参附注射液对大鼠胰腺移植受体小肠肠粘膜屏障的保护作用

目的探讨参附注射液（SF）对大鼠胰腺移植受体肠粘膜屏障的保护作用及机制。方法24只糖尿病大鼠随机分为缺血再灌注组（IR组。n=12），参附注射液预处理组（SF组．n=12），12只正常大鼠为对照组，IR组和SF组大鼠均接受胰腺移植，再灌注后5d检测小肠通透性和吸收功能，检测血清TNF-α、NO、SOD和淀粉酶活性，取受体空肠粘膜组织检测小肠粘膜粘膜湿重、微绒毛高度及宽度、MDA含量及MPO活性，同时取肠系膜静脉血、肠系膜淋巴结、肝及脾组织进行细菌培养，观察细菌易位情况。结果再灌注后SF组血清TNF—α含量（P〈0．01）、淀粉酶活性（P〈0．01）、MDA含量（P〈0．01）、MPO活性（P〈0．01）、小肠通透性（P〈0．01）、细菌易位率（P〈0．01）和小肠粘膜损伤程度均低于IR组；血清NO和SOD含量、小肠吸收功能均高于IR组（P〈0．01）。结论SF预处理可保护大鼠胰腺移植受体小肠肠粘膜屏障，降低细菌易位率，机制可能与降低胰酶活性、减少TNF—α生成、减轻PMNs粘附与聚集、增加NO和SOD含量有关。     

Von Willebrand factor, platelets and endothelial cell interactions

Summary.  The adhesive protein von Willebrand factor (VWF) contributes to platelet function by mediating the initiation and progression of thrombus formation at sites of vascular injury. In recent years there has been considerable progress in explaining the biological properties of VWF, including the structural and functional characteristics of specific domains. The mechanism of interaction between the VWF A1 domain and glycoprotein Ibα has been elucidated in detail, bringing us closer to understanding how this adhesive bond can oppose the fluid dynamic effects of rapidly flowing blood contributing to platelet adhesion and activation. Moreover, novel findings have been obtained on the link between regulation of VWF multimer size and microvascular thrombosis. This progress in basic research has provided critical information to define with greater precision the role of VWF in vascular biology and pathology, including its possible involvement in the onset of atherosclerosis and its acute thrombotic complications.     

急诊左半结肠一期切除吻合术25例治疗体会

目的探讨急诊左半结肠切除一期肠吻合的可行性。方法腹腔探查完后，用布带结扎横结肠，游离肠系膜后，于预切除肠段的上端切开作肠外减压，挤压排空粪便，切除病变肠管，端端吻合，术后作肛管扩张，停留肛管引流，胃肠减压。结果全部病人预期痊愈出院，无发生吻合口漏和腹腔污染。结论该法有利于吻合口的愈合，增加左半结肠一期切除吻合的安全性，减少第2次手术痛苦，可推荐为左半结肠急诊切除一期吻合的良好方法。     

组织工程心肌补片对黑山羊陈旧性心肌梗死心功能和建立侧支循环的影响

目的探讨自体骨髓间充质干细胞(m arrow m esenchym a l stem ce lls,M SC s)-小肠黏膜下层(sm a llin testina l subm ucosa,S IS)构建的组织工程心肌补片,移植于陈旧性心肌梗死区后对心功能及缺血区建立侧支循环的影响。方法将已建立急性心肌梗死模型后6周的黑山羊16只,随机分为实验组和对照组,实验组抽取自体骨髓,经体外分离M SC s,进行培养、传代,以第3代细胞行5-B rdU标记并与S IS支架材料复合培养5 d,制备M SC s-S IS组织工程心肌补片。将其缝合至陈旧性心肌梗死区;对照组仅行假手术处理。于植入后6周,采用超声心动图观察两组动物心功能变化,数字减影血管造影选择性左冠状动脉造影观察缺血心肌侧支循环的建立。结果术后6周实验组及对照组:心博出量、左心室射血分数分别为42.81±4.91、37.06±4.75 m l和59.20%±5.41%和44.56%±4.23%,组间差异均有统计学意义(P<0.05);左心室舒张末期容积、左室收缩末期容积分别为72.55±8.13、83.31±8.61 m l和29.75±5.98、46.25±6.68 m l,组间差异均有统计学意义(P<0.05);左心室舒张功能各项指标分别为:E峰最大速度分别为54.85±6.35 cm/s和43.14±4.81cm/s(P<0.01);A峰最大速度分别为52.33±6.65 cm/s和56.91±6.34 cm/s(P>0.05)。超声心动图显示对照组左室腔扩张明显,室壁运动明显减弱,梗死区呈瘤样扩张,局部室壁反常运动;实验组左室腔明显小于对照组,室壁运动较对照组强,心尖梗死区扩张不明显。选择性左冠状动脉造影见实验组左冠状动脉前降支远端与回旋支间明显侧支循环建立。结论M SC s-S IS构建的组织工程心肌补片移植于黑山羊陈旧性心肌梗死区后侧支循环建立,心功能有明显改善作用。     

细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义

目的探讨ICAM—1在大鼠弥漫性脑损伤中的表达及意义。方法采用Marmarou方法获得大鼠弥漫性脑损伤模型．实时定量RT—PCR、S—P免疫组化法分别测定ICAM—1蛋白和mRNA在外伤后不同时间点的表达变化．干湿重法测脑组织含水量．组织切片苏木精一伊红染色观测炎性细胞浸润情况。结果外伤组与假手术对照组比较，ICAM—1蛋白表达分别于伤后6h明显升高．72h达到高峰（P〈0.05），ICAM—ImRNA表达3h即明显升高，72h达最高峰，其后下降。7d时仍高于假手术对照组（P〈0．01）。伤后脑组织含水量较假手术对照组高，同时炎性细胞大量聚集。结论大鼠脑外伤诱导了ICAM—1的表达．ICAM—1通过介导炎性细胞的浸润可能参与了伤后脑水肿的形成过程．     

血管细胞粘附分子调控造血的研究进展

本文简述了血管细胞粘附分子 (Vascularcelladhesionmolecule 1,VCAM 1)的结构和生物学功能 ,总结了VCAM 1在恶性血液病骨髓基质中的表达和意义 ,探讨了VCAM 1在造血干细胞动员和归巢中的作用 ,指出VCAM 1作用机制的深入研究将对恶性血液病的治疗提供更为有效的方法。     

Kkay小鼠糖尿病肾病时ICAM-1的表达

目的:观察糖尿病肾病时(DN)细胞间黏附分子-1(ICAM-1)表达的变化。方法:22～24周龄:Kkay糖尿病鼠(KA)7只和Kkay非糖尿病鼠(KB)8只,测定血糖,以PAS染色观察各组:DN病变;对肾脏ICAM-1表达进行免疫组化染色和半定量图像分析;并以RT-PCR检测。肾脏ICAM-1 mRNA表达水平。结果:KA组出现明显糖尿病肾脏病变,其肾小球硬化指数(GI)240.00,明显高于KB对照组(118.36,P<0.05);免疫组化显示Kkay小鼠ICAM-1的表达与病理变化一致,其ICAM-1阳性着色面积(15.22％)高于对照组(4.38％,P<0.01),KA组ICAM-1 mRNA表达水平也高于KB组。结论:Kkay小鼠出现糖尿病肾病时伴有ICAM-1表达水平的增高,推测ICAM-1在糖尿病肾病发生发展中起一定作用。     

Reduced expression of CD69 and adhesion molecules of T lymphocytes in asthmatic children receiving immunotherapy

T lymphocytes play a fundamental role in the initiation and regulation of chronic inflammatory responses in patients with asthma. CD69 is an early marker of T‐cell activation. The levels of intercellular adhesion molecule‐1 (ICAM‐1, CD54) and L ‐selectin have been reported to increase in patients with allergic diseases and asthma. The present study was therefore undertaken to investigate the expression of CD69, CD54, and L ‐selectin by T lymphocytes of children with asthma, before and after immunotherapy. Eighteen children newly diagnosed with asthma, 11 good and nine poor responders to immunotherapy, and 16 normal subjects, were enrolled in this study. The percentages of CD69⁺, CD54⁺, and CD62L⁺ cells in T lymphocytes were measured by using flow cytometry. The levels of CD69, CD54, and CD62L in serum and culture supernatants were determined by using enzyme‐linked immunosorbent assay (ELISA). The expression of CD69 and CD54 on CD3⁺ T lymphocytes was significantly higher in children with asthma than in control patients. All the patient groups expressed (spontaneously and following stimulation with phorbol myristate acetate and ionomycin together with mite‐extract proteins) greater amounts of CD69 and CD54 than did control subjects. With long‐term immunotherapy, the percentages of CD69⁺ and CD54⁺ T lymphocytes were significantly lower in patients with a good response to immunotherapy. Our results also showed significantly lower serum L ‐selectin levels following immunotherapy. In conclusion, successful immunotherapy resulted in decreased expression and production of CD69 and CD54. These results may explain, in part, the clinical efficacy of immunotherapy.     

胃癌及肠化组织的微卫星不稳定性

目的 :探讨微卫星不稳定性 (MSI)在胃癌及肠化组织中的发生规律及其在胃癌发生过程中的作用。方法 :对 30例胃癌、4 0例肠上皮化生的石蜡标本分别提取病变及相应正常组织的DNA ,应用银染PCR SSCP技术检测 5个微卫星位点的不稳定性。结果 :胃癌组织MSI的发生率为2 3 3% ,胃窦癌MSI的发生率显著高于贲门癌 (P =0 0 4 4 )。肠化组织MSI发生率 2 0 % ,MSI全部出现在中度以上肠化组织中 (P =0 0 13) ,且更多见于女性 (P =0 0 4 4 )。结论 :MSI是胃癌多步骤发生过程中的早期分子事件 ,在胃癌的发生中可能具有重要作用。     

Monocyte adhesion molecule expression in interstitial inflammation in patients with renal failure.

BACKGROUND: Patients with renal failure have an increased susceptibility to infections. We therefore studied the recruitment of monocytes and their expression of adhesion molecules CD11b and CD62L at the site of interstitial inflammation in patients with renal failure. Furthermore, we studied if the capacity of monocytes to up-regulate CD11b in interstitial inflammation was determined by the interstitial concentration of chemotactic factors. METHODS: Three intensities of interstitial inflammation (0, intermediate and intense) were established in skin blister chambers. Leukocyte count, CD11b/CD62L expression, monocyte chemotactic protein-1 (MCP-1) and blister activity in terms of CD11b mobilization were determined. RESULTS: The CD62L expression on monocytes was lower in the peripheral circulation in patients with renal failure compared with healthy subjects (P<0.005 and P<0.001). At the site of interstitial inflammation patients had a higher expression of CD62L (intermediate, P<0.05; intense, P<0.005). Furthermore, monocytes from patients had an impaired capacity to mobilize CD11b both in the peripheral circulation (P<0.005) and at the intermediate and intense sites of interstitial inflammation (P<0.005 and P<0.001, respectively) compared with cells collected from healthy subjects. We incubated monocytes in blister exudates, in order to explore whether this phenomenon is caused by cellular factors and/or to the interstitial concentration of chemotactic mediators. The expression of CD11b on monocytes from healthy blood donors incubated in blister exudates from either patients or healthy subjects in vitro was similar. The interstitial concentration of MCP-1 at the site of intermediate inflammation was significantly lower in patients with renal failure compared with the corresponding blister exudate collected from healthy subjects (P<0.05), but no differences were observed at the site of intense inflammation. Furthermore, neutralizing the action of MCP-1 in blister exudates with monoclonal antibodies did not have any impact on monocyte CD11b expression following incubation in blister exudates. CONCLUSION: These studies indicate that the impaired capacity of monocytes to mobilize CD11b at the site of inflammation in patients with renal failure is more dependent on constitutive cellular factors than the concentration of CD11b mobilizing factors in the interstitium.