[On the substitution of the esophagus with intrathoracically displaced intestine (jejunum or colon). Experiences with 41 surgical cases].
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An increase in the percentage of antibiotic resistant and hemolysin-producing enterobacteria occurring in the process of the development of postradiation intestinal dysbacteriosis was due to a sharp increase in the number of such bacteria among the representatives of the genera inhabiting the large intestine of mice (E. coli, E. aerogenes, E. cloacae, P. morganii) and to the appearance of antibiotic-resistant and hemolysin-producing strains in the intestinal tract; these strains belonged to the genera which had not been detected in the intestines of the animals before irradiation. In postirradiation dysbacteriosis a considerable decrease in the percentage of colicin-producing strains was observed. The dissemination of enterobacteria in the small intestine of irradiated mice occurred as the result of exogenous and endogenous infection.
CT of the retroperitoneum in 70 patients (98 scans) who had undergone previous nephrectomy for renal cell carcinoma was reviewed. The interval between surgical operation and CT scanning were 15 days-7 years. In 59 cases (84%), CT scans were performed within the first 2 years. After nephrectomy, the emptied renal fossae were filled with adjacent organs, such as colon (27), small intestine (21), liver (14), inferior vena cava (3), adrenal gland (2) on the right side, and spleen (28) small intestine (33), colon (15), tail of pancreas (11), adrenal gland (2) on the left. In 47 cases, where CT scans were done within 4 months after operation, there were abscess/hematoma (8) and soft tissue thickening caused by post-operative edema and or inflammation (6). Most of the early post-operative complications gradually reduced in size in the follow-up scans. Local recurrences or metastases were detected by CT scan in 15 cases, with recurrence at the excision site (5), renal bed (6), adrenal gland (4), retroperitoneal lymph nodes (7) and contralateral kidney (1). 7 patients had solitary lesions and 8 patients had multiple recurrences. In 2 patients, local recurrences were detected by routine follow-up CT scanning. In 4 cases, recurrences were proved by surgery, and the others by clinical follow-up. Local recurrences were assessed within 2 years in 10/15 cases (67%), and 4 cases within 6 months. 9 cases had venous thrombosis (IVC 9, renal vein 3), the size of which was reduced after radiotherapy in 1 case. CT is the most preferred imaging technique in evaluating post-nephrectomy patients for renal cell carcinoma.
The authors analyze x-ray findings in 194 patients with colonic diverticulosis and its inflammatory complications. Findings of preoperative irrigoscopy were correlated with dates of morphological investigations. Roentgenomorphological and functional changes were assessed in different clinical types of colonic diverticulosis. Correlation was received between this changes and clinical sings of disease. Authors determined risk-groups of inflammatory complications of colonic diverticulosis.
Massive small bowel resection results in a short bowel syndrome, characterized by malabsorption, weight loss, diarrhea and steatorrhea. Different surgical techniques have been used to slow down intestinal transit time or to increase the area of absorption. Techniques for the deceleration of intestinal transit are reconstruction of the ileocecal-valve, antiperistaltic intestinal segments, colon interposition, recirculating intestinal loops and intestinal pacing. For increase of the area of absorption growth of neomucosa, mucosal autotransplantation, intestinal lengthening and small bowel transplantation have been performed. All these procedures are still at different experimental levels. Due to inconsistent results so far the surgical therapy of the short bowel syndrom cannot be recommended for routine use. However, some techniques offer hope of a successful surgical development.
In order to investigate the protective effects of intestinal trefoil factor (ITF) on colonic mucosa in experimental colitis of rats, ITF was detected by RT-PCR and immunohistochemistry at different time points. Three days after colitis induction, rats were treated with either 0.9% saline solution or rhITF. Pathological changes and the expression of iNOS mRNA, NO, MDA and SOD were measured respectively. It was found that ITF was mainly located in goblet cells, significantly higher in model group than in normal group (P<0.05). rhITF could increase the iNOS mRNA expression and NO contents, and there was statistically significant difference between rhITF group and model group (P<0.05). rhITF also caused an increase of MDA and a decrease of SOD, but there was no significant difference between two groups. These results indicated that ITF has apparent therapeutic effects in ulcerative colitis, which may be associated with iNOS and NO.
Intestinal Behcet's disease in a 38-year-old woman was diagnosed because of the history of recurrent oral aphthous ulcers, erythema nodosum-like eruptions, genital ulcer, and endoscopic findings of esophageal and ileocolonic punched-out ulcers with colonic longitudinal ulcers. Esophageal lesions and colonic longitudinal ulcers are rarely seen in intestinal Behcet's disease. The ulcers of esophagus and ileocolon healed with 3 wk of treatment with prednisolone and mesalazine without any adverse effect. Mesalazine may decrease the total dose of prednisolone required to treat the disease.
The ability of frequent feeding of bovine milk diets to prevent the colonization of the small intestines of newborn guinea-pigs with orally inoculated Escherichia coli was tested. At 3--4 days small intestinal samples from suckled controls were frequently sterile or were colonized with only very low numbers of Esch. coli. No bovine milk diet exhibited a significant "protective" effect but the diets could, however, be ranged in order of effectiveness in decreasing colonization by Esch. coli. Raw, fresh bovine milk was best, followed by milk pasteurized at 56 degrees or 63 degrees, then boiled milk; frozen milk was the worst. Because of this last finding, neither the bacteriostatic lactoferrin-dependent activity nor the lactoperoxidase could be correlated with the ability to decrease the colonization of the small intestines by Esch. coli.
Fucose-containing glycoproteins and glycolipids were compared in three human colon cancer cell lines and five human fetal intestinal epithelial cell lines. Cells were labeled by culturing cells in the presence of L-[3H]-fucose. Fucose was incorporated into both the membrane and cytoplasmic fractions of all three colon cancer cell lines to a much lesser extent than into fetal cells. When the relative fucose labeling of glycolipids and glycoproteins were examined, a much greater proportion of fucose labeling in the membrane was associated with lipid in colon cancer cells (11.6-16.7%) compared to fetal intestinal cells (1.3-2.5%). Fluorographic analysis of SDS-polyacrylamide gel electrophoresis of fucose-labeled glycoproteins revealed a rather uniform labeling pattern of fetal intestinal cells which was distinct from those of colon cancer cells. Thin-layer chromatographic analysis of fucose labeled glycolipids of all three colon cancer cell lines indicated the presence of fucose-containing glycolipids with carbohydrate chain lengths greater than five sugars. Glycolipids of the SKCO-1 cells in particular appear to consist predominantly of complex fucose-containing glycolipids. These results indicate that significant qualitative differences in the fucose-containing glycoproteins and glycolipids exist between the membranes of human colon cancer cells and fetal intestinal cells and that complex fuco-glycolipids with long carbohydrate side chains are present in the three human colon cancer cell lines.
SPARC is a glycoprotein of the extracellular matrix that exhibits a number of biological functions such as disruption of cell adhesion and modulation of matrix metalloprotease expression. These properties, in concert with the expression of the molecule during development, repair, and neoplastic progression, suggest that SPARC has an important role in remodeling in a variety of tissues. However, the role of SPARC in the intestine is unclear since the development expression and tissular origin of SPARC in this organ appears to be species-dependent. As a first step to investigate the function of SPARC in the tissues of the intestine, we have analyzed its expression at the protein and mRNA levels in the human fetal and adult small intestinal and colonic mucosa as well as in intestinal cell models. Our results show that SPARC expression is differentially regulated during development and along the length of the human intestine. In the colon, SPARC was predominantly found at the epithelial-mesenchymal interface at the fetal stage, below detection levels in the normal adult, but re-expressed in the stroma of colonic tumors. In the small intestine, low levels of SPARC expression were observed at an early stage of morphogenesis (between 9 and 11 weeks) but expression was not detected at subsequent developmental stages nor was it induced in the mucosa of Crohn's disease. While SPARC appeared to be produced mainly by mesenchymal and stromal cells in the intact intestine it was not detected in colon cancer cells. Taken together, these results indicate that SPARC is subject to an onco-fetal pattern of expression in the stroma of the colonic mucosa while its expression is much more restricted in the small intestine, suggesting a differential involvement of this molecule in the extracellular matrix remodeling occurring along the length of the developing and diseased human intestinal mucosa.
To investigate whether simple transit measurements based on scintigraphy performed only 0, 2, 4 and 24 h after intake of a radiolabelled meal can be used to predict the mean transit time values for the stomach, the small intestine, and the colon, a study was conducted in 16 healthy volunteers. After ingestion of a meal containing 111indium-labelled water and 99mtechnetium-labelled omelette, imaging was performed at intervals of 30 min until all radioactivity was located in the colon and henceforth at intervals of 24 h until all radioactivity had cleared from the colon. Gastric, small intestinal and colonic mean transit times were calculated for both markers and compared with fractional gastric emptying at 2 h, fractional colonic filling at 4 h, and geometric centre of colonic content at 24 h, respectively. Highly significant correlations were found between gastric mean transit time and fractional gastric emptying at 2 h (111In: r=0.95, P<0.00001; 99mTc: r=0.96, P<0.00001), between small intestinal mean transit time and fractional colonic filling at 4 h (111In: r=-0.97, P<0.00001; 99mTc: r=-0.89, P<0. 00001), and between colonic mean transit time and geometric centre of colonic content at 24 h (111In: r=- 0.88, P<0.00001). We therefore conclude that reliable regional gastrointestinal transit times can be estimated from scintigraphic images taken 0, 2, 4 and 24 h after intake of radiolabelled markers.
The effect of diet on intestinal ecology was studied in germ-free mice that were inoculated orogastrically with predominant intestinal flora components isolated from the feces of breast-fed human infants. The flora components colonized the intestines of mice and persisted at fixed population levels. Groups of flora- associated mice were fed either human milk, bovine milk, whey-dominant formula, or formula modifications exclusively for 2 weeks, and then examined for changes in small intestinal and cecal flora composition, cecal pH, and resistance to intestinal colonization with Salmonella typhimurium. Dietary variations influenced the composition of the flora to a moderate degree but the differences were generally not statistically significant. However, the addition of bovine lactoferrin to the whey-dominant formula resulted in significantly greater counts of Bifidobacterium, Bacteroides, Enterococcus and total aerobes in the small intestine when compared with mice fed unsupplemented formula. Bifidobacterium was present in large numbers in both the ceca and small intestines of mice fed the lactoferrin-supplemented formula. Despite similarities in intestinal flora patterns among mice fed the various diets, human milk consumption resulted in a lower pH of cecal contents and a greater resistance to colonization by Salmonella typhimurium after orogastric challenge than the consumption of the other diets.
The ability of Escherichia coli to survive stress during growth in different environments is, in large part, dependent on rpoS and the genes that comprise the rpoS regulon. E. coli BJ4 and an isogenic BJ4 rpoS mutant were used to examine the influence of the rpoS gene on E. coli colonization of the streptomycin-treated mouse large intestine. Colonization experiments in which the wild-type E. coli BJ4 and its rpoS mutant were fed individually as well as simultaneously to mice suggested that E. coli BJ4 does not face prolonged periods of nutrient starvation in the mouse large intestine and that the rpoS regulon is not expressed during long-term colonization after adaptation of the bacteria to the gut environment.
Colonic administration of a hapten, 2,4,6-trinitrobenzene sulphonic acid (TNBS) has been shown to induce colitis in rats. We are using this model to investigate the role of colonic antigens in the immunopathology. In this study, we show that colitis can be suppressed by oral administration of haptenized colonic antigens prior to the TNBS enema. Moreover, our data suggest that haptenization of the colonic antigens is not essential because oral feeding of non haptenized colonic antigens too protects rats from TNBS-induced colitis. Thus, unmodified colonic antigens may be involved in the induction of oral tolerance, and possibly in the pathogenesis in this model of colitis. Further, we show that the protective immunity or oral tolerance induced by non haptenized colonic antigens can be passively transferred to naïve rats by mesenteric T lymphocytes. Interestingly, oral feeding of small intestinal antigens, haptenized and non haptenized, does not protect rats from colitis, suggesting a specific role for colonic antigens. These data underscore the usefulness of this rat model in the identification of pathogenic antigens in colitis and in the development of therapeutic strategies based on oral tolerance.