海藻多糖对γ射线照射小鼠腹腔巨噬细胞免疫功能的影响

目的观察海藻多糖对γ射线照射损伤小鼠巨噬细胞免疫功能的影响。方法通过测定小鼠腹腔巨噬细胞吞噬功能、产生IL-1和NO能力,考察海藻多糖对γ射线照射小鼠巨噬细胞免疫功能的影响。结果海藻多糖处理组小鼠腹腔巨噬细胞吞噬功能、产生IL-1和NO能力较未给药照射组明显增强(P均<0.05)。结论海藻多糖对辐射所致的巨噬细胞免疫功能损伤有明显的拮抗作用。     

鼻咽癌放疗后张口困难的临床研究

[目的]探讨导致鼻咽癌放疗后张口困难的因素。[方法]对1998年1月￣2001年12月鼻咽癌患者109例,分析性别、年龄、原发灶范围、照射剂量和颈部纤维化对张口困难的影响。[结果]全组张口困难发生率为45.1%(49/109),Ⅰ级25例,Ⅱ级17例,Ⅲ级7例,Ⅳ级0,各占51.0%、34.7%、14.3%和0,张口困难出现中位时间27.0个月(4￣64个月),颞颌关节受照剂量59.8Gy￣79.9Gy,≥65Gy者张口困难发生率56.7%(38/67),<65Gy者则为26.2%(11/42),两者有显著差异(P<0.01),有/无颈纤维化者张口困难发生率分别为78.3%(36/46)、20.6%(13/63),有显著差异(P<0.01)。[结论]颞颌关节剂量≥65Gy和颈部纤维化可能是导致鼻咽癌放疗后张口困难重要因素。     

沙棘油和亚硒酸钠对汞诱导的大鼠肝肾氧化损伤的影响

目的通过汞诱导大鼠肝肾氧化损伤,观察沙棘油(Sea Buckthorn Oil,SBO)和亚硒酸钠(Na2SeO3)干预效应。方法Wister大鼠随机分成对照组、单纯染汞组、SBO和Na2SeO3处理组。测定肝、肾及尿中汞含量,肝、肾中GSH、MDA、蛋白含量和SOD、GSH-PX活力。结果与单纯染汞组相比,SBO处理组尿汞含量增加(P<0.05),肝GSH-PX活力升高(P<0.01);Na2SeO3处理组肝汞增加,肾和尿汞含量下降,肝GSH-PX活力、GSH含量均升高(P<0.01),肝SOD活力和肾GSH-PX活力均增加(P<0.05),肾MDA含量下降(P<0.05)。结论沙棘油具有促进汞从肾脏排出的作用,对汞诱导的肝氧化损伤具有一定保护作用,对肾氧化损伤未表现出明显的保护作用。Na2SeO3可有效拮抗汞诱导的肝肾氧化损伤作用。     

带胫后动脉蒂逆行岛状皮瓣急诊一期修复足跟部软组织缺损13例

目的 回顾分析应用带胫后动脉蒂逆行岛状皮瓣急诊一期修复足跟部软组织缺损的疗效,以探讨足跟部软组织缺损的有效治疗方法 .方法 经临床应用带胫后动脉蒂逆行岛状皮瓣急诊一期修复13例足跟部软组织缺损患者,供区应用单纯游离植皮修复伤口,术后应用“三抗”治疗.结果13例足跟部软组织缺损患者术后伤口愈合和功能全部达到优良,经随访1～18个月,结果 全部恢复自由行走功能,无麻木和行走痛等并发症.结论 应用带胫后动脉蒂逆行岛状皮瓣是急诊一期修复足跟部软组织缺损的一种有效的治疗方法 .     

糖耐量减低患者尿微量白蛋白排泄的探讨

目的探讨糖耐量减低(IGT)时尿微量蛋白(mALB)排泄与血压、血糖的关系。方法对83例IGT和64例NGT行空腹血糖(FBG)、餐后2h血糖(2hBG)和尿mALB检测,并依血压高低分组比较。结果各组间FBG、2hBG、尿mALB水平均有显著性差异,均P<0.01,IGT血压升高组分别依次显著高于IGT血压正常组、NGT血压升高组和NGT血压正常组。结论IGT患者已存在早期微血管病变所致的肾损害,预防糖尿病及并发症,干预应从IGT开始。     

疏肝化瘀汤对实验性动物肝损伤保护作用的研究

研究疏肝化瘀汤对实验性动物肝损伤的保护作用，并为临床应用提供理论依据：方法 利用四氯化碳造成小鼠、大鼠肝损伤模型，分别观察空白对照组、疏肝化瘀汤组、西药对照组、肝损伤模型组的肝功能、胆汁流量的变化。结果 疏肝化瘀汤组胆红素、谷丙转氨酶显著降低（P〈0．005），而白蛋白与A／G值明升高（P〈0．01）结论疏肝化瘀汤对四氯化碳造成的实验性动物肝损伤有保护作用。     

烧伤后“休克心”的研究

目的 探讨烧伤后休克心及其发生机制。方法 动物实验与临床研究相结合。采用心功能、心肌细胞损伤、细胞膜及骨架结构损伤、心肌生物力学、心肌病理等指标观测心肌损伤程度;通过心肌营养性血流量、心肌细胞氧利用、能量代谢及其释放的细胞因子等指标探讨其机制。靖暴严重烧伤后心功能、心肌力学指标、心肌营养性血流量、心肌细胞氧利用及能量代谢、心肌细胞黏弹性等均显降低,细胞膜及骨架结构受损,心肌纤维灶性溶解、断裂,血浆肌球蛋白轻链1、肌钙蛋白T及心肌组织细胞因子显增高。结论 严重烧伤休克期心肌即发生明显器质性损害,心肌缺血再灌流损伤、心肌细胞氧利用及能量代谢障碍、心肌组织水肿、失控性炎症反应等是发生休克心的主要机制。     

白藜芦醇和抗坏血酸对预防非典型肺炎方剂Ⅰ和Ⅵ所致小鼠外周血液淋巴细胞DNA损伤的保护作用

目的研究白藜芦醇和抗坏血酸对预防非典型肺炎方剂Ⅰ和Ⅵ致小鼠外周血液淋巴细胞DNA损伤的保护作用.方法采用单细胞凝胶电泳方法研究白藜芦醇和抗坏血酸对预防非典型肺炎方剂Ⅰ和Ⅵ致小鼠外周血液淋巴细胞DNA损伤的保护作用.结果白藜芦醇(50,100,200 mg/kg×3 d)和抗坏血酸(50,100,200 mg/kg×3 d)对方剂Ⅰ和Ⅵ(临床等效量×3 d)所致的小鼠外周血液淋巴细胞DNA损伤呈剂量依赖性的保护作用(P＜0.05).结论白藜芦醇和抗坏血酸能够保护预防非典型肺炎方剂J和Ⅵ对小鼠外周血液淋巴细胞DNA的损伤.     

轮状病毒胃肠炎患儿并发心肌损伤的研究

目的 :了解轮状病毒 (RV)胃肠炎并发心肌损伤的几率及探讨在大量补液过程中心功能不全的防治措施。方法 :测定 44例急性期RV胃肠炎患儿血清肌酸激酶同工酶 (CK -MB)和谷草转氨酶 (AST)浓度 ,并将CK -MB与可能导致其升高的相关临床因素进行统计学处理。结果 :急性期RV胃肠炎患儿中有 5 7%CK -MB超过正常值 ,显著增高者占 7% ;有 82 %AST超过正常值 ,显著增高者占 16.9% ;CK -MB升高与腹泻和脱水无明显相关性 ,与发热程度有相关性。结论 :部分RV胃肠炎患儿存在心肌损伤 ,心肌损伤可能与RV感染有关 ,正确处理RV腹泻大量补液与患儿心肌损伤需限制液量之间的矛盾是十分重要的     

Relationship between neuronal loss and interictal glucose metabolism during the chronic phase of the lithium-pilocarpine model of epilepsy in the immature and adult rat

The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. After having studied the metabolic changes occurring during the silent phase, in the present study, we explored the relationship between interictal metabolic changes and neuronal loss during the chronic phase following status epilepticus (SE) induced by Li-Pilo in 10-day-old (P10), 21-day-old (P21), and adult rats. Rats were observed and their EEG was recorded to detect the occurrence of spontaneous recurrent seizures (SRS). Local cerebral glucose utilization was measured during the interictal period of the chronic phase, between 2 and 7 months after SE, by the [(14)C]2-deoxyglucose method in rats subjected to SE at P10, P21, or as adults. Neuronal damage was assessed by cell counting on adjacent cresyl violet stained sections. When SE was induced at P10, rats did not become epileptic, did not develop lesions and cerebral glucose utilization was in the normal range 7 months later. When SE was induced in adult rats, they all became epileptic after a mean duration of 25 days and developed lesions in the forebrain limbic areas, which were hypometabolic during the interictal period of the chronic phase, 2 months after SE. When SE was induced in P21 rats, 24% developed SRS, and in 43% seizures could be triggered (TS) by handling, after a mean delay of 74 days in both cases. The remaining 33% did not become epileptic (NS). The three groups of P21 rats developed quite comparable lesions mainly in the hilus of the dentate gyrus, lateral thalamus, and entorhinal cortex; at 6 months after SE, the forebrain was hypometabolic in NS and TS rats while it was normo- to slightly hypermetabolic in SRS rats. These data show that interictal metabolic changes are age-dependent. Moreover, there is no obvious correlation, in this model, between interictal hypometabolism and neuronal loss, as reported previously in human temporal lobe epilepsy.