[The preoperative temporary suppression of colon flora and its significance in colon surgery].
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Colon↗
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[A rare anomaly and volvulus of the large intestine].
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Colon↗
[Preparation for surgery of the colon. Purging of large intestine with X-prep].
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Aged↗
Endorectal pull-through of transplanted colon as part of intestinal transplantation.
BACKGROUND: Two children with life-threatening disorders underwent intestinal transplantation; one multivisceral transplantation excluding the liver, and the second transplantation of the liver, small bowel, and colon. METHODS: Involvement of the native rectum necessitated resection and replacement with the transplanted allograft. To prevent a permanent colostomy, a pull-through of the allograft colon was performed. RESULTS: Both patients had a stormy early postoperative course, mainly because of the complexities of intestinal transplantation, but with eventual recovery, including improvement of rectal function. CONCLUSIONS: These are the first two known cases in which a transplanted large intestine was used for a pull-through procedure.
Colon↗
The detection and prevalence of Clostridium botulinum in pig intestinal samples.
To determine the prevalence of Clostridium botulinum types A, B, E, and/or F in pig intestinal samples, different PCR-based methods were compared using artificially contaminated faeces. The methods included a multiplex PCR targeted to botulinum neurotoxin genes A, B, E, and F or a nested PCR targeted to toxin genes B, E, and F, combined with different pre-enrichment protocols and forms of templates. A method including the two-step enrichment followed by DNA extraction and multiplex PCR yielded the highest number of positives. This assay protocol was employed to investigate 100 pig intestinal samples. The sample materials studied included colon wall, intestinal content, and mucus peeled from the colon wall. Three pigs (3%) were positive for C. botulinum type B, and no other toxinotypes were detected in any sample. The number of positive samples was higher when colon wall or peeled mucus was analyzed compared to the intestinal content. C. botulinum was isolated from two PCR-positive samples and confirmed to be type B by PCR. Both isolates were shown to be proteolytic and thus to represent C. botulinum group I.
Animals↗
Influence of trichlorfon and fractionated irradiation on hydroproteolytic activity of pancreas and intestinal tissues of rats.
Investigations into the hydroproteolytic activity of pancreas and intestinal tissues (small intestine and colon) of rats after fractionated irradiation (5 X 150 R) were carried out. There was found marked postirradiation enhancement of lipase activity in pancreas and duodenal part of intestine and increase of B-glucuronidase and acid phosphatase activity in nearly all parts of the examined intestinal tissues. Fractionated irradiation resulted in an increase of pancreatic catheptic (proteolytic) activity causing simultaneous decrease of proteolytic activity in intestine and colon. Preventive administration of Trichlorfon (ten days before irradiation) in the dose of 10 mg or 30 mg/kg evoked modification of hydroproteolytic activity in intestinal tissues of healthy and irradiated rats. Trichlorfon applied in the dose of 30 mg/kg exerted antilipolytic and anticatheptic effects in pancreas and intestinal tissues of irradiated rats.
Acid Phosphatase↗
Effect of epidermal growth factor administration on intestinal cell proliferation, crypt fission and polyp formation in multiple intestinal neoplasia (Min) mice.
Recombinant epidermal growth factor (EGF) may be useful to treat severe ulcerative gastrointestinal injury. There is concern, however, that systemic use of this potent mitogen might increase tumour development and/or progression in susceptible subjects. We therefore examined the effect of chronic administration of systemic EGF to multiple intestinal neoplasia (Min ) mice, who have a genetic defect in the adenomatous polyposis coli (APC) gene, leading to increased polyp development. Min mice (n =26) and wild-type littermates (n =26) received saline or EGF (223 microg of EGF/kg per day) for 4 weeks using subcutaneous osmotic mini-pumps. Cell proliferation and crypt fission were analysed using microdissection techniques and the number and size of polyps in the small and large intestines were determined. EGF increased wet weight and crypt cell proliferation rate by approx. 20% (all P <0.01 compared with the relevant control) in the small intestine and colon of both control and Min mice. In both groups, EGF reduced the colonic fission index by approx. 40% (P <0.01), but did not affect crypt fission in the small intestine. In Min mice, administration of EGF did not increase numbers of polyps or degree of dysplasia, but resulted in a 40% increase in the polyp size in the proximal intestine (P <0.02), but not in the remainder of the small intestine or colon. No polyps were found in control mice given EGF. EGF did not initiate polyp formation in control or Min mice. However, as polyp size is an important determinant for subsequent risk of malignant change in human colon cancer, further studies appear justified.
Adenomatous Polyposis Coli↗
Phenotype-stratified genetic linkage study demonstrates that IBD2 is an extensive ulcerative colitis locus.
OBJECTIVES: The complete elucidation of genetic variants that contribute to inflammatory bowel disease (IBD) will likely include variants that increase risk to both Crohn's disease and ulcerative colitis as well as variants that increase risk for particular phenotypic subsets. The purpose of this study was to assess phenotypic subsets that contribute to the major IBD susceptibility loci. METHODS: This linkage study encompassed 904 affected relative pairs, representing the largest combined phenotyped cohort to date, and allowing for meaningful subset analyses. Genetic linkage data were stratified by disease location and age at diagnosis. RESULTS: We establish that some loci, notably the IBD3 and chromosome 3q linkage regions demonstrate contributions from both small intestine and colon cohorts, whereas others, notably the IBD1 (NOD2/CARD15) and IBD2 regions increase risk for small intestine or colon inflammation, respectively. The strongest linkage evidence in this study was for the subset of extensive ulcerative colitis in the region of IBD2 (lod 3.27; p < 0.001). Evidence for linkage in the region of NOD2/CARD15 (IBD1) was stronger for the subset of Crohn's patients with ileal disease (lod 2.56; p= 0.035) compared to the overall Crohn's group, consistent with previous findings that NOD2/CARD15 variants are associated with ileal disease. CONCLUSIONS: Analyses incorporating disease location in IBD increase the power and enhance the accuracy of genomic localization. Our data provide strong evidence that extensive ulcerative colitis represents a pathophysiologic subset of IBD.
Adaptor Proteins, Signal Transducing↗
Localization of [3H]GABA-labelled nerve fibre networks in the rat intestinal mucosa.
Laminar preparations of the rat colonic mucosa were treated for [3H]GABA (5 x 10(-8) M) autoradiography. Under conditions specific for high-affinity labelling of neuronal elements, a network of fibres overlying the base of the mucosal crypts and a second network coursing in close association with the crypts, were intensely labelled. Along the course of the overlying network of fibres, were dense accumulations of silver grains reminiscent of junctions for fibres projecting into the mucosa. All labelling could be prevented by the specific neuronal uptake inhibitor, L-DABA (10(-3) M).
Aminobutyrates↗
Amino acid transport by small and large intestine of newborn pig.
Unidirectional fluxes of different amino acids have been determined across newborn pig small intestine and colon. The systems responsible for amino acid transport are present in the same proportion in both tissues. Colonic transport of amino acids appears to represent a transient overspill function of the small intestine.
Amino Acids↗
Pharmacokinetics in mice and growth-inhibitory properties of the putative cancer chemopreventive agent resveratrol and the synthetic analogue trans 3,4,5,4'-tetramethoxystilbene.
Resveratrol (trans-3,5,4'-trihydroxystilbene) is a naturally occurring polyphenol with cancer chemopreventive properties in preclinical models of carcinogenesis, including those of colorectal cancer. Recently, a variety of analogues of resveratrol have been synthesised and investigated in in vitro assays. One analogue, 3,4,5,4'-tetramethoxystilbene (DMU 212), showed preferential growth-inhibitory and proapoptotic properties in transformed cells, when compared with their untransformed counterparts. As part of a chemoprevention drug development programme, the pharmacokinetic properties of DMU 212 were compared with those of resveratrol in the plasma, liver, kidney, lung, heart, brain and small intestinal and colonic mucosa of mice. DMU 212 or resveratrol (240 mg kg(-1)) were administered intragastrically, and drug concentrations were measured by HPLC. Metabolites were characterised by cochromatography with authentic reference compounds and were identified by mass spectrometry. The ratios of area of plasma or tissue concentration vs time curves of resveratrol over DMU 212 (AUC(res)/AUC(DMU212)) for the plasma, liver, small intestinal and colonic mucosa were 3.5, 5, 0.1 and 0.15, respectively. Thus, resveratrol afforded significantly higher levels than DMU 212 in the plasma and liver, while DMU 212 exhibited superior availability compared to resveratrol in the small intestine and colon. Resveratrol was metabolised to its sulphate or glucuronate conjugates, while DMU 212 underwent metabolic hydroxylation or single and double O-demethylation. DMU 212 and resveratrol inhibited the growth of human-derived colon cancer cells HCA-7 and HT-29 in vitro with IC(50) values of between 6 and 26 microM. In the light of the superior levels achieved in the gastrointestinal tract after the administration of DMU 212, when compared to resveratrol, the results provide a good rationale to evaluate DMU 212 as a colorectal cancer chemopreventive agent.
Animals↗
Small intestinal differentiation in human colon carcinoma HT29 cells has distinct effects on the lateral diffusion of lipids (ganglioside GM1) and proteins (HLA class 1, HLA class 2, and neoplastic epithelial antigens) in the apical cell membrane.
We have studied the effect of maturation to small intestinal-like epithelial cells of the human colonic carcinoma cell line HT29 on the lateral mobility of different representative membrane components (lipid, proteins), as assessed with fluorescence recovery after photobleaching (FRAP). Maturation was induced in vitro in the HT29 cells by replacing glucose (Glu) with galactose (Gal) in the growth medium (DMEM) during a 21-day period. Scanning electron microscopy revealed an increased number of microvilli in the apical cell membrane, and enzyme analyses (alkaline phosphatase, aminopeptidase) in combination with aqueous countercurrent distribution, indicated that maturation was induced with DMEM-Gal. In comparison to control cells grown in DMEM-Glu medium, the more small intestinal-like cells grown in DMEM-Gal displayed no alteration of the lateral mobility of either cholera toxin (B subunit)-labelled ganglioside GM1 (diffusion coefficient, D [x 10(8)] = 0.8-0.9 cm2s-1; mobile fraction, R = 50-60%) or antibody-stained Class 2 histocompatibility (HLA-DR) antigen (D [x 10(9)] = 2 cm2s-1; R = 60-70%). However, antibody-labelled beta 2-microglobulin of HLA Class 1 antigen displayed increased mobility in HT29-Gal cells; D was x 1.4 and R x 1.8 larger in the HT29-Gal cells. By contrast, the mobility of a neoplastic antigen was reduced; D and R were x0.60 and x0.69 of the values seen in HT29-Glu cells. It is thus concluded that DMEM-Gal-induced differentiation in confluent HT29 cells is accompanied by specific rather than general effects on the lateral mobility of different membrane components.
Carcinoma↗
Decreased expression of the gut-enriched Krüppel-like factor gene in intestinal adenomas of multiple intestinal neoplasia mice and in colonic adenomas of familial adenomatous polyposis patients.
Gut-enriched Krüppel-like factor (GKLF) is a zinc finger-containing transcription factor, the expression of which is associated with growth arrest. We compared Gklf expression in intestinal and colonic adenomas to normal mucosa in multiple intestinal neoplasia (Min) mice and familial adenomatous polyposis (FAP) patients, respectively, using semi-quantitative RT-PCR. In Min mice, the level of Gklf transcript is highest in normal-appearing intestinal tissues and decreases as the size of the adenoma increases. In FAP patients, the level of GKLF transcript is lower in adenomas compared to paired normal-appearing mucosa from the same patient or normal colonic mucosa from control individuals without FAP. The possibility of DNA methylation as a cause for the decreased expression of Gklf in adenomas of Min mice was investigated by methylation-specific PCR. Results indicate that the Gklf gene is not methylated in either normal or tumorous tissues. The findings of our study are therefore consistent with the potential role of GKLF as a negative growth regulator of gut epithelial cells.
Adenoma↗
A Vibrio cholerae relaxed (relA) mutant expresses major virulence factors, exhibits biofilm formation and motility, and colonizes the suckling mouse intestine.
We have constructed a relaxed mutant of El Tor biotype Vibrio cholerae strain C7258 by disruption of the RelA catalytic domain. The ability of the V. cholerae relaxed mutant to biosynthesize guanosine tetraphosphate and pentaphosphate was severely affected; the mutant showed a reduced growth rate in minimal medium that could be reversed by the addition of Casamino Acids, and it was thermosensitive. Contrary to published findings, the new relA mutant still produced significant cholera toxin and toxin-coregulated pilus. The V. cholerae relA mutant was motile, produced normal biofilms, and colonized the suckling mouse intestine. Our data suggest that levels of basal guanosine nucleotides pppGpp and ppGpp, rather than the availability of a stringent response, could influence expression of virulence factors, depending on strain and culture conditions. Production of hemagglutinin (HA)/protease, which requires HapR, RpoS, and the cyclic AMP receptor protein, was not strongly affected. Nevertheless, overexpression of RelA protein from an isopropyl-beta-d-thiogalactopyranoside-inducible promoter posttranscriptionally diminished production of HA/protease.
Animals↗
Efa1 influences colonization of the bovine intestine by shiga toxin-producing Escherichia coli serotypes O5 and O111.
Shiga toxin-producing Escherichia coli (STEC) comprises a broad group of bacteria, some of which cause attaching and effacing (AE) lesions and enteritis in animals and humans. Non-O157 STEC serotypes contain a gene (efa1) that mediates attachment to cultured epithelial cells. An almost-identical gene in enteropathogenic E. coli (lifA) encodes lymphostatin, which inhibits the proliferation of mitogen-activated lymphocytes and the synthesis of proinflammatory cytokines. We have investigated the role of the efa1 gene in colonization of 4- and 11-day-old conventional calves by STEC serotypes O5 and O111. Our findings show that Efa1 is required for efficient colonization of the bovine intestinal tract by STEC, since efa1 deletion and insertion mutants were shed in the feces in significantly lower numbers. In addition, efa1 mutations dramatically reduced the number of bacteria associated with the intestinal epithelium. Expression and secretion of locus for enterocyte effacement-encoded type III secreted proteins that are required for adhesion and AE-lesion formation were impaired by mutation of efa1 in STEC but not by mutation of lifA in enteropathogenic E. coli. However, STEC efa1 mutants retain the ability to nucleate filamentous actin under sites of bacterial attachment to cultured eukaryotic cells. Efa1 is only the second STEC factor shown to influence carriage of the bacteria in the bovine intestine. Our data may have implications for strategies to reduce the prevalence of STEC in cattle.
Animals↗
Prostaglandins in the gut and their relationship to non-steroidal anti-inflammatory drugs.
Prostaglandins are long-chain, saturated, oxygenated fatty acids. Relatively large quantities of prostaglandins have been found in gut mucosa, suggesting that these substances play an important role in gastrointestinal physiology. Non-steroidal anti-inflammatory drugs (NSAIDs) cause damage to the gastric, intestinal, and colonic mucosa in experimental animals and in humans. Prostaglandins protect the gastric mucosa against injury induced by NSAIDs, and this property has been labelled cytoprotection. The mechanisms of cytoprotection have been extensively evaluated and are probably multifactorial, including effects on the gastric mucosal barrier, gastric blood flow, mucus, bicarbonate, and fluid section, ionic transport, cyclic AMP, and surface-active phospholipids. Prostaglandins may also prevent NSAID-induced injury in the small intestine and colon. The mechanisms responsible for prostaglandin protection in the lower gut against injurious agents are unknown. Further studies of the role of prostaglandins in the gut and their relationship to the effects of NSAIDs are needed. The results of these investigations may lead to a better understanding of the importance of prostaglandins in the physiology of the gastrointestinal tract, and may provide information regarding actions of NSAIDs on the functional integrity of the gastric, intestinal, and colonic mucosa.
Anti-Inflammatory Agents, Non-Steroidal↗
Diffuse colonic varices: an uncommon cause of intestinal bleeding.
Varices of the colon are uncommon and when present they are usually segmental. The cause of these segmental varices is usually portal hypertension. Diffuse variceal involvement of the colon is even more uncommon and up until now the two cases described in the literature have had an idiopathic etiology. We describe herein the third such case, while pointing out that the diffuseness implies an unknown cause.
Adult↗
Colonization of the mouse intestine with Escherichia coli.
Young albino Swiss mice, of the NCS and NCS-D colonies, proved highly susceptible to the establishment of intestinal infection with an enteropathogenic strain of E. coli administered per os or by stomach tube. The period of highest susceptibility was rather short, extending from the day of birth to approximately 2 weeks of age. Adult NCS and NCS-D mice failed to become experimentally colonized with E. coli, even when large doses were administered per os on 3 consecutive days. The extent of colonization of the various parts of the gastrointestinal tract was related to the size of the infective dose. Many of the young mice died within 2 to 3 days following per os infection with large doses of enteropathogenic E. coli. However, practically all the animals which survived cleared their intestinal infection at approximately the same age. For example, in mice infected with 23 x 10(6) bacteria, colonization of the intestinal tract usually came to an abrupt end when the animals were 24 to 28 days old, irrespective of the age at which they had been infected. There is suggestive evidence that the acquisition of resistance with age, and the ability of adult animals to control the intestinal infection, are related to the development in the gastrointestinal tract of a microbiota which is antagonistic to E. coli.
Aging↗