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.     

Rouviere沟引导定位与传统定位腹腔镜胆囊切除术的比较研究

[目的]分析Rouviere沟引导定位腹腔镜胆囊切除术(LC)与传统定位LC手术的效果.[方法]选择2015年4月至2016年4月于我院行腹腔镜胆囊切除术患者108例,将其随机分为对照组和观察组,每组各54例,对照组予以传统定位,观察组予以Rouviere沟引导定位,比较两组治疗后肝功能[总胆红素(TBIL)、谷草转氨酶(AST)、谷丙转氨酶(ALT)],手术时间和并发症率.[结果]术前两组患者肝功能指标TBIL、AST、ALT比较,差异无统计学意义(P>0.05);经LC术后,两组血清TBIL、AST、ALT水平均高于术前,观察组低于对照组,差异均具有统计学意义(均P<0.05).对照组手术时间(67.54±7.42)min显著高于观察组(47.38±5.69)min,差异具有统计学意义(P<0.05).对照组胆漏、胆管损伤各有4例,并发症发生率为14.82%(8/54);观察组有2例胆漏,其并发症发生率为3.70%(2/54),两组比较差异具有统计学意义(P<0.05).[结论]Rouviere沟引导定位LC手术的临床效果优于传统定位LC手术.     

老年人结肠癌并急性肠梗阻86例外科处理分析

目的探讨老年人结肠癌并发急性肠梗阻的特点、诊断、外科处理方法与预后。方法回顾性分析我院2000年1月—2009年8月86例年龄〉60岁的老年患者手术治疗的结肠癌并发急性肠梗阻病人的临床资料,其中一期切除吻合58例（右半结肠一期切除吻合39例,左半结肠一期切除吻合19例）,分期手术19例（右半结肠4例,左半结肠15例）,行Hartmann手术。肿瘤无法切除行单纯结肠造瘘和捷径手术9例。结果术后出现并发症8例,发生率为9.3%,其中切口感染3例,腹腔感染2例,肺部感染2例,感染性休克1例,1例死亡,病死率1.2%,85例痊愈出院。结论老年人结肠癌致肠梗阻的外科治疗要根据老年病人的具体情况选择合理的术式,准确的早期诊断,恰当的围术期处理,正确的手术方式的选择,是提高其预后的关键。     

甲状腺癌合并桥本甲状腺炎分析研究

甲状腺癌合并桥本甲状腺炎（Hashimoto’sthyroiditis,HT）的发病率呈上升趋势,2者之间的相关性已成为研究热点。现将解放军第八五医院2001年至2012年经手术治疗、病理证实的24例甲状腺癌合并HT的临床表现、病理特征报道分析如下。     

少见原因肠梗阻的诊断与治疗

目的　探讨少见肠梗阻的病因、诊断及治疗。方法　结合文献分析了我院收治的 6例少见肠梗阻的临床资料。结果　 6例中 ,3例胆石性肠梗阻 ,1例腹茧症 ,1例全小肠扭转 ,均经手术治愈。 1例为重金属中毒 (铅中毒 )引起的不全性肠梗阻 ,经非手术治疗治愈。结论　对于少见原因引起的肠梗阻 ,应有一定的认识 ,采取正确的治疗方法 ,防止误诊误治。     

胃浆膜面海绵状淋巴管瘤1例

患者女,63岁。5年前开始出现右上腹痛,每次持续0.5~2h,经对症处理后缓解,此后患者在进食物过多时右上腹痛、腹胀症状加重;经饮食控制与对症处理后好转。半月前患者上述症状加重,伴恶心与呕吐,为胃内容物,在当地医院查上腹部CT示:上腹部肿块,腹膜囊肿可能。为进一步诊治转入我科     

保留乳头乳晕复合体乳房切除加一期假体植入术的应用

目的研究保留乳头乳晕复合体乳房切除加一期假体植入术（NSM—IBRWI）应用于早期乳腺癌的安全性与有效性。方法1999年6月至2006年10月，对13例患者的14只乳房实施NSM-IBRWI手术，主要采用沿乳晕上或下的180。弧形切口，完整切除乳房，保留乳头乳晕复合体，在胸大肌下或皮下植入硅凝胶假体，同时乳腺癌患者另取胸大肌外缘切口行腋窝淋巴结清扫术。结果13例患者共植入14只假体，其中1例患者（单侧）因假体植入皮下后引流液2个月以上不减少而导致伤口无法愈合，被迫取出假体。手术成功率为92．9％（13／14）。术后6个月自我满意度良好者9例，一般者3例（其中不对称2例，疼痛1例），较差者1例（假体取出者）。13例中有原位癌1例，浸润性导管癌10例。所有患者的中位随访时间为27个月。1例患者（T1N1M0）术后9个月出现肺、骨转移，继而出现脑转移，术后15个月死亡，其余10例患者均无病生存至今。术后主要问题是伤口不愈合、不对称和疼痛。结论NSM—IBRWI是一种安全有效治疗早期乳腺癌的新方式，它可与保乳手术取长补短。