细胞黏附分子在多器官功能障碍综合征中的表达变化及意义

全身炎症反应综合征（SIRS）是MODS形成中的重要病理基础。而炎症反应对组织和器官的损伤是由于白细胞与血管内皮细胞相互作用、黏附增加，导致白细胞附壁和渗出引起。介导白细胞一内皮细胞黏附的分子基础是细胞黏附分子（CAMs），所以，了解CAMs在MODS中的表达变化，对于进一步认识M（）DS的发生机制及其防治有重要意义。     

内皮祖细胞在创伤后多器官功能障碍中的变化及意义

Objective To investigate characteristics of changes in bone marrow endothelial progenitor cells (EPCs) and implications on multiple organ dysfunction syndrome (MODS) as a result of trauma.Methods Eighteen mini-pigs were randomized into two groups: MODS group (n=9) and control group (n=9).The animal models of MODS were reproduced by "two-hit" injury with hemorrhagic shock and lipopolysaccharide (LPS) injection.Bone marrow and peripheral blood of them were collected at five time points: normal condition (T1), before injection of LPS (T2), and 0 (T3), 24 (T4) and 48 hours (T5) after injection of LPS.Erythrocytic lysate was added to the samples, and the number of leucocytes in every sample was counted.The rate of EPCs in each sample was determined by flow cytometry.Number of EPCs in bone marrow and peripheral blood were calculated, and the results were analyzed statistically.Results The number of EPCs (×106/L) in bone marrow of control group at T1-5 was 7.64±0.68,7.32±0.55, 7.58±1.13, 7.77±0.70, and 7.88±0.84, respectively, and in peripheral blood control group was 3.54±0.26,4.06±0.64, 3.74±0.55, 3.61±0.37, and 3.98±0.63, respectively.The number of EPCs (×106/L) in bone marrow in the experimental group was 7.45 ± 1.55, 6.58 ± 0.80, 11.27 ± 1.20, 10.88±1.15, and 8.36 ± 2.88, respectively.The number of EPCa (× 106/L) in peripheral blood in the experimental group was 3.21±0.48, 8.71±2.04, 5.98±0.77, 1.27±0.91, and 2.14±0.96, respectively.The number of EPCs in bone marrow of experimental group was larger than that of control group at T3, T4, T5.The number of EPCs in the experimental group in peripheral blood was larger than that of control group at T2, T3, T4, T5.The number of EPCs in bone marrow was larger than that in peripheral blood at every time point (all P＜0.05).Conclusion The number of EPCs in peripheral blood elevates sharply in the earlier period, then plummetes quickly during MODS after a trauma.While the number of EPCs in bone marrow descends mildly at first, then rises obviously.Along with the aggravation of MODS, a declination of EPCs in bone marrow emerges.The change in bone marrow EPCs plays an important role in recovery of MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

Endothelial progenitor cells modulated by IL-1β in multiple organ dysfunction syndrome in porcine

Objective To investigate the modulation of EPCs by interleukin 1β (IL-1β) and p38 mitogen activated protein kinase (p38MAPK) and the pathogenesis resulting from their dysdifferenfiation after trauma.Method Thirty pigs were divided into a control group (n = 15) and a multiple organ dysfimction syndrome (MODS) group (n = 15), the latter of which were subjected to a "two-hit" injury including hemon'hagic shock and endotoxemia. Phosphorylation of p38MAPK in peripheral blood mononuclear cells was monitored by western blotting. The concentration of IL-1β in peripheral blood plasma was determined by ELISA and the numbers of EPCs with FCM in peripheral blood plasma were monitored. The morbidity rates in the two groups were compared by chi square test. The levels of phosphorylation of p38MAPK in peripheral blood mononuclear cells, the concentmtions of IL-1β in peripheral blood plasma and the numbers of EPCs in the peripheral blood were compared between groups using with Student's t lest. Results The level of p38MAPK phosphorylation was more augmented and the concen-tration of IL-1β higher in peripheral blood mononuelear cells and plasma from MODS pigs compared with those from control pigs; nevertheless the mauler of EPC conspicuously decreased in the peripheral blood (P <0.01). The morbidity rate in the MODS group was much higher than that in the control group (P < 0.01). There were fewer EPCs in the peripheral blood of animals in group M than in the peripheral blood of animals in group C (P <0.01). Conclusions p38MAPK phosphorylation is important for the pathogenesis of MODS. p38MAPK phospho-rylation might cause the concentration of IL-1β in the peripheral blood plasma to rise and could cause a drop in the numbers of EPCs, thereby aggravating the inflanmmatory reaction in MODS.     

肝部分切除+定容失血性休克大鼠肝脏cDNA表达谱芯片结果分析

目的 利用cDNA表达谱芯片分析肝部分切除+定容失血性休克前和休克后24小时大鼠肝脏差异基因,并初步分析差异基因信号通路和网络调控. 方法 11只大鼠接受肝左外叶切除和2.5ml/100g体重定容失血性休克,选其中3只存活大鼠麻醉后失血前切除肝左外叶(A组),对于存活24小时的大鼠再次取肝脏(B组)行cDNA表达谱芯片(含21793个基因)分析.对差异基因行Pathway、Go、Network分析.使用RT-PCR对两组中基因Aldh1a1、Aldh1a7、Aoc3、Cyp26a1、Hdc1、Ephx2和Beta-actin进行分析,验证cDNA芯片的准确性. 结果 4只大鼠存活24小时,表达谱芯片筛查出两组差异表达下调基因634个,表达上调基因513个.差异基因涉及主要信号通路包括胆固醇代谢、细胞外刺激反应、甾醇代谢、激素刺激反应、甾体类激素刺激反应、类固醇代谢、内源性刺激反应、氧化还原反应、有机物质反应、脂肪酸代谢.结论 氧化还原和脂代谢信号通路在创伤失血性休克病理过程中起重要作用.     

围绕主题主线 积极创新发展 努力开创军队疾病预防控制机构建设新局面

通过全面系统总结,展示了"十一五"以来军队疾控机构建设取得的五个方面成绩和进步;指出了"十二五"时期军队疾控机构建设面临的四方面形势:(1)胡主席主题主线重大战略思想,为军队疾控机构建设发展指明了正确方向;(2)加强军事斗争准备和完成多样化军事任务,要求军队疾控机构建设必须提高保障能力;(3)日趋复杂的全球疫情形势和不断增长的官兵合理健康需求,要求军队疾控机构建设必须拓展服务功能;(4)一些深层次的矛盾问题尚未解决,要求军队疾控机构必须勇于改革创新。明确了"十二五"军队疾控机构建设的总体思路,提出了"十二五"期间军队疾控机构建设的五大任务:一是全力抓好战备和应急工作;二是着力完善疾控体制机制;三是切实强化人才学科建设;四是积极改善工作支撑条件;五是大力加强依法科学管理。     

内镜乳头括约肌切开术后出血的原因及外科处理

目的探讨内镜下乳头括约肌切开(endoscopic sphincterotomy,EST)取石术后大出血的原因及外科处理方法.方法Kocher切口游离十二指肠降部并纵行切开之,显露乳头创面出血点,检查出血原因,细丝线缝扎止血后缝闭十二指肠切口,行减压性胃造瘘.结果在本组1030例EST患者中,术后出现出血398例,需外科手术处理的2例,均为细小动脉出血,其中1例为切开部位出现变异血管,1例为切开部位有误,均经手术止血后而治愈.结论EST术后出现持续性出血多为动脉性出血,保守治疗无效者及时外科手术是必要的.     

胃癌腹腔化疗毒副反应的观察和处理

目的 评价胃癌腹腔化疗的毒副反应，并探讨其处理方法。方法 将156例胃癌病人进行随机分组。分为术中即时低渗温热腹腔化疗联合术后早期腹腔化疗组（治疗组），单纯术中即时低渗温热腹腔化疗组（对照组1），未行腹腔化疗组（对照组2），共三组，观察化疗的安全性和毒副反应。结果 治疗组化学性腹膜炎、消化道反应、骨髓抑制和肝功能异常的发生率明显高于两个对照组。结论 应用术中即时，低渗温热腹腔化疗联合术后早期腹腔化疗时化学性腹膜炎的防治不容忽视。     

提高股疝手术成功率的临床策略(附97例报告)

目的探讨股疝诊断要点和手术方法。方法 对我院经治的97例股疝临床资料进行回顾性总结。本组均经查体触及腹股沟韧带下方肿块及影像学检查确诊,除1例急诊死亡,其余均行手术治疗。经腹股沟上入路手术87例,经腹股沟下入路1例,经下腹部探查切口8例。68例(70.83%)行McVay疝修补术;13例(13.54%)行单纯高位结扎;14例(14.58%)行无张力疝修补术;1例(1.04%)采用经腹股沟下股疝修补术。所有患者术后常规应用抗生素。结果本组96例手术者中,94例痊愈,2例因术后心、肺功能衰竭而死亡,病死率3.09%。94例随访6个月～5年,1年后复发1例,余病例未见异常。结论股疝嵌顿绞窄发生率较高,仔细查体和超声检查可明确诊断,尽早手术是治疗股疝的有效手段,以减少并发症及死亡率。