[Chronic severe intestinal obstruction of the small intestine caused by nonspecific inflammation].
Explore the source record for details and available documents.
Aged↗
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.
The effect of low molecular weight dextran on intestinal survival in experimental small intestinal ischemia.
Explore the source record for details and available documents.
Animals↗
The effect of heparin on intestinal survival in experimental small intestinal ischemia.
Explore the source record for details and available documents.
Animals↗
[Effect of Tween 80 (a surface-active agent) on the enzymes of the intestinal mucosa of the small intestine and low absorption indices].
Explore the source record for details and available documents.
Adult↗
[Adaptive changes in intestinal mucosa of the small intestine as a result of intraluminal stress].
Under physiological conditions, the intestinal mucosa is the site of a delicate balance between cell proliferation in the crypt region and cell desquamation at the villus tips. This balance can be deranged by a number of endogenous or exogenous factors, oneof which is the intraluminal contents. This review discusses the effects of different modifications of the luminal milieu on the structure and function of the mucosa. Following intestinal resection or loop transposition, the contents reaching the remnant or the transposed loop differ markedly from those with which they come into contact under normal conditions. Hyperplasia without zonal transformation then develops in the experimental loop. The villi do not become wider, and changes in the strucutre of the epithelium are not observed. There are conflicting resutls in the literature concerning the enzyme activities in the individual enterocytes resulting from this hyperplasia. However, the epithelium its functionally immature, since transport capacities measured in vitro are reduced. On the other hand, the hyperplasia of the mucosa is such that absorptive capacities in vivo, when expressed in terms of intestinal length, are larger than normal. When the intestine is subjected to prolonged infusion of lactic acid, the enterocytes are damaged and increased exfoliation results. A similar result is obtained in the blind-loop syndrome, where the accumulation of bile acids and bacteria provides the stress responsible for the destruction of the enterocytes, and in non-tropical spure, where the epithelium is attacked by noxious peptides in the diet. The first consequence of the accelerated desquamation is epithelial hyperplasia without zonal transformation, though the enterocytes are damaged - in contrast to those of the resected intestine - and apparently possess reduced enzyme activities. If the application of the stress is continued, a stage is reached in which the cell proliferation does not suffice to counteract the cell loss at the villus tips. Then a zonal transformation occurs whereby, despite the lengthened crypts, the villi become shorter and wider until, in extreme cases, the mucosa is completely devoid of villi. The transport capacity in vitro and in vivo - even when expressed in terms of unit-length is reduced, and good correlations exist between the reduction in function and the diminution in surface area of the intestine. In a self-emptying blind loop, the intestine is devoid of all contact with nutritional material. Under these circumstances, hypoplasia of the mucosa develops in which the enterocytes appear unchanged, though in extreme cases they may possess reduced enzyme levels, and the absorption capacity in vivo is consequently reduced.
Adaptation, Physiological↗
Intestinal bile acid absorption. Na(+)-dependent bile acid transport activity in rabbit small intestine correlates with the coexpression of an integral 93-kDa and a peripheral 14-kDa bile acid-binding membrane protein along the duodenum-ileum axis.
The anatomical localization of the Na+/bile acid cotransport system from rabbit small intestine was determined using brush border membrane vesicles prepared from eight different segments of the small intestine. Na(+)-dependent transport activity for bile acids, both for [3H]taurocholate and [3H]cholate, was found in the distal segment 8 only representing the terminal 12% of the small intestine. In contrast, the Na(+)-dependent D-glucose transporter and the H(+)-dependent oligopeptide transporter were found over the whole length of rabbit small intestine in all segments. Photoaffinity labeling with 7,7-azo- and 3,3-azo-derivatives of taurocholate with subsequent fluorographic detection of labeled polypeptides after one- and two-dimensional gel electrophoresis showed that an integral membrane polypeptide of M(r) 87,000 is present in the entire small intestine, whereas an integral membrane protein of M(r) 93,000 together with a peripheral membrane protein of M(r) 14,000 are exclusively expressed in the distal small intestine correlating with Na(+)-dependent bile acid transport activity. Photoaffinity labeling with the cationic bile acid derivative 1-(7,7-azo-3 alpha,12 alpha-dihydroxy-5 beta[3 beta-3H]cholan-24-oyl)-1,2- diaminoethane hydrochloride and 7,7-azo-3 alpha,12 beta-dihydroxy-5 beta[12 alpha-3H]cholan-24-oic acid did not result in a specific labeling of the above mentioned proteins, demonstrating their specificity for physiological bile acids. Photoaffinity labeling of the 93- and 14-kDa bile acid-binding proteins was strongly Na(+)-dependent. Significant labeling of the 93- and 14-kDa proteins occurred only in the presence of Na+ ions with maximal labeling above 100 mM [Na+] showing a parallel [Na+] dependence to transport activity. Inactivation of Na(+)-dependent [3H]taurocholate uptake by treatment of ileal brush border membrane vesicles with 4-nitrobenzo-2-oxa-1,3-diazol chloride led to a parallel decrease in the extent of photoaffinity labeling of both the 93- and 14-kDa protein. Sequence analysis of the membrane-bound 14-kDa bile acid-binding protein surprisingly revealed its identity with gastrotropin, a hydrophobic ligand-binding protein exclusively found in the cytosol from ileocytes and thought to be involved in the intracellular transport of bile acids from the brush border membrane to the basolateral pole of the ileocyte. In conclusion, the present studies suggest that both an integral 93- and a peripheral 14-kDa membrane protein, identified as gastrotropin, and both exclusively expressed in the terminal ileum, are essential components of the Na+/bile acid cotransport system in rabbit terminal ileum.
Affinity Labels↗
On the difference between colonic and small intestinal alkaline phosphatase.
Colonic and small intestinal alkaline phosphatase extracts were studied biochemically and electrophoretically to elucidate the source of a reported difference in cellulose acetate electrophoretic mobility. Both preparations were inactivated with 0.5 mmol/L L-phenylalanine but retained full activity in the presence of 1.0 mmol/L tetramisole. Treatment with neuraminidase changed a minor fraction of the small intestinal but the major portion of the colonic alkaline phosphatase to a cathodically migrating form. The most likely explanation for our findings is that the colon and small intestinal alkaline phosphatase are mixtures of the same multiple forms but in different proportions.
Alkaline Phosphatase↗
Cryptdins: antimicrobial defensins of the murine small intestine.
Paneth cells are specialized small intestine epithelial cells that contain lysozyme, possess phagocytic properties, and secrete cytoplasmic granules into the intestinal crypt lumen after the entry of bacteria. Recent studies by Ouellette and associates (A. J. Ouellette, R. M. Greco, M. James, D. Frederick, J. Naftilan, and J. T. Fallon, J. Cell Biol. 108:1687-1695, 1989) indicated that murine Paneth cells produce prodefensin mRNA, but the properties of its peptide product were not reported. We purified two closely related defensins, cryptdin 1 and cryptdin 2, from a subcellular fraction of murine small intestine cells that was enriched in Paneth cells. Both peptides contained 35 amino acid residues, including the characteristic defensin "signature" of six invariantly conserved cysteines. Cryptdins 1 and 2 were approximately 90 to 95% homologous to each other and to the carboxy-terminal domain of the 93-amino-acid defensin precursor, cryptdin A, described by Ouellette and associates (Ouellette et al., J. Cell Biol. 108:1687-1695, 1989). Both cryptdins exerted bactericidal activity against Listeria monocytogenes EGD and Escherichia coli ML-35p in vitro. Their potency exceeded that of human neutrophil defensin HNP-1 but was considerably lower than that of NP-1, a defensin produced by rabbit neutrophils and alveolar macrophages. Both cryptdins killed mouse-avirulent Salmonella typhimurium 7953S (phoP) much more effectively than its phoP+, mouse-virulent, isogenic counterpart, S. typhimurium 14028S. Our data indicate that mouse intestinal prodefensins are processed into 35-amino-acid mature defensins (cryptdins) with broad-spectrum antimicrobial properties. The production of defensins and lysozyme by Paneth cells may enable them to protect the small intestine from bacterial overgrowth by autochthonous flora and from invasion by potential pathogens that cause infection via the peroral route, such as L. monocytogenes and Salmonella species.
Amino Acid Sequence↗
Distribution of vasoactive intestinal polypeptide and substance P receptors in human colon and small intestine.
Vasoactive intestinal polypeptide (VIP) and substance P are found in neurons in the lamina propria and submucosa and muscularis propria of human small intestine and colon. VIP receptors coupled to adenylate cyclase are present on epithelial, smooth muscle, and mononuclear cells. This study analyzes the distribution of [125I]VIP binding and [125I]substance P in human colon and small intestine using autoradiographic techniques. [125I]VIP binding was present in high density in the mucosal layer of colon and small intestine. [125I]VIP binding was not significantly greater than nonspecific binding in smooth muscle layers or the lymphoid follicles. In contrast, [125I]substance P binding was present in high density over the colonic muscle but was not present over the mucosal layer. In human colon cancer, [125I]VIP grain density over the malignant tissue was only slightly higher than background. These autoradiographic studies of [125I]VIP binding indicate that the highest density of VIP receptors was found in the small intestine and superficial colonic mucosa, whereas the density of substance P receptors was highest over the smooth muscle layers. These findings suggest a mismatch between immunochemical content of the peptide and autoradiographic density of the receptor.
Autoradiography↗
Immunoproliferative small intestinal disease associated with Campylobacter jejuni.
BACKGROUND: Immunoproliferative small intestinal disease (also known as alpha chain disease) is a form of lymphoma that arises in small intestinal mucosa-associated lymphoid tissue (MALT) and is associated with the expression of a monotypic truncated immunoglobulin alpha heavy chain without an associated light chain. Early-stage disease responds to antibiotics, suggesting a bacterial origin. We attempted to identify a causative agent. METHODS: We performed polymerase chain reaction (PCR), DNA sequencing, fluorescence in situ hybridization, and immunohistochemical studies on intestinal-biopsy specimens from a series of patients with immunoproliferative small intestinal disease. RESULTS: Analysis of frozen intestinal tissue obtained from an index patient with immunoproliferative small intestinal disease who had a dramatic response to antibiotics revealed the presence of Campylobacter jejuni. A follow-up retrospective analysis of archival intestinal-biopsy specimens disclosed campylobacter species in four of six additional patients with immunoproliferative small intestinal disease. CONCLUSIONS: These results indicate that campylobacter and immunoproliferative small intestinal disease are associated and that C. jejuni should be added to the growing list of human pathogens responsible for immunoproliferative states.
Anti-Bacterial Agents↗
P-glycoprotein content and mediation of vincristine efflux: correlation with the level of differentiation in luminal epithelium of mouse small intestine.
Luminal epithelium from mouse small intestine was fractionated into four distinct components ranging from the most differentiated (absorptive epithelial cells, fraction I) to the least differentiated (proliferative crypt cells, fraction IV). Immunoblot analysis of these fractions with monoclonal antibodies to P-glycoprotein, C219, and HYB-241, indicated that the amount of P-glycoprotein increased in cells as they progressed in level of differentiation from crypt to the villar surface of the lumen of the small intestine. P-glycoprotein in these normal intestinal cells functioned as a transporter of vincristine, one of a group of cancer chemotherapeutic agents to which cells can develop multidrug resistance. Transport ability was shown by efflux studies with vincristine as substrate. Efflux increased with differentiation and correlated with the increase in the amount of P-glycoprotein. Fraction I cells effluxed vincristine about seven times more rapidly than fraction IV cells. Efflux of vincristine was almost entirely inhibited from fraction I cells after treatment with antibody HYB-241, which recognizes an external epitope of P-glycoprotein. This finding would appear to demonstrate that P-glycoprotein was directly responsible for at least the majority of efflux of vincristine in these cells. The observed Mr of P-glycoprotein in fraction I cells was 140,000 when cells were solubilized with sodium dodecyl sulfate at room temperature before electrophoresis and immunoblot analysis. When solubilized fraction I protein was heated with 2-mercaptoethanol before electrophoresis, P-glycoprotein was seen by immunochemical procedures as an Mr 50,000-55,000 protein. No Mr 170,000 or 180,000 forms of P-glycoprotein (forms that are found in multidrug-resistant cell lines and are stable to heat or sulhydryl agents) were detected in any fraction of these epithelial cells under the conditions used. Functional P-glycoprotein was, therefore, associated with differentiation of luminal epithelium in small intestine, and the P-glycoprotein produced by these cells may be a type not previously described.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Adherence targets of Vibrio parahaemolyticus in human small intestines.
Formalin-fixed human small intestinal mucosa with mucus coating, villi, and lymphoid follicle epithelium at the mucosal surface was used to test the adherence sites of clinically isolated (Kanagawa phenomenon-positive) strains of Vibrio parahaemolyticus. V. parahaemolyticus strains grown on CFA agar (supplemented with 3% NaCl) for ca. 3 h at 37 degrees C possessed various levels of cell-associated hemagglutinins (HAs) which were detected with human or guinea pig erythrocytes. The observed adherence abilities of V. parahaemolyticus strains to human small intestinal mucosa correlated roughly with the HA levels of the strains. Under the test conditions, ileal lymphoid follicle epithelium (especially M cells) provided the best adherence target for V. parahaemolyticus. Adherence to villus absorptive cells or to mucus coating was observed at lower levels. In addition, all 3-h-grown V. parahaemolyticus strains tested produced high levels of HAs as detected with rabbit erythrocytes. The strains were all strikingly motile. In contrast, V. parahaemolyticus strains grown on CFA agar (supplemented with 3% NaCl) for ca. 20 h at 37 degrees C had much lower levels of HAs, adherence abilities, and motility. In contrast to the above observations, piliation of V. parahaemolyticus was more extensive at ca. 20 h of incubation at 37 degrees C than at ca. 3 h of incubation at 37 degrees C. The remarkable ability of V. parahaemolyticus to adhere to lymphoid follicle epithelium was also confirmed by using rabbit small intestinal mucosa.
Animals↗
[Protective and repair processes in the small intestine during radiation exposure].
The small intestine as a complex heterostructural organ possesses morphofunctional defence-regenerative mechanisms. All elements of this mechanism suffer in irradiation of the organ especially at ionizing radiation doses causing the acute intestinal syndrome. Regenerative processes in the small intestine are suppressed not only by ionizing radiation but also by the toxic products of exo- and endogenous origin resulting from irradiation of the body.
Animals↗
Age-related human small intestine methylation: evidence for stem cell niches.
BACKGROUND: The small intestine is constructed of many crypts and villi, and mouse studies suggest that each crypt contains multiple stem cells. Very little is known about human small intestines because mouse fate mapping strategies are impractical in humans. However, it is theoretically possible that stem cell histories are inherently written within their genomes. Genomes appear to record histories (as exemplified by use of molecular clocks), and therefore it may be possible to reconstruct somatic cell dynamics from somatic cell errors. Recent human colon studies suggest that random somatic epigenetic errors record stem cell histories (ancestry and total numbers of divisions). Potentially age-related methylation also occurs in human small intestines, which would allow characterization of their stem cells and comparisons with the colon. METHODS: Methylation patterns in individual crypts from 13 small intestines (17 to 78 years old) were measured by bisulfite sequencing. The methylation patterns were analyzed by a quantitative model to distinguish between immortal or niche stem cell lineages. RESULTS: Age-related methylation was observed in the human small intestines. Crypt methylation patterns were more consistent with stem cell niches than immortal stem cell lineages. Human large and small intestine crypt niches appeared to have similar stem cell dynamics, but relatively less methylation accumulated with age in the small intestines. There were no apparent stem cell differences between the duodenum and ileum, and stem cell survival did not appear to decline with aging. CONCLUSION: Crypt niches containing multiple stem cells appear to maintain human small intestines. Crypt niches appear similar in the colon and small intestine, and the small intestinal stem cell mitotic rate is the same as or perhaps slower than that of the colon. Although further studies are needed, age-related methylation appears to record somatic cell histories, and a somatic epigenetic molecular clock strategy may potentially be applied to other human tissues to reconstruct otherwise occult stem cell histories.
Adolescent↗
Neonatal intestinal perforation caused by congenital defect of the small intestinal musculature: report of one case.
Congenital defect of the small intestinal musculature is a rare cause of neonatal spontaneous intestinal obstruction or perforation. Its etiology and pathogenesis are still controversial. A male infant presented with intestinal obstruction at two days of age and rapidly progressed to perforation and septic shock. He died at seven days of age. Autopsy finding revealed a perforation hole at twenty-five cm proximal to ileocecal valve. Histology examination demonstrates multifocal deficiency of the inner circular muscle layer three cm around the perforation site. The clinical and histological characteristics are reviewed and discussed. We propose that the muscle defect of small intestine, especially ileum, is secondary to ischemic injury rather than an embryological malformation.
Diseases in Twins↗
Luminal bacteria and small-intestinal permeability.
BACKGROUND: The influence of luminal bacteria on small-intestinal permeability has not been fully assessed. This study addressed this issue. METHODS: Thirty-four subjects (mean age 64 years; range 22-95 years) were investigated for possible small-intestinal bacterial overgrowth (SIBO) with culture of a small-intestinal aspirate. A lactulose/mannitol small-intestinal permeability test was performed, small-intestinal histology assessed and serum vitamin B12 concentrations measured in all subjects. Permeability was also assessed in a control group of 34 asymptomatic volunteers. RESULTS: Urinary lactulose/mannitol ratios were significantly increased in subjects with SIBO with colonic-type flora (P < 0.0005), even in the absence of villous atrophy. Urinary lactulose/mannitol ratios were increased in this group due to significantly increased urinary lactulose concentrations (P < 0.0005) rather than reduced urinary mannitol levels, after correcting for inter-subject variations in renal function. Counts of intraepithelial lymphocytes of CD8 phenotype were significantly increased in this group (P = 0.003). Although a significant correlation was found between intraepithelial lymphocyte counts and small-intestinal permeability overall (P < 0.002), these counts were not significantly different in subjects with SIBO with colonic-type flora whose permeability values were < or = > 0.028, the upper limit of normal in asymptomatic controls. Serum vitamin B12 concentrations did not differ significantly between groups (P > 0.5). Ageing did not independently influence small-intestinal permeability (P > 0.5). CONCLUSIONS: Small-intestinal permeability is increased in subjects with SIBO with colonic-type bacteria. This effect is independent of ageing and not mediated by vitamin B12 deficiency. Although counts of intraepithelial lymphocytes of CD8 phenotype are increased in this disorder, it is also unlikely that these cells play an important causative role in this process. Routine light microscopic assessment underestimates the prevalence of small-intestinal functional disturbance in this disorder.
Bacterial Infections↗
Myoelectric activity in the intestine of cows with strangulating obstruction of the distal small intestine.
Myoelectric activity in 2 cows instrumented with permanent electrodes in the ileum, cecum, proximal loop of the ascending colon (PLAC), and spiral colon was analyzed after an obstruction developed in the distal small intestine. Results were compared with patterns from a group of 7 normal cows. Myoelectric activity in the ileum immediately orad to the occlusion was characterized by abolition of the migrating myoelectric complex (MMC) and a constant pattern of strong spike bursts of long duration. Cyclic activity was present in all parts of the large intestine, and propagation of phase III activity was evident from proximal to distal. A slight degree of disorganization in phase III propagation was restricted to the spiral colon. Activity cycles tended to be shorter in the cecum and PLAC of both cows with colic than in normal cows, and the intensity of spiking activity was generally lower. Changes in duration of the MMC in the spiral colon (bovine colonic MMC, bcMMC) were inconsistent, but the intensity of spiking activity tended to be lower in phases I and II of both cows compared to controls. The organization of phase III in several spindles typical of the bovine spiral colon was not disrupted, but phase IV of the bcMMC occurred only infrequently. Organized cyclic activity occurred in the large intestine of both cows despite complete disruption of the small intestinal MMC, indicating the presence of mechanisms able to initiate and regulate coordinated myoelectric patterns in the large intestine independent of the small intestine.
Animals↗
Immunoproliferative small intestinal disease: current concepts.
Immunoproliferative small intestinal disease is a distinctive lymphoproliferative disorder. Among these disorders, it is the only disease associated with a specific and characteristic abnormal protein, and also an identifiable, at least in some patients, early phase with a benign-looking histo-pathologic expression. Whether the disease at this stage is malignant or not is not known. Treatment of this early phase with antibiotics may cause remission in some patients. This observation is significant and raises the question of chemoprevention in lymphomas. In contrast to primary nonimmunoproliferative small intestinal lymphomas, in which the pathology in the intestine is usually focal and involving specific segments of the intestine and leaving the segments between the involved areas free of disease, the pathology in immunoproliferative small intestinal disease is diffuse, with a mucosal cellular infiltrate involving large segments of the intestine and sometimes the entire length of the intestine, thus producing malabsorption. Preliminary recent epidemiological data have shown a decrease in the incidence of this disease in endemic areas, and therefore environmental factors are suspected to play a major role in its pathogenesis. Additional research is indicated not only to understand this specific lymphoproliferative disorder but also to understand lymphomas in general.
Humans↗