[Massive venous infarct of colon & small intestine caused by complete thrombosis of upper & lower mesenteric venous arbor during recurrent venous thromboses].
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High levels of dietary fat caused a significant reduction in HMG CoA reductase activity in the liver of germ-free rats whereas significantly elevated small intestinal enzyme activity was observed. Dietary fat had no significant effect on HMG CoA reductase activity in any tissue studied in the conventional rat. No significant change in colonic HMG CoA reductase activity was observed between any of the experimental groups. Rats fed a high-fat diet tended to exhibit higher cytochrome P450 levels in all tissues studied, regardless of the presence of intestinal microflora.
Colon cancer is a leading cause of cancer death and its prevention is of great interest throughout the world. This study was conducted to examine the efficacy of different doses of dietary caraway (Carum carvi L.) on tissue lipid peroxidation (LPO) and antioxidant profile in rat colon carcinogenesis. Wistar male rats were divided into 6 groups and were fed a modified pellet diet for the whole of 30 weeks. To induce colon cancer, rats were given a weekly subcutaneous injection of 1,2-dimethylhydrazine (DMH) at a dose of 20 mg kg(-1) (based on body weight) for the first 15 weeks. Caraway was supplemented every day orally at doses of 30, 60 and 90 mg kg(-1) for different groups of rats for the total period of 30 weeks. All rats were sacrificed at the end of 30 weeks, the colons were examined visually for masses and were subsequently evaluated histologically. The results showed diminished levels of intestinal, colonic and caecal LPO products, such as conjugated dienes (CD), lipid hydroperoxides (LOOH) and thiobarbituric acid reactive substances (TBARS) and also the antioxidants superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione reductase (GR) in DMH treated rats, which were significantly reversed (P<0.05) on caraway supplementation. Moreover, enhanced activity of intestinal, colonic and caecal glutathione peroxidase (GPx), glutathione S-transferase (GST) and colonic ascorbic acid and alpha-tocopherol levels were observed in carcinogen-treated rats, which were significantly (P<0.05) reduced on caraway supplementation. Thus, our study showed that caraway supplementation at a dose of 60 mg kg(-1) had a modulatory role on tissue LPO, antioxidant profile and prevented DMH-induced histopathological lesions in colon cancer rats.
Vasoactive intestinal polypeptide (VIP) is a 28 amino acid peptide which is localised in both the central and peripheral nervous system. In the human colon VIP is found in all layers and the highest concentrations have been found in the myenteric plexus. It is known that VIP has various effects on intestinal functions: i) it is a potent stimulant of mucosal water and electrolyte secretion; ii) it is involved in the peristaltic reflex; and iii) plays an inhibitory role on immune cell function. Based on these biological effects it has been hypothesized that the intestinal mucosal immune system and inflammation may be influenced by alterations in the tissue concentrations of VIP. Some authors have demonstrated no changes in the VIP colonic content of patients with ulcerative colitis, whereas others have demonstrated a reduction. Our results, using specific radioimmunoassay, showed that there is a significant decrease of VIP in both rectal and colonic mucosa of patients with ulcerative colitis as compared to controls. The VIP decrease is selective since substance P and calcitonin gene-related peptide were unchanged in the mucosal tissue of ulcerative colitis patients and furthermore the VIP alteration is correlated to the degree of mucosal inflammation. These findings suggest that the reduction of VIP mucosal content, even if it represents a non-specific event, could influence local inflammatory response and the activity of the disease.
Barium examinations of the large and small bowel were analyzed in six of seven patients who had adenocarcinoma in areas of the intestine affected with Crohn disease; radiographic changes were correlated with clinical, surgical, and pathologic findings. Radiographic examinations were available in five of these patients at the time of diagnosis of tumor. Two of the five patients demonstrated classic radiographic changes associated with carcinoma. In the other three cases, the radiographic changes were atypical for carcinoma and demonstrated progression of disease over time to include more portions of the bowel and presence of fistulas, strictures, and obstruction. The most frequent clinical presentation of adenocarcinoma in these patients was a recrudescence of symptoms after a long quiescent period. In patients with long-standing Crohn disease plus these clinical features and the above radiographic findings, the diagnosis of a coexisting carcinoma should be considered.
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Hepatocyte nuclear factor-4alpha (HNF4alpha) exists in multiple isoforms that are generated by alternative promoter (P1 and P2) usage and splicing. Here we establish monoclonal antibodies (mAbs) for detecting P1 and P2 promoter-driven HNF4alpha, and evaluate their expression in normal adult human tissues and surgically resected carcinomas of different origins. Using immunohistochemical analysis, we demonstrate that, while P1 promoter-driven HNF4alpha is expressed in hepatocytes, small intestine, colon, kidney and epididymis, P2 promoter-driven HNF4alpha is expressed in bile duct, pancreas, stomach, small intestine, colon and epididymis. Altered expression patterns of P1 and P2 promoter-driven HNF4alpha were observed in gastric, hepatocellular and colorectal carcinomas. HNF4alpha was expressed in lung metastases from renal cell, hepatocellular and colorectal carcinoma but was not observed in lung tumours. The P1 and P2 promoter-driven HNF4alpha expression pattern of tumour metastases correlated with the primary site of origin. P1 promoter-driven HNF4alpha was also found in intestinal metaplasia of the stomach. These data provide evidence for the tissue distribution of P1 and P2 promoter-driven HNF4alpha at the protein level and suggest that HNF4alpha may be a novel diagnostic marker for metastases of unknown primary. We propose that the dysregulation of alternative promoter usage of HNF4alpha is associated with the pathogenesis of certain cancers.
Vasoactive intestinal peptide is a neuropeptide with potent modulatory activity on intestinal immunity and may be implicated in the pathogenesis of inflammatory bowel disease (IBD). Previous studies have reported abnormal morphology of vasoactive intestinal peptide-stained enteric nerves, in addition to increased, normal or decreased levels of extractable peptide in Crohn's disease (CD) and ulcerative colitis (UC) tissues. These observations have not been correlated with the amount of enteric nerve fibers or the degree of mucosal inflammation. The investigation was intended to determine whether abnormalities of vasoactive intestinal peptide in IBD are related to quantitative changes of enteric nerve fibers or mucosal inflammation, and whether they are specific for CD or UC. To do this, digitized morphometric analysis was applied to a large number of IBD and control colonic surgical specimens that were immunostained for vasoactive intestinal peptide and S100 protein and scored for severity of inflammation. The results showed that, as compared with controls, there is a marked decrease of vasoactive intestinal peptide-immunoreactive nerve fibers in the lamina propria and submucosa (P less than 0.0001), and of S100-immunoreactive nerve fibers in the lamina propria (P less than 0.0001) of patients with IBD. In the lamina propria but not the submucosa, the variation of decrease is significantly associated with the severity (P less than 0.0001) but not the type (P greater than 0.9) of IBD because it is detected in both CD and UC. We conclude that in IBD there is loss of mucosal neuropeptidic innervation that is intimately associated with inflammation. This loss probably represents a nonspecific event subsequent to damage to enteric nerve fibers but may contribute to disruption of local immunoregulation.
From the clinical data of the 199 patients with carcinoma of the uterine cervix from August 1978 to December 1982 using external irradiation and RALS, the tolerance dose of rectum and sigmoid colon were considered as 65 Gy and 70 Gy, respectively. On the other hand, from the review of 86 patients who had been treated for paraaortic lymph node based on a survey of Kansai Cancer Therapist Group, the tolerance doses of small intestine were considered as 40-50 Gy. For further reassessment of tolerance dose, the analysis of volume factor and basic research for pathogenesis of complication are essential.
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Campylobacter jejuni has often been responsible for human gastroenteritis. Poultry have often been implicated as a source for these human infections. Intestinal colonization of C. jejuni in the chicken plays a role in carcass contamination during slaughter. Thus, reducing C. jejuni colonization in chickens can potentially reduce the incidence of C. jejuni infections in humans. The use of probiotics to competitively exclude the colonization of intestinal pathogens has been proposed for poultry. Hence, the purpose of this study was to evaluate the use of an avian-specific probiotic containing Lactobacillus acidophilus and Streptococcus faecium for reducing the shedding and colonization of C. jejuni in the chicken intestinal tract. Day-old chicks were randomly allocated into either a probiotic-treated group or a control group. The treated group was given probiotic from day 1 to day 3, and the control group was not given any probiotic. Six hours after the first oral administration of probiotics (treatment) or double distilled water (control), these chicks were challenged with C. jejuni. The frequency of the C. jejuni shedding was monitored until market age. Intestinal colonization was determined for the two experimental groups at slaughter. Results indicated that chickens given probiotics from day 1 to day 3 had a 70% reduction in the frequency of C. jejuni shedding in colonized chicks (P = 0.0001) and a 27% reduction in jejunal colonization in colonized chicks (P = 0.0001) at slaughter when compared with the control group. Thus, the use of the avian-specific probiotic containing L. acidophilus and S. faecium can reduce the colonization and frequency of fecal shedding of C. jejuni in market-aged broilers.
The human colon carcinoma cell line Caco-2 was used as an enterocyte model to study the expression of the facilitative glucose transporters GLUT-1 and GLUT-2, and of the putative hexose transporter GLUT-5, which are expressed specifically in the gut. Northern blots indicate that Caco-2 cells express GLUT-1 and GLUT-5 mRNAs but not the mRNA coding for the basolateral glucose transporter GLUT-2. The level of GLUT-5 mRNA is growth dependent, being detectable only in postconfluent differentiated cells. In addition, the expression of GLUT-5 increases with the number of cell passages and is approximately 10 times higher in later passages (passage 184) than in early ones (passage 26). With the use of polyclonal antibodies directed against the COOH-terminus of GLUT-5, indirect immunofluorescence and Western blotting indicate that GLUT-5 is mainly localized to the brush border of Caco-2 cells. GLUT-5 is also found to be associated with the brush border of epithelial cells from fetal and normal adult human small intestine, but is absent from the colon.
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