防旋股骨近端髓内钉内固定治疗股骨近端骨折效果观察

目的探讨股骨近端防旋髓内钉内固定术(PFNA)治疗股骨近端骨折的效果。方法选取2015-01—2018-09间收治的72例股骨近端骨折患者,根据不同术式分为2组,各36例。对照组行动力髋螺钉内固定术(DSH),观察组行PFNA。结果观察组手术时间、术中出血量及术后完全负重时间、骨折愈合时间和关节功能(Harris)评分等指标均优于对照组,差异有统计学意义(P<0.05)。结论PFNA治疗股骨近端骨折,创伤小,患者术后恢复快,有利于改善关节功能。     

创伤后应激障碍及其遗传易感性研究

目前有关创伤后应激障碍(PTSD)及其发病机制的研究很多,但遗传因素对其影响尚不清楚。PTSD的遗传学研究尚处于起步阶段,研究的数量较少,且多停留在单个基因、单个位点的多态分析。由于PTSD本身在临床上具有高度异质性,应结合表观遗传学与传统遗传学两种研究方法,从PTSD的遗传易感性与环境的相互作用方面探讨其发病机制。本文就PTSD的遗传易感性及相关易感基因进行综述,并对有关研究方法进行了分析。     

脂多糖诱导小鼠肝组织白细胞介素6表达的动态变化及意义

目的:探讨不同剂量脂多糖诱导肝组织中白细胞介素6(Interleukin-6,IL-6)水平的动态变化及意义。方法:40只清洁级健康昆明种小鼠按每组4只随机分组为:脂多糖尾静脉注射3h的量效关系:正常对照组和低(1mg/kg)、中(5mg/kg)、高(10mg/kg)3个脂多糖剂量组;注射5mg/kg脂多糖的时效关系:正常对照,0.5,1,3,5,8h组。然后处死动物取肝脏,采用酶联免疫吸附测定法(Enzyme-linkedimmunosorbentassay,ELISA)检测不同剂量脂多糖诱导肝组织中IL-6水平的动态变化。结果:注射脂多糖3h,肝组织中IL-6水平随内毒素剂量的增加,表现为先升高后降低,中剂量组IL-6水平(ng/g)达峰值。低(1mg/kg)、中(5mg/kg)、高(10mg/kg)3剂量组IL-6水平(79.4±1.2),(112.0±1.4),(82.1±0.5)ng/g与正常对照组(44.3±1.2)ng/g相比较差异有显著性意义(t=6.058,P<0.01)。肝组织中IL-6水平随时间的推移表现为先升高后降低,用5mg/kg脂多糖处理后3hIL-6水平达峰值。各时相点IL-6水平犤0.5,1,3,5,8h:(53.5±1.3),(62.0±0.5),(112.0±1.4),(103.0±0.7),(80.9±0.5)ng/g犦与正常对照组(44.3±1.2)ng/g相比较差异有显著性意义(t=4.218,P<0.01)。在注射5mg/kg脂多糖后3h,肝组织IL-6的水平达峰值。结论:不同剂量的脂多糖均在一定程度上促进IL-6的表达,且脂多     

脂多糖诱导小鼠肝组织白细胞介素6表达的动态变化及意义

目的：探讨不同剂量脂多糖诱导肝组织中自细胞介素6(Interleukin-6，IL-6)水平的动态变化及意义。方法：40只清洁级健康昆明种小鼠按每组4只随机分组为：脂多糖尾静脉注射3h的量效关系；正常对照组和低(1mg／kg)、中(5mg／kg)、高(10mg／kg)3个脂多糖剂量组；注射5mg／kg脂多糖的时效关系；正常对照，0．5，1，3，5，8h组。然后处死动物取肝脏，采用酶联免疫吸附测定法(Enzyme-1inked immtmosorbent assay，ELISA)检测不同剂量脂多糖诱导肝组织中IL-6水平的动态变化。结果：注射脂多糖3h，肝组织中IL-6水平随内毒素剂量的增加，表现为先升高后降低，中剂量组IL-6水平(ng／g)达峰值。低(1mg／ks)、中(5mg／ks)、高(10mg／kg)3剂量组IL-6水平(79．4&;#177;1．2)，(112．0&;#177;1．4)，(82．1&;#177;0．5)ng／g与正常对照组(44．3&;#177;1．2)ng／g相比较差异有显著性意义(t=6．058，P&;lt;0．01)。肝组织中IL-6水平随时间的推移表现为先升高后降低，用5mg／kg脂多糖处理后3h IL-6水平达峰值。各时相点IL-6水平[0.5，1，3，5，8h．(53.5&;#177;1.3)，(62．0&;#177;0.5)，(112.0&;#177;1.4)，(103．0&;#177;0．7)，(80．9&;#177;0．5)ng／g]与正常对照组(44．3&;#177;1．2)ng／g相比较差异有显著性意义(t=4．218，P&;lt;0．01)。在注射5mg／kg脂多糖后3h，肝组织IL-6的水平达峰值。结论：不同剂量的脂多糖均在一定程度上促进IL-6的表达，且脂多糖感染后3h为肌体炎症反应从效应性向防御性转化的转折点，此时采取必要的药物治疗，可缓解过度炎症反应，促进肌体康复。     

白细胞介素-10在内毒素诱发肝损伤中的作用

本文简要综述了白细胞介素 10的结构特点、生物学效应及其在内毒素诱发肝损伤中的作用及在肝损伤免疫治疗方面的进展。     

Expression of NF-κB in Schwann cells and its effect on motor neuron apoptosis in spinal cord following sciatic nerves injury in rats

Objective: To explore the expression of nuclear factor-kappa B (NF-κB) in Schwann cells (SCs) and its effect on motor neuron apoptosis in spinal cord following sciatic nerves injury in adult rats. Methods: Thirty-six adult Sprague-Dawley (SD) rats were divided randomly into normal control group (n=6), and sciatic nerves crushing group (n=30). and the later was further equally randomized into 5 subgroups: 1. 3. 7. 11. and 21 d post-injury groups. The expression of NF-κB of normal and injured nerves were examined by immunohistochemistry staining, and the apoptosis of motor neurons in spinal cord of lumbar 4 to lumbar 6 (L4-L6) was investigated by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNED assay. Both were quantitated by image analysis. Results: In crushing group, except 21 d post-injury group, the expression of NF-κB was markedly higher than that in the normal control group (P<0. 05,P<0. 01). At 1 d after sciatic nerves crushing, the expression of NF-κB was obviously up-regulated, reached peak at 3 d. and recovered at 21 d. The same trend was observed in the time-course on motor neuron apoptosis after sciatic nerves injury. Correlation analyses revealed that motor neuron apoptosis was significantly and positively correlated with the expression of NF-κB following sciatic nerves injury (r=0. 976 0,P<0. 01). Conclusion: After injury of sciatic nerves, the presence and up-regulation of NF-κB in SCs may be involved in motor neuron apoptosis in L4-L6 spinal cord.     

β2-MG新型酶免疫分析方法研究

本文将通用固相二抗和生物素-亲和素系统应用于酶免疫分析中,成功地建立了β2-MG新型酶免疫分析方法.该方法的各项指标均可满足临床检测的要求,其优点是:二抗包被板可以通用、保存期长、节省抗体,检测方法的灵敏度高、精密性好.     

Activation of NF-κB and its regulation on IL-6 expression during LPS-induced liver injury

Objective： To explore the kinetics of the activation of nuclear factor-kappa B （NF-κB） and its regulation of interleukin-6 （IL-6） expression during LPS induced liver injury. Methods： Kunming mice were randomly divided into 4 groups in order to observe the does effect relationship at 3h： normal saline solution （control） group, low （1 mg/kg）, middle （5 mg/kg）, and high （10 mg/kg） LPS-induced groups; 6 groups in order to observe the time-effect relationship of 5 mg/kg LPS injection： normal saline solution （control） group, 0.5, 1, 3, 5 and 8 h groups ; pyrrolidine dithiocarbamate （PDTC） intervened groups （3 h）： normal saline solution （control） group, 5 mg/kg LPS, 200 mg/kg PDTC, and 200 mg/kg PDTC＋5 mg/kg LPS groups. NF-κB activities of Kupffer cells were determined with electrophoretic mobility shift assay （EMSA） and expression levels of IL-6 were measured with enzyme-linked immunosorbent assay （ELISA）. Results： Does-effect of NF-κB activities in Kupffer cells after LPS injection 3 h： NF-κB activation could be detected in 1 mg/kg LPS group, reached the highest level in 5 mg/kg LPS group, and persisted in 10 mg/kg LPS group; time-course after 5 mg/kg LPS injection： the DNA-binding activity was observable at 0.5 h after LPS injection, increased significantly at 3 h, and persisted for at least 8 h; in addition, antioxidant PDTC could inhibit the activation of NF-κB significantly. The kinetics of IL-6 level in liver tissues during LPS-induced liver injury were that IL-6 level after 3 h of injection increased first and then reduced; the same trend was observed in the time-course on IL-6 level after LPS injection; PDTC could significantly inhibit the release of IL-6. Correlation analyses revealed that IL-6 level was significantly and positively correlated with the activation of NF-κB. Conclusion ： NF-κB in Kupffer cells can be activitied during LPS-induced liver injury to some extent, and NF-κB may have some regulation on the expression of IL-6.     

C1-通道在溶血磷脂酸引起的血管平滑肌细胞增殖中的作用

目的 探讨C1-通道在溶血磷脂酸(LPA)引起的血管平滑肌细胞(VSMC)增殖中的作用.方法 采用细胞计数和氚标胸腺嘧啶脱氧核苷掺入实验,并结合激光共聚焦显微镜上测定细胞内Ca2 浓度等技术,研究不同C1-通道阻断剂对LPA促大鼠血管平滑肌细胞增殖的影响.结果 C1-通道阻断剂DIDS(二异硫氰酸二丙乙烯二磺酸,0.01～O.1mmol/L)可浓度依赖式的抑制溶血磷脂酸引起的血管平滑肌细胞增殖,其他C1-通道阻断剂如5-硝基苯丙氨基苯甲(NPPB)、4乙酰氨基4异硫氰酸2,2二磺酸(SITs)、二苯丙氨基2,2二羧酸(DPC)(浓度均为10-7～10-3mol/L)和速尿(浓度均为10-5～10-3mol/L)等均无此作用,且DIDS对电压依赖性钙通道没有直接的影响.结论 溶血磷脂酸可以开放DIDS敏感的C1-通道,且该通道可能在溶血磷脂酸引起的血管平滑肌细胞增殖的调控上起一定的作用.