Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “colonization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources
PubMed1989

Association between postprandial changes in colonic intraluminal pressure and transit.

The aim of this study was to correlate the movement of colonic luminal contents with the changes in intraluminal pressure. Studies were performed in 9 healthy volunteers. Intraluminal pressure was measured with perfused catheter ports in the transverse, splenic flexure, descending, and sigmoid colon. Movement of the luminal contents was measured by following the movement of technetium 99m-ethylenetriamine-pentaacetic acid that was instilled as a bolus in the splenic flexure. During fasting there was very little change in pressure or in the movement of intraluminal contents. After eating a 1000-kcal meal, the tracer moved from the splenic flexure into the transverse colon and the sigmoid colon. Nonpropagating colonic motor activity increased in all colonic segments immediately after eating the meal (p less than 0.05). The increase in motility was significantly greater in the descending colon than in the transverse and sigmoid colon (p less than 0.05). In one-half of the subjects propagating contractions occurred postprandially. The movement of the intraluminal tracer occurred during both types of motility. The nonpropagating contractions were associated with a gradual movement of the luminal contents. The direction of the movement of the contents was determined by the differences in pressure in the different segments of the colon. The propagating contractions were associated with a rapid movement of intraluminal contents. These studies suggest that (a) colonic motility and transit are quiescent during fasting and (b) the transverse colon acts as a mixing and storage area, as retrograde transit into the transverse colon is the characteristic postprandial pattern.

Adult↗
PubMed1999

Functional expression of costimulatory molecule CD86 on epithelial cells in the inflamed colonic mucosa.

BACKGROUND & AIMS: Costimulatory signals are essential for T-cell activation. The aim of this study was to demonstrate expression of costimulatory molecules CD86 and CD80 in human colonic epithelial cells and assess their functional roles in the activation of T cells in inflamed colonic mucosa. METHODS: CD86 and CD80 expression was assessed by immunohistochemistry of colonic mucosa, reverse-transcription polymerase chain reaction, and flow cytometric analysis of isolated colonic epithelial cells and cell lines. Costimulatory effect of CD86-expressing colonic epithelial cells on purified CD4(+) T-cell proliferation was also assessed at suboptimal phytohemagglutinin stimulation. RESULTS: CD86 and CD80 messenger RNA was detected in isolated colonic epithelial cells from normal and inflamed mucosa of patients with ulcerative colitis. Immunohistochemistry and flow cytometric analysis of colonic epithelial cells confirmed cell surface expression of CD86 protein in inflamed colonic mucosa. Cell surface expression of CD86 protein was increased in the colonic epithelial cell line HT29-18-N2 after interferon gamma stimulation. Purified CD4(+) T cells proliferated in response to suboptimal phytohemagglutinin costimulated with interferon gamma-stimulated HT29-18-N2, and these proliferative responses were efficiently inhibited by the addition of anti-CD86 monoclonal antibody. Costimulatory effect of CD86-expressing colonic epithelial cells isolated from inflamed mucosa of ulcerative colitis was also demonstrated at suboptimal phytohemagglutinin stimulation in CD4(+) T cells. CONCLUSIONS: Colonic epithelial cells may act as antigen-presenting cells, and contribute to the activation of T cells through costimulatory molecule CD86 expression in inflamed colonic mucosa.

Antigen-Presenting Cells↗
PubMed2002

A rat colon cancer model induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, PhIP.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is one of the most abundant heterocyclic amines contained in cooked meat and fish, and induces aberrant crypt foci (ACF), putative preneoplastic lesions of the colon, and colon cancers in male rats when administered orally. As has been reported previously, F344 rats are susceptible to induction of ACF by PhIP, while ACI rats being relatively resistant. Approximately one-fourth of ACF induced by PhIP in F344 rats are dysplastic; exhibiting lesions with structural distortion of the crypt, decrease of goblet cells, nuclear stratification and enlargement of nuclei. Dysplastic ACF demonstrate beta-catenin accumulation, mainly in the cytoplasm, and increased cell proliferation in crypts. These dysplastic ACF are, therefore, strongly considered to be putative preneoplastic lesions of the colon.A genetic trait affecting the susceptibility to colon carcinogenesis in F344 rats was mapped to chromosome 16, between D16Rat17 and D16Wox3, using the number of ACF as a surrogate biomarker for colon carcinogenesis. Since the number of dysplastic lesions is well correlated with the total number of ACF, being approximately one-fourth of the total ACF as described above in F344 rats and will be described elsewhere in ACI rats, the gene involved in the susceptibility to ACF induction may possibly be partly responsible for the susceptibility to colon carcinogenesis by PhIP. We, thus, tentatively referred the name of the candidate susceptibility gene on rat chromosome 16 as susceptibility to colon tumor (Sct). In the present study, the colonic lesions induced by PhIP were well refined histologically and genetically, and the multi-step profiles of colon cancer development by PhIP were well characterized and revealed to be similar to the multi-step model of colon carcinogenesis in humans. The PhIP-induced colon cancer model in rats, thus contributes as a relevant tool to elucidate genetic factors responsible for susceptibility to colon carcinogenesis in human. Other unknown genetic or epigenetic alterations, which are essential for the development of early lesions of colon carcinogenesis, could also be clarified using this system.

Animals↗
PubMed2000

Neural and muscular receptors for motilin in the rabbit colon.

Motilin receptors were classically recognized in the gastroduodenal area, where they help to regulate interdigestive motility. More recently, motilin receptors were identified in the colon where their biologic significance remains unclear. We aimed here to characterize the motilin receptors of the rabbit colon. Distal colon and duodenum were obtained from sacrificed rabbits. Tissues homogenized by Polytron were submitted to differential centrifugation to obtain neural synaptosomes or smooth muscle plasma membranes enriched solutions. Motilin binding to these membranes was determined by the displacement of (125)I MOT by the native peptide MOT 1-22, or by peptide analogues MOT 1-12 [CH(2)NH](10-11) or GM-109 and by erythromycin derivative GM-611. Motilin binding capacity was maximum in colon nerves (49.5 +/- 6.5 fmol/mg protein vs. 19.9 +/- 2.5 in colon muscles or 9.4 +/- 2.8 and 6.6 +/- 1.2 in duodenal muscles and antral nerves respectively); all tissues expressed similar affinity for MOT 1-22, and the motilin agonist GM-611 bound equally to neural or muscle tissues from the rabbit colon; the synthetic antagonist MOT 1-12 [CH(2)NH](10-11) showed greater affinity for colon nerves than for colon muscles (plC50: 7.23 +/- 0.07 vs. 6.75 +/- 0.03). Similar results were obtained with the peptide antagonist GM-109; receptor affinity toward MOT 1-12 [CH(2)NH(10-11)] was always five times superior in neural tissues, whether they came from the colon or the antrum, than in muscle tissues, whether they were obtained from colon or from duodenum. Motilin receptors are found in very high concentration in nerves and in muscles from rabbit colon; specific motilin receptor subtypes are identified in nerves (N) and muscles (M) of the rabbit colon; N and M receptor subtypes seem independent of the organ location.

Animals↗
PubMed1997

Absence of p53 gene mutations in rat colon carcinomas induced through the synergistic interaction between methylazoxymethanol and X-irradiation.

p53 is one the most frequently mutated genes found in human colonic tumors. Because colonic neoplasms induced in rats by certain chemical carcinogens are similar to human colonic tumors in their histological features and proliferation characteristics, the rat has been used as an experimental model to study the pathogenesis of colon cancer. However, p53 mutations were not detected in the chemically induced colonic tumors analyzed for p53 mutations. X-irradiation has also been shown to induce colonic neoplasms in rats that resemble human colonic tumors histopathologically. Because the incidence of colonic tumors induced by methylazoxymethanol (MAM) in rats was shown to be enhanced by X-irradiation, we immunohistochemically analyzed these colonic carcinomas for the presence of p53 gene mutations. The immunohistochemical analyses clearly showed the absence of nuclear immunoreactivity in all ten tumors examined. The results from the present study indicate that point mutations in p53, at least in the coding region, are not involved in the development of colon cancer induced by the combination of MAM and X-irradiation. Our observations, together with the data from previous studies, further suggest that rat colon carcinogenesis, unlike human colon cancer, may not involve p53 mutation as an obligatory event.

Adenocarcinoma↗
PubMed2002

Inferior mesenteric artery reimplantation does not guarantee colon viability in aortic surgery.

Reimplantation of the inferior mesenteric artery (IMA) at the time of aortic surgery has been advocated to prevent colon ischemia in patients deemed to have inadequate perfusion of the left colon. The purpose of this study was to determine whether IMA reimplantation is globally protective against colon necrosis. We reviewed the medical records of all patients who were diagnosed with colon ischemia after aortic surgery during a 10-year period. Cases were indexed from the institution's operative database and from the vascular morbidity and mortality registry. Ten patients (eight men, two women; mean age 71 +/- 9 years) were identified during the study period. Five patients (50%) underwent successful IMA reimplantation for inadequate Doppler signals on the antimesenteric border of the sigmoid colon. Five other patients (50%) did not undergo IMA reimplantation because they were deemed to have adequate colon perfusion. Transmural colon necrosis occurred in 6 of the 10 study patients, 4 of whom had IMA reimplantation. Five of the six patients had intraoperative hypotension. Three of the four patients with colon ischemia presenting less than 24 hours after aortic revascularization survived (mortality 25%), but both patients with late colon ischemia died of multisystem organ failure (mortality 100%). Four patients developed mucosal ischemia and did not undergo colectomy. Only one of these had IMA reimplantation. Colon ischemia was detected more than 1 week postoperatively in three patients. All four patients were treated with supportive therapy and antibiotics, and all four survived to discharge after a mean length of stay of 14 +/- 10 days. These data show that IMA reimplantation does not ensure colon viability in aortic surgery. Transmural colon necrosis tends to present sooner than mucosal ischemia and may be attributable to nonanatomic variables such as intraoperative hypotension. Although transmural necrosis is a highly morbid complication after aortic surgery, timely colectomy may lead to survival in some patients.

Aged↗
PubMed2001

Effects of short chain fatty acids on colonic Na+ absorption and enzyme activity.

Short chain fatty acids (SCFA) stimulate colonic Na+ absorption and inhibit cAMP and cGMP-mediated Cl- secretion. It is uncertain whether SCFA have equivalent effects on absorption and whether SCFA inhibition of Cl- secretion involves effects on mucosal enzymes. Unidirectional Na+ fluxes were measured across stripped colonic segments in the Ussing chamber. Enzyme activity was measured in cell fractions of scraped colonic mucosa. Mucosal 50 mM acetate, propionate, butyrate and poorly metabolized isobutyrate stimulated proximal colon Na+ absorption equally (300%). Neither 2-bromo-octanoate, an inhibitor of beta-oxidation, nor carbonic anhydrase inhibition affected this stimulation. All SCFA except acetate stimulated distal colon Na+ absorption 200%. Only one SCFA affected proximal colon cGMP phosphodiesterase (PDE) (18% inhibition by 50 mM butyrate). All SCFA at 50 mM stimulated distal colon cAMP PDE (24-43%) and decreased forskolin-stimulated mucosal cAMP content. None of the SCFA affected forskolin-stimulated adenylyl cyclase in distal colon or ST(a)-stimulated guanylyl cyclase in proximal colon. Na+-K+-ATPase in distal colon was inhibited 23-51% by the SCFA at 50 mM. We conclude that all SCFA (except acetate in distal colon) stimulate colonic Na+ absorption equally, and the mechanism does not involve mucosal SCFA metabolism or carbonic anhydrase. SCFA inhibition of cAMP-mediated secretion may involve SCFA stimulation of PDE and inhibition of Na+-K+-ATPase.

Adenylyl Cyclases↗
PubMed1990

Metabolism of 15N-labelled urea in the functioning and defunctioned human colon.

1. The luminal metabolism of urea was studied using double-labelled urea ([15N2]urea) which was placed in the lumen of the colon through a colostomy. The recovery of label was measured as [15N2]urea or [14N, 15N]urea in urine and as 15N in stool. 2. Five patients with a loop colostomy allowed a comparison of the right functioning colon with the left defunctioned colon in the same individual. Five subjects with a left end-colostomy enabled a comparison of the right with the left functioning colon. 3. A significantly greater proportion of labelled urea was recovered as [15N2]urea in the urine when the dose was placed in the left defunctioned colon (29%) compared with either the left or the right functioning colon (9 and 4%, respectively). This is interpreted as being a result of a decrease in the bacterial activity and concomitant urea hydrolysis in the defunctioned colon. 4. On average more than half of the label was retained in the body, regardless of whether the urea was placed in the functioning or the defunctioned colon, on the left or on the right. 5. The data confirm that the colon is permeable to the intact urea molecule. Intraluminal urea is readily hydrolysed in the functioning colon. A large proportion of the nitrogen released by urea hydrolysis may be retained within the metabolic nitrogen pool of the host. There are significant differences in the handling of urea nitrogen in the defunctioned colon relative to the functioning colon.

Aged↗
PubMed2000

Limited exposure of the healthy distal colon to orally-dosed formulation is further exaggerated in active left-sided ulcerative colitis.

BACKGROUND: Active distal ulcerative colitis is often resistant to topically acting oral formulations. We speculated that the left side of the colon is underexposed to orally-dosed topical agents in patients with active distal colitis. METHODS: Twenty-two healthy volunteers (12 males, aged 22-47 years), and 10 patients (6 males, aged 33-73 years) with active left-sided ulcerative colitis ingested a Eudragit-coated gelatine capsule containing 111In-labelled amberlite resin on four successive days. Regional colonic distribution, transit times and percentage of daily dose resident were calculated from the average of four serial gamma camera images on the 4th day. RESULTS: (mean [95% CI]). When compared to controls, patients with colitis had significantly faster total colon transit (24.3 h [9.5-39.1] vs. 51.7 h [41.1-62.3]) as well as faster proximal colon transit (18.7 h [9.1-28.3] vs. 36.7 [28.5-44.9]), and distal colon transit (3.1 h [-0.5 to 6.8] vs. 15.0 h [10.5-19.5]), respectively (all P < 0.01). Material was asymmetrically distributed in health (proximal colon 69% [63-76] vs. distal colon 31% [24-37]). This asymmetry was more extreme in colitis, with corresponding values of 91% [85-96] vs. 9% [4-15]. As a result colitics had less material in the left-sided colon (9% [4-15] vs. 31% [24-37]), P < 0. 001. Colitics had a significantly lower percentage of the daily dose resident within the left side of the colon compared to controls (13% [-2 to 28] vs. 63% [44-81]), P < 0.01. CONCLUSIONS: Delayed release oral formulation is asymmetrically distributed within the colon in health. This asymmetry is exaggerated in active left-sided ulcerative colitis and, together with faster colonic transit, results in reduced exposure of the distal colon to orally-dosed topical agents.

Administration, Oral↗
PubMedDate not supplied

Interstitial cells of cajal in patients with constipation due to total colonic inertia.

Colonic wall contains interstitial cells of Cajal. In view of studies demonstrating that Cajal cells generate electric waves which are presumably responsible for colonic motor activity, and that these waves are absent in total colonic inertia, we investigated the hypothesis that colonic Cajal cells might be disordered in patients with total colonic inertia. The study comprised 28 patients (age 41.6 +/- 8.2 SD years, 19 women, 9 men) with total colonic inertia in whom total colectomy was performed. Colonic specimens obtained from normal segments of the excised colon of 24 cancer patients acted as controls. Specimens were subjected to c-kit immunohistochemistry. Controls for antisera specificity consisted of tissue incubated with normal rabbit serum that had been substituted for the primary antiserum. C-kit-positive branched Cajal-like cells were detected in the musculature of the normal colonic segments. They were distinguishable from the C-kit-negative smooth muscle cells and the C-kit-positive but unbranched mast cells. No Cajal cells were detected in colon of total colonic inertia patients. The absence of Cajal cells in patients with total colonic inertia can be assumed to explain the absence of electric waves and motile activity previously reported in these patients. Further studies are needed to investigate the cause of Cajal-cell absence.

Adult↗
PubMed1996

Platelet-derived endothelial cell growth factor in human colon cancer angiogenesis: role of infiltrating cells.

BACKGROUND: Development of new blood vessels is essential for tumor growth and metastasis and depends on the production of angiogenic factors by tumor and/or infiltrating cells. We previously showed that vascular endothelial growth factor (VEGF) expression and vessel count correlate with metastasis in human colon cancer. Although most tumors with high vessel counts express high levels of VEGF, some do not. Recently, platelet-derived endothelial cell growth factor (PD-ECGF), another potent angiogenic factor, has been reported to be expressed in colon cancer. PURPOSE: In this study, we examined the role of PD-ECGF in colon cancer angiogenesis and whether PD-ECGF is derived from the tumor or infiltrating cells. METHODS: Immunostaining for PD-ECGF was performed on 96 colon cancer specimens, some of which were previously stained for VEGF and factor VIII, a marker that is specific for endothelial cells. Double staining was done by using antibodies to PD-ECGF and to CD68 (macrophage specific) or CD3 (lymphocyte specific) to confirm which infiltrating cells produce PD-ECGF. Northern blot analysis for PD-ECGF messenger RNA (mRNA) was performed on four colon cancer specimens and corresponding normal colon mucosae (same patients) and four human colon cancer cell lines (KM12SM, SW620, HT29, and NCI-H508) to determine whether colon cancer epithelium expresses PD-ECGF. RESULTS: Immunohistochemical analysis demonstrated that PD-ECGF was expressed in infiltrating cells in most of the colon cancer specimens (80 [83%] of 96) but rarely in tumor epithelium (five [5%] of 96). Double staining demonstrated that infiltrating cells staining positive for both PD-ECGF and CD68 were more predominant than those staining positive for both PD-ECGF and CD3. The intensity of staining for PD-ECGF in infiltrating cells correlated with vessel counts (Spearman's rank correlation coefficient (R) = .29; P = .004), but did not correlate with the intensity of VEGF staining (R = .176, P = .086) or metastasis (Mann-Whitney U test, P = .253). PD-ECGF staining intensity was higher in specimens with a high vessel count (> 50 at high magnification) and low VEGF-staining intensity (< or = 2+) than in specimens with a high vessel count (again, > 50) and high VEGF-staining intensity (3+). Northern blot analysis revealed that colon cancer specimens and normal mucosae expressed relatively high levels of PD-ECGF mRNA, whereas PD-ECGF mRNA transcripts were not detectable in colon cancer cell lines. CONCLUSIONS AND IMPLICATIONS: PD-ECGF expression in human colon cancer specimens is associated with vessel count and may be responsible for tumor vascularity in those tumors with low VEGF expression. Infiltrating cells expressing PD-ECGF may contribute to angiogenesis, thus providing an additional mechanism for tumor neovascularization.

Blotting, Northern↗
PubMed1997

Methods to enhance in vivo urothelial growth on seromuscular colonic segments in the dog.

PURPOSE: We demonstrated survival and expansion in vivo of urothelial free autografts on demucosalized seromuscular segments. MATERIALS AND METHODS: Four methods of in vivo urothelial expansion were investigated on demucosalized colonic segments in the canine model. Group 1 underwent colonic mucosal removal by manual stripping, group 2 underwent removal of colonic mucosa and submucosa, and group 3 underwent manual stripping of the colonic mucosa followed by treatment with protamine sulfate and urea. In the 3 groups urothelial autografts were then placed on the seromuscular segment and tubularized over a balloon splint. In group 4 the colonic mucosa was removed but the grafts were not tubularized. Instead the colonic segment was sutured to the parietal peritoneum. RESULTS: Group 4 grafts had no epithelial growth and shrinkage of the bowel segment. Group 1 grafts had minimal growth with no expansion and colonic mucosal regrowth. Group 2 grafts demonstrated growth and expansion, although these colonic segments had a significant inflammatory response and fibrosis. Group 3 grafts had the best growth and expansion with the least inflammatory response, and 1 colonic segment was almost completely covered with urothelium. CONCLUSIONS: We demonstrated in vivo expansion of urothelial autografts grown on seromuscular colonic segments. Preservation of the submucosa is essential to prevent fibrosis of the seromuscular colonic segment and a balloon stent is crucial to prevent graft contraction. Treatment of the demucosalized segment with protamine sulfate and urea results in better urothelial expansion and less colonic mucosal regrowth.

Animals↗
PubMed2006

Functional CD4+CD25high regulatory T cells are enriched in the colonic mucosa of patients with active ulcerative colitis and increase with disease activity.

BACKGROUND: Factors determining the extension and degree of inflammation in the colonic mucosa of patients with ulcerative colitis (UC) are largely unknown, but CD4+CD25high regulatory T cells (Tregs) have been implicated to play an important role in suppressing inflammation. Therefore, the aims of this study were to determine whether colonic Tregs have suppressive effects on colonic effector T cells in UC and to analyze the association between segmental colonic Treg distribution and disease activity. MATERIALS AND METHODS: The suppressive activity of colonic CD4+CD25high Tregs from patients with active UC was determined in coculture assays measuring proliferation and cytokine production. The frequency of Tregs and the expression of the Treg marker FOXP3 were analyzed with flow cytometry and RT-PCR in isolated cells and the whole mucosa from patients with active and inactive disease, as well as healthy mucosa. RESULTS: Colonic CD4+CD25high T cells from patients with UC suppressed the proliferation and cytokine secretion of colonic effector CD4+ T cells. Healthy controls but not patients with UC had lower Treg frequencies in the sigmoid than in the ascending colon. Patients with UC with active disease had increased frequency of colonic Tregs. The frequency of Tregs was positively correlated with colonic disease activity and serum C-reactive protein. CONCLUSIONS: Colonic CD4+CD25high Tregs are able to suppress colonic effector T cell activity in vitro, and the Treg frequency in the inflamed intestine increases with disease activity in patients with active UC. This suggests that Tregs may be outnumbered by other inflammatory cells or that their suppressive activity may be influenced by the in vivo environment.

Adult↗
PubMed2003

Colon injury after blunt abdominal trauma: results of the EAST Multi-Institutional Hollow Viscus Injury Study.

BACKGROUND: Blunt injury to the colon is rare. Few studies of adequate size and design exist to allow clinically useful conclusions. The Eastern Association for the Surgery of Trauma Multi-institutional Hollow Viscus Injury (HVI) Study presents a unique opportunity to definitively study these injuries. METHODS: Patients with blunt HVI were identified from the registries of 95 trauma centers over 2 years (1998-1999). Patients with colon injuries (cases) were compared with blunt trauma patient undergoing a negative laparotomy (controls). Data were abstracted by chart review. RESULTS: Of the 227,972 patients represented, 2,632 (1.0%) had an HVI and 798 had a colonic/rectal injury (0.3%). Of patients diagnosed with HVI, 30.2% had a colon injury. No physical findings or imaging modalities were able to discriminate colonic injury. Logistic regression modeling yielded no clinically useful combination of findings that would reliably predict colonic injury. In patients undergoing laparotomy, presence of colon injury was associated with a higher risk of some complications but not mortality. Colon injury was associated with increased hospital (17.4 vs. 13.1, p < 0.001) and intensive care unit (9.7 vs. 6.9, p = 0.003) length of stay. Almost all colon patients (92.0%) underwent laparotomy within 24 hours of injury. CONCLUSION: Colonic injury after blunt trauma is rare and difficult to diagnose. No diagnostic test or combination of findings reliably excluded blunt colonic injury. Despite the inadequacy of current diagnostic tests, almost all patients with colonic injury were taken to the operating room within 24 hours. Even with relatively prompt surgery, patients with colon injury were at significantly higher risk for serious complications and increased length of stay. In contrast to small bowel perforation, delay in operative intervention appears to be less common but is still associated with serious morbidity.

Colon↗
PubMed2004

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats.

Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c)9,trans(t)11,c13-18:3 as conjugated linolenic acids (CLN). Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in c9,t11,t13-CLN, inhibited the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM). In this study, we investigated the effect of dietary PGO on the development of AOM-induced colonic malignancies and compared it with that of conjugated linoleic acid (CLA). To induce colonic tumors, 6-week old male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks. One week before the AOM treatment they were started on diet containing 0.01%, 0.1%, or 1% PGO or 1% CLA for 32 weeks. Upon termination of the bioassay (32 weeks) colon tumors were evaluated histopathologically. AOM exposure produced colonic adenocarcinoma with an incidence of 81% and multiplicity of 1.88 +/- 1.54 at week 32. Administration of PGO in the diet significantly inhibited the incidence (AOM + 0.01% PGO, 44%, P < 0.05; AOM + 0.1% PGO, 38%, P < 0.01; AOM + 1% PGO, 56%) and the multiplicity (AOM + 0.01% PGO, 0.56 +/- 0.73, P < 0.01; AOM + 0.1% PGO, 0.50 +/- 0.73, P < 0.005; AOM + 1% PGO, 0.88 +/- 0.96, P < 0.05) of colonic adenocarcinomas, although a clear dose-response relationship was not observed at these dose levels. CLA feeding also slightly, but not significantly, reduced the incidence and multiplicity of colonic adenocarcinomas. The inhibition of colonic tumors by PGO was associated with an increased content of CLA (c9,t11-18:2) in the lipid fraction of colonic mucosa and liver. Also, administration of PGO in the diet elevated expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the non-tumor mucosa. These results suggest that PGO rich in c9,t11,c13-CLN can suppress AOM-induced colon carcinogenesis, and the inhibition is associated in part with the increased content of CLA in the colon and liver and/or increased expression of PPARgamma protein in the colon mucosa.

Animals↗
PubMed2006

Influence of acute serotonin reuptake inhibition on colonic sensorimotor function in man.

BACKGROUND: It is unclear whether decreased serotonin transporter function contributes to sensorimotor abnormalities in irritable bowel syndrome. AIM: To study the influence of acute serotonin transporter inhibition on colonic sensorimotor function in man. METHODS: Ten healthy subjects (five men, aged 20-29 years) underwent a combined manometry/barostat study of the descending colon on two occasions. Stepwise distentions by 2 mmHg increments were performed until discomfort. Subsequently, placebo or citalopram 20 mg were administered i.v. over 20 min and distentions were repeated. Afterwards, isobaric tone measurements were performed 30 min before and 90 min after ingestion of a meal. High-amplitude propagated contractions, colonic motility index, colonic compliance, sensitivity and colonic response to a meal after placebo or citalopram were compared by t-test and two-way ANOVA. RESULTS: Citalopram induced a significant increase in colonic motility index (5.6 +/- 0.9 to 0.8 +/- 1.9 mL*min, P < 0.005) and high-amplitude propagated contractions (32 after citalopram vs. 2 after placebo, P < 0.05), which were associated with abdominal cramping. Administration of citalopram increased colonic compliance (10.3 +/- 1.5 vs. 14.5 +/- 2.2 mL/mmHg, P < 0.01) and inhibited colonic response to a meal (volume decrease 48 +/- 12 vs. 16 +/- 12 mL, P < 0.01). CONCLUSIONS: Acute serotonin transporter inhibition in man increases colonic phasic contractility and the occurrence of high-amplitude propagated contractions, increases colonic compliance and suppresses the colonic tonic response to a meal. These data suggest that both release and elimination of 5-hydroxytryptamine by serotonin transporter are involved in the control of colonic motility in man.

Adult↗
PubMed1985

Regional variation in the sensitivity of longitudinal smooth muscle to histamine at H1-receptors in guinea-pig ileum and colon.

The sensitivity of the distal ileum, proximal colon, medial colon, and distal colon of the guinea-pig to histamine has been evaluated. The rank order of sensitivity was ileum greater than medial colon greater than proximal colon approximately equal to distal colon. The mean -logEC50 values at receptors in the ileum, medial, proximal, and distal colon were 6.74, 6.18, 5.79, and 5.72, respectively. The apparent dissociation constant for the interaction of histamine with receptors in the various regions was determined. The -log Kd values at receptors in the ileum, proximal colon, medial colon, and distal colon were 4.68, 4.65, 4.62, and 4.44, respectively. The mean apparent -log Kd values for the antagonism of histamine by mepyramine were 9.0, 9.0, 9.1, and 8.9 for receptors on the ileum, proximal, medial, and distal colon, respectively. The results of these experiments provide no evidence that histamine receptors in the colon are distinguishable from H1-receptors as characterized on the ileum. The differences in sensitivity to histamine in the various regions of the intestine may be due to differences in the density of H1-receptors.

Animals↗
PubMed1990

Differences in control of descending inhibition in the proximal and distal regions of rat colon.

1. Descending inhibition in the proximal and distal portions of rat colon was studied separately, in vitro. 2. In the proximal colon, localized distension with a small balloon caused three types of response (contraction; relaxation; relaxation, then contraction) of the circular muscle on the anal side of the distended region. 3. Distension caused descending relaxation of circular muscle in all segments of the proximal colon, although for this prostaglandin F2 alpha (PGF 2 alpha) was necessary in some segments to increase muscle tone. 4. Atropine and guanethidine did not inhibit this descending relaxation, but tetrodotoxin did. 5. Hexamethonium inhibited the descending relaxation in 14 of 17 preparations of proximal colon tested, but not in the others. 6. In the distal colon, distension consistently caused an increase in the tone of the circular muscles. Descending relaxation was observed only after development of higher tone. Atropine and guanethidine did not inhibit the relaxation, but tetrodotoxin did. 7. Hexamethonium did not inhibit the descending relaxation in most of the preparations of distal colon examined. 8. AF64A, an inhibitor of choline uptake, inhibited the response mediated by cholinergic neurons in vitro to electrical transmural stimulation of the longitudinal muscle of proximal colon. 9. Treatment of colonic preparations with AF64A in vitro resulted in inhibition of descending relaxation in those of proximal, but not those of distal, colon. 10. The participation of intrinsic cholinergic neurones in the descending neuronal pathway is strongly suggested by the results in the proximal colon, but less so in the distal colon. 11. The tone and spontaneous contractile activity of colonic circular muscles are discussed in relation to their neuronal control.

Animals↗