新麦纤散对溃疡性结肠炎大鼠结肠黏膜炎症及相关免疫因子表达的影响

麦纤散是郑红斌教授运用麦芽纤维防治溃疡性结肠炎（UC）这一访日留学研究成果，结合临床经验配伍而成。本实验旨在探讨在此基础上酌加白及组成的新麦纤散对UC大鼠结肠黏膜炎症及血清白介素（IL）-34、IL-35的影响。

结肠黏膜炎症、便秘及肠源性内毒素与帕金森病相关性研究

目的:探讨结肠粘膜炎症、便秘及肠源性内毒素与帕金森疾病的相关性,为早期鉴别帕金森病寻找有效的发病机制,为实验提供依据。方法:在2016年9月—2017年9月这段期间内,采用问卷调查方式对113例帕金森患者进行调查,并对其便秘进行分析。分析帕金森病患者年龄、运用症状病程以及便秘病程与患者便秘分型间的关系。结果:在此次所选的113例研究帕金森研究对象中,便秘人数30例,占26.55%,不便秘人数83例;占73.45%;便秘人数远多于不便秘人数,相互间比较具有统计学意义。同时在患有便秘的患者,有32例慢性输障碍型便秘,有14例进出口障碍型便秘,有37例混合型便秘。在81例帕金森患者中,其肠源性内毒素≥0.1EU/ml患者有17例;0.1—0.01EU/ml之间的患者有31例;低于0.01EU/ml患者有23例。由此可见,患者肠源性内毒素增高和患者便秘具有较大的关联性(P<0.05)。结论:结肠粘膜炎症、便秘和肠源性内毒素和帕金森疾病之间具有较大的相关性,后期还需要加大对各个要素的研究,寻找期间的联系性,为尽早地诊断出帕金森病提供合理的参考依据。

升阳除湿法治疗溃疡性结肠炎理论依据和机制

升阳除湿法治疗溃疡性结肠炎的机制一方面通过改善结肠黏膜炎症对溃疡性结肠炎起治疗作用,另一方面可能通过调节肠黏膜通透性缓解炎症反应。升阳除湿法升提脾胃阳气,使清气得升,湿浊得降,郁阳舒展,湿气得化,进而对溃疡性结肠炎发挥治疗作用。

Persistence of gene expression changes in noninflamed and inflamed colonic mucosa in ulcerative colitis and their presence in colonic carcinoma

AIM： A few studies have applied genomic-wide gene expression analysis in inflamed colon tissue sample in ulcerative colitis （UC）. We reported the first study of non-inflamed mucosal gene expression in UC and explored its clinical implication. METHODS： Non-inflamed mucosa was obtained from 6 UC patients who received total colectomy. The gene expression of UC in noninflamed mucosa was monitored with a microarray. For a selected gene, RT-PCR was performed to verify array results and to further examine expression pattern in inflamed mucosa of UC, colorectal cancer tissue and normal mucosa using additional matched pairs. RESULTS： Two genes showing 2.5-fold decreased expression with significance set at in UC samples were borneo box a4 （HOXa4） and mads box transcription enhancer factor 2, polypeptide B （MEF2b）. RT-PCR showed that MEF2b expression in non-inflamed mucosa was significantly downregulated, whereas the expression of MEF2b increased in accordance with the severity of mucosal inflammation. HOXa4 expression both in inflamed and non-inflamed mucosa in UC was consistently downregulated, and the downregulation of HOXa4 was also found in colorectal carcinoma. CONCLUSION： It is suggested that the MEF2b expression in UC which increase in accordance with inflammation may be induced by the inflammatory mediator. In contrast the downregulation of HOXa4 may be partly involved in the pathogenesis of disease including UC and UC-related carcinogenesis.

Intestinal alkaline phosphatase in the colonic mucosa of children with inflammatory bowel disease

AIM： To investigate intestinal alkaline phosphatase （iAP） in the intestinal mucosa of children with inflammatory bowel disease （IBD）. METHODS： Colonic biopsy samples were taken from 15 newly diagnosed IBD patients and from 10 healthy controls. In IBD patients, specimens were obtainedboth from inflamed and non-inflamed areas. The lAP mRNA and protein expression was determined by reverse transcription-polymerase chain reaction and Western blotting analysis, respectively. Tissue localiza- tion of lAP and Toll-like receptor （TLR） 4 was investi- gated by immunofluorescent staining. RESULTS： The lAP protein level in the inflamed muco- sa of children with Crohn＇s disease （CD） and ulcerative colitis （UC） was significantly decreased when compared with controls （both P 〈 0.05）. Similarly, we found a significantly decreased level of lAP protein in the in- flamed mucosa in CD compared with non-inflamed mucosa in CD （P 〈 0.05）. In addition, the iAP protein level in inflamed colonic mucosa in patients with UC was decreased compared with non-inflamed mucosa in patients with CD （P 〈 0.05）. lAP protein levels in the non-inflamed mucosa of patients with CD were similar to controls, lAP mRNA expression in inflamed colonic mucosa of children with CD and UC was not significant- ly different from that in non-inflamed colonic mucosa with CD. Expression of lAP mRNA in patients with non- inflamed mucosa and in controls were similar. Co-local- ization of lAP with TLR4 showed intense staining with a dotted-like pattern, lAP was present in the inflamed and non-inflamed mucosa of patients with CD, UC, and in control biopsy specimens, irrespective of whether it was present in the terminal ileum or in the colon. However, the fluorescent signal of TLR4 was more pro- nounced in the colon compared with the terminal ileum in all groups studied. CONCLUSION： Lower than normal lAP protein levels in inflamed mucosa of IBD patients may indicate a role for lAP in inflammatory lesions in IBD. Based on our results, administration of exogenous lAP enzyme to pa- tients with the active form of IBD may be a therapeutic option.

B1a lymphocytes in the rectal mucosa of ulcerative colitis patients

AIM:To assess B1a cell expression in the rectal mucosa of ulcerative colitis (UC) patients in comparison with healthy controls.METHODS:Rectal mucosa biopsies were collected from 15 UC patients and 17 healthy controls.CD5 + B cells were analysed by three colour flow cytometry from rectal mucosal samples after mechanical disaggregation by Medimachine.Immunohistochemical analysis of B and T lymphocytes was also performed.Correlations between,on the one hand,rectal B1a cell concentrations and,on the other,erythrocyte sedimentation rate and C-reactive protein levels and clinical,endoscopic and histological disease activity indices were evaluated.RESULTS:Rectal B-lymphocyte (CD19 + /CD45 +) rate and concentration were higher in UC patients compared with those in healthy controls (47.85% ± 3.12% vs 26.10% ± 3.40%,P=0.001 and 501 ± 91 cells/mm 2 vs 117 ± 18 cells/mm 2,P < 0.001);Rectal B1a cell density (CD5 + CD19 +) was higher in UC patients than in healthy controls (85 ± 15 cells/mm 2 vs 31 ± 6.7 cells/mm 2,P=0.009).Rectal B1a cell (CD5/CD19 +) rate correlated inversely with endoscopic classification (Rs=-0.637,P < 0.05).CONCLUSION:B1a lymphocytes seem to be involved in the pathogenesis of UC,however,the role they play in its early phases and in disease activity,have yet to be defined.

Mucosa-associated bacteria in two middle-aged women diagnosed with collagenous colitis

AIM:To characterize the colon microbiota in two women histologically diagnosed with collagenous colitis using a culture-independent method.METHODS:Biopsies were taken from the ascending colon and the total DNA was extracted.Universal bacterial primers were used to amplify the bacterial 16S rRNA genes.The amplicons were then cloned into competent Escherichia coli cells.The clones were sequenced and identified by comparison to known sequences.RESULTS:The clones could be divided into 44 different phylotypes.The microbiota was dominated by Firmicutes and Bacteroidetes.Seven phylotypes werefound in both patients and constituted 47.5% of the total number of clones.Of these,the most dominating were clones similar to Bacteroides cellulosilyticus,Bacteroides caccae,Bacteroides thetaiotaomicron,Bacteroides uniformis and Bacteroides dorei within Bacteroidetes.Sequences similar to Faecalibacterium prausnitzii and Clostridium citroniae were also found in both patients.CONCLUSION:A predominance of potentially pathogenic Bacteroides spp.,and the presence of clones showing similarity to Clostridium clostridioforme were found but the overall colon microbiota showed similarities to a healthy one.Etiologies for collagenous colitis other than an adverse bacterial flora must also be considered.

Lansoprazole-associated collagenous colitis:Diffuse mucosal cloudiness mimicking ulcerative colitis

There have only been a few reports on lansoprazole-associated collagenous colitis. Colonic mucosa of collagenous colitis is known to be endoscopically normal. We present a case of collagenous colitis where the mucosa showed diffuse cloudiness mimicking ulcerative colitis. A 70-year-old woman developed watery diarrhea four to nine times a day. She had interstitial pneumonia at 67 and reflux esophagitis at 70 years. Lansoprazole 30 mg/d had been prescribed for reflux esophagitis for nearly 6 mo. Lansoprazole was withdrawn due to its possible side effect of diarrhea. Colonoscopy disclosed diffuse cloudiness of the mucosa which suggested ulcerative colitis. Consequently sulfasalazine 2 g/d was started. The patient's diarrhea dramatically disappeared on the following day. However, biopsy specimens showed subepithelial collagenous thickening and infi ltration of inflammatory cells in the lamina propria, confirming the diagnosis of collagenous colitis. One month after sulfasalazine therapy was initiated, colonoscopic and histological abnormalities resolved completely. Five months later the diarrhea recurred. The findings on colonoscopy and histology were the same as before, confirming a diagnosis of collagenous colitis relapse. We found that the patient had begun to take lansoprazole again 3 mo ahead of the recent diarrhea. Withdrawal of lansoprazole promptly resolved the diarrhea. Endoscopic and histological abnormalities were also completely resolved, similar to the first episode. Retrospectively, the date of commencement of sulfasalazine and discontinuation of lansoprazole in the first episode was found to be the same. We conclude that this patient had lansoprazole-associated collagenous colitis.