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At least 451 records · Page 25Linked to original sources
PubMed1980

Effect of bile acid perfusion on colonic motor function in patients with the irritable colon syndrome.

A study was performed to determine the effect of bile acid perfusion on motility in the sigmoid colon of patients with the irritable colon syndrome compared with normal subjects. Deoxycholic acid (15 mM) statistically significantly increased motility in normal subjects (control 25.0 +/- 6.4%, perfusion 71.4 +/- 7.2%, P < 0.05) but neither chenodeoxycholic acid nor cholic acid had any apparent effect. In patients with the irritable colon syndrome, however, deoxycholic acid at 5 mM concentration (control 29.8 +/- 4.2%, during perfusion 57.4 +/- 6.5%, P < 0.05) as well as at 15 mM concentration (control 19.4 +/- 5.7+, perfusion 57.8 +/- 9.6%, P < 0.05) statistically significantly increased rectosigmoid motility. Patients with the irritable colon syndrome had a high resting 0.033-0.066 Hz (2-4 c/m) electrical activity, whereas in normal subjects 0.1-0.15 Hz (6-9 c/m) activity was greater. However, there was no statistically significant alteration in either electrical rhythm during the period of bile acid perfusion. In conclusion, additional evidence is presented to suggest that deoxycholic acid is the only bile acid likely to be implicated in the motor disorder of the irritable colon syndrome.

Bile Acids and Salts↗
PubMed2000

Effect of colonic luminal components on induction of apoptosis in human colonic cell lines.

Apoptosis is central to cell number regulation in the colonic epithelium, and interest in its role in colon carcinogenesis has been growing rapidly. It thus becomes of interest to characterize luminal components, possibly of dietary origin, that may influence this process. We have investigated the sensitivity of two human colonic cell lines, the human adenocarcinoma cell line (HT-29) and the human fetal colonic mucosa cell line (FHC), to induction of apoptosis by sodium butyrate, bile acids, and human fecal water fractions. The apoptotic effect has been studied by 1) morphological changes in cells examined by fluorescence microscopy, 2) DNA fragmentation analysis by gel electrophoresis, 3) flow cytometry analysis of DNA strand breaks assessed by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay (TUNEL), and 4) poly(ADP-ribose) polymerase cleavage by Western blot. Sodium butyrate and bile acids induced a time- and concentration-dependent apoptosis in both cell lines. Quantitation of this effect, by use of the TUNEL assay, indicated that deoxycholic acid was most effective in inducing this effect at lower concentrations and at shorter times. Apoptotic effects were also observed, in both cell lines, when the cells were exposed to intact human fecal waters (the fecal fraction in direct contact with the epithelium) and their lipid extracts, with the intact samples being more effective. Although all fecal waters examined induced apoptosis, quantitation of the effect by the TUNEL assay indicated that the ability to induce apoptosis differed markedly between samples. Induction of apoptosis by the fecal waters was not correlated to cytotoxicity but was negatively correlated to the pH of the samples. Interestingly, the cells derived from the fetal mucosa (FHC) were consistently less sensitive to apoptotic effects of the luminal components than the tumor-derived cells (HT-29). Thus human fecal water fractions induce apoptosis in colonic cells, and this effect is not due to lipid components alone.

Apoptosis↗
PubMed2003

Selenium supplementation enhances low selenium levels and stimulates glutathione peroxidase activity in peripheral blood and distal colon mucosa in past and present carriers of colon adenomas.

Selenoproteins such as glutathione peroxidases (GPx), thioredoxin reductases (TrxR), and selenoprotein P (SePP) contain molecular selenium in form of selenocysteines within their active center. They are involved in the defense of reactive oxygen species, which otherwise may cause DNA damage and alterations of protein function. Selenium intake has been linked to colon carcinogenesis in epidemiological and interventional studies. In a double-blinded, placebo-controlled trial, we demonstrate that carriers of colon adenomas present with low basal serum levels of selenium and plasma glutathione peroxidase (pGPx) activity before treatment, but both parameters can be normalized by interventional selenium supplementation. GPx activity in colon mucosa was enhanced in the verum group, albeit this had only borderline significance. No change of activity was observed for mucosal TrxR activity on selenium supplementation. In summary, our results confirm the existence of low selenium levels in patients prone to colon adenomas and show that by selenium supplementation this can be normalized. If prospective trials confirm that selenium supplementation reduces colon cancer incidence rates, it may be concluded that selenium supplementation should be recommended for patients at risk.

Adenoma↗
PubMed2001

[Effect of nonsteroidal antiinflammatory drugs on colonic lipoxygenase and cyclooxygenase activities from patients with colonic neoplasia].

Lysine clonixinate (LC) is a nonsteroidal anti-inflammatory drug (NSAID) with good gastrointestinal tolerance. Treatment with LC at levels equivalent to those found in plasma following therapeutic doses resulted in significant inhibition of both cyclooxygenase 2 (COX-2) and production of 5 hydroxy-eicosatetraeonic acid (5-HETE) and slightly affected levels of cyclooxygenase 1 (COX-1) in in vitro studies carried out on human tissues. This study deals with the in vivo effect of the drug on human colon segments. Experiment 1: Five patients about to undergo hemicholectomy due to colon neoplasia were treated preoperatively with a continuous infusion of LC, to achieve a steady-state concentration between 4 and 6 mg/ml. Human colon segments from the five patients and from another five control patients receiving no treatment with [14C]-arachidonic acid were incubated. Human colon segments treated with LC showed significant inhibition of PGE2, the only prostaglandin (PG) synthesised by the tissue, as well as of 5-HETE. Experiment 2: Fifteen patients received an i.v. bolus of LC 100 mg (n1 = 5); LC 200 mg (n2 = 5) or indomethacin (INDO) 50 mg (n3 = 5). Both doses of LC showed greater inhibition of PGE2 synthesis than the INDO bolus. Both NSAIDs studied proved to have different effects on the production of 5-HETE; while treatment with LC elicited significant inhibition, levels with INDO remained unchanged. Western blotting analysis showed expression of both COX isoforms in colon segments, COX-2 levels being 20% higher. Both types of in vivo studies conducted continuous infusion and i.v. bolus, revealed that LC exerted significant inhibition of basal synthesis of PGE2 and 5-HETE.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Variability of spectra of laser-induced fluorescence of colonic mucosa: its significance for fluorescence detection of colonic neoplasia.

To determine the extent of a natural variability of the spectra of the autofluorescence and its significance for a reproducibility of different approaches typically used in studies on fluorescence detection of colonic lesions. Two independent series of experiments have been conducted during three years in the same laboratory. Macroscopic tissue specimens obtained during operations of patients with colonic cancers were studied in vitro. The tissues were excited using UV lines of c.w. He-Cd laser and pulsed nitrogen laser and the autofluorescence spectra were recorded for areas visually diagnosed as normal or pathologically changed mucosa. Natural variability of the autofluorescence spectra of colonic tissues seems to be most important factor limiting sensitivity and specificity of the diagnostic algorithms. The mean fluorescence spectra obtained for normal mucosa and its neoplastic lesions differ significantly but the differences are difficult to observe because of the high natural variability among the individual spectra. Further studies of biological basis of the colonic autofluorescence are necessary for a progress in the field of fluorescence detection of colonic neoplastic lesions.

Colon↗
PubMed1990

Histologic similarity of murine colonic graft-versus-host disease (GVHD) to human colonic GVHD and inflammatory bowel disease.

In a study designed to determine which T-cell subsets are involved in the development of murine graft-versus-host disease (GVHD), a prospective histologic analysis of gastrointestinal involvement was performed. In C57BL/6JXDBA/2F1 (B6D2F1) recipients of DBA/2 donor spleen and bone marrow cells, the colonic histologic findings were found to be similar in many respects to the histologic findings reported in human colonic GVHD and were much more severe and diffuse than were the abnormalities of the small intestine. Host irradiation before transplantation was found to play an additive or synergistic role in the development of GVHD. Furthermore the histologic features noted in DBA/2----B6D2F1 murine colonic GVHD suggest that bone marrow and spleen cell transplantation in this strain combination may be a useful model for studying the immunologic mechanisms involved in human inflammatory bowel disease. Thus severe colonic disease noted during the course of DBA/2----B6D2F1 murine GVHD was found to have significant histopathologic similarities to both human GVHD enteropathy and other inflammatory diseases of the human colon.

Animals↗
PubMed1990

A morphometric study of the canine colon: comparison of control dogs and cases of colonic disease.

The microstructure of the canine colon was described morphometrically. The artifacts induced by administration of enemas and biopsy technique were studied by comparing biopsy specimens to tissues obtained at necropsy from 15 normal dogs. Biopsies from control dogs and clinical cases of colonic disease were then evaluated quantitatively, and histological abnormalities which might clarify mechanisms underlying large bowel dysfunction in the dog were sought. In control dogs, gland length and diameter, epithelial, goblet cell and mucosal mast cell numbers, and intraepithelial lymphocyte and mitotic indices were remarkably uniform throughout the colon. Minor variations were found in the proximal and distal regions of the colon. An apparent shortening of glands, and a reduction in mucous goblets and intraepithelial lymphocytes in biopsies were attributed to suboptimal orientation and irritation caused by enemas. The only significant difference from controls identified by morphometric analysis of biopsies from clinical cases was fewer epithelial cells lining longitudinal sections of glands. It was concluded that failure to identify morphometric variations in the colonic mucosa of clinical cases might reflect either a biased, homogeneously mild clinical syndrome in this group, or the possibility that in many of the clinical cases, a functional rather than physical abnormality was involved. The proprial inflammatory cell population was not examined quantitatively; further investigation of this component is merited.

Animals↗
PubMed1987

[Effects of medicinal fiber on colonic transit in patients with irritable colon syndrome].

Twenty patients suffering from irritable bowel syndrome, 14 patients with pain and constipation and 6 patients with pain and diarrhoea, were studied in order to: a) Evaluate the symptomatic response to a Plantago Ovatae fiber medicine. b) Study with radio-opaque markers the colonic transit modifications that could explain the therapeutic responses. There were observed the following results: 1) Pain decreased or disappeared in 80% of the patients. 2) Constipation decreased or disappeared in 78.6% of the patients. 3) Diarrhoea decreased or disappeared in 5 of the 6 patients that were studied. 4) There was a significative increase of the feces weight without changes of the dry residue. 5) Taking all the patients as a whole the number of the retained radio-opaque markers was the same before and after the active treatment. If we evaluate the patients with constipation and the patients with diarrhoea separately the first group shows an acceleration of the colonic transit (fewer retained markers) and the second group shows a decrease of the colonic transit (more retained markers). We draw the conclusion that the Plantago Ovatae fiber regulates or moderates the colon motility and enables a physiological balance of the colonic transit.

Adult↗
PubMed1985

Effects of carcinogen dosage on experimental colonic carcinogenesis by azoxymethane: an ultrastructural study of grossly normal colonic mucosa.

The transmission electron microscopic features of grossly normal colonic mucosa in the azoxymethane [(AOM) CAS: 25843-45-2]-treated rat model of colonic carcinogenesis were studied by the method of concomitant variation. Ten-week-old male F344 rats were given 10 weekly sc injections of AOM at doses of 3, 7, or 14 mg/kg body weight and were killed 1 week or 15 weeks after the last AOM dose. Grossly normal distal left colon was examined using transmission electron microscopy. Three transient dose-dependent features of colonic epithelial cells were identified: a) mitochondrial injury, b) nuclear pleomorphism and loss of polarity, and c) increased numbers of mitotic figures in the lower third of the crypts. Because these dose-dependent features were present only shortly after AOM administration, they appeared to be manifestations of carcinogen toxicity and associated reactive, regenerative epithelial changes. By contrast, four persistent dose-dependent features were identified: a) increased numbers of epithelial cells with enlarged nucleoli, b) increased numbers of mitotic figures in the middle third of crypts, c) reduced numbers of goblet cells, and d) reduced numbers of apical cytoplasmic vacuoles in the upper third of the crypts. Because these features persisted in a dose-dependent manner for many weeks after the last dose of AOM and were present after the latent period to tumor formation, they appear to be morphologic precursors to colonic carcinogenesis in the model.

Animals↗
PubMed1985

Nifedipine reduces the colonic motor response to eating in patients with the irritable colon syndrome.

Patients with the irritable colon syndrome have an exaggerated and/or prolonged colonic motor response to eating. This is believed to be the cause of their postprandial complaints. Since the flux of calcium ions across cell membranes plays a major role in the contractions of the gastrointestinal smooth muscle, we investigated the effect of nifedipine, a calcium channel blocker, on the gastrocolonic response in nine patients with the irritable colon syndrome. Colonic myoelectric and contractile activity was recorded during fasting and after a 1000-cal mixed meal, either with or without nifedipine (20 mg sublingually) administration. Nifedipine reduced the postprandial increase of both spike potential activity and motility index. This effect of acute administration of the drug provides rational support to test nifedipine in clinical trials as a possible means for treating the irritable colon syndrome.

Action Potentials↗
PubMed1985

Neoplastic modulation of extracellular matrix. Colon carcinoma cells release polypeptides that alter proteoglycan metabolism in colon fibroblasts.

Despite the growing evidence implicating proteoglycans in the control of cell proliferation and differentiation, little is known about the factors that control their metabolism in neoplasia or the mechanisms through which these macromolecules may influence neoplastic growth. The primary objective of the present study was to test whether human colon carcinoma cells released soluble mediators capable of stimulating the synthesis of proteoglycans in normal colon fibroblasts in vitro. Serum-free medium conditioned by colon carcinoma cells (TCM) was capable of stimulating several-fold the synthesis and secretion of proteoglycans in normal colon fibroblasts without inducing a mitogenic response. This effect was a true stimulation of proteoglycan biosynthesis since the kinetics of turnover were identical in the presence or absence of TCM. Characterization of the proteoglycans synthesized in the absence of TCM revealed that colon fibroblasts synthesized at least three species of proteoglycans including a heparan sulfate proteoglycan which was associated primarily with the cell layer and two populations of proteoglycans which were predominantly released into the medium and contained chondroitin-dermatan sulfate side chains. When fibroblasts were exposed to TCM, they synthesized and released higher amounts of proteoglycans which had overall similar density, molecular weight, and polydispersity but differed from controls in that they contained significantly higher proportions of chondroitin sulfate side chains. Partial characterization of TCM strongly indicated that the stimulatory activity comprised a family of polypeptides, with molecular weight between 5.4 and 6.0 X 10(5), which were heat stable and acid/alkali labile. Neoplastic modulation of proteoglycan metabolism in normal mesenchymal cells may represent an additional mechanism through which tumor cells can alter their surrounding environment.

Animals↗
PubMed1984

Classification and risk assessment of individuals with familial polyposis, Gardner's syndrome, and familial non-polyposis colon cancer from [3H]thymidine labeling patterns in colonic epithelial cells.

A probabilistic analysis has been developed to assist the binary classification and risk assessment of members of familial colon cancer kindreds. The analysis is based on the microautoradiographic observation of [3H]thymidine-labeled epithelial cells in colonic mucosa of the kindred members. From biopsies of colonic mucosa which are labeled with [3H]thymidine in vitro, the degree of similarity of each subject's cell-labeling pattern measured over entire crypts was automatically compared to the labeling patterns of high-risk and low-risk reference populations. Each individual was then presumptively classified and assigned to one of the reference populations, and a degree of risk for the classification was provided. In carrying out the analysis, a linear score was calculated for each individual relative to each of the reference populations, and the classification was based on the polarity of the score difference; the degree of risk was then quantitated from the magnitude of the score difference. When the method was applied to kindreds having either familial polyposis or familial non-polyposis colon cancer, it effectively segregated individuals affected with disease from others at low risk, with sensitivity and specificity ranging from 71 to 92%. Further application of the method to asymptomatic family members believed to be at 50% risk on the basis of pedigree evaluation revealed a biomodal distribution to nearly zero or full risk. The accuracy and simplicity of this approach and its capability of revealing early stages of abnormal colonic epithelial cell development indicate potential for preclinical screening of subjects at risk in cancer-prone kindreds and for assisting the analysis of modes of inheritance.

Colonic Neoplasms↗
PubMed1982

Isolation and characterization of proteoglycans synthesized by human colon and colon carcinoma.

The biosynthesis of proteoglycans in short term organ culture of human colon and colon carcinoma was studied. Proteoglycans, labeled with [35S]sulfate and [3H]serine, were extracted with either 4 M or 0.5 M guanidine HCl in the presence of protease inhibitors and sequentially purified by associative and dissociative CsCl density gradient ultracentrifugation. Normal colon synthesized two polydisperse classes of proteoglycans: a large heparan sulfate-containing monomer, with a Kav of 0.48 on Sepharose CL-2B and a small dermatan sulfate-containing monomer with a Kav of 0.65. A portion (25%) of the proteoglycans was found as aggregate when chromatographed under associative conditions, and the larger monomers interacted with hyaluronic acid to an extent greater than the smaller proteoglycans. Following papain or alkali treatment, the free glycosaminoglycan side chains of both monomers eluted as a single broad peak (Kav = 0.5) from Sepharose CL-6B, with an estimated Mr of 20 X 10(3). In contrast, colon carcinoma synthesized only one proteoglycan monomer, which aggregated to a limited extent (12%). This proteoglycan population, with a Kav of 0.7 on CL-2B, contained chondroitin sulfate as the major glycosaminoglycan (greater than 81%), with small amounts of dermatan sulfate. The glycosaminoglycans had an estimated Mr of 9 X 10(3), and the disaccharides released by chondroitinase ABC consisted of 32% 4-sulfate and 68% 6-sulfate. Electron microscopy of mixed proteoglycancytochrome c monolayers from the associative fractions of normal and neoplastic colon revealed aggregated complexes which were similar in over structure, although smaller than the proteoglycan aggregates from cartilage.

Amino Acids↗
PubMed1995

Histochemical alterations of mucin in normal colon, inflammatory bowel disease and colonic adenocarcinoma.

Loss of sialic acid o-acyl substitutions in colonic mucus was studied using specific histochemical techniques in individuals with a variety of large-bowel diseases and in a control population. Changes found included a focal or field (diffuse) loss of side-chain substitutions which were qualitatively similar in all groups studied. The results were tested statistically using a variety of assumptions that field and/or focal loss of o-acyl substitution may be either abnormal or a normal variant. No statistically significant differences in the prevalence of substitutions were detected between normal males and females or between normal individuals aged 0-29 years and 30-80 years. Significant differences were found between ascending and descending colon in both normal individuals and in the non-neoplastic mucosa of patients with cancer. There were also significant differences between the normal descending colon and cases with cancer of the descending colon. These differences seem unlikely to be due to non-specific factors, since for most assumptions there were also differences between colons containing cancer and those from patients with inflammatory bowel disease. In agreement with the work of other investigators, it seems likely that focal loss of o-acetylation results from an acquired gene mutation. It is not clear whether or not this plays a role in carcinogenesis.

Adenocarcinoma↗
PubMed1998

Extracellular matrix modulates expression of growth factors and growth-factor receptors in liver-colonizing colon-cancer cell lines.

Site-specific metastasis is determined by the extracellular matrix (ECM) of the colonized organ. We have shown that hepatocyte-derived ECM stimulated proliferation of colon-cancer cells via induction of autocrine growth factors and their receptors. The ECM component responsible was heparin proteoglycan. We therefore investigated the effect of exogenously added heparin on colon cell lines of varying liver-colonizing potential. The cells were grown on typical liver matrix components, such as fibronectin and collagens type I and IV. We assessed the effect of these matrix components on clonal growth, proliferation and expression of autocrine growth factors and their receptors. The clonal growth of the KM12 cells was not affected by heparin, while the other cell lines were inhibited by heparin. Cell proliferation in weakly metastatic KM12, but not in strongly metastatic KM12SM, was inhibited by heparin on plastic. Weakly metastatic LS174T, but not strongly metastatic LiM6, was inhibited by heparin on fibronectin. Expression of erb-B2 was also differently modulated by heparin in weakly metastatic vs. highly metastatic cells. In weakly metastatic cells, heparin reduced erb-B2 levels when cells were on plastic and fibronectin, while in strongly metastatic cells, erb-B2 was induced by heparin. In all 4 cell lines, mRNA for cripto was induced by heparin when the cells were grown on fibronectin. In KM12SM cells, amphiregulin was induced by heparin in cells on fibronectin and collagen IV. We show that soluble heparin, similar in its carbohydrate chemistry to liver heparin proteoglycan, regulates the growth of colon-cancer cells. This effect depends on other matrix components found in the liver and is mediated in part by EGF family members.

Amphiregulin↗
PubMed1977

Metabolic epidemiology of colon cancer. Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps.

Because of potential significance of bile acids and cholesterol metabolites in the pathogenesis of colon cancer, fecal neutral sterols, and bile acids were determined in patients with colon cancer, adenomatous polyps or other digestive diseases and American or Japanese controls. The fecal excretion of cholesterol, coprostanol, coprostanone, total bile acids, deoxycholic acid, lithocholic acid was higher in patients with colon cancer and patients with adenomatous polyps compared to normal American and Japanese controls as well as patients with other digestive diseases. Patients with other digestive diseases excreted comparable levels of fecal bile acids and cholesterol metabolites compared to normal American controls; Japanese controls excreted reduced levels compared to normal American controls. These findings suggest that possible interactions between bile acids and cholesterol metabolites and colonic epithelial cells may be relevant in colon carcinogenesis.

Adult↗
PubMed1985

In vitro cellular cytotoxicity for a human colon cancer cell line by mucosal mononuclear cells of patients with colon cancer and other disorders.

In vitro cellular cytotoxicity of mononuclear cells of intestinal mucosa and peripheral blood for a colon cancer cell target was measured in patients with colon cancer and other disorders requiring resection. Four- and 24-hour cytotoxicity assays were conducted using selenium 75 (75Se)-labeled RPMI-4788 human colon cancer target cells grown in culture. In the cancer group mean cytotoxicity was 30.4% at 24 hours for peripheral blood effectors and 8.0% for effectors from normal mucosa. Values in patients with Crohn's disease were 10.4% for blood and 17.2% for effectors from normal mucosa, and 13.6% and 18.5%, respectively, for blood and abnormal mucosa. Values in patients with other diseases were 25% for blood and 14.7% for mucosa. Mean cytotoxicity at 4 hours did not exceed 6.4% for any group, and assays in autologous serum gave results similar to tests in calf serum. In additional studies, K 562 chronic leukemia cells were somewhat more sensitive to lysis than RPMI-4788 by blood mononuclear cells, but there was no lysis of K 562 by mucosal populations that were cytotoxic for RPMI-4788. There was no competitive inhibition by either target cell for the other. It was concluded that 75Se RPMI-4788 colon cancer cells are suitable targets for evaluating in vitro cytotoxicity by intestinal mucosal cells and that mucosal cytotoxicity in patients with colon cancer is depressed compared to cytotoxicity by peripheral blood effectors.

Adolescent↗
PubMed2005

Peroxisome proliferator-activated receptor gamma agonist troglitazone induces colon tumors in normal C57BL/6J mice and enhances colonic carcinogenesis in Apc1638 N/+ Mlh1+/- double mutant mice.

The role of the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in colon tumorigenesis remains controversial. Notwithstanding evidence that PPAR-gamma ligands impede murine colorectal carcinogenesis, PPAR-gamma agonists have been shown to enhance in vivo tumor formation in mouse models of human colon cancer. Our study was designed to determine whether troglitazone (TGZ) induces colonic tumor formation in normal C57BL/6J mice and enhances colorectal carcinogenesis in double mutant Apc1638N/+ Mlh1+/- mice fed a standard AIN-76A diet. We report herein that not only does TGZ enhance carcinogenesis in the large intestine of mutant mice predisposed to intestinal carcinogenesis but TGZ also induces colonic tumors in normal mice without gene targeting or carcinogen administration. This observation indicates that preexisting mutational events are not necessary for induction of colonic tumors by activated PPAR-gamma in vivo.

Adaptor Proteins, Signal Transducing↗