弥漫性轴索损伤后内质网钙释放对轴突内早期钙离子浓度的影响

目的研究弥漫性轴索损伤(diffuse axonal injury,DAI)后内质网(endoplasmic reticulum,ER)钙释放的变化,以及对轴突内早期钙离子浓度的影响,并探讨造成ER钙释放的可能分子机制。方法使用体外培养7¹2d的小鼠神经元行轴突牵拉损伤建立体外DAI模型,根据是否行牵拉损伤分为损伤组及对照组。使用ER Tracker Red标记ER,观察ER在轴突损伤前后的分布。通过Fluo-4AM钙探针及激光共聚焦钙成像技术测量单个轴突内钙离子浓度的变化,并使用20mmol/L咖啡因作用于细胞,使ER内钙离子快速排空,测量轴突部位咖啡因作用前后的钙离子浓度变化,从而间接观察ER内钙存量的变化。结果 ER Tracker Red荧光结果显示ER存在于神经元轴突部位中,损伤后的轴突肿胀部位存在ER聚集的现象。神经元牵拉损伤后,被牵拉的轴突钙离子浓度明显升高,与对照组比较,差异有统计学意义(P<0.05),受损的轴突表现出肿胀及"串珠样"变性等病理学改变。除损伤后2min外,使用无钙细胞外液虽然明显降低了牵拉损伤导致的轴突的钙离子浓度升高,但在212d的小鼠神经元行轴突牵拉损伤建立体外DAI模型,根据是否行牵拉损伤分为损伤组及对照组。使用ER Tracker Red标记ER,观察ER在轴突损伤前后的分布。通过Fluo-4AM钙探针及激光共聚焦钙成像技术测量单个轴突内钙离子浓度的变化,并使用20mmol/L咖啡因作用于细胞,使ER内钙离子快速排空,测量轴突部位咖啡因作用前后的钙离子浓度变化,从而间接观察ER内钙存量的变化。结果 ER Tracker Red荧光结果显示ER存在于神经元轴突部位中,损伤后的轴突肿胀部位存在ER聚集的现象。神经元牵拉损伤后,被牵拉的轴突钙离子浓度明显升高,与对照组比较,差异有统计学意义(P<0.05),受损的轴突表现出肿胀及"串珠样"变性等病理学改变。除损伤后2min外,使用无钙细胞外液虽然明显降低了牵拉损伤导致的轴突的钙离子浓度升高,但在2³0min时间段中钙离子浓度升高依然存在,与对照组比较,差异有统计学意义(P<0.05)。对照组中未经牵拉损伤的神经元轴突可被20mmol/L咖啡因激起一个明显的轴突钙离子浓度升高,而牵拉损伤后的轴突对咖啡因的这种钙升高反应程度明显下降,与对照组比较,差异有统计学意义(P<0.05)。结论 DAI后的轴突钙离子浓度升高不仅由细胞外钙内流引起,细胞内钙释放同样参与其中。ER是引起这种DAI后轴突内钙释放的细胞器来源。     

Protective effect of glutamine pretreatment on ischemia-reperfusion injury of spinal cord in rabbits

Objective To investigate the effect of glutamine (Gln) on the content of reduced glutathione hormone (GSH) and aminoglutaminic acid (Glu) of spinal cord following ischemia-reperfusion injury. Methods Totally 40 healthy adult male rabbits were randomly divided into five groups: sham-operation group (S group), ischemia-reperfusion injury group (I/R group), low-dose glutamine group (L Gln group), median-dose glutamine group (M Gln group) and high-dose glutamine group (H Gln group). After glutamine preconditioning, the model of spinal cord ischemia-reporfasion injury was established according to Zivin's method. The general status of animals was observed and the changes of Jacobs scoring were recorded in each group. Malondialdehydes (MDA), GSH, Glu and superoxide dismutase (SOD) activity in lumbar spinal cord tissues were determined using chemical colorimetry. The neuron number and deviation rate in spinal cord anterior horn were observed histopathologically. Results There was no significant difference between L Gin group and I/R group in behavior scoring, SOD activity, content of MDA and Glu, neuron number and deviation rate of spinal cord (P>0.05); however, there was a significant difference in GSH content of spinal cord (P<0.05). M Gln group and I/R group differed significantly (P<0.05) in behavior scoring, SOD activity, content of MDA, Glu, GSH, neuron number and deviation rate of spinal cord. Between H Gln group and M Gln group, there was no significant difference in behavior scoring, content of MDA and Glu, SOD activity, neuron number and aberration rate in spinal cord (P>0.05), whereas there was a significant difference in SOD activity and Giu content (P<0.05). Conclusion Pretreatment with medium-dose glutamine has a protective effect on spinal cord ischemia-reporfasion injury in rabbits, which may be related to the maintenance of GSH content, increase of SOD activity and reduction of MDA.     

Effect of ulinastatin on hepatic ischemia-reperfusion injury in rats

Objective To investigate the effect of ulinastatin (UTI) on hepatic ischemia-reperfusion injury in rats. Methods Totally 24 adult Sprague-Dawley rats were randomly divided into 3 groups: sham-operated control group (SO group), ischemia-reperfusion group (I/R group) and ulinastatin group (UTI group). Liver in I/R group underwent 1 h of reperfasion after 30 min of ischemia. In UTI group, UTI (2×104 U/kg) was administered to rats 30 min before modeling. The levels of alanine aminotransferase, aspartate aminotransferase and tumor necrosis factor-alpha (TNF-α) in serum were measured and the levels of nitric oxide and malondialdehyde in liver were determined. The histological changes of liver were observed. Results The levels of alanine aminotransferase, aspartate aminotransferase and TNF-α in serum were significantly increased in I/R group compared with those in UTI group (P<0.05). The levels of nitric oxide and malondialdehyde in liver were significantly higher in I/R group than in UTI group (P<0.05).Histological examination of liver indicated that the damages were more severe in I/R group than in UTI group.Conclusion UTI has the ability to inhibit the production of TNF-α and oxyradical, and ameliorate microcirculatory dysfunction in rats with hepatic ischemia-reperfasion injury.     

SBS改性沥青粘结防水层的作用和施工控制

通过作者在高速公路大中修的实践,分析SBS改性沥青粘结防水层在预防水损坏起到的作用和施工过程的控制.     

考虑潜在类别的老年行人交通事故严重程度致因分析

人口老龄化问题日益突出，老年行人的出行安全同样引起各界重视。本文基于潜在类别聚类分析和随机参数Logit模型相结合的两步法深入探究影响老年行人交通事故严重程度的诱因。对北卡罗来纳州2007—2019年65岁及以上老年行人与机动车的碰撞数据进行清洗。为消除碰撞数据中固有的未观察到的异质性，首先进行潜在类别聚类分析，依据拟合优度指标确定最佳聚类数，将数据分成3个集群，分别对每个集群进行特征描述。然后，分别对每个集群建立随机参数Logit模型，以进一步探索集群内部未观察到的异质性，同时计算各显著变量的边际效应，量化其对事故严重程度概率的影响。结果显示，随机参数Logit模型具有更好的拟合优度；不同集群参数估计结果有所差异，一些变量只在特定集群内是显著的；集群1中，“救护车援助”为随机变量，集群2中“事故发生在城市”为随机变量，集群3中未发现随机变量，退化为多项Logit模型。本文研究结果可为交通工程师和政策制定者提供更可靠准确的老年行人交通事故严重程度诱因信息，为老年行人出行安全改善方案的制定提供理论支撑和技术支持。     

五仁醇对慢性肝损伤的保护作用

本实验证明五仁醇可使慢性肝损伤大白鼠LDH_5和SGPT 下降,清蛋白增多,r-球蛋白减少,清、球蛋白比率增高,肝中胶元含量明显降低,病理改变减缓.以上结果说明五仁醇对慢性肝损伤具有保护作用。     

3,6-(二甲氨基)-二苯并碘杂六环葡萄糖酸盐对大鼠缺血再灌注心肌的保护作用

目的　观察 3,6 (二甲氨基 ) 二苯并碘杂六环葡萄糖酸盐 (IHC 93)对大鼠缺血再灌注的保护作用。方法　选用健康SD大鼠 ,结扎和松解冠状动脉制备心肌缺血再灌注模型。结果　IHC 930 .12 5、0 .2 5、0 .5mg·kg-1能明显缩小缺血再灌注心肌梗死范围 ;可不同程度地减少心肌CK和CK MB的释放 ;减少心肌ET 1的产生 ;IHC 930 .2 5、0 .5mg·kg-1明显降低心肌肿胀度。结论　IHC 93对大鼠心肌缺血再灌注损伤具有保护作用。     

TNF-α基因表达在大鼠急性重症胰腺炎肺损伤中的作用

目的　探讨急性重症胰腺炎 (ASP)大鼠肺组织肿瘤坏死因子 α(TNF α)基因表达在肺损伤中所起的作用。方法　将ASP大鼠分别在 1、3、5、7、9h点剖杀 ,取肺组织行病理观察、微血管通透性、组织含水量及髓过氧化物酶(MPO)活性测定 ,RT PCR法检测肺组织TNF α基因表达。结果　制模后肺组织TNF α基因表达在 1h后逐渐上升 ,至9h达到峰值 (P <0 .0 5 )。同时肺损伤程度逐渐加重 ,肺组织微血管通透性、组织含水量及MPO活性逐渐升高。结论　ASP大鼠肺组织TNF α基因过度表达 ,且与肺损伤严重程度相关     

碱性成纤维细胞因子在博莱霉素致肺纤维化肺血管损伤中的作用

目的探讨碱性成纤维细胞因子(bFGF)在博莱霉素(BLM)致大鼠肺纤维化肺组织中的表达及其在肺血管损伤中的作用。方法于大鼠气管内注射BLM以复制其肺纤维化模型,应用bFGF多克隆抗体按SABC法行免疫组织化学染色,定量图像分析。结果BLM组动物支气管上皮细胞胞浆内、支气管和肺小动脉肌层以及肺泡巨噬细胞胞浆内可见较多棕黄色细颗粒状bFGF阳性表达产物,显著高于对照组(P<0.05)。结论在BLM致大鼠肺纤维化过程中bFGF表达上调,提示bFGF可能参与肺间质纤维化的发病过程。     

超氧化物歧化酶对心肌线粒体再给氧损伤的作用

本文目的是观察大鼠离体心脏缺氧后再给氧心肌线粒体呼吸功能的改变及超氧化物歧化酶(SOD)的作用。结果表明,心肌缺氧40min后再给氧20min,线粒体呼吸功能(呼吸控制率RCR,P/O比值)及线粒体琥珀酸脱氢酶(SDH)、细胞色素氧化酶(CCO)活性显著降低;应用SOD,可明显提高RCR、P/O值,保护SDH、CCO活性。