[A case of gastrointestinal situs inversus with mesenterium commune, dextrocardia, colonic diverticulosis and intestinal cancer].
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Abnormalities, Multiple↗
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Intestinal Oxalobacter formigenes colonization in calcium oxalate stone formers and its relation to urinary oxalate.
BACKGROUND AND PURPOSE: Oxalobacter formigenes is an anaerobic commensal colonic bacterium capable of degrading oxalate through the enzyme oxalyl-CoA decarboxylase. It has been theorized that individuals who lack this bacterium have higher intestinal oxalate absorption, leading to a higher urinary oxalate concentration and an increased risk of calcium oxalate urolithiasis. We performed a prospective, controlled study to evaluate O. formigenes colonization in calcium oxalate stone formers and to correlate colonization with urinary oxalate and other standard urinary stone risk factors. PATIENTS AND METHODS: Thirty-five first-time calcium oxalate stone formers were compared with 10 control subjects having no history of urolithiasis and a normal renal ultrasound scan. All subjects underwent standard metabolic testing by submitting serum and 24-hour urine specimens. In addition, all subjects submitted stool samples for culture and detection of O. formigenes by Xentr(ix) O. formigenes Monitor. RESULTS: Intestinal Oxalobacter was detected in only 26% of the stone formers compared with 60% of the controls (p < 0.05). Overall, the average urinary oxalate excretion by the two groups was similar (38.6 mg/day v 40.8 mg/day). Among stone formers, however, there were statistically higher urinary oxalate concentrations in O. formigenes-negative patients compared with those testing positive (41.7 mg/day v 29.4 mg/day) (p = 0.03). Furthermore, all 10 stone formers with hyperoxaluria (>44 mg/day) tested negative for O. formigenes (p < 0.05). CONCLUSIONS: Calcium oxalate stone formers have a low rate of colonization with O. formigenes. Among stone formers, absence of intestinal Oxalobacter correlates with higher urinary oxalate concentration and an increased risk of hyperoxaluria. Introduction of the Oxalobacter bacterium or an analog of its enzyme oxalyl-CoA decarboxylase into the intestinal tract may be a treatment for calcium oxalate stone disease.
Adult↗
[Intestinal preparation for colon enema with fleet sodium phosphate: comparative study with the conventional method].
PURPOSE: To evaluate the possible optimization of a well-tolerated and versatile method of intestinal preparation able to adequately free the lumen and consequently improve diagnostic results with a lower risk of prolonged hospital stay for incorrectly prepared patients. MATERIAL AND METHODS: We examined 40 patients, namely 20 men (mean age 70 years, range 52-87) and 20 women (mean age 68 years, range 49-81) referred to the Institute of Radiology of the Università Cattolica del Sacro Cuore, Gastrointestinal tract Unit, to undergo double contrast colonic enema. The patients were divided into two groups by one-to-one randomization: group 1 was prepared with the conventional method and group 2 with the new protocol for intestinal preparation. On the two days before the examination a low-residue diet was administered; the day before the examination a phial of Fosfo-soda fleet was administered in two times (at 8 am and 4.30 pm), which was diluted with half a glass of water. Bread, pasta and vegetables were strictly forbidden at lunch and soup or milk at supper; the patients were fasted on the examination day. Two evaluations were performed: one to assess tolerance to the preparation and the other, a radiographic study, to assess the grade of intestinal preparation, the presence of secretions/bubbles, and the degree of painting. RESULTS: Of the 20 patients given X-prep, 3 had to discontinue it and 4 exhibited severe side-effects, but completed the treatment; tolerance was satisfactory in the remaining 13 patients. The grade of intestinal preparation, the presence of secretions/bubbles, and the degree of painting were considered satisfactory in 9, 17 and 16 patients respectively. None of the patients given Fosfo-soda fleet had to discontinue it and tolerance was satisfactory in 19 patients. The grade of intestinal preparation, the presence of secretions/bubbles, and the degree of painting were considered satisfactory in 15, 18 and 18 patients respectively. The statistical analysis of all data was performed with Wilcoxon test. DISCUSSION: Intestinal preparation with Fosfo-soda fleet appeared to be definitely better than the conventional method relative to tolerance (p = .02, a statistically significant difference), while providing similarly satisfactory data relative to the other parameters. CONCLUSIONS: Our results, coupled with the versatility of Fosfo-soda fleet (possible application in colonoscopy) and its ease of use recommend this preparation not only for inpatients but also for outpatients in whom self-administration is feasible.
Aged↗
5-(N,N-Dimethyl)-amiloride to discriminate the Unidirectional electrolyte transports in rat small intestine and proximal colon in vivo.
The effect of dimethyl-amiloride (DMA), a selective Na+/H+ exchange blocker, was studied on electrolyte net fluxes and unidirectional fluxes of Na and Cl at four levels of rat intestine in vivo in basal conditions. DMA was applied intraluminally at concentrations of 10(-4) and 10(-3) M in the model of ligated loops prepared from duodenum, proximal jejunum, distal ileum and ascending colon in fasted Sprague Dawley rats. Two iso-osmotic test solutions were used: (1) hypo-ionic: Na+ 80 mM and (2) iso-ionic: Na+ 148 mM, pH 8.2. 22Na was placed in the loop and 36Cl was given by intravenous route at the beginning of the experiment. Na+/H+ was calculated by two different means, one was based on pH variation following amiloride inhibition of Na influx, the other on the calculation of the passive Na transport. The quantitative evaluation shows that Na/H exchange largely contributes to the electroneutral absorption and luminal pH regulation. The exchanger activity decreases from duodenum, jejunum, ileum and colon where it is completed by K/H exchange to assure low colon luminal pH.
Amiloride↗
Small intestinal malabsorption and colonic fermentation of resistant starch and resistant peptides to short-chain fatty acids.
Some starch and protein, as well as fiber, remains unabsorbed in the small intestine and is degraded by anaerobic bacteria to short-chain fatty acids, hydrogen, methane, and carbon dioxide in the large intestine. The production of butyrate from starch has received the most attention, because butyrate seems to possess several important functions in the large bowel, including antineoplastic properties. In 16.6% fecal homogenates, starch polysaccharides, whether digestible or resistant to in vitro hydrolysis by amylase, pectin, and glucose, were all completely degraded to equal amounts of short-chain fatty acids (mean 60 wt/wt%; range 49-67 wt/wt%). However, starch that was resistant to hydrolysis by amylase was much more slowly fermented with the production of proportionally less butyrate and propionate than digestible starch (butyrate, 15 and 33%, respectively; propionate, 3 and 20%, respectively). The daily intake of 35 g resistant starch (100 g amylomaize starch) by 7 ileostomy subjects increased ileal dry-matter effluent by 38 +/- 2 g/day, due exclusively to increased excretion of carbohydrates of nonfiber origin (starch-polysaccharides and oligo- and monosaccharides) from 14 +/- 1 to 51 +/- 2 g/day, with no change in excreted nonstarch polysaccharides, nitrogen, and ileal volume. The ileal excreted resistant starch increased the formation of total short-chain fatty acids by 50% in fecal homogenates incubated with ileal dry matter from the amylomaize starch period, with comparatively little effect on the ratio of produced butyrate.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effects of p53 mutations on apoptosis in mouse intestinal and human colonic adenomas.
We have examined the effects of inactivation of the p53 tumor suppressor gene on the incidence of apoptotic cell death in two stages of the adenoma-to-carcinoma progression in the intestine: in early adenomas where p53 mutations are rare and in highly dysplastic adenomas where loss of p53 occurs frequently. Homozygosity for an inactivating germ-line mutation of p53 had no effect on the incidence or the rate of progression of ApcMin/+-induced adenomas in mice and also did not affect the frequency of apoptosis in the cells of these adenomas. To examine the effect of p53 loss on apoptosis in late-stage adenomas, we compared the incidence of apoptotic cell death before and after the appearance of highly dysplastic cells in human colonic adenomas. The appearance of highly dysplastic cells, which usually coincides during colon tumor progression with loss of heterozygosity at the p53 locus, did not correlate with a reduction in the incidence of apoptosis. These studies suggest that p53 is only one of the genes that determine the incidence of apoptotic in colon carcinomas and that wild-type p53 retards the progression of many benign colonic adenoma to malignant carcinomas by mechanism(s) other than the promotion of apoptosis.
Adenoma↗
Use of beta-lactamase-producing anaerobes to prevent ceftriaxone from degrading intestinal resistance to colonization.
Six adult volunteers were given 1 g/d of intravenous ceftriaxone for 5 d (consecutive). Ceftriaxone and beta-lactamase activities were assayed in fecal samples obtained before and during drug administration, and anaerobic bacteria, Enterobacteriaceae, and fungi were counted. In two volunteers, no fecal beta-lactamase activity was detected, but ceftriaxone was present during treatment at concentrations of 1.8-2.0 mg/g of feces. Concomitantly, fecal counts of anaerobes in these volunteers dropped from 10.5 to less than 8 log10 colony-forming units (cfu)/g of feces, and those of Candida species increased more than 100-fold. However, in the feces of the four other volunteers, beta-lactamase activity was high during ceftriaxone administration, but no ceftriaxone was detected. In these volunteers, ceftriaxone administration was not followed by any significant change in counts of anaerobes or Candida species. This appeared to be due to the intraintestinal hydrolysis of ceftriaxone by resident beta-lactamase-producing anaerobes. In gnotobiotic mice associated with a human fecal flora containing no beta-lactamase-producing anaerobes, it was possible to prevent the deleterious effects of ceftriaxone on intestinal microbial composition and on colonization resistance (against a strain of Candida albicans and one of ceftriaxone-resistant Enterobacter cloacae) by feeding the animals with an association of four beta-lactamase-producing anaerobic strains.
Adult↗
[Intestinal neuronal dysplasia in adults as a cause of chronic constipation: morphometric characterization of colon innervation].
Intestinal neuronal dysplasia (IND) was initially described as a developmental abnormality of the submucous plexus in children. In recent years this abnormality has also been observed in adults with chronic constipation. The aim of this study was a morphometric characterization of this disease. The investigation was performed with 10 adults with IND, compared with 10 healthy control probands. The best diagnostic indicator of IND proved to be the detection of 6-10 giant ganglia with more than 7 nerve cells in 15 biopsy sections. IND is an interesting cause of chronic constipation which can be histologically verified.
Adult↗
Voltage-clamp experiments reveal receptor type-dependent modulation of chloride secretion in the guinea pig colonic mucosa by intestinal opioids.
The influence of four opioid antagonists on short circuit current (Isc), transepithelial potential difference (Pdo) and tissue conductance (Gt) in the guinea pig colonic mucosa was investigated in vitro under both basal and PGE1 plus theophylline-stimulated conditions. The experiments aimed at identifying the opioid receptor type(s) endogenously activated to control chloride secretion. Under blockade of sodium-dependent Isc by amiloride (100 mumol/l), net anion secretion was regarded to equal the lumen-negative shift in Isc upon addition of 1 mumol/l PGE1 plus 100 mumol/l theophylline. It was significantly elevated by 100 nmol/l of the kappa-selective antagonist nor-binaltorphimine (nor-BNI). This augmenting effect was totally abolished in amiloride-free buffer or by omission of chloride. 1 mumol/l TTX completely prevented the effect of both PGE1 plus theophylline and nor-BNI. Both the kappa agonist U 69593 (10 nmol/l) and the calcium channel agonist Bay K 8644 (1 mumol/l) significantly depressed net anion secretion stimulated by PGE1 plus theophylline. Nor-BNI at 10 nmol/l prevented the suppressive effect of both Bay K 8644 and U 69593. This suggests release of endogenous opioids by the calcium channel agonist Bay K 8644 and competition between the kappa agonist U 69593 and the kappa antagonist nor-BNI. In contrast to the kappa antagonist nor-BNI, the mu antagonist CTOP-NH2 at 100 nmol/l significantly impaired, while the mu-selective agonist DAGO at 0.2 nmol/l augmented, net anion secretion stimulated by PGE1 plus theophylline. The effect of CTOP-NH2 was abolished in chloride-free buffer.(ABSTRACT TRUNCATED AT 250 WORDS)
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Colonic and small intestinal response to intravenous prostaglandin F2 alpha and E2 in man.
The effects of intravenous infusions of prostaglandins (PGs) F2 alpha(0-4 or 0-8 mug kg-1 min-1) or E2 (0-08 or 0-1 mug kg-1 min equals1) on net colonic movement of water and electrolytes and on ileal flow were measured in eight healthy males by simultaneous ileal and colonic perfusion. Ileal flow was increased by PGF2 alpha (six subjects) from a mean of 1-69 ml min-1 to 4-63 ml min-1 (P smaller than 0-01); it also increased in the two subjects given PGE2. Colonic absorptive function was not significantly diminished by either prostaglandin. These results suggest that diarrhoea due to prostaglandins originates in the small intestine.
Adult↗
Histochemical changes in the digestive tract in irradiated rats.
Wistar rats (110-125 g) were irradiated with a single dose of 500 R. Histochemical studies were done concerning the glycoproteins (GP) of sublingual glands, gastric, small intestine and colon mucosa, and some intestinal enzymes: acid and alkaline phosphatase (ACP, ALP) leucineaminopeptidase (LAP), Mg-dependent ATP-ase, NADH-diaphorase, lactic dehydrogenase (LDH). After irradiation all these reactions were diminished, with a maximal effect between 3-5 days. This impairment is in accord with the maximal lethality in this interval after such a degree of irradiation that produced the gastrointestinal syndrome. Cocarboxylase, a radioprotector, improved these changes regarding the structures of the small intestine and also the GP of sublingual glands, stomach, small intestine and colon, demonstrating there its efficiency.
Animals↗
[The voice of laryngectomized patients after receiving colonic or other intestinal transplant].
This study reports the experience of our Rehabilitation Centre for laryngectomees un Albi regarding the acquisition of an esophageal voice in cases of circular total pharyngolaryngectomy, with restoration of continuity through intestinal or colic transplantation. Among eight rehabilitated patients, we obtained six good results with a voice allowing a conversation easily understood by relatives and friends. Thus, we think this continuity restoration method gives good phoniatric results.
Colectomy↗
Adrenergic and cholinergic contributions to decreased gastric emptying, small intestinal transit, and colonic transit in the postoperative ileus rat.
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Animals↗
Age-dependent effect of secretagogues during colonic maturation.
Intestinal secretory response is altered during colonic development. The aim of this report was to study the developmental changes of the Ca(2+)- and cAMP-induced regulatory pathways with special attention to the direct and indirect effect of secretagogues on the colonic epithelium. We investigated the effect of bethanechol, 5-hydroxytryptamine (5-HT), and histamine on Cl(-) secretion and stimulation of intracellular Ca(2+) ([Ca(2+)](i)) and cAMP in the distal colon of suckling, weanling and adult rats. In the presence of tetrodotoxin, immature colon of suckling and weanling rats displayed higher potency (EC(50)) of 5-HT to stimulate Cl(-) secretion, whereas the potency of histamine was not changed during development. The potency of bethanechol was reduced during weaning and partially restored in adulthood. 5-HT increased cAMP level similarly in both neonatal and adult colonic crypts, but the adults had higher basal level of cAMP than suckling rats. Also the effect of bethanechol on [Ca(2+)](i) was independent of colonic maturation. The results suggest that colonic Cl(-) secretion displays developmental changes of regulation depending on the non-neural secretagogue-signalling pathway and that these developmental changes seem to be localized somewhere outside colonocytes.
Age Factors↗
Isolation of nonchemotactic mutants of Campylobacter jejuni and their colonization of the mouse intestinal tract.
Three nonchemotactic mutants (D54, Y14, and N74) of Campylobacter jejuni were isolated from wild-type strain FUM158432 by either the negative swarming or liquid gradient method with brucella broth as the attractive substance. Strains D54 and Y14 were isolated after mutagenesis with methyl methanesulfonate, and N74 was isolated from a nonmutagenized culture. These mutants all failed to swarm on a semisolid medium and did not show any chemotactic behavior in the hard-agar plus assay method for any of the chemicals which act as attractants for the wild-type strain. They had intact flagella and were actively motile. Swimming behavior examined by a video tracking technique showed that the mutants swim only straight, without any tumbling. When suckling mice were challenged orally with approximately 10(5) CFU of these mutant strains, all of the mutants were cleared from the intestinal tract by 48 h. In contrast, the wild-type strain colonized the intestinal tracts of all mice challenged with 10(2) CFU. We concluded that chemotactic movement is important for colonization of the intestinal tract of suckling mice by C. jejuni.
Animals↗
TGF-beta1 gene transfer to the mouse colon leads to intestinal fibrosis.
Crohn's disease (CD) is a chronic, relapsing inflammatory bowel disease, characterized by transmural inflammation. In CD, the recurrent inflammatory injury and tissue repair that occurs in the intestine can progress uncontrollably, leading to the proliferation of mesenchymal cells as well as fibrosis, characterized by excessive extracellular matrix deposition. These processes thicken the bowel wall, reducing flexibility, and often culminate in obstructive strictures. Because no effective measures are currently available to specifically treat or prevent intestinal stricturing, we sought to gain a better understanding of its pathogenesis by developing a mouse model of intestinal fibrosis. Because transforming growth factor (TGF)-beta1 can mediate both fibrosis and mesenchymal cell proliferation; we studied the effects of delivering adenoviral vectors encoding spontaneously active TGF-beta1 into the colons of mice. We first demonstrated that enema delivery of marker adenoviral vectors led to the transfection of the colonic epithelium and transient transgene expression. Histologically, control vectors caused an acute inflammatory response, involving the recruitment of neutrophils and mononuclear cells into the colonic lamina propria; however, infection caused little if any fibrosis. In contrast, the TGF-beta1 vector caused a more severe and prolonged inflammatory response as well as localized collagen deposition, leading to severe and progressive fibrosis. This was accompanied by the emergence of cells with a myofibroblast phenotype. Ultimately the fibrosis resulted in many of the TGF-beta1-transfected mice developing profound colonic obstruction. Through adenoviral gene transfer technology, we describe a novel mouse model of colitis and implicate TGF-beta1 in the pathogenesis of obstructive intestinal fibrosis.
Adenoviridae↗
Effect of high-risk diets for colon carcinogenesis on intestinal mucosal and bacterial beta-glucuronidase activity in F344 rats.
The effect of high-protein (beef or soybean protein) and high-fat (beef fat, corn oil, or lard) diets on large intestinal bacterial and intestinal mucosal beta-glucuronidase was studied in female F344 rats maintained on these diets for two generations. Animals fed a 20% corn oil or 20% lard and 20% casein diet had a higher beta-glucuronidase activity in the contents of cecum and colon than did rats fed a 5% corn oil or lard and 20% casein diet. The cecal bacterial beta-glucuronidase activity was higher in animals fed diets with high levels of beef protein (40%) and beef fat (23%) or with high levels of soybean protein (39%) and corn oil (24%) than it was in rats fed diets containing 18.5% beef protein and 6.5% beef fat or 19% soybean protein and 5.4% corn oil. Animals fed diets containing high levels of beef protein and fat or high levels of soybean protein and corn oil had a higher small intestinal mucosal beta-glucuronidase activity than did the other groups. No significant difference was observed in the colonic mucosal beta-glucuronidase activity among the animals fed beef and soybean diets. It is concluded that diets high in fat and high or normal in protein are associated with elevated levels of bacterial beta-glucuronidase activity in the large intestine of rats.
Animals↗
[Injuries of the large intestine resulting from colonic contrast media administration].
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Aged↗