E—钙粘附蛋白在溃疡生结肠炎发病中的作用

目的 通过研究Ｅ－钙粘附蛋白在性结肠炎中的表达，探讨Ｅ－ＣＤ在ＵＣ发病中的作用。方法 应用免疫组织化学方法，研究正常结肠和ＵＣ标本中的Ｅ－ＣＤ表达。结果 正常组和ＵＣ组中Ｅ－ＣＤ水平无显著性差异（Ｐ〉０．０５）；ＵＣ组中Ｅ－ＣＤ民病情程度不相关（Ｐ〉０．０５）．结论 Ｅ－ＣＤ在ＵＣ进展阶段不起主作用，Ｅ－ＣＤ在ＵＣ触发阶段的作用尚须进一步研究。     

糖皮质激素对重度溃疡性结肠炎患者淋巴细胞粘附分子表达的影响

目的：研究糖皮质激素在分子水平抑制溃疡性结肠炎（ＵＣ）免疫反应和白细胞粘附的机制。方法：采用双标记免疫荧光染色和流式细胞仪，分析２０例中重度ＵＣ患者应用泼尼松治疗前后淋巴细胞粘附分子表型的变化。结果：①中重度ＵＣ患者ＣＤ＋４ＣＤ＋２９、ＣＤ＋８ＣＤ＋１１ａ、ＣＤ＋８ＣＤ＋１８、ＣＤ＋２０ＣＤ＋５４细胞均明显高于正常对照组（Ｐ均＜０．０１）；好转治愈组１６例治疗后上述指标明显下降；除ＣＤ＋２０ＣＤ＋５４细胞外，其余指标与正常对照组比较均无显著性差异（Ｐ均＞０．０５）；无效恶化组４例治疗前后上述指标均无明显变化（Ｐ均＞０．０５），且仍明显高于正常对照组（Ｐ均＜０．０１）。②中重度ＵＣ患者ＣＤ＋４ＣＤ＋１１ａ、ＣＤ＋４ＣＤ＋１８细胞均较正常对照组明显降低（Ｐ均＜０．０１）；好转治愈组治疗后均显著升高（Ｐ均＜０．０１），与正常对照组比较差异均无显著性（Ｐ均＞０．０５）。无效恶化组治疗后上述指标均无明显变化（Ｐ均＞０．０５），仍显著低于正常对照组（Ｐ均＜０．０１）。结论：糖皮质激素可能通过抑制部分淋巴细胞粘附分子的表达来抑制ＵＣ患者自体免疫过程，控制炎症     

ⅡCD34抗原表达与对化疗药物的敏感性

体外细胞毒法（四唑盐法）检测３６例急性髓系白血病（ＡＭＬ）细胞对阿糖胞苷（Ａｒａ－Ｃ）、高三尖杉酯碱（ＨＨｒ）、柔红霉素（ＤＮＲ）、阿克拉霉素（Ａｃｌａ）、长春新碱（ＶＣＲ）、足叶乙甙（ＶＰ－１６）的敏感性，同时用碱性磷酸酶抗碱性磷酸酶（ＡＰＡＡＰ）法检测其ＣＤ＿（３４）抗原，并与临床化疗疗效比较。发现Ａｒａ－Ｃ、ＨＨｒ、ＶＰ－１６中敏组ＣＤ＿（３４）抗原的表达较高敏组高（Ｐ＜０．０５），ＤＮＲ、Ａｃｌａ、ＶＣＲ耐药组较中敏组高，差异亦显著（Ｐ＜０．０５），六种化疗药物耐药组ＣＤ＿（３４）抗原的表达均较高敏组高（Ｐ＜０．０５）。诱导化疗第一疗程后骨髓原始细胞减少指数（ＭＢＤＩ）值＜４０组，４０～６０组及＞６０组组间ＣＤ＿（３４）抗原的表达差异显著（Ｐ＜０．０５）。ＡＭＬ化疗完全缓解，部分缓解与未缓解组组间ＣＤ＿（３４）抗原表达差异亦显著（Ｐ＜０．０５）。复发患者ＣＤ＿（３４）抗原的表达较初诊者高（Ｐ＜０．０５）。ＣＤ＿（３４）阳性白血病细胞对化疗药物具有抗药性，除因其处于静止期（Ｇ＿０期）外，可能与多药耐药基因（ＭＤＲ１）的高水平表达有关。     

消化性溃疡病人的食管粘膜与动力学研究

应用内和多功能消化道检测仪对１００例ＤＵ、４３例ＧＵ的食管粘膜和食管动力学进行研究，并以２００名正常人作对照结果显示：（１）ＰＵ易并发ＲＥＩ，ＤＵ组（２２％）高于ＧＵ组（１４％，Ｐ〈０．０５）。（２）ＤＵ组的ＬＥＳＰ明显低于正常组（Ｐ〈０．０１），提示ＬＥＳ功能障碍是ＤＵ易俣并ＲＥＩ的原因之一。ＧＵ组食管动力学各项指标与正常组相比无明显差异（Ｐ〉０．０５），提示ＧＵ合并ＲＥＩ与食管运动功能无关，可     

尿酶对碘造影剂肾毒性的早期评估

前瞻性观察１６例肾功能正常患者造影前、造影后２４，４８ｈ肾功能动态变化。造影后２４ｈ血尿素氮（ＢＵＮ）、血清肌酐（ＳＣｒ）无显著变化（Ｐ＞０．０５）、尿谷氨酰转肽酶（γ－ＧＴ）、Ｎ－乙酰基－β－Ｄ氨基葡萄糖苷酶（ＮＡＧ）、乳酸脱氢酶（ＬＤＨ）较造影前显著增高（Ｐ＜０．０１）。造影后４８ｈＢＵＮ，ＳＣｒ显著增高（Ｐ＜０．０ｌ），尿γ－ＧＴ，ＮＡＧ，ＬＤＨ显著恢复（Ｐ＜０．０５）；但仍明显高于造影前，差异有显著性（分别Ｐ＜０．０１，０．０１，０．０５）。提示在肾功能正常患者泛影葡胺对肾小管损害呈一过性，尿γ－ＧＴ是评估碘造影剂肾毒性亚临床期敏感指标     

冠状动脉病变程度与血脂及其亚组分、超氧化物歧化酶关系的研究

目的：探讨血脂、脂蛋白及超氧化物歧化酶（ＳＯＤ）与冠状动脉病变程度的关系。方法：选择冠状动脉造影患者３０例，分为正常组（１１例）、单支组（１０例）和多支组（９例）；测定胆固醇、甘油三酯、脂蛋白及其亚组分和ＳＯＤ含量。结果：３组患者间血清甘油三酯和胆固醇水平相近；多支组高密度脂蛋白胆固醇／低密度脂蛋白胆固醇（ＨＤＬＣ／ＬＤＬＣ）比值低于正常组（Ｐ＜０．０５）。单支组和多支组ＨＤＬＣ均低于正常组（Ｐ均＜０．０１），而ＬＤＬＣ均高于正常组（Ｐ＜０．０５或Ｐ＜０．０１）。正常组ＳＯＤ为（２０３．４±５７．７）ｋＵ／Ｌ，高于单支组〔（１２９．４±７１．６）ｋＵ／Ｌ，Ｐ＜０．０５〕和多支组〔（９５．９±５３．３）ｋＵ／Ｌ，Ｐ＜０．０１〕。ＳＯＤ与ＬＤＬ呈中度负相关（ｒ＝－０．４４８，Ｐ＜０．０５），ＳＯＤ与ＨＤＬ（ｒ＝０．６９６，Ｐ＜０．０１）和ＳＯＤ与ＨＤＬＣ（ｒ＝０．３９９，Ｐ＜０．０５）均呈正相关。结论：血脂、脂蛋白、脂蛋白亚组分及ＳＯＤ与冠状动脉病变程度有一定的联系，ＨＤＬ、ＨＤＬＣ、ＬＤＬ、ＬＤＬＣ和ＨＤＬＣ／ＬＤＬＣ是预测冠状动脉粥样硬化性心脏病发病的重要易患因子。     

急性出血性脑血管病并发多脏器功能失常综合征患者血浆内皮素-1及降钙素基因相关肽水平的观察

目的：探讨血浆内皮素１（ＥＴ１）和降钙素基因相关肽（ＣＧＲＰ）在急性出血性脑血管病（ＡＨＣＶＤ）并发多脏器功能失常综合征（ＭＯＤＳ）发病中的作用。方法：采用放射免疫法分别测定２１例ＡＨＣＶＤ合并ＭＯＤＳ患者（ＭＯＤＳ组）、２０例ＡＨＣＶＤ患者（ＡＨＣＶＤ组）及３０例正常人（正常对照组）血浆中ＥＴ１和ＣＧＲＰ水平。结果：ＭＯＤＳ组及ＡＨＣＶＤ组血浆ＥＴ１水平明显高于正常对照组（Ｐ均＜０．０１），ＭＯＤＳ组ＥＴ１水平又明显高于ＡＨＣＶＤ组（Ｐ＜０．０１）。ＡＨＣＶＤ组血浆ＣＧＲＰ水平高于正常对照组，但无显著性差异（Ｐ＞０．０５）。而ＭＯＤＳ组血浆ＣＧＲＰ水平明显低于正常对照组，ＥＴ１／ＣＧＲＰ（Ｅ／Ｃ）比值明显高于ＡＨＣＶＤ组及正常对照组（Ｐ均＜０．０１）。结论：血浆ＥＴ１水平升高、ＣＧＲＰ水平降低、Ｅ／Ｃ比值严重失衡与ＭＯＤＳ的发生相关；检测血浆ＥＴ１和ＣＧＲＰ水平对评估ＡＨＣＶＤ患者预后有一定意义     

急性肺损伤环氧合酶同工酶mRNA表达的变化及地塞米松的影响

目的 探讨急性肺损伤（ＡＬＩ）环氧合酶（ＣＯＸ）同工酶的变化及地塞米松（ＤＥＸ）的影响。方法 用内毒素（ＬＰＳ）复制ＡＬＩ模型,用逆转录多聚酶链反应（ＲＴ－ＰＣＲ）测定ＣＯＸ－１和ＣＯＸ－２的ｍＲＮＡ表达。结果 ＣＯＸ－１ｍＲＮＡ表达在对照组、ＬＰＳ组、ＤＥＸ组之间无显著差别（Ｐ〉０．０５）,而ＣＯＸ－２ｍＲＮＡ表达ＬＰＳ组显著高于对照组（３倍）（Ｐ〈０．０１）,ＤＥＸ干预组显著低ＬＰＳ组（Ｐ〈０     

口服猪脾转移因子对正常,化疗,荷瘤小鼠DNCB皮肤DTH的影响

本实验结果表明，二硝基氯苯（ＤＮＣＢ）能致敏正常小鼠产生皮肤迟发型超敏反应（ＤＴＨ），而化疗，荷瘤小鼠皮肤ＤＴＨ受到明显抑制（Ｐ＜０．００１）；当ＤＮＣＢ致敏的正常，化疗，荷瘤小鼠同时口服与腹注猪脾转移因子（ＰＳ－ＴＦ）一定剂量后，对正常小鼠皮肤ＤＨＴ无明显影响（Ｐ＞０．０５）；对化疗，荷瘤小鼠皮肤ＤＴＨ有明显增强作用（＜０．０５－０．００１）。表明，ＰＳ－ＴＦ对化疗和肿瘤所致的细胞免疫功能下降有     

二十碳五烯酸对卵巢切除小鼠骨髓造血干细胞及基质细胞分化增殖功能的调节作用

以卵巢切除（ＯＶＸ）小鼠模型，观察二十碳五烯酸（ＥＰＡ）对骨髓造血干细胞和基质细胞分化增殖功能的调节作用，结果ＯＶＸ组骨髓造血干细胞培养（ＣＦＵ－ＧＭ）明显增高（Ｐ＜０．０５），ＥＰＡ具有降低ＯＶＸ组骨髓ＣＦＵ－ＧＭ和提高骨髓丛质细胞培养（ＣＦＵ－Ｆ）的作用，但无促ＯＶＸ小鼠子宫生长发育作用。     

溃疡性结肠炎结肠粘膜HLA－DR抗原表达

本文检测了６０例溃疡性结肠炎和３０例正常结肠粘膜上皮细胞ＨＬＡ－ＤＲ抗原表达。结果显示，３０例正常结肠粘膜上皮及腺体不表达ＨＬＡ－ＤＲ抗原；而６０例ＵＣ中有３２例结肠粘膜上皮和腺体不同程度表达该抗原。其中，４２例活动性ＵＣ中２９例表达，１８例非活动性ＵＣ仅３例表达。同时发现ＵＣ结肠粘膜上皮表达ＨＬＡ－ＤＲ抗原还与粘膜炎症程度成正比。结果提示，细胞免疫机制在ＵＣ的发病机理中起重要作用。     

溃疡性结肠炎大鼠C04^＋CD25^＋T细胞的改变

目的 探讨CD4＋CD25^＋T细胞的异常在大鼠溃疡性结肠炎动物模型发病机制中的作用。方法 40只Wistar大鼠分为正常对照组和溃疡性结肠炎模型组，应用三硝基苯磺酸／乙醇法建立溃疡性结肠炎的大鼠模型，进行粪便细菌培养，流式细胞仪分析其外周血单个核细胞（PBMC）和肠系膜淋巴结（MLN）中的CD4^＋CD25^＋T细胞和CD4^＋T细胞的比例，实时荧光PCR测定Foxp3 mRNA的含量。结果 （1）溃疡性结肠炎模型组大鼠PBMC中CD4^＋CD25^＋T细胞的比例明显高于正常（P〈0．05），CD4^＋T细胞的比例明显下降（P〈0．05），MLN中CD4^＋CD25^＋T细胞的比例明显低于正常（P〈0．05），CD4^＋T细胞的比例明显增高（P〈0．05）；（2）模型组大鼠PBMC中Foxp3 mRNA的含量明显增高（P〈0．05）；而MLN中Foxp3 mRNA的含量明显下降（P〈0.05）；（3）模型纽大鼠肠道菌群较正常对照有显著改变（P〈0．05）。结论 CD4^＋CD25^＋T细胞的异常在溃疡性结肠炎的发病机制中起重要作用，其异常可能与肠道菌群的改变有关。     

Appendiceal lesion in ulcerative colitis

Recently, there has been a resurgence in the interest of the role of the appendix in ulcerative colitis. The lesion of appendix in ulcerative colitis is reviewed. Surgical studies were mainly reported in western countries and endoscopic studies were mainly reported in Japan. Epidemiological and experimental studies suggest a central role of the appendix in development of ulcerative colitis. It was considered that understanding of the significance of a skip lesion in the appendix would contribute to the elucidation of the pathogenesis of ulcerative colitis.     

Phospholipase A2 in serum and colonic mucosa in ulcerative colitis.

Group II phospholipase A2 is involved in the pathogenesis of various inflammatory diseases and in the host defence against bacteria. The enzyme is expressed in the epithelial cells of colonic mucosa in ulcerative colitis. In this study, we measured the concentration of group II phospholipase A2 in serum and colonic mucosa of patients with ulcerative colitis of different severity and of control patients without any inflammatory disease. The activity of ulcerative colitis was assessed by endoscopy. The concentration of group II phospholipase A2 was measured with an immunoassay. The concentrations of group II phospholipase A2 in serum and colonic mucosa were significantly higher in patients with active and inactive ulcerative colitis than in controls. However, the group II phospholipase A2 levels did not separate patients with different disease activity. The concentration of group II phospholipase A2 in colonic mucosa corresponded with the mucosal inflammatory activity (higher in active colonic areas) intra-individually, but not between different patients with ulcerative colitis. Serum group II phospholipase A2 values were above the normal reference range more often than the values of 11 standard laboratory blood tests widely used for the follow-up of inflammatory activity in ulcerative colitis. These results indicate that the concentration of group II phospholipase A2 is increased in serum and colonic mucosa of patients with ulcerative colitis. The clinical value of the measurement of group II phospholipase A2 in the follow-up of ulcerative colitis remains to be clarified.     

Macrophage migration inhibitory factor in the sera and at the colonic mucosa in patients with ulcerative colitis: clinical implications and pathogenic significance

BACKGROUND: Inflammatory cytokines produced by activated macrophages are implicated in the pathogenesis of ulcerative colitis (UC). With the theory that macrophage migration inhibitory factor (MIF) may have a role in the accumulation of macrophages, we studied MIF in UC. MATERIALS AND METHODS: A total of 27 patients with UC, 14 patients with Crohn's diseases (CD), 11 patients with other forms of colitis and 26 normal controls were enrolled in the study. The levels of MIF in the sera and culture supernatant were measured by an enzyme-linked immunosorbent assay. MIF, macrophages and T cells were localized at the colonic mucosa by immunohistochemistry. RESULTS: The levels of MIF in the sera were significantly higher in UC than in normal controls (P < 0.05), in serum C-reactive protein (CRP) -positive cases with UC than in CRP-negative cases with UC (P < 0.05), and in patients with severe colitis with UC than in mild colitis with UC (P < 0.05). There was a positive relationship between serum MIF levels with the CRP levels and activities of colitis. However, the levels of MIF in patients with CD and other forms of colitis were not significantly different from their levels in normal controls and UC. Infiltrating cells at the colonic mucosa in UC and CD expressed MIF. CONCLUSIONS: These data suggest a role of MIF in the pathogenesis of UC. MIF may be used as a marker of disease activity in UC and control of MIF production may have therapeutic implications.     

CD44拼接变异体V6与上皮钙粘附素在胰腺癌中的表达及意义

目的探讨CD44拼接变异体V6（CD44 Splicevarint V6，CD44V6）和上皮钙粘附素（E-Cadherin，E-CD）在胰腺癌中表达及与胰腺癌浸润、转移的关系，评价CD44V6和E-CD在胰腺癌浸润转移中的作用。方法采用SP免疫组化染色方法，检测43例胰腺癌组织中CD44V6和E-CD的表达情况。结果正常胰腺导管上皮细胞CD44V6呈阴性表达，胰腺癌组织中CD44V6阳性表达率达58．1％（25／43），CD44V6阳性表达与胰腺癌浸润深度、淋巴结转移情况密切相关（P〈0．05），与胰腺癌组织分化程度无关（P〉0．05）。正常胰腺导管上皮细胞E-CD呈强阳性表达，60．5％（26／43）的胰腺癌组织中E-CD呈异常表达，E-CD的异常表达与胰腺癌组织分化程度、浸润程度、淋巴结转移情况关系密切（P〈0．01）。CD44V6和E-CD在胰腺癌中的表达无明显相关性（P〉0．05）。结论CD44V6阳性表达和E-CD异常表达与胰腺癌浸润、转移关系密切，检测CD44V6和E-CD表达有助于对胰腺癌浸润转移潜能的判断，二者可以作为胰腺癌浸润转移的生物学指标。     

溃疡性结肠炎大鼠肠组织NF—κB P^65表达的意义

目的探讨溃疡性结肠炎（ulcerative colitis,uc）大鼠结肠组织核因子-κB（NF-κB） P^65的表达的意义。方法雌性SD大鼠随机分为正常对照组、模型组,每组7只。模型组用三硝基苯磺酸（TNBS）／乙醇溶液灌肠复制UC模型。评价2组实验大鼠大体及组织病理学改变、采用蛋白质印迹杂交法检测结肠组织核因子（NF）-κB P^65蛋白的表达。结果与正常组比较,模型组大鼠结肠大体形态评分、组织学评分明显升高（0．00±0．00）Vs（5．43±1．27）,（1．29±0．49）Vs（6．71±0．95）,P〈0．01）;与正常组比较,模型组结肠组织NF—κB蛋白区带加宽。结论NF—κB与UC发病关系密切。     

Treatment of ulcerative colitis and Crohn's disease with monoclonal antibody

Ulcerative colitis and Crohn's disease are nonspecific inflammatory diseases of unknown etiology. Recent immunological studies have shown that proinflammatory cytokines and adhesion molecules play an important role in the pathogenesis of ulcerative colitis and Crohn's disease. Therefore, monoclonal antibodies to proinflammatory cytokines and adhesion molecules are used to suppress the mucosal inflammatory response in experimental colitis and ulcerative colitis and Crohn's disease. Anti-TNF alpha antibody and anti-alpha 4 beta 7 integrin antibody are well-tolerated and effective for treatment of patients with Crohn's disease. This review described clinical features and immunopathophysiology of ulcerative colitis and Crohn's disease, proinflammatory cytokines and immunosuppressive cytokines and adhesion molecules involved in the pathogenesis of both disease, and treatment of both diseases with monoclonal antibodies.     

Extra-intestinal complications of ulcerative colitis: arteriovenous thrombosis/embolism

Thromboembolic episode is a well known extraintestinal complications of ulcerative colitis, but it is a rare complication in clinically. In the literature there are some interesting observations concerning the factors, may play a major role both in the pathogenesis and in the hypercoagulability in ulcerative colitis. However the exact mechanism of hypercoagulability in patients with ulcerative colitis is still unknown. We reviewed the incidence, the activity and severity of the basic disease, the pathogenesis, the treatment, the prognosis of thromboembolic phenomena in patients with ulcerative colitis.     

E—CD的表达和胰腺癌浸润、转移的关系

目的：探讨E－CD（E－Cadherin)在胰腺中表达及与腺癌浸润,转移的关系,评价E－CD在胰腺癌浸润转移中的作用。方法：采用SP免疫组化染色方法,检测43例胰腺癌组织中E－CD的表达情况。结果：正常胰腺导管上皮细胞E－CD呈强阳性表达,60．5％（26／43）的胰腺癌组织中E－CD呈异常表达,E－CD的异常表达与胰腺癌组织分化程度、浸润程度、淋转移情况关系密切（P＜0．05）／。结论E－CD异常表达与胰腺癌浸润、转移关系密切,检测E－CD表达有助于对胰腺癌浸润转移潜能的判断,其可以作为胰腺癌浸润转移的生物学指标。