结肠癌患者肿瘤组织及外周血ICAM-1和VCAM-1表达的研究

目的:检测结肠癌患者肿瘤组织中细胞间粘附分子-1(intercellular adhension molecular-1,I-CAM-1)和血管细胞粘附分子-1(vascular cell adhesion molecular-1,VCAM-1)的表达,同时测定血清中可溶性ICAM-1(sICAM-l)和可溶性VCAM-1(sVCAM-1)水平,探讨二者与结肠癌生物学特性及预后的关系。方法:应用免疫组化SP法对32例结肠癌组织、17例溃疡性结肠炎组织和21例正常结肠组织标本进行ICAM-1与VCAM-1表达检测,分析其与结肠癌临床病理指标的关系。ELISA法检测结肠癌患者手术前后外周血sICAM-1和sVCAM-1含量,分析治疗前后水平的变化。结果:结肠癌组织ICAM-1和VCAM-1的阳性表达率显著高于溃疡性结肠炎组织(P<0.05)及正常结肠组织(P<0.01),其表达水平与患者年龄、性别、肿瘤大小和病理学分级无关(P>0.05),与肿瘤分期及有无远处转移有关(P<0.05);结肠癌患者外周血sICAM-1和sVCAM-1水平明显高于溃疡性结肠炎患者(P<0.05)及正常对照组(P<0.01),结肠癌患者术后1周sICAM-1及sVCAM-1水平明显下降(P<0.01,P<0.01)。结论:结肠癌患者肿瘤组织及外周血ICAM-1和VCAM-1的表达可能与结肠癌的浸润转移有关;sICAM-1、sVCAM-1的检测可能成为监测结肠癌病情进展和评价治疗效果的有价值指标。     

大鼠急性胰腺炎时ICAM-1在胰、肺组织的表达特征与作用的观察

目的：探讨急性坏死性胰腺炎（ANP）时细胞间粘附分子-1（ICAM-1）在胰腺及肺组织的表达特征和作用。方法。用3.5%的牛磺胆酸钠逆行胰胆管注射制备ANP模型，采用免疫组化技术等方法动态观察ANP时胰腺、肺组织ICAM-1的表达改变和PMN组织聚集的变化。结果：胰腺及肺组织ICAM-1的表达分别在ANP造模后3H、6h明显增强，并于12h达高峰。结论：ICAM-1介导的PMN大量组织聚集可能是ANP早期胰腺及肺组织损伤的重要参与因素。     

急性胆管炎时肝微循环的变化及其细胞间粘附分子-1和E-选择素的作用

为探讨细胞间粘附分子１ （ Ｉ Ｃ Ａ Ｍ１） 和 Ｅ选择素 （ Ｅｓｅｌｅｃｔｉｎ） 在急性胆管炎肝微循环变化中的作用, 对急性胆管炎时肝脏组织学、肝脏血流量及肝组织伊文思蓝 （ Ｅ Ｂ） 含量的变化, 以及 Ｉ Ｃ Ａ Ｍ１ 和 Ｅ选择素单抗预处理对以上变化的影响进行了观察。结果： 急性胆管炎时肝窦内皮细胞及肝细胞出现变性和结构破坏, 肝窦及肝细胞周围多形核粒细胞 （ Ｐ Ｍ Ｎ） 数量显著增多, 肝微血管血流量明显减少, 肝组织 Ｅ Ｂ含量显著增高, 肝窦通透性增高; 而抗 Ｉ Ｃ Ａ Ｍ１ 及 Ｅ选择素单抗预处理使以上损害均明显减轻。由此表明, Ｉ Ｃ Ａ Ｍ １ 及 Ｅ选择素在肝脏微循环障碍的发生发展中起重要作用。     

急性胆管炎时肝微循环的变化及其细胞间粘附分子—1和E …

为探讨细胞间粘附分子和Ｅ－选择素在急性胆管炎肝微循环变化中的作用，对急性胆管炎时肝脏组织学，肝脏血流量及肝组织伊文思蓝含量的变化，以及ＩＣＡＭ－１和Ｅ－选择素单抗预处理对以上变化的影响进行了观察。结果：急性胆管炎时肝窦内皮细胞及肝细胞出现变性和结构破坏，肝窦及肝细胞周围多形核粒细胞数量显著增多，肝微血管血流量明显减少，肝组织ＥＢ含量显著增高，肝窦通透性增高；     

肝组织ICAM-1及LFA-1表达对急性排斥反应的诊断价值

目的 探讨大鼠移植肝组织内细胞间粘附分子-1（ICAM-1）和淋巴细胞功能相关抗原-1（LFA-1）和淋巴细胞功能相关抗原-1（LFA-1）与急性排斥反应的关系。方法 将SD大鼠、Listar大鼠随机分为正常对照组、同种同基因移植组、同种异基因移植组。分别对正常肝组织及移植后2，4，7d肝组织进行活检，用单克隆抗体免疫组化染色，然后进行图像半定量分析，以检测正常及移植肝组织中ICAM-1和LFA-1的表达水平。结果 同种异基因移植组大鼠肝组织ICAM-1和LFA-1分子表达水平显著高于同种同基因移植组及正常对照组，且其升高与移植术后的时间呈正相关。结论 移植肝组织中ICAM-1和LFA-1表达的检测对肝移植术后急性排斥反应的诊断具有参考价值。     

大鼠移植肾组织ICAM-1/LFA-1分子表达与急性排斥反应的关系

目的探讨移植肾组织内细胞间粘附分子－１（ＩＣＡＭ－１）／淋巴细胞功能相关抗原－１（ＬＦＡ－１）的异常表达与移植排斥的关系。方法采用改进的大鼠原位肾移植模型，分五个实验组，在不同的时间段、观测受体鼠存活、肾功能；以及移植肾组织用单克隆抗体免疫组织化学染色后，图象分析法定量测定移植肾组织ＩＣＡＭ－１／ＬＦＡ－１分子表达的水平。结果移植肾急性排斥组ＩＣＡＭ－１／ＬＦＡ－１分子水平显著高于同品系移植对照组和药物治疗组。结论移植肾组织活检同时检测组织内ＩＣＡＭ－１／ＬＦＡ－１分子的表达，在肾移植急性排斥的诊断和治疗方面具有极其重要的临床意义。     

TNF-α单克隆抗体对急性胰腺炎胰腺组织中ICAM-1的表达的影响

目的 探讨急性胰腺炎(AP)胰腺组织中细胞间粘附分子-1(ICAM-1)的表达与炎症发生发展的关系，以及肿瘤坏死因子-α单克隆抗体(TNF-αMCAb)预处理后的影响。方法 采用免疫组化技术结合多媒体图像分析系统检测AP大鼠胰腺组织中ICAM-1的表达与炎症轻重程度的关系，以及应用TNF-αMCAb对ICAM-1的表达的影响。结果 正常胰腺组织仅少量ICAM-1阳性表达，随着炎症程度的加重，ICAM-1表达逐渐升高，与炎症程度呈正相关。应用TNF-αMCAb预处理后胰腺组织ICAM-1表达明显减弱，炎症程度明显减轻。结论 急性胰腺炎ICAM-1的表达在炎症的发生发展中起着重要的作用，TNF-αMCAb通过抑制ICAM-1的表达，减轻了胰腺组织炎症反应，对胰腺组织有明显的保护作用。     

TNF-α单克隆抗体对急性胰腺炎胰腺组织中ICAM-1的表达的影响

目的　探讨急性胰腺炎 (AP)胰腺组织中细胞间粘附分子 1(ICAM 1)的表达与炎症发生发展的关系 ,以及肿瘤坏死因子 α单克隆抗体 (TNF αMCAb)预处理后的影响。方法　采用免疫组化技术结合多媒体图像分析系统检测AP大鼠胰腺组织中ICAM 1的表达与炎症轻重程度的关系 ,以及应用TNF αMCAb对ICAM 1的表达的影响。结果　正常胰腺组织仅少量ICAM 1阳性表达 ,随着炎症程度的加重 ,ICAM 1表达逐渐升高 ,与炎症程度呈正相关。应用TNF αMCAb预处理后胰腺组织I CAM 1表达明显减弱 ,炎症程度明显减轻。结论　急性胰腺炎ICAM 1的表达在炎症的发生发展中起着重要的作用 ,TNF αMCAb通过抑制ICAM 1的表达 ,减轻了胰腺组织炎症反应 ,对胰腺组织有明显的保护作用     

大鼠创伤失血性休克/复苏后肺、肠组织iNOS、ICAM-1的mRNA表达变化及山莨菪碱的调节作用

目的探讨大鼠创伤失血性休克/复苏后肺、肠组织中诱导型一氧化氮合成酶(iNOS)和细胞间粘附分子-1(ICAM-1)的mRNA表达变化及山莨菪碱的调节作用。方法制作创伤失血性休克大鼠模型,48只SD大鼠随机均分为空白对照组(S组)、创伤失血性休克/复苏组(R1组)、复苏联合山莨菪碱治疗组(R2组)。分别于模型完成后24h处死大鼠,取出大鼠左上肺叶、肠管(取离盲肠末端约10cm处的回肠2cm)标本,以RT-PCR法测定各组大鼠肺、肠组织中iNOS和ICAM-1mRNA的相对表达量。结果在肺、肠组织中iNOS、ICAM-1的mRNA相对表达量上,R1组比S组明显增加(P<0.01),R2组比R1组都有不同程度的降低(P<0.01)。结论大鼠创伤失血性休克/复苏后肺、肠组织中炎症介质和粘附分子表达上调,由此介导中性粒细胞(PMN)在组织中扣押,引起组织损伤。复苏早期应用山莨菪碱,能够使这两种关键的炎症介质iNOS、ICAM-1的mRNA表达量得到一定程度的抑制,从而在一定程度上抑制了过度的炎症反应,减少机体受损害的程度。     

休克期切痂对大鼠肝组织ICAM-1及TNF-αmRNA表达的影响

目的研究烧伤后肝组织细胞间粘附分子-1(ICAM-1)、肿瘤坏死因子-α(TNF-α)表达及肝组织髓过氧化物酶(MPO)变化的规律,探讨实施休克期切痂对上述指标变化的影响,论证及早切除焦痂的重要性.方法Wistar大鼠176只,30%Ⅲ°烫伤,采用逆转录PCR方法分别观察伤后不同时相点及不同时机切痂后肝组织ICAM-1、TNF-α mRNA的表达及肝组织MPO活性变化.结果烫伤后肝组织ICAM-1及TNF-α的mRNA表达在伤后4h即已升高,分别在伤后12h和24h达到高峰;8h和24h切痂组动物切痂后再次出现一峰值,但低于第一个峰值,伤后96h恢复正常;未切痂组和96h切痂组在伤后7天仍未恢复正常.休克期切痂组MPO活性96时恢复正常,未切痂组和非休克期切痂组伤后7天仍未恢复正常.结论及早切痂去除了坏死组织,阻断了炎症介质及细菌毒素的释放,避免了内皮细胞大量合成ICAM-1等粘附分子,减轻了由粘附分子介导的中性粒细胞对内皮细胞的进一步损害.     

烧伤大鼠早期切痂对内皮细胞间粘附分子-1及E-选择素 mRNA表达影响

目的　研究烧伤血清对体外培养的内皮细胞的细胞间粘附分子１（ＩＣＡＭ１）及Ｅ选择素（Ｅｓｅｌｅｃｔｉｎ）ｍＲＮＡ表达的影响,探讨实施休克期切痂上述指标的变化。　方法　Ｗｉｓｔａｒ 大鼠１７６ 只,３０％ Ⅲ度烫伤,收集不同时间点血清,采用逆转录ＰＣＲ 方法分别观察伤后不同时相点血清刺激内皮细胞ＩＣＡＭ１、Ｅｓｅｌｅｃｔｉｎ ｍＲＮＡ表达的规律。　结果　烫伤后血清可刺激内皮细胞ＩＣＡＭ１ 、ＥｓｅｌｅｃｔｉｎｍＲＮＡ表达上调,而且表达量与伤后时间呈正相关。伤后８ 及２４ 小时切痂动物血清不引起内皮细胞的上述变化,９６ 小时切痂（１－６０±０－１７）、（１－２０ ±０－０９） 效果不及休克期切痂组（０－９３ ±０－１４） 、（０－９３ ±０－２２）。　结论　及早切痂去除了坏死组织,避免了内皮细胞大量合成ＩＣＡＭ１、Ｅｓｅｌｅｃｔｉｎ 等粘附分子,减轻了由粘附分子介导的中性粒细胞对内皮细胞的进一步损害。     

Ⅱ度烧伤病人皮肤角朊细胞ICAM-1的表达

目的探讨Ⅱ度烧伤创面愈合过程中角朊细胞间粘附分子１（ＩＣＡＭ１）的表达及其意义。方法应用免疫组织化学染色技术,对烧伤后不同时间Ⅱ度烧伤皮肤组织角朊细胞ＩＣＡＭ１的表达进行动态观察。８例健康人皮肤,６例烧伤病人正常皮肤及８例Ⅱ度烧伤愈合后增生性瘢痕组织为对照组。结果健康人正常皮肤基底层细胞ＩＣＡＭ１可低表达,烧伤病人正常皮肤基底层细胞ＩＣＡＭ１可表达增强。Ⅱ度创面基底层细胞伤后１周内ＩＣＡＭ１表达轻度增高,２周内明显增强,２～４周稳定高表达,ＩＣＡＭ１呈极性分布,新生上皮多层角朊细胞ＩＣＡＭ１表达显著增强,ＩＣＡＭ１阳性细胞呈长柱状排列。结论Ⅱ度烧伤皮肤角朊细胞ＩＣＡＭ１表达增强可能与创基炎性细胞浸润相关,具有诱导角朊细胞增殖、迁移,加速上皮化的作用。     

急性化脓性胆管炎外科的临床特征与治疗变迁

目的了解急性化脓性胆管炎外科治疗30年来的变化情况.方法收集我院1970年1月～1999年12月急性化脓性胆管炎手术治疗的病例共288例,从其年龄、休克率、发病原因、手术方式及治疗预后等资料分析,并按70、80及90等三个年代进行排列比较.结果(1)青幼年下降,老年人上升;(2)胆囊穿孔、休克及病死率下降;(3)胆道蛔虫及细菌感染下降,胆结石上升.结论随着社会的发展及医疗水平的提高,急性化脓性胆管炎的发病率及病死率均明显下降.早期诊断早期治疗,是减少其死亡及并发症的主要措施.     

Unusual cases of acute cholecystitis and cholangitis: Tokyo Guidelines

Unusual cases of acute cholecystitis and cholangitis include (1) pediatric biliary tract infections, (2) geriatric biliary tract infections, (3) acalculous cholecystitis, (4) acute and intrahepatic cholangitis accompanying hepatolithiasis (5) acute biliary tract infection accompanying malignant pancreatic-biliary tumor, (6) postoperative biliary tract infection, (7) acute biliary tract infection accompanying congenital biliary dilatation and pancreaticobiliary maljunction, and (8) primary sclerosing cholangitis. Pediatric biliary tract infection is characterized by great differences in causes from those of adult acute biliary tract infection, and severe cases should be immediately referred to a specialist pediatric surgical unit. Because biliary tract infection in elderly patients, who often have serious systemic conditions and complications, is likely to progress to a serious form, early surgery or biliary drainage is necessary. Acalculous cholangitis, which often occurs in patients with serious concomitant conditions, such as those in intensive care units (ICUs) and those with disturbed cardiac, pulmonary, and nephric function, has a high mortality and poor prognosis. Cholangitis accompanying hepatolithiasis includes recurrent pyogenic cholangitis, an epidemic disease in Southeast Asia. Biliary tract infections, which often occur after a biliary tract operation and treatment of the biliary tract, may have a fatal outcome, and should be carefully observed. The causes of acute cholangitis associated with pancreaticobiliary maljunction differ before and after operation. Direct cholangiography is most useful in the diagnosis of primary sclerosing cholangitis. If cholangiography visualizes a typical bile duct, differentiation from acute pyogenic cholangitis is easy. This article discusses the individual characteristics, diagnostic criteria, treatment guidelines, and prognosis of these unusual types of biliary tract infection.     

Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines

This article discusses the definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis. Acute cholangitis and cholecystitis mostly originate from stones in the bile ducts and gallbladder. Acute cholecystitis also has other causes, such as ischemia; chemicals that enter biliary secretions; motility disorders associated with drugs; infections with microorganisms, protozoa, and parasites; collagen disease; and allergic reactions. Acute acalculous cholecystitis is associated with a recent operation, trauma, burns, multisystem organ failure, and parenteral nutrition. Factors associated with the onset of cholelithiasis include obesity, age, and drugs such as oral contraceptives. The reported mortality of less than 10% for acute cholecystitis gives an impression that it is not a fatal disease, except for the elderly and/or patients with acalculous disease. However, there are reports of high mortality for cholangitis, although the mortality differs greatly depending on the year of the report and the severity of the disease. Even reports published in and after the 1980s indicate high mortality, ranging from 10% to 30% in the patients, with multiorgan failure as a major cause of death. Because many of the reports on acute cholecystitis and cholangitis use different standards, comparisons are difficult. Variations in treatment and risk factors influencing the mortality rates indicate the necessity for standardized diagnostic, treatment, and severity assessment criteria.     

Deficient expression ofO 6-Methylguanine-DNA methyltransferase combined with mismatch-repair proteins hMLH1 and hMSH2 is related to poor prognosis in human biliary tract carcinoma

Background O ⁶-Methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that transfers methyl groups fromO ⁶-methylguanine to itself. Alkylation of DNA at theO ⁶ position of guanine is an important step in the induction of mutations in the organism by alkylating agents. TheO ⁶-methyl G:T mismatch is recognized by the mismatch-repair (MMR) pathway. The biliary duct is highly exposed to alkylating agents because of its anatomical location. Methods We examined 39 surgically resected gallbladder carcinomas and 35 extrahepatic bile duct carcinomas and evaluated the expression of MGMT and MMR protein (hMLH1 and hMSH2) by immunohistochemical staining. Results MGMT-negative staining was detected in 59.0% of gallbladder carcinoma specimens and 60.0% of extrahepatic bile duct carcinoma specimens. In gallbladder carcinoma, hMLH1- and hMSH2-negative staining was observed in 51.3% and 59.0%, respectively, whereas in extrahepatic bile duct carcinoma, the respective values were 57.1% and 65.7%. MGMT-negative staining correlated with hepatic invasion in gallbladder carcinoma and with poor prognosis in both types of tumor. Furthermore, a combined MGMT and MMR status was shown to be a more significant prognostic biomarker in both tumor types. Conclusions Combined MGMT and MMR is a possible prognostic marker that probably reflects an accumulation of genetic mutations.     

Modulation of ICAM‐1 tissue expression in patients with liver transplantation (LT) and acute rejection (AR) after glucocorticoid treatment

Abstract Acute rejection (AR) is a frequent complication following liver transplantation (LT). ICAM‐1 may be involved in its pathogenesis. High doses of glucocorticoids are the standard treatment in these patients. The aim of this study was to describe corticoid effects on ICAM‐1 tissue expression in liver biopsies of patients with LT and AR. The study included liver biopsies performed before and after treatment in 12 patients with LT and proven AR. In 10 patients AR was reversible and in 2, was steroid resistant. For immunohistochemistry, an indirect immunoperoxidase technique was used. Each histology section was semiquantitatively evaluated as follows: 0: <10% staining, 1: 10‐25%, 2: 25‐50%, 3: >50%. The control group comprised nine patients with LT and normal liver biopsies. In pre‐treatment liver biopsy samples, ICAM‐1 was markedly expressed on sinusoidal cells (2.41 ± 0.66), and there was also expression on periportal (0.66 ± 0.65) and perivenular hepatocytes (0.83 ± 0.57). By contrast, in the liver tissue from the control group, sinusoidal ICAM‐1 reactivity was significantly lower (0.88 ± 0.33; P < 0.05), and hepatocytes showed no reliable ICAM‐1 expression. After steroid treatment the intensity of ICAM‐1 decreased significantly in sinusoids (1.5 ± 0.67; P < 0.05) and in perivenular hepatocytes (0.25 ± 0.86; P < 0.05). Additionally, we also observed a decreased ICAM‐1 reactivity in portal hepatocytes (0.25 ± 0.62), but these differences did not reach statistical significance. Remarkably, after treatment, hepatocytes did not show ICAM‐1 reactivity in resolved AR, but in corticoid‐resistant patients AR did not change or increase. In conclusion, in patients with LT and AR, ICAM‐1 was expressed in hepatocytes and with more intensity in sinusoid cells. Additionally, a down‐regulation of the ICAM‐1 tissue expression after corticoid treatment may exist, although in corticoid‐resistant AR no modulation on ICAM‐1 tissue expression was observed.