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At least 1,225 records · Page 68Linked to original sources
PubMed1991

The ability of rifampin-resistant Escherichia coli to colonize the mouse intestine is enhanced by the presence of a plasmid-encoded aerobactin-iron(III) uptake system.

Rifampin-resistant Escherichia coli are known to be poor colonizers of the animal intestine. In this report, we show that the colonizing ability of rifampin-resistant E. coli cells is increased dramatically in the presence of the aerobactin-mediated iron(III) uptake system. In contrast, the colonization by nalidixic acid-resistant E. coli does neither depend on the aerobactin-iron(III) nor on the dicitrate-iron(III) uptake system. Likewise, it does not depend on the production of the siderophore enterochelin.

Animals↗
PubMedDate not supplied

Gastrointestinal stromal tumour of the colon presenting with intestinal obstruction.

Gastrointestinal Stromal Tumours are the commonest mesenchymal tumors of the gastrointestinal tract, the stomach and small intestine being the favored sites. They rarely occur in the colon and rectum and esophagus. The diagnosis is difficult, especially in the rarer sites, since there are no pathognomic features to suggest GIST on preoperative clinical examination and investigations, and only a detailed histopathological analysis of the specimen reveals their true nature. The case of a young female patient who presented with intestinal obstruction due a GIST of the transverse colon is reported. The relevant literature is briefly reviewed.

Adolescent↗
PubMed2001

Rearrangement of diflunisal acyl glucuronide into its beta-glucuronidase-resistant isomers facilitates transport through the small intestine to the colon of the rat.

Many non-steroidal anti-inflammatory drugs (NSAIDs) which form acyl glucuronide conjugates as major metabolites have shown an antiproliferative effect on colorectal tumors. This study assesses the extent to which rearrangement of an acyl glucuronide metabolite of a model NSAID into beta-glucuronidase-resistant isomers facilitates its passage through the small intestine to reach the colon. Rats were dosed orally with diflunisal (DF), its acyl glucuronide (DAG) and a mixture of rearrangement isomers (iso-DAG) at 10 mg DF equivalents/kg. The parent drug DF appeared in plasma after all doses, with maximum concentrations of 20.5+/-2.5, 28.8+/-8.3 and 11.0+/-1.6 microg DF/ml respectively, obtained at 3.8+/-0.3, 3.6+/-1.8 and 7.5+/-0.9 hr after the DF, DAG and iso-DAG doses respectively. At 48 hr, 16.2+/-3.3, 19.8+/-0.8 and 42.9+/-10.1% of the doses respectively were recovered in feces, with < or = 1% remaining in the intestine. About half of each dose was recovered as DF and metabolites in 48 hr urine: for DF and DAG doses, the majority was in the first 24 hr urine, whereas for iso-DAG doses, recoveries in the first and second 24 hr periods were similar. The results show that hydrolysis of both DAG and iso-DAG, and absorption of liberated DF, occur during passage through the gut, but that these processes occur more slowly and to a lesser degree for iso-DAG. The intrinsic hydrolytic capacities of various intestinal segments (including contents) towards DAG and iso-DAG were obtained by incubating homogenates under saturating concentrations of DAG/iso-DAG at 37 degrees C. Upper small intestine, lower small intestine, caecum and colon released 2400, 3200, 9200 and 22800 microg DF/hr/g tissue plus contents respectively from DAG substrate, and 18, 10, 140 and 120 microg DF/hr/g tissue plus contents respectively from iso-DAG substrate. The much greater resistance of iso-DAG to hydrolysis appears attributable to its resistance to beta-glucuronidases. The data suggest that in rats dosed with DF, DAG excreted in bile would be substantially hydrolysed in the small intestine and liberated DF reabsorbed, but that portion which rearranges to iso-DAG would likely reach the colon.

Animals↗
PubMed1989

Consumption of raw potato starch alters intestinal function and colonic cell proliferation in the rat.

Raw potato starch (RPS) may escape complete digestion to enter the colon and produce alterations in colonic function, while cooked potato starch (CPS) is nearly completely digested in the rat small intestine. Effects of RPS and CPS on colonic function [fecal weight, transmit time and thymidine kinase (TK) activity (a marker for cell proliferation)] were contrasted in a 6-wk feeding study. Male F344 rats consumed either dextrose/sucrose (DS; control), 30% CPS or 30% RPS diet. RPS feeding resulted in a 3-fold increase in fecal weight and a 30% prolongation in transit time, as well as elevated levels of colonic mucosal total protein (50%) and TK activity (4- to 7-fold) compared to DS-fed rats. A second study revealed normal large intestinal histology in rats fed CPS or RPS, with elongated colonic crypts (33% increased over CPS) in group RPS. Large intestinal contents were heavier in group RPS than in group CPS. These studies demonstrate that RPS feeding significantly enhances fecal weight yet prolongs total gastrointestinal transit time. Enhanced colonic TK and elongated colonic crypts suggest that RPS stimulates colonic mucosal growth.

Analysis of Variance↗
PubMed1993

Motor dysfunction of the small bowel and colon in patients with the carcinoid syndrome and diarrhea.

BACKGROUND AND METHODS: The pathophysiology of diarrhea in patients with the carcinoid syndrome is not understood. Possible causes include tumor production of neurohumoral substances, such as serotonin and substance P, which stimulate small-bowel and colonic motility, and intestinal abnormalities, such as lymphangiectasia and bacterial overgrowth. We undertook this study to determine whether carcinoid diarrhea is associated with abnormal motor function in the small intestine and colon. We measured the gastric, small-bowel, and colonic transit of radiolabeled solid residue and estimated the volume of the ascending colon in 16 patients with the carcinoid syndrome and diarrhea and 16 normal subjects. We also measured colonic tone and phasic pressure activity by intracolonic multilumen manometry and with an electronic barostat in seven patients and six normal subjects. RESULTS: The patients with the carcinoid syndrome had elevated 24-hour urinary excretion of 5-hydroxyindoleacetic acid and elevated fasting plasma serotonin concentrations. Transit times in the small bowel and colon were two times (P < 0.001) and six times (P = 0.001) faster in the patients than in the normal subjects. The volume of the ascending colon was approximately 50 percent smaller in the patients than in the normal subjects (P < 0.001). The patients had normal fasting colonic tone; their mean postprandial colonic tone was markedly increased as compared with the values in the normal subjects (mean increase, 41 percent vs. 24 percent; P = 0.03). CONCLUSIONS: Patients with the carcinoid syndrome who have diarrhea have major alterations in gut motor function that affect both the small intestine and colon.

Adult↗
PubMed1992

Glucose absorption by the interposed colon segment after intestinal resection.

One of the proposed surgical treatments of Short Bowel Syndrome is the interposition of a distal colon segment between two portions of the remnant small intestine. This method proved to reverse the nutritional disorders caused by this morbid entity. Surgical technique consisted in an 80% small bowel resection and the interposition of a 3 cm segment of distal colon between the remaining jejunum and ileum. After 70 days, the animals were reoperated and the interposed and the distal colon were isolated and tied. By using the method of rapid and successive absorptions of a glucose solution through the intestinal lumen, the relations between the absorption curves of the interposed and the normal colon could be drawn. Results show that the interposed colon segment absorbs more glucose (mean = 1.43 +/- 1.16 mg/dl) than the distal colon (mean = 0.37 +/- 0.29 mg/dl) and that its absorption pattern is similar to the small bowel rather than the colon. These results allow the use of this method for further studies in which the interposed colon adaptation is studied with other nutrients and/or under specific conditions.

Animals↗
PubMed2004

A wheat-based diet enhances colonization with the intestinal spirochaete Brachyspira intermedia in experimentally infected laying hens.

This study investigated the influence of feeding diets based on cereals with different non-starch polysaccharide content on colonization with the intestinal spirochaete Brachyspira intermedia in experimentally infected laying hens. The diets were based on wheat, barley, or barley and sorghum, all with or without supplementation with exogenous dietary enzymes. Six groups of 12 individually caged laying hens were fed the respective diets for 2 weeks, and then challenged at 20 weeks of age by crop tube with 10(8) to 10(9) colony forming units of active motile spirochaetes on five successive days. Eggs were collected daily. The birds were weighed weekly, and caecal faeces collected for assessment of water content. Every 3 to 4 days cloacal swabs were collected and subjected to culture and subsequent polymerase chain reaction for B. intermedia. The birds were killed at 27 weeks of age. Caecal contents were cultured for spirochaetes, and the viscosity of the ileal and rectal contents assessed. Dietary soluble non-starch polysaccharide content was not a consistent predictor of viscosity in the ileum, and the addition of enzymes did not significantly reduce the viscosity. A dietary influence on colonization was observed, with birds fed wheat having significantly more colonization than the birds fed the other diets. No significant association was found between either dietary soluble non-starch polysaccharide content or ileal viscosity and colonization with B. intermedia, as assessed by faecal excretion of the spirochaete. Dietary enzymes did not consistently or significantly reduce colonization. It was not established how wheat enhances colonization by B. intermedia, but the results suggest that wheat-based diets should be avoided in flocks infected with B. intermedia.

Animal Feed↗
PubMed1996

Mutagenicity of high fat diets in the colon and small intestine of transgenic mice.

Dietary fat has been implicated as a cause of colon cancer by epidemiological studies. Unfortunately, these studies are compatible with high fat as either initiator or promoter. Since initiators are normally mutagenic, we have tested the mutagenicity of high fat diets in the intestinal epithelium at two loci. The Dlb-1 assay, used in the small intestine, detects a wide spectrum of mutations. The lacI assay (Big Blue Mouse assay) is not as sensitive to some types of mutation as is Dlb-1 but was used in the colonic epithelium. Mice suitable for both assays were fed isocaloric high fat diets and subsequently assayed for somatic mutation. The diets consisted of: (i) a mixture of beef tallow, butter and lard totalling to 31% w/w of the diet (AIN-76A) up to 17 weeks; and (ii) corn oil, beef tallow, lard or butter individually, at 31% w/w of the diet for 5 and 9 weeks. These diets provided 50% of the calories from fat. The weights of the experimental and control mice were similar throughout the experiment. No significant increases in mutant frequencies were observed on any high fat diet compared to controls, so we conclude that uncooked fats are not mutagenic and are not initiators of carcinogenesis in the intestinal epithelium.

Animals↗
PubMed2000

Intestinal trefoil factor confers colonic epithelial resistance to apoptosis.

Intestinal trefoil factor (ITF) is an essential regulator of colonic epithelial restitution, the rapid migration of colonocytes over mucosal wounds. High levels of ITF are frequently present in colorectal cancers and derived cell lines. Mucosal restitution requires the detachment of epithelium from substrate, which would be expected to induce apoptosis. However, mice deficient in ITF showed an increase in colonocyte apoptosis unaccompanied by changes in expression of receptor-related (TNFR/Fas) or stress-related (Bcl-family) cell death regulators. An ITF-expressing colonic (HT-ITF1) cell line was resistant to apoptosis induced by serum starvation and ceramide. Exogenous ITF also protected another human colonic carcinoma-derived cell line (HCT116) and a nontransformed rat intestinal epithelial cell line (IEC-6) from apoptosis. This effect was abrogated by wortmannin and tyrphostin A25, indicating the potential involvement of phosphatidylinositol 3-kinase and epidermal growth factor (EGF) receptor activation. Expression of phosphorylated Akt, which lies downstream of phosphatidylinositol 3-kinase activation, was elevated in this HT-29-ITF line. p53-dependent cell death in the AGS human gastric cancer cell line after etoposide was similarly inhibited by transient expression of ITF but not a C-terminal truncation mutant of ITF, and it required functional phosphatidylinositol 3-kinase and EGF receptor. These findings support a central role for ITF in the maintenance of intestinal mucosal continuity, and conversely demonstrate the potential for ITF expression to confer resistance of colorectal tumors to therapy.

3-Phosphoinositide-Dependent Protein Kinases↗
PubMed1990

Effect of the feeding practices on the establishment of bacterial interactions in the intestine of the newborn delivered by cesarean section.

The purpose of this study was to clarify the role of the intestinal anaerobe bacteria colonizing the intestine of the newborn delivered by cesarean section. The intestinal bacterial colonization of 18 newborns delivered by cesarean section was assessed sequentially over the first 14 days of life. Emphasis is placed on C. perfringens and upon interaction to other bacteria. Correlation was made with the infant feeding mode. Microbial studies were realized in anaerobic conditions using Columbia blood agar simple and supplemented with antibiotics. Artificial alimentation seemed to favour C. perfringens installation, in contrast to the maternal one which promote B. bifidum proliferation. Antagonism between these bacteria seems to be established in the newborn intestine, via the alimentation.

Bifidobacterium↗
PubMed2003

Primary cervical adenocarcinoma with intestinal differentiation and colonic carcinoma metastatic to cervix: an investigation using Cdx-2 and a limited immunohistochemical panel.

CONTEXT: Cdx-2 is expressed in normal colonic epithelia and in most colorectal adenocarcinomas. No data exist on Cdx-2 expression in primary cervical adenocarcinoma with colonic differentiation. OBJECTIVE: To ascertain the utility of Cdx-2 and a limited immunohistochemical panel in differentiating between primary cervical adenocarcinoma with intestinal differentiation and secondary (colonic) cervical adenocarcinoma, which call for different surgical and chemotherapeutic treatment protocols. DESIGN: We examined cervical tract adenocarcinomas in women with previously negative medical histories for neoplastic disease and in women with colonic carcinoma. An immunohistochemical panel consisting of cytokeratin 7, cytokeratin 20, carcinoembryonic antigen, and a new marker, Cdx-2, was evaluated in all cases. The clinical data, the morphologic features, and the immunohistochemical staining patterns were compared. RESULTS: Of the tumors diagnosed as metastatic intestinal adenocarcinoma of the cervix, based on clinical data and hematoxylin-eosin-stained sections, all were Cdx-2 positive, whereas Cdx-2 was not expressed in any of our cases of primary cervical adenocarcinoma with colonic differentiation. Carcinoembryonic antigen was expressed both in primary cervical tumor and in secondary (intestinal) cervical adenocarcinoma. Cytokeratin 20 was not expressed in our cases of cervical adenocarcinoma, and it was not expressed in 7.15% of cervical metastases from intestinal carcinoma. Immunostaining with cytokeratin 7 was positive in cervical adenocarcinoma, but was negative in secondary (intestinal) cervical adenocarcinoma. CONCLUSIONS: Our immunohistochemical analysis shows that Cdx-2 has good specificity and would be a good marker to use in a limited panel of immunohistochemical markers, such as cytokeratin 7, cytokeratin 20, and carcinoembryonic antigen, to distinguish primary cervical adenocarcinoma from intestinal metastases to the cervix.

Adenocarcinoma↗
PubMed1991

Absorption mechanisms of secondary aliphatic amines in rat colon and small intestine.

This study is intended to be a further and conclusive validation of the bihyperbolic model equation proposed by Plá-Delfina and Moreno to describe passive intestinal absorption mechanisms through the analysis of absorption-lipophilicity correlations for homologous series of xenobiotics and drugs. Secondary aliphatic amines, largely differing from previously tested substances, were selected as model compounds. Evidence is given which demonstrates that a minimum lipophilicity value exists for absorption in small intestine, instead of a maximum, as probabilistic theories predict. Moreover, bihyperbolic equation provides an excellent fit, with AIC figures up to -29. Aqueous pore absorption was small, presumably due to ionic interactions with pore charges (kp approximately 1.0 h-1), whereas membrane penetration was highly lucrative (km approximately 7.4 h-1), thus indicating that some part of the lipophilic ionic species is capable of penetrating "per se" the lipoidal membrane. As model predicts, bihyperbolic equation collapses to monohyperbolic for colonic absorption, where AIC figures up to -39 were found, with a km value of about 4.0 h-1. Membrane absorption efficiency was, surprisingly, similar in colon and small intestine for the tested solutes; it was attributed to the basic character of the compounds associated with working pH and ion absorption. This latter effect would deserve further investigation in oral sustained-release medication with basic drugs having similar pKa values.

Amines↗