Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An antigen has been isolated from a human signet-ring cell carcinoma serially growing in hamsters, GW-39, by saline, PCA, or phenol extraction, and has been found immunologically identical to a similarly extracted substance in normal human or hamster colon. No other hamster or human tissues or cells were found to contain this antigen, for which reason we have termed it colon-specific antigen, or CSA. CSA has been found to be distinct from the major blood group-specific antigens and from othercolon tumor-associated antigens, such as CEA, CCA-II, and CCA-III. It thus seems that a colon organ-specific antigen can be synthesized by this particular human tumor system. Hamsters immunized with CSA could reject cheek pouch grafts of GW-39 tumors, and tumor rejection by these animals correlated with their anti-CSA antibody titers. Preliminary characterization of CSA suggested that it is a glycoprotein on the cell surface having a molecular size of 30,000 to 50,000 daltons. It is proposed that CSA may play a role in the diagnosis of mucin-producing adenocarcinoma of the colon and in ulcerative colitis.
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PMID:Identification of a colon-specific antigen (CSA) in normal and neoplastic tissues. 4 58

Differential counts of the faecal flora of patients with ulcerative colitis showed a dysbiotic flora with a 100-fold increase of group-D streptococci and a reduction of bifidobacteria in comparison with the stable eubiotic flora of healthy subjects. The increase in number in group-D streptococci was accompanied by an increase in variety. About four different varieties of enterococci were found in faeces from patients compared with one or two in samples from healthy subjects. The strains isolated from patients were more active in mucin breakdown, and only strains from patients were able to break down hyaluronic acid. Lactic acid could be formed from these substrates. The increased secretion of mucin in colitis and the presence of unprotected hyaluronic acid in ulcers seem to select these organisms which are probably the cause of the high lactic-acid content of the faeces in such patients.
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PMID:The faecal flora in ulcerative colitis. 81 97

A 41-year-old female with a history of total ulcerative colitis for 15 years is presented. After eight years, she was enrolled in a colonoscopic surveillance program with regular examinations every second year and with biopsy sampling for histologic assessment of dysplasia as well as for flow cytometric analysis. Neither dysplasia nor DNA aneupoloidy developed during the course of the follow-up, but, after seven years, the patient developed a rapidly growing malignant stricture in the lower rectum. At the time of diagnosis, a local gluteal metastasis was found. Following preoperative radiation therapy, laparotomy disclosed a rectal cancer with local growth in the pelvis. Despite an attempt to perform curative surgery, the patient deteriorated and died within four months after the diagnosis. The carcinoma was of a poorly differentiated, mucinous, signet ring cell type, and DNA analyses of both the tumor and its metastases were diploid. Retrospective analyses of mucin content in colonoscopic biopsies showed a gradual shift from sulfated mucin to sialomucin. This case underlines the fact that even rigorous follow-ups offer no absolute guarantee against incurable malignancy in surveillance programs for ulcerative colitis despite the inclusion of DNA analyses.
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PMID:Highly malignant carcinoma in chronic ulcerative colitis without preceding dysplasia or DNA aneuploidy. Report of a case. 131 Feb 71

Three human mucin cDNAs (Muc-1, Muc-2, Muc-3) have recently been cloned and sequenced. The major portion of each mucin consists of sequences repeated in tandem along the protein. Three mucins are distinct due to differences in tandem repeat length, lack of sequence homology and different chromosomal locations of their genes. Since altered mucin glycosylation occurs in cancer resulting in exposure of core carbohydrate, we postulated that increased exposure or other alteration of core peptide structure may occur in cancerous tissues. Antibodies against Muc-1, Muc-2, Muc-3 tandem repeats were used for immunohistochemical analysis of normal, non-malignant and cancer tissues. The results indicate that in normal tissues, only Muc-2 expressed, while in cancerous tissues all three mucin core peptides were significantly accumulated, All of the three mucin core peptides increasingly expressed in adenoma, dysplasia epithelium and active ulcerative colitis (pre-malignant lesions), but not in the hyperplastic polyps, ischemic colitis and quiescent ulcerative colitis (non-malignant diseases).
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PMID:[Mucin core peptide expression in malignant and non-malignant colorectal tissues]. 132 1

1. Normal colonic mucin is heavily sulphated and this increases its resistance to degradation by bacterial enzymes. Any defect in mucus sulphation could therefore be important in the pathogenesis of ulcerative colitis. 2. Rectal biopsies taken at colonoscopy from patients with ulcerative colitis (n = 9), patients with Crohn's disease (n = 6) and control subjects (n = 16) were cultured for 24 h in the presence of N-[3H]acetylglucosamine and [35S]sulphate. Mucin was then extracted and purified, and the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into pure mucin was assessed. 3. The ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin was significantly reduced in rectal biopsies taken from patients with ulcerative colitis (0.463, 0.305-0.703, geometric mean and 95% confidence intervals) compared with control subjects (0.857, 0.959-1.111, P < 0.01). In patients with Crohn's disease the reduction in this ratio (0.559, 0.378-0.829) did not quite reach statistical significance (P = 0.06). There was no difference between the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin in Crohn's disease and that in ulcerative colitis (P = 0.26). 4. In control subjects the ratio of [35S]sulphate to N-[3H]acetylglucosamine incorporated into mucin was higher in the rectal biopsies (0.882, 0.618-1.022) than in their paired proximal colonic biopsies (0.602, 0.421-0.861; P < 0.01), but this regional variation was not observed in either ulcerative colitis (rectum: 0.450, 0.262-0.773; right colon: 0.470, 0.321-0.690, P = 0.3) or Crohn's disease (rectum: 0.459, 0.260-0.815; right colon: 0.492, 0.260-0.929, P = 0.8).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sulphation of colonic and rectal mucin in inflammatory bowel disease: reduced sulphation of rectal mucus in ulcerative colitis. 848 52

Ultrastructural changes that occurred in chronic active ulcerative colitis and Crohn's disease were investigated and compared to normal as well as to higher grades of dysplasia in adenomas and carcinomas. A greater number of immature absorptive cells, undifferentiated and intermediate cells were seen as compared to normal. One case of Crohn's and two cases of chronic ulcerative colitis including one with coexisting carcinoma showed increased number of vesicles and electron-dense bodies (EDB) in the absorptive cells and increased heterogeneity of mucin droplets in goblet cells and presence of atypical secretory cells (ASC). Higher grades of dysplasia characterised by large numbers of atypical secretory cells were not seen in the present series and provide no relationship between the atypical ultrastructural features and increased risk of malignancy. However, the number of cases investigated is too small and a large series is required to clarify the significance of observations such as increased number of electron-dense bodies and vesicles in the apical cytoplasm and presence of atypical secretory cells.
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PMID:Ultrastructural study of inflammatory bowel disease. 145 81

Normal human faeces and effluent from terminal ileostomies in patients with ulcerative colitis were collected. The results for ileostomy effluent given as g/24 h (mean +/- SD; n = 12) were as follows: wet weight, 897 +/- 120; total dry weight, 84 +/- 8; non-diffusible dry weight 46 +/- 5. The corresponding results for faeces (n = 6) were 104 +/- 24; 26 +/- 6; 19 +/- 5. Whereas approximately 15% of the total dry weight of ileostomy effluent appeared to consist of mucin-derived material, only trace amounts of such material could be detected in faeces.
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PMID:The glycoconjugate content of human faeces and ileostomy effluents. 177 83

To determine the prognostic importance of microscopic rectal inflammation we followed up 82 patients (aged 21 to 78 years, 44 men) with chronic quiescent ulcerative colitis over 12 months. At trial entry each patient underwent a rectal biopsy and sections were graded independently by two histopathologists. A chronic inflammatory cell infiltrate of varying severity was present in all biopsy specimens, and 58% had crypt architectural irregularities. In addition, 32% had evidence of acute inflammatory activity: 28% acute inflammatory cell infiltrate, 11% crypt abscesses, and 22% mucin depletion. Agreement between the two histopathologists for the presence of each of these features was 94% (90-98%). During the 12 month follow up 27 patients (33%) relapsed after a mean interval of 18 weeks (range 3-44 weeks). Relapse rates were unrelated to duration or extent of disease or to the type of maintenance drug treatment. In patients with an acute inflammatory cell infiltrate 52% relapsed, whereas in the absence of such an infiltrate only 25% relapsed (p = 0.02). Similarly, relapse rates were higher in the presence of crypt abscesses (78% v 27%, p less than 0.005), mucin depletion (56% v p less than 0.02), and breaches in the surface epithelium (75% v 31%, p = 0.1). The presence of a chronic inflammatory cell infiltrate or crypt architectural irregularities, however, bore no relation to the frequency of colitis relapse.
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PMID:Microscopic activity in ulcerative colitis: what does it mean? 186 37

MUC-2, the first described intestinal mucin gene, has become important as a prototype for secreted mucins in several organ systems. However, little is known about its protein backbone structure and hence its role in diseases such as colon cancer, ulcerative colitis, and cystic fibrosis, which are known to have mucin abnormalities. Studies in this manuscript show that MUC-2 contains two distinct regions with a high degree of internal homology, but the two regions bear no significant homology to each other. Region 1 consists mostly of 48-bp repeats which are interrupted in places by 21-24-bp segments. Several of these interrupting sequences show similarity to each other, creating larger composite repeat units. Region 1 has no length polymorphisms. Region 2 is composed of 69-bp tandem repeats arranged in an uninterrupted array of up to 115 individual units. Southern analysis of genomic DNA samples using TaqI and HinfI reveals both length and sequence polymorphisms which occur within region 2. The sequence polymorphisms have different ethnic distributions, while the length polymorphisms are due to variable numbers of tandem repeats.
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PMID:MUC-2 human small intestinal mucin gene structure. Repeated arrays and polymorphism. 188 63

Previous reports of a selective mucin subclass defect in ulcerative colitis have been reassessed using high performance chromatography (Superose 6 and Mono Q) for mucin purification and fractionation coupled with analysis of the fractions obtained using a combination of enzyme linked lectin and mucin antibody assays. Mucin samples purified from snap frozen rectal biopsy specimens obtained from patients with ulcerative colitis (n = 12), Crohn's disease (n = 5), and non-inflammatory bowel disease control subjects (n = 9) were subject to ion exchange chromatography using a continuous 0-0.35 mol/l NaCl salt gradient with a final 2.5 mol/l NaCl step. In all samples the major proportion (mean (SD) 86.7 (8.9)%) of the mucin detectable by wheat germ agglutinin binding eluted between 0.15 and 0.35 mol/l NaCl with no significant difference in elution profile between ulcerative colitis and control subjects. Significant elution of glycoprotein at less than 0.15 mol/l NaCl did occur, however, when a lower molecular weight mucin containing fraction which contained concanavalin A positive (glucose or mannose containing) material was analysed similarly. Similar ion exchange profiles were obtained when (3H)N-acetylglucosamine labelled mucins were studied after tissue culture of rectal biopsy specimens. No significant alteration in the ion exchange profile of purified mucins in ulcerative colitis has been shown in these studies. It is possible that the previously reported relative depletion of mucin subclass IV (eluting with 0.20 mol/l NaCl) may simply have reflected mucin depletion.
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PMID:Ion exchange chromatography of purified colonic mucus glycoproteins in inflammatory bowel disease: absence of a selective subclass defect. 195 68


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