人结肠粘膜Mr40KD蛋白的提取、纯化及免疫学特性鉴定

目的 探索非特异性溃疡性结肠炎(UC)血清学诊断方法。方法 采用DE-52离子交换层折及cNBr-Sepharose 4B亲和层析技术从人结肠粘膜组织中提取一种蛋白组分，经10％SDS-PAGE、IEF、CIE及Westem blot技术，对该蛋白分子量、等电点及免疫学等进行鉴定。结果 产物PI为5．8，分子量为40KD，免疫学鉴定发现其主要与UC患者血清起反应。结论 人结肠40KD蛋白可能是UC的一种自身抗原，血清中ACA可以作为UC的一个特异性指标。     

溃疡性结肠炎所致肠梗阻3例误诊分析

溃肠性结肠炎(ulcerativecolitis,UC)又称非特异性或特发性溃疡性结肠炎,是一种原因不明的慢性结肠炎症性病变,主要限于大肠黏膜及黏膜下层,以溃疡病变为主.多累及直肠和乙状结肠,也可遍及整个结肠及末端回肠.[1]UC在欧美发达国家多见,亚洲国家发病率远低于欧美国家,近年来,很多国家报道UC的发病率呈上升趋势.[2]肠腔狭窄和肠梗阻是此病的并发症之一,但发生机率很低,而且随着近年来对此病的内科治疗进展迅速,绝大多数病情经内科治疗都能有效控制,原则上不需外科手术.近两年来,我科共收治溃疡性结肠炎所致的肠梗阻3例,术前均误诊,现报告如下.     

溃疡性结肠炎治疗进展

溃疡性结肠炎是一种原因不明的炎症性病变,主要发生在结肠粘膜层,以溃疡糜烂为主要表现,主要累及直肠、乙状结肠、亦可向上扩展至左半结肠和右半结肠,甚至全结肠。 1 病因 本病病因迄今尚未明了,近年来由于免疫学和遗传学研究的发展,对溃疡性结肠炎的病因学探索初见端倪。     

锡类散、云南白药、氟哌酸、地塞米松等混合液保留灌肠治疗溃疡性结肠炎25例

我们自1992年以来,在我科门诊与住院病人中采用中药锡类散、云南白药与氟哌酸、地塞米松混合液保留灌肠治疗轻、中度、活动期、初发型、慢性复发型、慢性持续性溃疡性结肠炎25例。 25例均按照1993年太原全国慢性非感染性肠道疾病学术研讨会所规定的溃疡性结肠(UC)诊断标准诊断。初发型9倒,慢性复发     

194例溃疡性结肠炎临床分析

目的：探讨溃疡性结肠炎（UC）的临床特征,深化本病认识并提高诊治水平。方法：回顾性分析我院2009年1月-2010年3月已确诊的194例UC患者的临床特征,结肠镜特点和病理学特征。结果：UC男性发病率高于女性,发病30—39岁最多发。本组患者临床特点以腹泻（93．8％）、脓血便（82．0％）、腹痛（77．8％）为主,这些临床表现的发生率随病变范围加大而增高,发病部位以直乙结肠型（30．4％）多见,病变呈连续性,严重者可累及全结肠。结论：UC有较明显的临床特征,其病变范围与病程关系密切且由结肠远端向近端发展;结肠镜检查和病理学特征有助于本病诊断。     

诱发溃疡性结肠炎动物模型化学方法及评价

溃疡性结肠炎（ulcerative colitis,UC）又称慢性非特异性溃疡性结肠炎,流行病学资料提示溃疡性结肠炎的发病率在国内外都有逐年增高的趋势,溃疡性结肠炎的研究越来越受到国际肠病学家的关注,所以建立接近于人类的稳定的溃疡性结肠炎动物模型尤为重要。本文综述了近几年常用的诱发溃疡性结肠炎动物模型的化学方法及评价,以期为基础与临床研究应用提供参考。     

中西药结合治疗溃疡性结肠炎42例疗效观察

目的:观察中西药结合治疗溃疡性结肠炎(UC)的疗效.方法:将80例患者随机分为治疗组对照组.治疗组给予柳氮磺胺吡啶、中药口服及灌肠,对照组给予柳氮磺胺吡啶口服.2组4周围一疗程.结果:治疗组总有效率为83.3%;对照组总有效率为52.6%,差异有显著性(P<0.05).结论:中西药结合治疗UC疗效显著.     

一例慢性非特异性溃疡性结肠炎病人的护理

慢性非特异性溃疡性结肠炎是一种原因尚未完全阐明的慢性结肠炎,以溃疡为主,病情复杂,目前现有西医治疗仅能缓解病情,未能使本病痊愈.为了进一步探究慢性非特异性溃疡性结肠炎的主要发病相关因素,本文探讨了针对慢性非特异性溃疡性结肠炎病人的护理方法及效果,以便更好地预防病情复发、减轻患者病痛、提高护理效果.通过对一例慢性非特异性溃疡性结肠炎病人的发病诱因、具体临床表现的观察,并且经过基础护理、饮食护理、心理护理、中医治疗护理四个方面的护理过程,患者病情基本得到控制并有所改善.说明提高各方面的护理工作水平对慢性非特异性溃疡性结肠炎病人的治疗乃至康复是非常重要的.     

溃疡性结肠炎患者血小板α颗粒膜蛋白和平均容积的检测及其临床意义

目的:探讨溃疡性结肠炎(UC)患者血小板α颗粒膜蛋白(GMP-140)含量与血小板平均容积(MPV)的变化及其在病情活动性与严重性评价中的意义.方法:采用ELISA法与自动血细胞分析系统,检测32例活动期UC患者、25例缓解期UC患者及30例健康对照者的GMP-140含量、MPV大小,并评价活动期患者病情轻重程度.结果:活动期UC患者GMP-140含量、MPV与缓解期患者和对照组分别有显著差异,分别为(P<0.01和P<0.05),缓解期患者与对照组比较,仍有明显差异P<0.05,且与UC病情活动性,病情分型均呈显著相关性.结论:活化的小容积血小板是UC患者的一个特点.GMP-140、MPV可作为UC患者病情活动性与严重性评价的参考指标.     

三七珍珠散治疗非特异性溃疡性结肠炎72例观察

非特异性溃疡性结肠炎(UC)的病因目前尚未完全明确,国内外多用免疫抑制剂及前列腺素合成抑制剂治疗,患者需长期服药,往往不能耐受,且有较重的副作用。我科于1984年5月至1992年12月应用三七珍珠散治疗136例患者,取得较好的疗效,现将观察情况及体会汇报如下:     

Inflammatory bowel disease unclassified

Objective  

Inflammatory bowel diseases (IBDs) are idiopathic, chronic, and inflammatory intestinal disorders. The two main types, ulcerative colitis (UC) and Crohn’s disease (CD), sometimes mimic each other and are not readily distinguishable. The purpose of this study was to present a series of hospitalized cases, which could not initially be classified as a subtype of IBD, and to try to note roles of the terms indeterminate colitis (IC) and inflammatory bowel disease unclassified (IBDU) when such a dilemma arises.     

抗人双特异性磷酸酶DUSP18单克隆抗体的制备及鉴定

双特异性磷酸酶（Dual Specificity Phosphatase）是酪氨酸磷酸酶家族中的一员,这个家族中的成员既能对磷酸化酪氨酸去磷酸化,也能对磷酸化丝／苏氨酸去磷酸化．此外,它们还在有丝分裂原激活蛋白磷酸酶信号途径（MAPK）中起重要生理功能．为了制备抗人双特异性磷酸酶的单克隆抗体（mAb）,以DUSP18重组蛋白为抗原免疫BALB／e小鼠,通过B淋巴细胞杂交瘤技术制备抗相应磷酸酶的mAb．用Western blot检测mAb对重组蛋白和细胞中天然磷酸酶的反应性,共获得6株可稳定分泌抗磷酸酶mAb的杂交瘤细胞株,为进一步研究双特异性磷酸酶的去磷酸化作用机理以及其在有丝分裂原激活蛋白磷酸酶信号途径（MAPK）中的信号转导提供强有力的工具．     

Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats

The histopathological features and the associated clinical findings of ulcerative colitis (UC) are due to persistent inflammatory response in the colon mucosa. Interventions that suppress this response benefit UC patients. We tested whether sodium arsenite (SA) benefits rats with dextran sulfate sodium (DSS)-colitis. The DSS-colitis was induced by 5% DSS in drinking water. SA (10 mg/kg; intraperitoneally) was given 8 h before DSS treatment and then every 48 h for 3 cycles of 7,14 or 21 d. At the end of each cycle rats were sacrificed and colon sections processed for histological examination. DSS induced diarrhea, loose stools, hemoccult positive stools, gross bleeding, loss of body weight, loss of epithelium, crypt damage, depletion of goblet cells and infiltration of inflammatory cells. The severity of these changes increased ir the order of Cycles 1,2 and 3. Treatment of rats with SA significantly reduced this severity and improved the weight gain.     

腹腔注射丁酸盐对大鼠乙酸性结肠炎的预防作用(英文)

目的:探索腹腔注射丁酸盐对防止乙酸性结肠炎的疗效。创新点:首次对大鼠进行腹腔注射丁酸盐,通过与直肠灌注和口服比较,探索三种不同给药方式对预防乙酸性结肠炎的疗效差异。方法:以40只Wistar大鼠为实验对象,分组进行连续7天的腹腔注射、直肠灌注和口服100 mg/kg丁酸钠(SB),第8天进行乙酸(AA)直肠灌注,48小时后处死。记录实验大鼠的临床症状,包括体重减少、腹泻、便血等。对结肠切片进行组织病理学观察,最后对试验数据进行统计分析。结论:腹腔注射、直肠灌注和口服丁酸盐均能明显缓解大鼠乙酸性结肠炎的炎症,其中以腹腔注射疗效最佳。     

抗-CCP抗体检测在类风湿关节炎诊断中的应用

目的探讨抗-CCP抗体检测在类风湿关节炎诊断中的作用。方法回顾性分析了125例疑为风湿疾病患者及33例类风湿关节炎（RA）患者抗-CCP抗体和RF检测结果。结果 125例疑为风湿疾病患者中,抗-CCP抗体阳性31例、RF阳性10例,其中确诊的33例RA患者抗-CCP抗体阳性31例、RF阳性9例。结论抗-CCP抗体检测是RA早期诊断一种十分有效的方法。     

溃疡性结肠炎模型的构建及其炎症反应机制研究

目的：构建2,4,6-三硝基苯磺酸（2,4,6-trinitrobenzene sulfonic acid,TNBS）以及恶唑酮（oxazolone,OXZ）诱导的小鼠溃疡性结肠炎（ulcerative colitis,UC）模型。方法：120只昆明小鼠（）随机分为4组（n=30）。Ⅰ组、Ⅱ组参照Morris及Walter的方法制备小鼠TNBS模型：Ⅰ组（TNBS溶剂对照组）,50%乙醇0.1 m L灌肠;Ⅱ组（TNBS模型组）,0.6%TNBS溶液0.1 m L灌肠;两组灌肠给药一次后在d 1、d 2、d 3、d 5、d 7每组处死6只。Ⅲ组、Ⅳ组参照Heller方法制备小鼠OXZ模型：Ⅲ组（OXZ溶剂对照组）,皮肤涂抹100%乙醇0.1 m L,每天一次,连续2 d,d 7以50%乙醇0.1 m L灌肠;Ⅳ组（OXZ模型组）,皮肤涂抹1%OXZ溶液（100%乙醇溶解）0.1 m L每天一次,连续2 d（致敏）,d 7以0.5%OXZ（50%乙醇溶解）0.1 m L灌肠;两组灌肠给药一次后在d 1~d 5每天处死6只小鼠。观察Ⅰ~Ⅳ组小鼠疾病活动指数（disease activity index,DAI）、结肠组织大体损伤指数（colon macroscopic damage index,CMDI）和病理组织学评分（histopathological score,HPS）,并检测小鼠结肠组织中髓过氧化物酶（myeloperoxidase,MPO）、白细胞介素-4（interleukin-4,IL-4）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）的水平。结果：两种模型组小鼠DAI,CMDI和HPS均较对照组有明显改变;TNBS和OXZ诱导的结肠炎均可导致MPO明显上升,TNBS结肠炎TNF-α明显上升,OXZ结肠炎IL-4明显下降。结论：TNBS及OXZ均能诱导小鼠溃疡性结肠炎模型。两种模型各有特点,其中TNBS诱导的小鼠溃疡性结肠炎以辅助性T1（helper1,Th1）型炎症反应为主,OXZ诱导的小鼠溃疡性结肠炎以辅助性T2（helper2,Th2）型炎症反应为主。     

上消化道出血49例胃超声影象分析

目的分析上消化道出血胃B超图象特征,探讨B超对上消化道出血及其病因诊断的意义.方法;选择上消化道出血活动期的位院患者49例,分别于空腹及饮水后依次探查贲门、胃体、胃窦、十二指肠及其邻近器官,记录图像,并结合内镜病理及X线结果进行分析.结果49例中.B超检出相关疾病41例,命中37例;检出率及准确率分别为83.7%和75.5%,X线报告32例,命中29例,检出率及准确率分别为65.3%和59.2%,统计分析结果显示该两种检查方法有显著差异(P＜0.05).结论B型超声可作为上消化道出血病因诊断较可靠的方法.     

Spirulina platensis aqueous extracts ameliorate colonic mucosal damage and modulate gut microbiota disorder in mice with ulcerative colitis by inhibiting inflammation and oxidative stress

Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease (IBD) that has become a major gastroenterologic problem during recent decades. Numerous complicating factors are involved in UC development such as oxidative stress, inflammation, and microbiota disorder. These factors exacerbate damage to the intestinal mucosal barrier. Spirulina platensis is a commercial alga with various biological activity that is widely used as a functional ingredient in food and beverage products. However, there have been few studies on the treatment of UC using S. platensis aqueous extracts (SP), and the underlying mechanism of action of SP against UC has not yet been elucidated. Herein, we aimed to investigate the modulatory effect of SP on microbiota disorders in UC mice and clarify the underlying mechanisms by which SP alleviates damage to the intestinal mucosal barrier. Dextran sulfate sodium (DSS) was used to establish a normal human colonic epithelial cell (NCM460) injury model and UC animal model. The mitochondrial membrane potential assay 3-‍‍(4,5-dimethylthiazol-2-yl)-2,‍5-diphenyltetrazolium bromide (MTT) and staining with Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) and Hoechst 33258 were carried out to determine the effects of SP on the NCM460 cell injury model. Moreover, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qPCR), western blot, and 16S ribosomal DNA (rDNA) sequencing were used to explore the effects and underlying mechanisms of action of SP on UC in C57BL/6 mice. In vitro studies showed that SP alleviated DSS-induced NCM460 cell injury. SP also significantly reduced the excessive generation of intracellular reactive oxygen species (ROS) and prevented mitochondrial membrane potential reduction after DSS challenge. In vivo studies indicated that SP administration could alleviate the severity of DSS-induced colonic mucosal damage compared with the control group. Inhibition of inflammation and oxidative stress was associated with increases in the activity of antioxidant enzymes and the expression of tight junction proteins (TJs) post-SP treatment. SP improved gut microbiota disorder mainly by increasing antioxidant enzyme activity and the expression of TJs in the colon. Our findings demonstrate that the protective effect of SP against UC is based on its inhibition of pro-inflammatory cytokine overproduction, inhibition of DSS-induced ROS production, and enhanced expression of antioxidant enzymes and TJs in the colonic mucosal barrier.