TAT和GMP-140在急性心肌梗塞患者溶栓治疗中的应用价值

目的探讨急性心肌梗塞溶栓治疗中凝血酶-抗凝血酶复合物(TAT)和血小板α-颗粒膜蛋白(GMP-140)动态变化及临床应用价值.方法以健康人为正常对照组(n=48),随机选择6h内急性心肌梗塞患者48例,用150万U尿激酶进行溶栓治疗,并按临床再通标准分为再通组(n=30),未通组(n=18),分别在溶栓前、溶栓后2h、4h、24h、48h采用酶联免疫吸附双抗体夹心法测定血浆TAT和GMP-140水平,观察其动态变化.结果患者组治疗前TAT水平(14.56±1.04)μg/L、GMP-140水平(12.50±1.05)ng/ml,较正常对照组(2.15±0.89)μg/L、(8.39±1.33)ng/ml显著升高(P<0.05),治疗后2h再通组GMP-140水平达到峰值(22.17±2.05)ng/ml,4h后TAT到达峰值(46.67±5.79)μg/L(P<0.05)后逐渐下降,持续至少3天,但仍高于正常对照组.未通组二项指标持续缓慢上升,48h达到峰值.结论急性心肌梗塞溶栓治疗前后TAT、GMP-140水平变化对判断疗效有一定指导意义.     

丝裂霉素C在复发性青光眼中的应用

目的 :观察丝裂霉素C(MMC)在抗青光眼手术中应用的近期及远期效果。方法 :4 2只复发性青光眼在二次手术中一次性应用MMC术后观察及随访。结果 :术前眼压 34.0 5± 4 .0 5mmHg ,明显高于随访半年期 13.13± 3.30mmHg以及随访 2年期 14 .33± 3.30mmHg ,差异有显著性 (P <0 .0 1)。术后近期眼压 6 .75± 1.4 3mmHg ,明显低于随访半年期 (P <0 .0 1)。功能性滤过泡所占比率为 95 .2 %。结论 :术中一次性应用MMC ,远期观察其降压效果明显 ,且无严重并发症发生     

全身麻醉插管术后院内获得性肺部感染探讨

全身麻醉气管插管术后下呼吸道感染具有较高发生率。分析５２６例手术时间超过４小时普外科病例，经ｕ检验发现全身麻醉气管插管术后患者肺部感染率明显高于持续性硬膜外麻醉术后患者，影响因素主要与全麻插管用具及麻醉机消毒情况有关，也与术前存在慢性阻塞性肺部疾患和术后保留气管插管有关。降低全麻术后肺部感染应重视无菌操作，尽可能对麻醉机管道进行常规消毒。     

椎动脉型颈椎病的彩色多普勒超声诊断

目的 :观察椎动脉型颈椎病的高频彩色多普勒表现和血流动力学变化。方法 :应用彩色多普勒超声诊断仪 (高频探头 ,频率 7～ 10MHz)检测 138例椎动脉型颈椎病患者 (颈椎病组 )的椎动脉 (VH)内径 (D)、血流速度 (V)和血流量 (Q)、阻力指数 (RI)和搏动指数 (PI) ,观察其形态结构、并与 10 0例 (对照组 )进行对照分析。结果 :颈椎病组VA的V(除平均血流速度外 )、D ,Q ,RI,PI与对照组比较差异有显著性 (P <0 0 1)。结论 :高频彩超显示的椎动脉形态和血流参数变化为临床评价椎动脉型颈椎病治疗效果提供了有价值的依据     

山莨菪碱、旋覆花素、苦碟子对过度训练致急性心肌损伤大鼠的影响

目的探讨山莨菪碱、旋覆花素、苦碟子对过度训练致急性心肌损伤大鼠的影响。方法雄性Wistar大鼠80只,体重200～220 g,随机分为5组:正常对照组(C组,n=8)、力竭对照组(E组, n=24)、山莨菪碱组(A组,n=16)、旋覆花素组(IB组,n=16)、苦碟子组(IS组,n=16)。采用游泳致力竭建立过度训练动物模型。A组于力竭前即刻腹腔注射山莨菪碱10 mg/kg,IB组于力竭前24 h和力竭前即刻口腔灌入旋覆花素25 ml/kg,IS组于力竭前即刻腹腔注射苦碟子20 ml/kg。取标本检测大鼠血清磷酸肌酸激酶(CK)及其同工酶(CK-MB)的活性,光镜观察心肌组织形态学,采用流式细胞术及TUNEL法检测大鼠心肌细胞凋亡,并计算心肌细胞凋亡率。结果与C组比较,E组、A组、IB组和IS组血清CK及CK-MB升高,心肌细胞凋亡率升高(P<0.05);与E组比较,A组、IB组及IS组大鼠血清CK及CK-MB及心肌细胞凋亡率均降低(P<0.05)。光镜下,E组的心肌细胞核深染,有固缩现象;而A组、IB组及IS组的心肌心肌组织学变化均未见异常。结论山莨菪碱、旋覆花素、苦碟子预先给药通过抑制心肌细胞的凋亡,可减轻过度训练致大鼠的心肌损伤。     

上海市外来人员肺结核病分布与临床特征

目的：了解上海市外来人口中肺结核病人的分布和临床特征。方法：对1996年1～12月全市外来人口活动性肺结核病报告登记资料进行分析。结果：外来人员肺结核病人总数达2279人，青壮年占总病例65％以上；男性病例为主；主要来源于江苏、浙江、安徽、四川、江西等省；登记病人来沪暂居地主要集中在市区及城乡地区，外来人口结核病管理重点在市区及城乡地区。病人分型以Ⅲ型为主。查痰率仅60．1％，但排菌率高达40％。外来人。的病例发现工作及治疗管理难度较大，目前登记病例规则化疗仅占10．4％。结论：有必要通过有关部门的共同协作，拟定切实可行的外来人口结核病管理办法。     

硝酸甘油β-环糊精包合物的研究

采用正交设计法对硝酸甘油包合物中硝酸甘油与β-环糊精(β-CD)的比例、包合温度、搅拌时间、搅拌强度进行研究,筛选出最佳包合工艺。线衍射分析、薄层色谱等证明该包合物质量是可靠的。     

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) – hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damage, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/ or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damage, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously. Received: 31 March 1995 / Revised, accepted: 27 November 1995     

基质金属蛋白酶与骨关节炎发生发展关系的研究进展

基质金属蛋白酶（matrix metalloproteinases, MMPs）因需要Ca2+、Zn2+等金属离子作为辅助因子而得名,其家族成员具有相似的结构,由5个功能不同的结构域组成。MMP-1、MMP-3、MMP-9、MMP-13是促软骨基质降解的核心物质,在骨关节炎（osteoarthritis, OA）发生发展过程中发挥了重要的作用。MMPs可通过降解软骨细胞细胞外基质蛋白、促进炎症发生等机制推进OA发展,逐渐受到医疗界的广泛关注。OA是常见的关节退行性疾病,与增龄、代谢、感染、遗传、运动等因素有关,引起患者发生关节酸痛、晨僵、关节活动受限等各种症状,严重影响患者生活质量。这种高度流行的疾病的致病机制尚不清楚,目前还没有有效的疾病改善治疗方法,未来选择性抑制关键酶MMPs或可成为一种有效的治疗方法。针对MMPs在OA中的致病作用,本文对MMPs在OA发生发展中的研究新进展作一综述。     

Cyclosporin A-mediated killing of <Emphasis Type="Italic">Leishmania major</Emphasis> by macrophages is independent of reactive nitrogen and endogenous TNF-α and is not inhibited by IL-10 and 13

Murine macrophages were treated with various doses of cyclosporin A (CsA) to enhance the killing of Leishmania major parasites. CsA reduced the rate of infected cells from 75% in non-treated controls to less than 15% with 1 micro g CsA/ml in a dose-dependent manner. The leishmanicidal effect was also observed when CsA was added 48 h after the infection of macrophages. In contrast, FK506, another structural non-related immunosuppressive drug with antiparasitic activities, showed no effect on the ability of macrophages to kill intracellular Leishmania parasites. Since nitric oxide has been identified as a key molecule for the leishmanicidal function of macrophages, we analyzed the role of this molecule. There was no influence on the leishmanicidal effect of CsA when L- N-(1-iminoethyl)lysine, a potent and selective inhibitor of mouse inducible nitric oxide synthase, was added. Furthermore, the presence of the macrophage-inhibiting cytokines interleukin (IL)-10 and IL-13 simultaneously or prior to CsA did not inhibit leishmania killing, while both cytokines completely prevented parasite killing by macrophages activated with gamma interferon and tumor necrosis factor (TNF). CsA was fully active on macrophages from TNF-receptor p55 knockout mice arguing against autocrine activation by TNF. We therefore conclude that the antileishmanial effect of CsA is independent of effector mechanisms employed by macrophage-activating cytokines.