PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Intestine, Small”

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 325 records · Page 18Linked to original sources
PubMedDate not supplied

[Microecological aspects of small intestinal bacterial overgrowth syndrome].

Small intestinal bacterial overgrowth syndrome (SIBOS) means chronic recurrent diarrhea with malabsorption, intoxication and increased risk of endogenous infection. This syndrome are accompanied by increase of overall bacterial burden in biotope >10(5) CFU/ml in adults and >10(4) CFU/ml in children, emergence of different species of enterobacteria, bacteroides, clostridia and fusobacteria et al. in small intestine. Such characteristics of the syndrome allow to consider it as syndrome of disturbances of intestinal microflora (dysbacteriosis). Microecological changes are accompanied by B12 vitamin deficiency anemia, hypovitaminosis, protein deficiency, translocation of bacteria and their toxins from intestine in blood, emergence of endotoxinemia and possible generalization of infection. SIBOS is diagnosed by concentration of hydrogen in expiratory flow (lactulosa load test) or by bacteriological study of aspirate from proximal part of small intestine. Complex treatment includes containing lacto- and bifidobacteria probiotics and, in more severe cases, antimicrobial agents (vancomycine, metronidazole, aminoglycosides, amoxicillin clavulanate, tetracycline, and cephalosporines of 2nd generation) with following correction of disturbed microbiocenosis by different probiotics.

Adult↗
PubMed1997

Genetic alterations in sporadic and Crohn's-associated adenocarcinomas of the small intestine.

BACKGROUND & AIMS: Small intestinal carcinomas are rare but occur with increased incidence in Crohn's disease. The aim of this study was to elucidate the genetic alterations. METHODS: Mutations and deletions involved in colorectal carcinoma were studied in sporadic and Crohn's-associated intestinal carcinomas and precursors. RESULTS: c-K-ras mutations were present in all four sporadic carcinomas with contiguous adenomas, in only 18% without adenomas (P = 0.01), in 43% of Crohn's-associated carcinomas, and in 14% of dysplasias. Overexpression of p53 gene product and/or 17p allelic loss were present in 47% of sporadic carcinomas and 33% of contiguous adenomas and in 71% of Crohn's-associated carcinomas and 43% of dysplasias. In contrast, allelic losses of 5q (adenomatous polyposis coli [APC] gene region) and 18q (deleted in colorectal cancer [DCC] gene region) were rare. DNA replication errors (RERs) were present in 13% of sporadic carcinomas and in the carcinoma and dysplasias of 1 patient with Crohn's disease (14%), but mutations in the transforming growth factor beta type II receptor (TGFbeta RII) gene were absent. CONCLUSIONS: Accumulation of ras and p53 alterations occurs during the adenoma/dysplasia-carcinoma sequence in small intestinal carcinogenesis, but a ras-independent pathway may also exist. The infrequent loss of the APC and DCC regions and the absence of TGFbeta RII gene mutation in RER-positive neoplasms contrast with colorectal carcinogenesis.

Adenocarcinoma↗
PubMed2005

Differences in the effects of age on intestinal proliferation, crypt fission and apoptosis on the small intestine and the colon of the rat.

The increase in gastrointestinal epithelial tissue mass and the development of the gut can occur through three main mechanisms, namely elevated cell production from the intestinal crypts, by raised crypt number, which occurs through the process of crypt fission or by altered apoptosis. The small bowel and the colon have various rates of these, which were studied in rats of various ages. Wistar rats were fed ad libitum, and were killed at 3, 4, 6, 9, 12, 18, 26 and 48 weeks of age. Tissue was later stained and microdissected and the number of native mitoses and apoptotic figures per crypt and the percentage of crypts in fission were determined. There was an almost linear increase in body weight from 3 to 9 weeks, followed by a more gradual rise until 18 weeks. The weight of the stomach and the small intestine reached maximum values at 9 weeks, whereas the caecum and the colon approached this at 12 weeks. Mitotic activity per crypt in the small intestine increased from 3.8 +/- 0.1 at 3 weeks to 7.8 +/- 0.4 mitoses per crypt (P < 0.001) at 9 weeks and then decreased slightly; crypt fission increased from 4.6% +/- 0.8 at 3 weeks to 8.4 +/- 0.9% at 6 weeks and then decreased gradually reaching a value of 1.5 +/- 0.4% at 48 weeks. Apoptosis also peaked at 6 weeks and was then very low. In the colon, the proliferation decreased from 4.2 +/- 0.2 mitoses per crypt in the young (3 weeks) rat and reached a plateau by 9 weeks (2.5 +/- 0.1 mitoses per crypt, P < 0.001). Crypt fission also declined rapidly in the first 9 weeks (from 67.6 +/- 4.2 to 23.1 +/- 4.6%, P < 0.01) and then continued to decline, although at a lower rate. The crypt fission index at 48 weeks was 9.8 +/- 1.0. Apoptosis in the colon persisted throughout the duration of the study, 0.19 +/- 0.06 apoptotic bodies per crypt were seen at week 48. The development of the small intestine is more dependent on cell proliferation, whereas in the colon crypt fission is far more predominant, with the colon having fission indices approximately six times greater than those of the small intestine. Proliferative activity in the colon was approximately half that of the small intestine.

Aging↗
PubMed2006

Increased antioxidant capacity of serum did not prevent lipid peroxidation in the intermittent ischemia-reperfusion of rat small intestine.

Changes in small molecular antioxidants were followed up in a model of small intestinal ischemia in Wistar rats to evaluate their possible role in ischemic preconditioning. The superior mesenteric artery was occluded either for 60 minutes only or for 60 minutes preceded by one to three 15-minute periods of ischemia with 5-minute reperfusion periods interposed. Total antioxidant capacity (TRAP) in serum, serum antioxidants (uric acid, ascorbic acid, bilirubin), and the thiobarbituric acid reactive substances in both serum and mucosa were measured. An increase in TRAP observed after 60 minutes of ischemia was prevented in preconditioned animals. Ascorbic and uric acid concentrations increased generally in comparison to intact controls, but this increase was not sufficient to prevent lipid peroxidation in serum and intestinal mucosa. In short, the small molecular antioxidants measured did not contribute to the phenomenon of ischemic preconditioning.

Analysis of Variance↗
PubMed2003

Association of vasoconstrictive exposures with risks of gastroschisis and small intestinal atresia.

BACKGROUND: Gastroschisis and small intestinal atresia are congenital anomalies that may arise from vascular disruption. It is hypothesized that maternal exposure to cocaine, amphetamines, decongestants and nicotine, all of which have vasoconstrictive actions, can contribute to these defects. The present study examined risks of gastroschisis and small intestinal atresia associated with combined exposure to vasoconstrictive drugs and cigarette smoking. METHODS: This was a retrospective study conducted from 1995 to 1999 in 15 cities across the United States and Canada. Mothers of 205 gastroschisis cases, 127 small intestinal atresia cases, 381 malformed controls and 416 nonmalformed controls were interviewed within 6 months of delivery. RESULTS: Reported vasoconstrictive drugs included pseudoephedrine, phenylpropanolamine, ephedrine and methylenedioxymethamphetamine. Combined exposure to vasoconstrictive drugs and cigarette smoking in the first 2.5 months of pregnancy was reported by 9% of gastroschisis cases, 9% of small intestinal atresia cases and 4% of controls. Multivariate-adjusted odds ratios, controlling for the effects of age, education, income, other drug use and alcohol intake, were 2.1 (95% confidence interval = 1.0-4.4) for gastroschisis and 2.8 (1.1-6.9) for small intestinal atresia. Risks of each defect increased with increasing level of cigarettes (P for trend = 0.019 and 0.012, respectively). Vasoconstrictive drug use among smokers of 20 or more cigarettes a day increased gastroschisis risk 3.6-fold (1.3-10.3) and small intestinal atresia risk 4.2-fold (1.1-16.2). CONCLUSIONS: These findings provide further evidence of vascular disruption as an etiology for gastroschisis and small intestinal atresia.

Adult↗
PubMed1998

Anti-inflammatory and antisecretory potential of histidine in Salmonella-challenged mouse small intestine.

Challenge of mouse small intestinal loops with Salmonella typhimurium invoked the accumulation of luminal fluid, acute inflammation, and extensive structural damage to the small intestinal mucosa, as determined by histology and electron microscopy. Intraperitoneal and intestinal luminal injection of L-histidine, a known antioxidant, reduced the amount of fluid accumulating in the intestinal lumen and protected the intestinal tissue from S. typhimurium-induced damage. The reduction in S. typhimurium-induced fluid accumulation by L-histidine was specific for the L-enantiomer because D-histidine had no significant protective effect. Efficacy of L-histidine in protecting the infected intestinal tissue was attributed to the capacity of the imidazole ring to scavenge reactive oxygen species (ROS) generated by cells in the intestine during the acute inflammatory response. Glutathione levels were markedly reduced in S. typhimurium-challenged, inflamed intestinal tissues as a result of ROS generation. Importantly, after dosing the S. typhimurium-challenged mice with L-histidine, the glutathione content of the small intestinal tissue was not significantly different from mock-challenged controls. Further evidence favoring this mechanism included the capacity of L-histidine to scavenge ROS produced as a result of lipopolysaccharide (LPS) exposure of mononuclear cells (U937), as demonstrated with a redox-sensitive fluorescent dye (2'7'-dichlorodihydrofluorescein [DCF]). Addition of L-histidine, and to a lesser extent D-histidine, to the culture media of U937 cells before LPS exposure, resulted in a significant dose-dependent reduction in LPS-induced intracellular DCF fluorescence, as measured quantitatively by flow cytometry. The potential therapeutic value of anti-inflammatory drugs containing an L-histidine-like structure could protect infected mucosal tissues irrespective of microbial etiology.

Amino Acids↗
PubMed1978

Alterations in cell surface membrane components of adapting rat small intestinal epithelium. Studies with lectins after massive proximal jejunoileal resection and jejunoileal transposition.

After proximal resection or transposition of intestinal segments, the small intestinal mucosa of rats was examined with fluorescein-conjugated lectins derived from Ricinus communis and Triticum vulgare (wheat germ). These agglutinins are thought to be specific for the nonreducing end-terminal carbohydrate residues, beta-D-galactose and beta-N-acetyl-D-glucosamine, respectively. After 70% proximal jejunoilealal resection as well as transposition of ileal segments to jejunum, ileal villus cell surface labeling by both lectins was changed to a pattern characteristic of normal rat proximal intestine. Alterations were not detected proximal to the surgical anastomosis after massive resection or in the jejunal segments transposed to ileum. Although the labeling pattern of goblet cell mucin differed in proximal duodenum from the remainder of control small intestine in normal animals, no differences were detected in goblet cell mucin labeling between normal and resected or transposed animals. This study confirms the previously reported differential lectin-labeling patterns of the small intestinal crypt and villus cells and further emphasizes the differences between cell surface carbohydrate and secretory mucins of goblet cells. Furthermore, the changes induced in the cell surface-labeling pattern by massive proximal jejunoileal resection and transposition suggest that cell surface and secretory components may be altered differently during adaptation of the small intestine.

Adaptation, Physiological↗
PubMed1984

Paraovarian-omental bands as a cause of small intestinal obstruction in cows.

Small intestinal obstruction caused by a fibrous band extending from the free edge of the greater omentum to the ovary or the tip of uterine horn was found in 4 cows. The band and distended small intestine were palpable per rectum in each cow. In 3 cows, severance of the fibrous band relieved the small intestinal obstruction and the cows recovered without complication. In the fourth cow, the compromised portion of intestine ruptured during manipulation and the animal was euthanatized.

Animals↗
PubMed1975

[Changes in blood pressure and impulse activity in intestinal nerves during exposure of small intestine interoreceptors to lactic acid].

I. a. administration of threshold concentration (0.2 ml 7.8 mM) of lactic acid into the small intestine was found to increase afferent and efferent impulsation in the intestinal nerves as well as the systemic arterial blood pressure in anesthetized cats. Increase in the lactic acid concentration up to 250 mM/l resulted in two-phasic augmentation of the nerve responses and of the pressor reflexes. In the range from 7.8 to 62.5 mM/l of lactic acid concentration the absolute magnitude of pressor reflexes was 2.3 +/- 0.6--4.2 +/- 0.5 mm Hg. Further increase in the lactic acid concentration (up to 250 mM/l) produced on augmentation in the reflexes magnitude up to 18 +/- 2.8 mm Hg. A possible functional role of afferent impulses generated by the tissue receptors following an increase in metabolites concentration in the organs, is discussed.

Animals↗
PubMed1993

Muscarinic cholinergic receptor density following small intestinal transplantation in rats.

After small intestinal transplantation, intestinal isografts can organize migrating myoelectric complexes, and we have shown that migrating myoelectric complex frequency in the fasted state was reduced compared with controls after transplantation of the distal 50% of small intestine. We hypothesized that changes in motor activity after transplantation were related to alteration of cholinergic nerve activity or receptor density. With use of standard microsurgical techniques, the distal 50% of small intestine was orthotopically transplanted in a Lewis-to-Lewis donor-recipient combination. Resection controls were prepared by resecting the proximal 50% of small intestine, and sham controls were prepared by performing a sham laparotomy. Two months after surgery, small intestine was harvested. Choline acetyltransferase activity among the three groups was similar, suggesting that intrinsic cholinergic nerves remained intact. There was a strong trend toward decreased acetylcholinesterase activity [analysis of variance (ANOVA), P = 0.16] after transplantation, consistent with loss of extrinsic vagal nerve fibers. There were no differences in histochemical distribution of acetylcholinesterase among these groups. Muscarinic receptor density, as determined by binding to [N-methyl-3H]scopolamine, was decreased after transplantation (ANOVA, P = 0.02). There was a trend toward decreased receptor density in animals with resected small intestine. Surgical interruption of intrinsic nerve pathways rather than ischemia or extrinsic denervation might be the mechanism for diminished receptor density after transplantation, and reduced small bowel motor activity may be related to decreased density of muscarinic cholinergic receptors.

Acetylcholine↗
PubMed1979

The assay and partial characterization of macromolecular heparin depolymerase activity in rat small intestine.

Homogenates of rat small intestine can depolymerize macromolecular rat skin heparin (RS heparin) to products similar in size to commercial heparin [Horner (1972) Proc. Natl. Acad. Sci. U.S.A. 69, 3469--3473]. This activity is attributed to an enzyme provisionally named 'macromolecular heparin depolymerase'. An assay for macromolecular heparin depolymerase activity in rat small intestine has been developed, based on the action of the enzyme on 35S-labelled macromolecular RS heparin. The depolymerized products are separated into two peaks by gel chromatography through columns of Bio-Gel A-15m. The amount of label in the second peak, expressed as a percentage of the total radioactivity, is the index of enzyme activity. The pH optimum was found to be 6.0 and the temperature optimum 45 degrees C. The enzyme was shown to be most stable in 50mM-Tris/maleate buffer containing 1 mM-EDTA. Macromolecular heparin depolymerase activity measured as a function of time and substrate concentration produced curves typical of an enzymic reaction. Evidence was obtained demonstrating that the activity did not originate from bacteria in the intestine. Macromolecular heparin depolymerase activity was increased by dilution and storage at 7 degrees C for 24 h. This suggests that homogenates of rat small intestine contain an unstable inhibitor of the enzyme.

Animals↗
PubMed1986

Effect of epidermal growth factor on growth and maturation of fetal and neonatal rat small intestine in organ culture.

Small intestinal explants from pre- and post-natal rats were incubated in an organ culture system in the absence and presence of epidermal growth factor (EGF). The rate of synthesis of small intestinal DNA and protein as well as the activity of lactase and alkaline phosphatase increased rapidly between 17 and 20-day gestational age, whereafter they declined. The maximal incorporation of 3H-thymidine and 14C-alanine into DNA and protein, respectively, was significantly stimulated by EGF (100 ng/ml). EGF had no effect on the activity of either lactase or alkaline phosphatase in the small intestinal explants.

Alkaline Phosphatase↗
PubMed2001

Activation of Paneth cell alpha-defensins in mouse small intestine.

Paneth cells in small intestine crypts secrete microbicidal alpha-defensins, termed cryptdins, as components of enteric innate immunity. The bactericidal activity of cryptdins requires proteolytic activation of precursors by matrix metalloproteinase-7 (MMP-7; matrilysin) (Wilson, C. L., Ouellette, A. J., Satchell, D. P., Ayabe, T., Lopez-Boado, Y. S., Stratman, J. L., Hultgren, S. J., Matrisian, L. M., and Parks, W. C. (1999) Science 286, 113-117). Here, we report on the intracellular processing of cryptdin proforms in mouse Paneth cells. Peptide sequencing of MMP-7 digests of purified natural procryptdins identified conserved cleavage sites in the proregion between Ser(43) and Val(44) as well as at the cryptdin peptide N terminus between Ser(58) and Leu(59). Immunostaining co-localized precursor prosegments and mature cryptdin peptides to Paneth cell granules, providing evidence of their secretion. Extensive MMP-7-dependent procryptdin processing occurs in Paneth cells, as shown by Western blot analyses of intestinal crypt proteins and proteins from granule-enriched subcellular fractions. The addition of soluble prosegments to in vitro antimicrobial peptide assays inhibited the bactericidal activities of cryptdin-3 and -4 in trans, suggesting possible cytoprotective effects by prosegments prior to secretion. Levels of activated cryptdins were normal in small bowel of germ-free mice and in sterile implants of fetal mouse small intestine grown subcutaneously. Thus, the initiation of procryptdin processing by MMP-7 does not require direct bacterial exposure, and the basal MMP-7 content of germ-free Paneth cells is sufficient to process and activate alpha-defensin precursors. MMP-7-dependent procryptdin activation in vivo provides mouse Paneth cells with functional peptides for apical secretion into the small intestine lumen.

Amino Acid Sequence↗
PubMed1974

The small intestine in dermatitis herpetiformis.

Small intestinal biopsies from 43 patients with dermatitis herpetiformis have been studied. The diagnosis of dermatitis herpetiformis was made on clinical and histological criteria and the presence of IgA deposits in the uninvolved skin. The macroscopic appearance of the intestinal biopsy was flat in 13, convoluted in 10, leaves only in eight, and fingers and leaves in 12. Twenty small intestinal biopsies from patients who did not have dermatitis herpetiformis or gastrointestinal disorder showed leaves only in three and fingers and leaves in 17. The mean total lymphocyte count per 1000 epithelial cells for this control group was 159 +/- SE 13; for the dermatitis herpetiformis patients with flat biopsies it was 464 +/- SE 27; for the convoluted biopsies 365 +/- SE 59; for leaves only 535 +/- SE 39; and for the fingers and leaves biopsies 301 +/- SE 31. The counts for all four groups are significantly greater than the control group (P < 0.001). Three of the 43 patients with dermatitis herpetiformis had lymphocyte counts below 200 per 1000 epithelial cells, and four of our controls had counts greater than 200 but none above 300. In the control group the mean counts for lymphocytes per 1000 epithelial cells in the basal position of the intestinal epithelium was 79 +/- SE 8; in the dermatitis herpetiformis flat biopsies it was 89 +/- SE 11; for the convoluted biopsies 93 +/- SE 12; for the leaves only biopsies 121 +/- SE 18 and for the fingers and leaves 98 +/- SE 13. However, the mean lymphocyte count in the perinuclear position was 81 +/- SE 7 for the controls, 362 +/- SE 23 for the flat dermatitis herpetiformis biopsies; 251 +/- SE 46 for the convoluted specimens; 402 +/- SE 43 for the leaves only specimens, and 195 +/- SE 25 for the fingers and leaves biopsies. The mean lymphocyte count for the supranuclear position was 0.55 +/- SE 0.22 for the control group; 13.7 +/- SE 2.3 for the flat dermatitis herpetiformis biopsies; 20.0 +/- SE 6.9 for the convoluted biopsies; 14.5 +/- SE 3.3 for the leaves only biopsies; and 8.3 +/- SE 2.6 for the fingers and leaves biopsies. Thus in gluten-sensitive enteropathy the increase in lymphocytes in the intestinal epithelium is in the perinuclear and supranuclear position. The ratio of basal lymphocytes to peri- and supranuclear lymphocytes appears to be 1:1 in normal intestinal epithelium, but approximately 1:4 in the gluten-sensitive enteropathy of dermatitis herpetiformis.

Adult↗
PubMed2001

PACAP-(6-38) inhibits the effects of vasoactive intestinal polypeptide, but not PACAP, on the small intestinal circular muscle.

Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating peptide-(1-38) (PACAP) have been found to stimulate distension-induced peristaltic motility in the guinea-pig isolated small intestine. In this study, we tested whether the putative VIP/PACAP receptor antagonist PACAP-(6-38) counteracts the properistaltic effect of VIP and PACAP in isolated segments of the guinea-pig small intestine. VIP (100 nM) and PACAP (30 nM) had a stimulatory effect, i.e., lowered the peristaltic pressure threshold at which peristaltic waves were triggered and enhanced the frequency of peristaltic waves. PACAP-(6-38) (3 microM) was per se without effect on peristalsis but prevented or reversed the peristaltic motor stimulation caused by VIP, when it was given before or after the agonist, respectively. PACAP-(6-38), however, failed to antagonize the properistaltic effect of PACAP. In ileal circular strips treated with tetrodotoxin (1 microM) and indomethacin (3 microM), spontaneous myogenic activity was inhibited by VIP (5-30 nM). This effect was significantly reduced by a pretreatment with PACAP-(6-38) (3 microM). A similar inhibition by PACAP-(1-38) (10-500 nM) was not influenced by the antagonist. It is concluded that PACAP-(6-38) is a VIP receptor antagonist, both in the peristaltic motor pathways and at the level of the circular muscle of the guinea-pig small intestine. The lack of a motor effect of PACAP-(6-38) on its own indicates that VIP acting on PACAP-(6-38)-sensitive receptors (located on neurons and/or the smooth muscle) is unlikely to participate in peristaltic motor regulation.

Animals↗
PubMed1991

[Roles of the sympathetic nervous system in the local release of vasoactive intestinal polypeptide (VIP) from the small intestine of anesthetized dogs].

To investigate roles of the sympathetic nervous system in the local release of VIP, pharmacological alpha (phenoxybenzamine), beta (propranolol) adrenergic blockade or surgical sympathectomy by the ganglionectomy of splanchnic plexus was performed in anesthetized dogs. Portal and venous plasma VIP levels during intrajejunal infusion of 0.1 N HCl solution at a rate 1.5 ml/min for 20 minutes were observed before and after these procedures. The plasma VIP levels during the intrajejunal HCl infusion were significantly increased after blocking of alpha-adrenoceptors and surgical sympathectomy but showed no change after blocking of beta-adrenoceptors. These results suggest the inhibitory mechanism of the sympathetic nervous system on the local release of VIP from the canine small intestine. In addition, the increase of portal blood flow and bile secretion, and the elevation of bicarbonate concentration in the secreted bile during the intrajejunal HCl infusion were significantly higher after surgical sympathectomy than before, and plasma VIP levels were also significantly higher.

Anesthesia↗