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If intestinal leiomyosarcoma is quite a rare tumour, the income of a double localisation: small intestine and 9 years after large bowel seams exceptional. This observation reminds us the case of that young patient.
Botulism is a rare disease with 4 naturally occurring syndromes: foodborne botulism is caused by ingestion of foods contaminated with botulinum toxin, wound botulism is caused by Clostridium botulinum colonization of a wound and in situ toxin production, infant botulism is caused by intestinal colonization and toxin production, and adult intestinal toxemia botulism is an even rarer form of intestinal colonization and toxin production in adults. Inhalational botulism could result from aerosolization of botulinum toxin, and iatrogenic botulism can result from injection of toxin. All forms of botulism produce the same distinct clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care (including mechanical ventilation, when necessary) and timely treatment with antitoxin.
BACKGROUND/AIMS: Colonic epithelium is considered to be relatively tight. The colonic "pore" diameter is 6 A; therefore, colonic epithelium has generally been considered to be impermeable to hydrophilic probes with a cross-sectional diameter of > 6 A. This study examined whether rat colon is permeable to inulin, a large hydrophilic macromolecule having a molecular weight of 5000 g/mol and a cross-sectional diameter of 15 A (hydration diameter, 20 A). METHODS: The colonic permeation of inulin (10 mumol/L) in vivo was investigated by perfusion of rat colonic segments. RESULTS: There was significant colonic permeation of inulin, but tissue retention of inulin was low. The net colonic flux of inulin was strongly dependent on net water flux, showing a strong solvent drag effect. Addition of 16,16-dimethyl prostaglandin E2 decreased water flux with a corresponding decrease in inulin flux; this process seemed to be mediated by 5'-cyclic adenosine monophosphate because both the phosphodiesterase inhibitor aminophylline and dibutyryl adenosine 5'-cyclic adenosine monophosphate decreased water and inulin flux in a parallel manner. Chenodeoxycholic and taurocholic acids decreased net mucosal-to-serosal water flux but increased inulin flux. The net colonic permeation rate of inulin was higher than the small intestinal permeation rate. CONCLUSIONS: Rat colon is permeable to inulin. The higher net colonic permeability may be caused by differences in mucosal surface, permselectivity, solvent drag effect, and differences in net water fluxes of the colon and small intestine.
Factors that stimulate gut mucosal proliferation may be beneficial during periods of gut disuse or atrophy. Recently glucagon-like peptide 2 (GLP-2) has been shown to stimulate small bowel growth. The purpose of our study was to compare the trophic effects of GLP-2 with those of neurotensin (NT), a potent gut trophic factor. Mice were randomized to receive either GLP-2, NT, or saline solution (control) for 10 days. The mice were killed on day 11, at which time the jejunum, ileum, and colon were removed, weighed, and DNA and protein content measured. Mice treated with GLP-2 showed a significant increase in the weight of the jejunum, ileum, and colon compared to both control and NT-treated mice. DNA content, a marker of cellular hyperplasia, was significantly increased in the small bowel and colon by treatment with GLP-2 and NT compared to control tissues. Small intestinal protein content, an indicator of cellular hypertrophy, was significantly increased by GLP-2 compared to both NT and control; protein content of the colon was greater in each of the treatment groups compared with control mice. We have demonstrated, for the first time, that GLP-2 stimulates colonic growth. In addition, GLP-2 is a potent trophic factor of normal small intestine with proliferative effects that are equal to or greater than those of NT. Administration of GLP-2 may be useful clinically to enhance small intestinal regeneration and adaptation during periods of disease and in the early phases of the short bowel syndrome.
Modern rearing conditions may cause stress to pigs. At the cellular level all animals respond to stress by synthesizing heat shock proteins (HSP), which protect cells from injury. The objective of this study was to examine the concentrations of stress-inducible HSP72 in porcine small intestine and colon, known to be stress sensitive tissues, and to compare the findings with HSP72 concentrations in serum and with conventional markers of stress, namely blood lactate and serum cortisol, glucose, free fatty acids and acute phase proteins. HSP72 in the colon correlated with serum HSP72 but there was a negative correlation with carcass weight (growth). The results suggest that the colon may be a significant source of serum HSP72, the concentration of which may reflect changes in the permeability of intestinal epithelium due to stressors, such as transport and handling.
1 The sites of action of 5-hydroxytryptamine (5-HT) were examined in isolated segments of guinea-pig intestine. Mechanical records were taken from the longitudinal muscle of the ileum and proximal colon and from the circular muscle of the ileum and distal colon.2 In order to examine direct actions of 5-HT, nerve-mediated responses were blocked with tetrodotoxin (0.2 mug/ml). There was a gradient in the responsiveness of the longitudinal muscle of the ileum; in the proximal ileum it was usually unresponsive, whereas in the distal ileum about 30% of the amplitude of contraction was caused by a direct effect on the muscle. In the circular muscle from all parts of the ileum, direct effects on the muscle were weak or absent. In the distal colon, the circular muscle was almost always unresponsive to direct effects of 5-HT even when concentrations of 5-HT as great as 100 mug/ml were used. All direct actions of 5-HT on intestinal muscle were blocked by methysergide (1 mug/ml), which itself did not affect nerve-mediated responses.3 Excitatory cholinergic nerves and excitatory and inhibitory nerves which released unidentified substances were all stimulated by 5-HT. The contractions mediated through cholinergic nerves were blocked by hyoscine (0.6 mug/ml).4 Tachyphylaxis to the action of 5-HT occurred both for effects mediated through nerves and for direct effects on the muscle. Responses returned promptly after 5-HT was washed from the organ bath.5 While 5-HT blocked its own action on neural receptors, it did not antagonize the stimulation of nicotinic receptors on cholinergic neurones by 1-1 dimethyl-4-phenylpiperazinium iodide (DMPP). Moreover, pentolinium markedly reduced contractions caused by DMPP without significantly affecting responses to 5-HT. In contrast, (+)-tubocurarine, another nicotinic receptor antagonist, was effective in reducing contractions caused by 5-HT.6 Phenyldiguanide, which has been reported to antagonize the stimulant action of 5-HT on cholinergic neurones in the mouse small intestine, did not cause any significant reduction in the action of 5-HT on cholinergic neurones in the guinea-pig ileum unless a concentration of 1 mg/ml was used. However, contractions elicited by carbachol and DMPP were antagonized to a similar extent by phenyldiguanide at this concentration. Antagonism of the action of 5-HT at neural receptors by bromolysergic acid and by tryptamine was found but it was not specific, these drugs causing comparable decreases in responses to 5-HT, carbachol and DMPP.7 The present results, which show that 5-HT has little or no direct effect on the circular muscle of the ileum and colon, imply that, if 5-HT is a transmitter in enteric reflexes, it must be released from interneurones.
Colon cancer is becoming increasingly common in Asian countries and still remains the second leading cause of cancer death in the United States. Ginger, a natural spice having both antioxidant and antimutagenic property, is known to inhibit chemical carcinogenesis. This study was designed to investigate the chemopreventive efficacy of ginger on the activity of bacterial enzymes in rats induced colon cancer by 1,2-dimethylhydrazine. Twenty milligrams per kilogram body weight of 1,2-dimethylhydrazine was administered subcutaneously once a week for the first 15 weeks and then discontinued. Ginger (50 mg/kg body weight/per day, oral) was given at the initiation and also at the postinitiation stages of carcinogenesis to 1,2-dimethylhydrazine-treated rats. The animals were killed at the end of 30 weeks. The macroscopic findings in the colon and the incidence of tumors were recorded in each group, and the activity of beta-glucuronidase and mucinase was estimated in the tissues and fecal contents of rats. After a total experimental period of 32 weeks (including 2 weeks of acclimatization), tumor incidence was 100% in 1,2-dimethylhydrazine-treated rats. The incidence of cancer as well as the number of tumors in the colon was significantly reduced both in the initiation and postinitiation stages of carcinogenesis on ginger administration. The activities of bacterial enzymes beta-glucuronidase (proximal colon, distal colon, intestines, liver and colon contents) and mucinase (colon and fecal contents) were significantly elevated in 1,2-dimethylhydrazine-treated rats as compared with the control rats. The increase in beta-glucuronidase activity may augment the hydrolysis of glucuronide conjugates, liberating the toxins, while the increase in the mucinase activity may enhance the hydrolysis of the protective mucins in the colon. Ginger administration to 1,2-dimethylhydrazine-treated rats significantly decreased the incidence and number of tumors as well as the activity of beta-glucuronidase and mucinase. Thus, ginger has a chemopreventive and anticarcinogenic effect against 1,2-dimethylhydrazine-induced colon cancer by virtue of its ability to lower the activities of the microbial enzymes beta-glucuronidase and mucinase.
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Bile acid uptake occurs via passive diffusion in all regions of the intestine and via active absorption in the ileum. Determination of the passive permeability coefficient for ionized monomers ((*)P(-)) demonstrated that permeability decreased by a factor of 3.4, 6.8, and 8.1 for the addition of a hydroxyl, glycine, or taurine group, respectively, to the steroid nucleus. Removal of the negative charge increased permeation by a factor of 4.4; however, permeability coefficients for the protonated monomers showed the same relative decrease with addition of a hydroxyl group. The calculated incremental free energies of solution (deltaDeltaF(W-->1)) associated with these additions equaled + 757 (hydroxyl), + 1178 (glycine), and + 1291 (taurine) cal/mole. Passive permeability coefficients for the transverse colon showed the same relative relationships among the various bile acids. After making appropriate corrections for passive permeability across the ileum, apparent values for the maximal transport velocity ((*)V(max)) and Michaelis constant ((*)K(m)) of the active transport system were measured. (*)V(max) depended upon the number of hydroxyl groups on the steroid nucleus; values for the trihydroxy bile acids were high (1543-1906 pmoles/min per cm) while those for the dihydroxy (114-512 pmoles/min per cm) and monohydroxy (45-57 pmoles/min per cm) acids were lower. In contrast, (*)K(m) values were related to whether the bile acid was conjugated; unconjugated bile acids had values ranging from 0.37 to 0.49 mM, while values for the conjugated bile acids were approximately half as high (0.12-0.23 mM).
Poultry are considered to be the primary reservoirs of Campylobacter jejuni for humans. Campylobacter jejuni can colonize the poultry intestinal tract and its subsequent shedding can result in environmental contamination, resulting in an increased risk of infection for the rest of the flock. At present, there is no information on the daily shedding pattern of C. jejuni in broiler chickens. Thus, the purpose of this study was to determine the daily shedding pattern of C. jejuni in broiler chickens and to correlate intestinal colonization with fecal shedding, which would aid in the development of intervention strategies such as the use of competitive exclusion products at 1 day of age. Twenty-four broiler chicks were orally inoculated with 1.6 x 10(7) colony-forming units of C. jejuni, and the reisolation rate of the organism was determined daily from day 1 to day 43. Fifty percent and 70% of the chicks were shedding C. jejuni within 24 and 48 hr postinoculation, respectively. The group collectively reached a peak excretion on days 13-19 postinoculation. There was a steady decline in fecal shedding after the third week. By market age, on day 43, only 37.5% (9/24) of the birds were shedding C. jejuni in their feces. Throughout the sampling period from days 1 to 43, a cyclic pattern of shedding was observed in individual birds. Individual birds excreted C. jejuni on an average of 25 out of 43 days. The C. jejuni isolate failed to colonize 16.6% (4/24) of the birds. A small percentage of the birds, 12.5% (3/24), were observed to be chronic shedders. Enumeration of C. jejuni in the crop, jejunum, and cecum on day 43 revealed that the cecum was the major colonization site, and 15 out of the 24 birds carried C. jejuni in their intestinal tract.
BACKGROUND: Subsets of myenteric neurons have been identified. To determine the proportional representation of neurons in each, it is necessary to relate the number of neurons in the subset to that of the complete set. Prior estimates of total numbers of neurons, obtained with many different markers, have varied widely. METHODS: Markers were compared for counting myenteric neurons in dissected laminar preparations of guinea pig duodenum, jejunum-ileum, and colon; the effect of stretching preparations on these counts was also determined. Markers included the visualization of single-stranded nucleic acid with cuprolinic blue and the immunocytochemical demonstration of neuron specific enolase (NSE), PGP9.5, S-100, and the constitutive expression of a Fos related antigen (FRA). RESULTS: Neurons could not be counted accurately by demonstrating NSE, PGP9.5, or S-100. The number of neurons detected by demonstrating FRA was consistently less than that determined with cuprolinic blue (approximately 65%). Cuprolinic blue-derived estimates of neuron numbers were higher than most reported in the literature, but comparable to those recently obtained with "a nerve cell body" antiserum. Ganglionic area was found to be stretch independent. The rank order of neurons/cm2 and ganglionic area/ unit resting length was colon > duodenum >> jejunum-ileum; more neurons were found in the myenteric plexus of the colon (7.3 x 10(6)) than in that of the entire small intestine (6.5 x 10(6)). CONCLUSIONS: Prior studies that have obtained denominators for estimating the proportions of myenteric neuronal subsets with markers that do not reveal the entire population should be re-evaluated. The guinea pig colon contains a surprisingly large number of neurons, the physiological significance of which must be determined.
The motor responses of the jejunum and colon to stimulation of alpha 2-adrenoceptors by medetomidine and clonidine were investigated in four dogs. In fasting dogs, medetomidine, at a dose rate of 30 micrograms/kg i.v., disrupted the migrating myoelectric complex (MMC) pattern of the small intestine for about 2 h. Similar, but shorter-lasting effects were also induced by clonidine (30 micrograms/kg i.v.) on the jejunum. The administration of alpha 2-agonists inhibited colonic motility in fasting dogs, although medetomidine-induced inhibition was preceded by a short period of increased muscle tone. All these effects were reversed by the alpha 2-antagonists atipamezole (0.15 mg/kg i.v.) and yohimbine (0.20 mg/kg i.v.). In fed dogs, medetomidine (30 micrograms/kg i.v.) induced a strong increase of the tone on the proximal colon, while the activity of the medium and distal colon was completely suppressed. Yohimbine (0.50 mg/kg i.v.) immediately restored the activity of the colon and induced a propagated giant contraction and defaecation by the animal. These data confirm the importance of alpha 2-adrenergic receptors in the control of intestinal and colonic motility in the dog.
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There is controversy regarding the presence of colonic mucosal abnormalities or mucosal invasion by Entamoeba histolytica in patients with "nondysenteric intestinal amebiasis." To determine the role of E. histolytica in causing symptoms and mucosal changes and to detect if mucosal invasion by E. histolytica is present in nondynsenteric intestinal amebiasis, we evaluated 24 E. histolytica-infected patients (stool microscopy positive for E. histolytica) and 12 noninfected controls who presented with chronic gastrointestinal symptoms, but without dysentery, to a clinic in Calcutta. The colonic mucosa was evaluated at colonoscopy, and mucosal biopsies obtained from the cecum, sigmoid colon, and rectum were evaluated by light microscopy, indirect immunofluorescence microscopy, and scanning electron microscopy. At colonoscopy mucosal ulcerations were absent in all the controls and all except one of the E. histolytica-infected patients. E. histolytica trophozoites or cysts were not seen in the lamina propria or on the luminal surface in any infected patient by light and immunofluorescence microscopy. On scanning electron microscopy, structures that resembled rounded E. histolytica trophozoites were seen on the luminal surface in two of 19 cecal specimens from the infected patients. Moderate or severe mucosal inflammation was frequent on light microscopy in both the E. histolytica-infected patients and the noninfected controls with the cecum involved in two thirds of both groups. Antibodies to E. histolytica were detected in serum of 25% of study patients and 58% of controls. Mucosal inflammation did not correlate with stool positivity for E. histolytica or seropositivity for ameba antibody.(ABSTRACT TRUNCATED AT 250 WORDS)