痹舒治疗腰椎间盘突出症临床疗效分析

用中药腰痹舒治疗腰椎间盘突出症 3 1例 ,治愈 2 8例 ,有效 3例。治疗后随访 6～ 1 8个月 ,无 1例复发。与牵引、按摩、秋水仙碱内服对照组比较 ,中药疗效显著优于对照组 (P<0 .0 5 )。经 CT检查 ,腰痹舒治愈后椎间盘的后突压迫、粘连均有不同程度的解除。提出可根据症状、体征将腰椎间盘出症的腰腿痛分为 1 0级。作为判断病情和疗程的主要指标。其治疗宜通经、化瘀散寒为主。     

同时检测两种运动神经元存活基因第7外显子缺失的简便方法及其临床应用

目的：建立同时检测运动神经元存活基因SMNT和SMNC第7外显子缺失的简便方法，用于儿童期起病的脊髓性肌萎缩症（SMA）的临床诊断。方法：应用聚合酶链反应（PCR）－限制性酶切技术，用一对引物同时扩增55例正常成年人和5例SMA患儿及其父母的SMN基因2个成员的第7外显子中的高度保守区，扩增产物经限制性内切酶酶切及非变性聚丙烯酰胺凝胶电泳。结果：此法可检测2个SMN基因第7外显子的缺失情况，经检测，55例正常成人均无SMNT基因第7外显子缺失，SMNC基因第7外显子缺失仅3例，5例SMA患儿的SMNT基因第7外显子均有缺失，患儿父母无SMNT基因和SMNC基因第7外显子缺失，结论：此法对检测2个SMN基因第7外显子的缺失提供了简便，特异，且适合临床特别是基层医院应用，优于PCRSSCP分析的方法。