Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestine, Small”

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 1,027 records · Page 57Linked to original sources
PubMed1976

Small intestinal transit in diabetics.

Small intestinal transit was assessed in diabetic patients and healthy controls by measuring the breath hydrogen appearance time after the ingestion of lactulose. Transit in diabetics with autonomic neuropathy was significantly slower than in diabetics without neuropathy and controls. Delayed transit is probably due to vagal denervation. These slower transit times would allow bacteria to proliferate, which might explain why some diabetics have diarrhoea. The test cannot be used in patients with bacteria in the small bowel because these may metabolise lactulose and release hydrogen prematurely.

Autonomic Nervous System↗
PubMedDate not supplied

[Congenital diverticulum of the small intestine: Meckel's diverticulum or intestinal duplication?].

A congenital diverticulum of the small intestine is a condition with only a low morbidity and is generally a Meckel's diverticulum. There is, however, another congenital malformation, which can closely resemble a Meckel's diverticulum, but has another etiology, the tubular duplication of the small intestine. The authors point out the embryologic, anatomic and histological findings between these different but very similar malformations. It seems that the diagnosis of duplication is not often considered when finding a diverticulum of the small intestine and such a malformation is too easily called a Meckel's diverticulum.

Adolescent↗
PubMed2000

Recurrent idiopathic perforations of the small intestine.

BACKGROUND/AIMS: Idiopathic perforation of the small intestine is extremely rare. The definition depends on the absence of any detectable pathology that could be responsible for the perforation. This study was undertaken to outline the criteria for determination of the condition. METHODS: Case report and review of the literature. RESULTS: A 50-year-old male patient underwent surgery including laparostomy and planned reexplorations for multiple recurrent small intestinal perforations of unknown origin; the patient made an uneventful recovery. Extensive investigations were carried out to search for any pathology that could explain the occurrence of perforations, but yielded no results. CONCLUSIONS: Further studies will possibly give more information concerning idiopathic perforation of the small intestine, provided that judicious criteria for its determination are applied.

Humans↗
PubMed1993

The motor response to intestinal resection: motor activity in the canine small intestine following distal resection.

BACKGROUND: The mucosal response to intestinal resection has been extensively studied; little is known of the motor response. Our aim was to evaluate motility in the intestinal remnant following distal resection. METHODS: Motor activity, duodenocecal transit, nutrition, and absorption were studied over a 3-month period in control animals (n = 9) and in groups of dogs who had undergone 25% (n = 6), 50% (n = 5), and 75% (n = 5) distal resection. RESULTS: Diarrhea and steatorrhea developed in each resection group, and the 75% group alone developed true short bowel syndrome. Resection did not affect migrating motor complex frequency or periodicity; phase 1 duration was shorter in the 75% group (control vs. 75%: 22 +/- 4 vs. 6 +/- 2 minutes, P < 0.03). The most striking motor effect was the development of prominent cluster activity in the distal part of the remnant in 25% and 50% resection animals and throughout the remaining intestine in the 75% group. Duodenocecal transit slowed during the study period from 13 +/- 1 to 20 +/- 2 minutes in the 50% and from 10 +/- 2 to 14 +/- 2 minutes in the 75% group (P < 0.05). CONCLUSIONS: The initial motor response to major resections of the distal small intestine is dominated by the development of abnormal patterns. This motor disruption may contribute to the symptomatology and clinical features of the short bowel syndrome.

Animals↗
PubMed2006

Modelling slow wave activity in the small intestine.

We have developed an anatomically based model to simulate slow wave activity in the small intestine. Geometric data for the human small intestine were obtained from the Visible Human project. These data were used to create a one-dimensional finite element mesh of the entire small intestine using an iterative fitting procedure. The electrically active components of the intestinal walls were modelled using a modified Fitzhugh-Nagumo cell model embedded within a longitudinal smooth muscle layer and a layer containing Interstitial Cells of Cajal. Within these layers, the monodomain equation was used to describe slow wave propagation. To solve the monodomain equation, a high-resolution finite difference grid, with an average spatial resolution of 0.95 mm, was embedded within each finite element. The resulting simulations of intestinal activity agree with the experimental observation that slow wave frequency gradually declines from 12 cycles per minute (cpm) in the duodenum to 8 cpm at the terminal ileum. Furthermore, the simulations demonstrated a decrease in conduction velocity with distance along the small intestine (10.7 cm/s in the duodenum, 5.1cm/s in the jejunum and 1.4 cm/s in the ileum), matching experimental recordings from the canine small intestine. We conclude that the framework presented here is capable of qualitatively simulating normal slow wave activity in an anatomical model of the small intestine.

Finite Element Analysis↗
PubMed2002

Starving affects CDX gene expression during small intestinal development in the chick.

The small intestine of the chicken undergoes intensive changes in the immediate posthatch period, increasing in size and developing crypts, villi and mature enterocytes. During this time, chicks are also transferring from nutrition based on the lipid-rich yolk to exogenous carbohydrate-rich feeds. The cdx homeobox genes participate in axial patterning and in definition of cell identity in embryos, and some cdx genes remain active postpartum in organs such as the intestine. In this study, the transcription patterns of two of these genes, cdxA and cdxB, were examined in the small intestine of the embryo and posthatch chick; in addition, the effects on these genes of starving for 48 h at hatch were examined. Both cdx transcription factors were upregulated toward the time of hatch and were observed in proliferating enterocytes; this enhanced expression continued posthatch. Distribution of cdxA changed with age and was found at higher concentrations in mature enterocytes. Starving from 0 to 48 h posthatch retarded growth and decreased enterocyte proliferation and expression of cdxA and cdxB. After access to feed, expression of cdx genes was enhanced. Chicken homeobox genes cdxA and cdxB are expressed in all enterocytes during embryonic and posthatch development; however, cdxA may have a role in enterocyte maturation posthatch. CdxB was expressed later in development then previously reported.

Animals↗
PubMed2004

Fetal bovine serum suppresses apoptosis in the small intestine after total ischemia and reperfusion in mice.

BACKGROUND/PURPOSE: Total ischemia/reperfusion (I/R) of the small intestine induces cellular apoptosis. In this study, the authors investigated the effects of fetal bovine serum (FBS) on apoptosis and related proapoptotic and antiapoptotic factors in the I/R-injured small intestine of mice. METHODS: The mice underwent total I/R of the small intestine and were treated with oral gavages of normal saline or FBS for 3 days, concluding with total ischemia of the small intestine. Samples of the I/R-injured small intestine, representing various predefined time-points post-I/R (immediately before and after 1 hour of total ischemia and at 1, 6, and 24 hours after initiation of reperfusion), were subjected to terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining to study the cellular apoptosis, and Western blot analysis to measure expression of p53, bcl-2 and bax, with caspase-activity assay used to determine the activity of caspase 3. RESULTS: For the saline-treated mice, increased cellular apoptosis, suppressed expression of p53 and bcl-2 (with decreased bcl-2 to bax ratio) and increased caspase-3 activity were found for the I/R-injured small intestine. By contrast, FBS treatment suppressed cellular apoptosis, producing up-regulation of p53 and bcl-2 (with increased bcl-2 to bax ratio to 5.4-fold of the saline-treated group) and inhibiting the activity of caspase 3 (P <.05). CONCLUSIONS: The results of our study suggest that I/R-induced apoptosis of the mouse small intestine may be related to p53 and bcl-2 suppression (with decreased bcl-2 to bax ratio) and activation of caspase 3 and that such apoptosis seems to be suppressed by FBS treatment.

Animals↗
PubMed1996

Increasing incidence of adenocarcinomas and carcinoid tumors of the small intestine in adults.

Malignant neoplasms of the small intestine are relatively rare and have received little study. We report on trends in the age-adjusted, sex-, and race-specific incidence rates of adenocarcinomas and carcinoid tumors of the small intestine in the United States from 1973 through 1991. Data were derived from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. There were statistically significant increases in the incidence rates of both adenocarcinomas and carcinoid tumors during the time frame of the study. Rates increased most dramatically in black males, with 2- and 4-fold increases in adenocarcinomas and carcinoid tumors, respectively. The only rates that remained relatively unchanged were those of adenocarcinoma among white females. It remains to be determined if changing environmental factors are important causes of these observed trends. If environmental factors are involved in the etiology of small intestine cancers, analytic studies conducted while the disease is increasing in incidence may provide useful insights.

Adenocarcinoma↗
PubMed1987

Purification and separation of two soluble fucosyltransferase activities of small intestinal mucosa.

1. Rat small intestinal soluble fucosyltransferase is purified more than 2000-fold using chromatographic procedures with DEAE-cellulose, CM-cellulose, GDP-Sepharose and Concanavalin A-Sepharose. 2. Chromatography on Sephadex G15 of the final enzymatic fraction clearly separates two activities: a first peak incorporates fucose on asialoserotransferrin and a second peak on asialofetuin. 3. The use of small saccharidic acceptors (phenylgalactose, lactose, lacto-N-fucopentaose I) and the analysis of fucosylated asialoglycoproteins indicate that the first activity corresponds to an alpha-(3/4)-fucosyltransferase and the second one to an alpha-(1-2)-fucosyltransferase. 4. Protein analysis by polyacrylamide gel electrophoresis in the presence of SDS for each enzyme shows two bands corresponding to a mol. wt of about 65,000 and 70,000. The two enzymes have the same sensitivity to the action of N-ethylmaleimide.

Animals↗
PubMed1994

Rapid reversible substrate regulation of fructose transporter expression in rat small intestine and kidney.

To understand the regulation of fructose transport in the small intestine and kidney, we provided rats with "control" diets (46% glucose as starch) and with diets enriched in fructose, glucose, or sucrose (60% each of simple carbohydrate) and measured the concentration of facilitative glucose transporter isoform (GLUT5) protein and mRNA in these tissues. The fructose-enriched diet resulted in a five- and eightfold increase in GLUT5 protein at 1 and 7 days, respectively, in the small intestine, which declined rapidly with reversion to control diet. No change in GLUT5 protein levels was seen after glucose- or sucrose-enriched diets. Glucose, and to a lesser extent fructose, feeding resulted in an increase in the basolateral GLUT2 protein. Feeding glucose to the rats caused a rise in sodium-dependent glucose transporter isoform (SGLT1) protein levels compared with the control diet. There was a transient increase in the small intestine GLUT5 mRNA 1 day after fructose feeding, which returned to normal by 7 days. In the kidney, both fructose and sucrose increased GLUT5 protein levels three- to fourfold, whereas glucose had no effect. Fructose-enriched diet did not increase the levels of GLUT5 protein or mRNA in a segment of small intestine that was isolated from the rest of the small intestine but continued to have mesenteric blood supply. The results suggest that the levels of GLUT5 protein are regulated by fructose, its in vivo substrate, in both the small intestine and kidney, and the regulation requires fructose to interact with the brush border of the small intestine, possibly stabilizing the protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Expression of cyclo-oxygenase 1 and 2, prostaglandin E synthase and transforming growth factor beta1, and their relationship with vascular endothelial growth factors A and C, in primary adenocarcinoma of the small intestine.

BACKGROUND: Primary adenocarcinomas of the small intestine are rare. The prostaglandin biosynthetic pathway plays a major role in carcinogenesis and is linked with angiogenesis in various tumours. Promotion of tumour growth by transforming growth factor (TGF) beta may be mediated through the prostaglandin pathway. METHODS: Expression of cyclo-oxygenase (COX) 1 and 2, prostaglandin E synthase (PGES), TGF-beta1 and vascular endothelial growth factor (VEGF) A and C genes was analysed in 54 primary adenocarcinomas of the small intestine and corresponding normal intestinal mucosa. All patients had undergone surgical resection without previous antineoplastic therapy. Target gene expression was analysed at the mRNA level by reverse transcriptase-polymerase chain reaction and correlated with clinicopathological parameters as well as survival. COX-2 protein expression was examined by immunohistochemistry. RESULTS: Expression of COX-2 protein was detected immunohistochemically in 98 per cent of the carcinomas. COX-1, COX-2, VEGF-A, VEGF-C, PGES and TGF-beta1 mRNA expression varied markedly in different tumours, but all were overexpressed compared with levels in normal intestinal mucosa. There were significant associations between levels of COX-1, COX-2, TGF-beta1 and PGES mRNAs and those of VEGF-A and VEGF-C. CONCLUSION: Correlations between levels of mRNA for COX-1, COX-2, TGF-beta1 and PGES and those for proangiogenic factors VEGF-A and VEGF-C suggest a role for these factors in the propagation of primary adenocarcinomas of the small intestine.

Adenocarcinoma↗
PubMed1994

Lamina propria macrophages involved in cell death (apoptosis) of enterocytes in the small intestine of rats.

In the rat small intestine, apoptotic enterocytes are exfoliated at the villus tip as a whole cell, in contrast to guinea pig enterocytes which are phagocytosed by macrophages in their cell body and shed off only in their apical cortex. While macrophages gather in the lamina propria of the intestinal villi in both species, their functions seem to differ. Unlike the guinea pig, lamina propria macrophages observed in the rat small intestine did not show morphological signs of phagocytosis, revealing few cellular elements in their phagosomes. At the "shoulder" of the villus, i.e., a certain distance proximal to the villus tip, subepithelial macrophages extended a thick process deep into the epithelium; their branched terminals penetrated the cytoplasm of enterocytes, resulting in the formation of excavated spaces in the cell body. Processes of macrophages frequently reached close to the brush border. At the shoulder of the villus, a few effete cells showed typical apoptotic signs and appeared to be pushed out into the lumen; still, the shedding of apoptotic enterocytes was recognized mainly at the very top of the villus, where no intraepithelial processes of macrophages could be seen. The present findings indicate that in the rat, lamina propria macrophages do not engulf aged enterocytes, but are involved in inducing their apoptosis.

Acid Phosphatase↗