PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Intestine, Large”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 235 records · Page 13Linked to original sources

Effects of enterally fed epidermal growth factor on the small and large intestine of the suckling rat.

Epidermal growth factor (EGF) has been shown to be present in the milk of several species, including the rat, and to have gastrointestinal effects when given parenterally or orally in pharmacologic doses. We investigated the effect of enteral EGF in physiologic doses on the small intestine and colon of suckling rats. Serum thyroxine (T4) levels were also measured. Rats were gavage-fed by hand with an artificial formula with or without added EGF every 3 h from 11 to 14 days of age. Intake was adjusted to deliver 30 kcal/100 g b.wt./day of formula and 16 micrograms/kg/day of EGF approximating the daily caloric intake, and about twice the estimated daily EGF intake for suckling rats. Weight gain did not differ between groups (fed EGF: 3.8 + 0.2 g; not fed EGF: 3.7 + 0.1 g). The protein content of the whole colon of rats fed an EGF-containing formula was significantly lower and the DNA content significantly higher, than in rats fed formula without added EGF. The protein/DNA ratio was therefore markedly higher in the animals fed formula without added EGF; these effects were most evident in the distal colon. In contrast, there was no effect of EGF on small intestinal protein and DNA content; lactase, sucrase, and maltase activities were likewise unaffected, as was serum T4. These data suggest a physiologic role for breast milk EGF in the development of the suckling rat colon.

Animals↗

Identification of enteric pathogens in the small and large intestine of children with diarrhea.

Enteric pathogens were identified in children with diarrhea from duodenal specimens obtained with a string capsule and from fecal specimens. Rotavirus was identified in stools of 43 of 100 children, and was recovered from the small intestine from nine (21%) children who were excreting this virus. Shigella was isolated from stools from 22, Salmonella from 17, enterotoxigenic Escherichia coli from eight, and Aeromonas hydrophila from one of 100 children with diarrhea. In contrast to rotavirus, Salmonella, Shigella, enterotoxigenic Escherichia coli, and A. hydrophila were not isolated from the small intestine. Nonenterotoxigenic Aeromonas species were recovered from the small intestine, but not the stool of five children. These children were also infected with Shigella or with rotavirus; this suggests that Aeromonas was not the cause of their diarrhea. None of 51 Escherichia coli isolated with the string capsules, or 67 isolated from stool that agglutinated in commercial enteropathogenic Escherichia coli antisera were of classical enteropathogenic Escherichia coli serotypes. One hundred and five of these 118 Escherichia coli did not hybridize with a deoxyribonucleic acid probe for plasmid mediated factors conferring adherence to HeLa cells. Examination of specimens collected with a string capsule from children with diarrhea did not identify any more enteric pathogens than examining stools. Furthermore testing Escherichia coli for agglutination in commercial enteropathogenic Escherichia coli antisera did not identify Escherichia coli of enteropathogenic serotypes.

Aeromonas↗

Aquaporins in chicken: localization of ck-AQP5 along the small and large intestine.

Aquaporins (AQPS) are transmembrane water channels poorly investigated in birds. Using degenerated primers and RT-PCR, we identified in kidney and gastrointestinal tract of Hubbard chickens (Gallus gallus) three fragments, corresponding to ck-AQP2, ck-AQP4, and ck-AQP5 mRNAs. Comparison of nucleotide ck-AQPs sequences to their rat and human orthologues revealed an overall identity of 75-90%. Expression in the renal and gastrointestinal systems of the three ck-AQPs mRNA was analysed by Northern assays. Transcript of ck-AQP2 was only identified in kidney. ck-AQP4 mRNA was highly expressed in brain, and to a lesser extent in kidney and stomach. ck-AQP5 mRNA was found in jejunum and ileum, and to a lesser extent in colon and lung. In situ hybridisation showed ck-AQP5 mRNA in the crypt cells of jejunum, ileum and colon, whereas it was absent from the cells lining the villi. Levels of ck-AQP5 mRNA (analyzed by Northern and in situ hybridisation assays) and protein (analysed by immunohistochemistry) decreased from the jejunum to the colon. This work confirmed the presence of AQPs in chicken, and showed that chicken and mammalian AQPs share a high degree of similarity in nucleotide sequence and tissue distribution.

Amino Acid Sequence↗

Neoplastic obstruction of the small and large intestine.

Obstructive symptoms due to small bowel tumors are the most common indication of primary malignant disease in the small intestine. Primary obstructing tumors of the small bowel are treated best by resection and primary anastomosis. Malignant lesions of the duodenum sometimes will require pancreaticoduodenectomy and those of the distal ileum, right hemicolectomy. Obstruction due to localized metastatic disease can be treated by resection and primary anastomosis but, more frequently, one or more side-to-side enteroenterostomies will be needed, especially in abdominal carcinomatosis. The complication of LBO due to colorectal cancer is an ominous sign. The less favorable prognosis is a result of the higher operative mortality, advanced stage of disease and lower resectability rate. Obstructing neoplasms of the right side of the colon are treated best by immediate resection and primary anastomosis. Left-sided colon obstruction due to malignancy traditionally is treated by preliminary diversion followed later by definitive resection. Insufficient data are available to evaluate any benefit on operative mortality and long-term survival with a more aggressive approach involving decompression and resection of the obstructing carcinoma at the initial operation. It is doubtful that any marked improvement in current mortality and survival figures will result from wide deviations of the current principles of operative managment. Early diagnosis of the cancer before obstruction occurs remains the primary means of improving survival rates. This involves not only primary means of improving survival rates. This involves not only patient education regarding presenting symptoms, but improvement of physician recognition and response to these complaints so that the appropriate tests are ordered and treatment is initiated.

Humans↗

Expression and motor effects of secretin in small and large intestine of the rat.

Immunocytochemistry and in situ hybridization revealed abundant secretin expressing cells on duodenal villi with a gradual decrease throughout the small intestines of the rat. They were absent in pancreas, stomach and colon. Secretin caused relaxation of rat intestinal longitudinal muscle in vitro. Studies on colon revealed that the secretin-evoked response was unaffected by apamin, tetrodotoxin, L-NAME, VIP or PACAP pretreatment; secretin itself caused desensitization. Addition of VIP or PACAP when the secretin-evoked relaxation was maximal evoked a further relaxation suggesting the presence of distinct receptors. Secretin causes relaxation via activation of secretin receptors located on the smooth muscle and not via any of the related VIP/PACAP receptors.

Acetylcholine↗

Gastric or rectal instillation of short-chain fatty acids stimulates epithelial cell proliferation of small and large intestine in rats.

Short-chain fatty acids stimulate gut epithelial cell proliferation in vivo, although the difference between oral and rectal routes is unknown. Accordingly, we examined the effect of oral or rectal administration of these acids. We instilled a mixture of acetic acid, propionic acid, and n-butyric acid (150, 60, and 60 mmol/liter, respectively; pH 6.5) or saline (270 mM, pH 6.5) into the stomach (2 ml) or rectum (1 ml) three times daily for five days in rats fed an elemental diet. We measured crypt cell production rate of the jejunum, ileum, and distal colon of these rats. The crypt cell production rate of these segments was higher in rats with gastric or rectal instillation of short-chain fatty acids than in saline controls. The rectal route was slightly more effective than the gastric route. The above results indicated that the instillation of short-chain fatty acids orally or rectally stimulated gut epithelial cell proliferation.

Acetic Acid↗

Differential absorption of amoxicillin from the human small and large intestine.

Differences in extent of amoxicillin absorption from various regions of the gastrointestinal tract were determined and compared with the same dose administered orally. Nine healthy men were intubated at a proximal (duodenum or jejunum) or distal (ileum or colon) site with use of a 15-foot double lumen nasointestinal tube. Amoxicillin solutions (375 mg in 120 ml water) were delivered on 2 successive days as a bolus or a 4-hour infusion. Subjects were reintubated at another site and amoxicillin administration was repeated. Subjects with colonic intubation received only infusions. Finally, all subjects received an oral dose of amoxicillin solution. Plasma samples were obtained at 16 time points over a 10-hour period and assayed for amoxicillin by use of an HPLC method. Area under the concentration-time curve and the maximum plasma concentration were computed to evaluate amoxicillin absorption. Amoxicillin absorption was rate and site dependent in the gastrointestinal tract. The drug was well absorbed in the duodenum and jejunum, with no significant differences in absorption when administered as a bolus or 4-hour infusion, but absorption was decreased and rate dependent in the ileum, where more drug was absorbed as an infusion compared with a bolus. Amoxicillin was unabsorbed when infused in all colonic regions.

Adult↗

Bcl-w is an important determinant of damage-induced apoptosis in epithelia of small and large intestine.

The potential role of the bcl-2 relative bcl-w as a physiological regulator of apoptosis in intestinal epithelia has been investigated. Immunoblots for bcl-w with new monoclonal antibodies revealed that it was expressed in the small intestine and colon, among other murine tissues, as well as in six human tumour cell lines of epithelial origin, including two colon carcinoma lines. To assess whether bcl-w regulates either spontaneous or damage-induced apoptosis in the small intestine or colon, apoptosis in intestinal crypts of bcl-w -/- and wild-type mice was quantified microscopically on a cell positional basis. Spontaneous apoptosis within crypt epithelia was not significantly increased by loss of bcl-w, in either the small intestine or midcolon. However, after treatment with the cytotoxic drug 5-fluorouracil or with gamma-radiation, the bcl-w-null animals exhibited substantially more apoptosis than their wild-type counterparts in both tissues. The greatest enhancement of apoptosis attributable to the absence of bcl-w (up to sixfold) occurred in the small intestine. Hence, bcl-w is an important determinant of damage-induced apoptosis in intestinal epithelia, and unlike bcl-2, which regulates only colonic apoptosis, plays a major role in small intestinal epithelium.

Animals↗