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At least 1,297 records · Page 72Linked to original sources
PubMed1997

Comparison of olestra absorption in guinea pigs with normal and compromised gastrointestinal tracts.

Female guinea pigs (12/group) were given a single dose of [14C]olestra by gavage after consuming either 3% poligeenan in tap water (Compromised group) or just tap water (Normal group) for 5 weeks. A Sentinel group (N = 2) was given 3% poligeenan for 5 weeks. Ten sentinel animals were killed 1 day before and 10 1 day after the other animals were dosed with [14C]olestra and their gastrointestinal tracts were examined by histology. The Compromised and Normal animals were endoscoped just before dosing with [14C]olestra. Urine and feces were collected continuously and CO2 was collected for 7 days after dosing. The samples were analyzed for 14C and urine was also analyzed for [14C]sucrose. Animals (3/group) were killed 1, 3, 7, and 21 days after dosing, and tissues were collected and assayed for 14C. Tissue lipids were extracted, fractionated by high-pressure liquid chromatography, and analyzed for [14C]olestra by liquid scintillation. Animals fed poligeenan showed mucosal edema, congestion, ulceration, and fibrin deposition within the distal colon and rectum. Histology revealed inflammation, epithelial degeneration, and multifocal ulceration of the cecum, distal colon, and rectum. The gastrointestinal mucosae of nonpoligeenan fed animals were normal. No [14C]olestra was detected in liver lipids and no [14C]sucrose was found in the urine for any animal in the Normal or Compromised groups, indicating that intact olestra was not absorbed. The amount, distribution, and elimination of absorbed 14C did not differ between guinea pigs with normal and compromised gastrointestinal tracts. The poligeenan-treated animals displayed mucosal damage similar to that seen in human inflammatory bowel diseases; therefore, these results suggest that patients with inflammatory bowel conditions will not absorb olestra to any greater extent than normal healthy people.

Administration, Oral↗
PubMed1992

Cell proliferation biomarkers in the gastrointestinal tract.

Measurements of epithelial cell proliferation in the mucosa of the gastrointestinal tract pointed out the existence of cell kinetic abnormalities which can be involved in the first steps of carcinogenesis. In particular, an increase in the cell proliferation rate and an abnormal distribution of proliferating cells were found both in animals exposed to carcinogens and in human subjects at high risk of gastrointestinal cancer. In some diseases which predispose to cancer (i.e., chronic atropic gastritis, hereditary gastrointestinal cancer, sporadic colorectal neoplasia, chronic ulcerative colitis) we observed an expansion of the proliferative compartment even when the mucosa was not affected by morphological abnormalities. This proliferative feature seems to be associated with the presence of defects in cell differentiation. The abnormality is well detected by the histological examination of the proliferative pattern using microautoradiography after incorporation of tritiated thymidine, or using immunohistochemistry after bromodeoxyuridine uptake. The literature, and our own results, indicate that the search for abnormalities of epithelial cell proliferation can be useful in studying the earliest mechanisms leading to gastrointestinal cancer, in detecting subjects at high cancer risk, and for pilot chemoprevention studies using these abnormalities as intermediate biomarkers of gastrointestinal cancer risk.

Animals↗
PubMed1994

Estimation of silver-binding nucleolar organizer regions (AgNORs) in lymphoproliferative disorders of gastrointestinal tract.

We quantified nucleolar organizer regions demonstrable by silver staining technique (AgNORs) in six cases of reactive lymphoid hyperplasia (RLH), and in 14 low-grade B-cell lymphomas (mucosa-associated lymphoid tissue (MALT) 5, centrocytic 3, centroblastic-centrocytic 6) and 49 high-grade B-cell lymphomas (centroblastic 44, immunoblastic 3, Burkitt's one, large cell anaplastic one). The pooled mean AgNOR number in low-grade B-cell lymphomas was significantly higher than that in RLH, and significantly lower than that in high-grade B-cell lymphomas. There was a statistically significant difference between RLH versus centroblastic-centrocytic lymphoma in pooled mean AgNOR number and in RLH versus centrocytic lymphoma but not in RLH versus MALT lymphoma. The AgNOR numbers in the cellular components of RLH were also analyzed. The follicle center centroblasts of RLH exhibited a significantly higher pooled mean AgNOR number than other kinds of lymphoid cells in RLH. Furthermore, AgNOR numbers of gastrointestinal lymphomas were compared with those of cellular elements in RLH. There was a statistically significant increased AgNOR number of centroblastic lymphoma when compared with neoplastic centroblasts in centroblastic-centrocytic lymphoma and follicular centroblasts in RLH. By contrast, there was no significant difference in AgNOR numbers between MALT lymphomas and interfollicular lymphocytes, mantle zone lymphocytes or follicular centrocytes in RLH, respectively. This study demonstrated a similar increase when non-Hodgkin's B-cell lymphomas in gastrointestinal tract were compared with histogenetically related cellular elements of RLH. AgNOR counting might be useful adjunct in the classification and grading of lymphoproliferative disorders in gastrointestinal tract.

Antibodies, Monoclonal↗
PubMed1989

Kallikrein-gene expression in the rat gastrointestinal tract.

The serine proteinase glandular kallikrein has been demonstrated in the gastrointestinal tract, although there is some doubt as to whether it is synthesized there or derives from exocrine-gland secretions. Using a rat pancreatic kallikrein cRNA probe we have demonstrated kallikrein-like gene expression in the corpus, duodenum, jejunum, ileum, caecum and colon, and compared the pattern of expression with that of the gastrointestinal peptides somatostatin, gastrin and glucagon. In addition, using a panel of oligonucleotide probes specific for various members of the rat kallikrein-gene family, we have shown that the kallikrein-like gene expressed appears to be expressed as true kallikrein.

Animals↗
PubMed1997

Sorbin in the porcine gastrointestinal tract and pancreas: an immunocytochemical analysis.

Sorbin is a 153-amino acid peptide that was initially discovered in the porcine duodenum. We have reported previously that this peptide regulates intestinal electrolyte transport and have described accumulation sites in the rat digestive tract. In the present study, we investigated the anatomical distribution and the site(s) of sorbin production in the porcine digestive tract using immunocytochemistry. The use of polyclonal antisera, which by cross-reaction studies were shown to be specific for different regions of the molecule, revealed a diversified distribution. Sorbin predominated in endocrine cells preferentially localized in the pyloric glands, duodenal crypts of Lieberkühn, and pancreatic islets; in the gastrointestinal tract, sorbin coexisted with Met-enkephalin or with substance P in a small fraction of serotonin-storing [enterochromaffin (ED)] cells, i.e. EC2 cells and EC1 cells, respectively; in the pancreas, sorbin coexisted with insulin in the beta-cells, also considered as serotonin-storing cells in the pig, and with EC cells in the exocrine pancreas. An enteric neuronal system containing sorbin was also reported. Our results demonstrate that sorbin is a component of the serotonin-storing cell type in the porcine gastrointestinal tract and pancreas, and suggest potential directions to investigate the functions of this new regulatory peptide.

Amino Acid Sequence↗
PubMed2001

The HER-2/neu oncogene in tumors of the gastrointestinal tract.

The HER-2/neu oncogene is localized to chromosome 17q and shares significant homology with the epidermal growth factor receptor. As a result of its potential role in the selection of therapy, HER-2/neu testing has reached near-standard-of-practice status in breast cancer. There is considerable interest in HER-2/neu as a prognostic factor and target of therapy in tumors of the gastrointestinal tract. In this review of HER-2/neu expression in esophageal squamous cell carcinoma and adenocarcinomas of the esophagus, stomach, and colon, a wide range of expression of HER-2/neu from 0 to 83% likely reflects both differences in methods and reagents, as well as study bias associated with patient selection (i.e., early versus advanced disease). For esophageal squamous cell carcinoma, little information exists as to the prognostic significance of HER-2/neu expression. In adenocarcinoma associated with Barrett's esophagus there is contradictory data. However, most of the information available indicates that this marker has significant prognostic value. In gastric adenocarcinoma, the wide expression range may truly reflect patient selection because HER-2/neu positivity appears linked to advanced rather than early disease with limited invasion. The majority of studies favor a significant prognostic value of HER-2/neu status for this tumor. Finally, in colorectal cancer HER-2/neu overexpression also appears to be a significant adverse outcome indicator as judged by the current published literature. In conclusion, given that either HER-2/neu protein overexpression or gene amplification is associated with approximately one-fourth of all gastrointestinal tract malignancies, strategies designed to employ the marker in therapy selection appear warranted. During the next several years it will not be surprising to see these tumors treated with antiHER-2/neu modalities such as Herceptin, likely in combination with other agents initially for patients with advanced disease, and possibly for individuals with high-risk lesions in an adjuvant setting.

Adenocarcinoma↗
PubMed1980

Lesions of the upper gastrointestinal tract in patients with chronic renal failure.

Endoscopy of the upper gastrointestinal tract was performed on 84 patients with end-stage chronic renal failure undergoing hemodialysis. Gastric acid secretion and fasting plasma gastrin levels were also examined in these patients. Hemorrhagic gastritis was most frequently observed (23 cases) followed by erosive gastritis (18 cases). No patients had gastric ulcers. Duodenal ulcers were observed in only two patients. Gastrointestinal bleeding was observed in 15 cases (17.9%). Thirteen of these 15 cases had hemorrhagic gastritis, one of which had a duodenal ulcer as a complication. Fasting plasma gastrin levels (359.6 +/- 336.5 pg/ml) were significantly higher than those of normal subjects (35.2 +/- 37.1 pg/ml), but no acceleration in gastric acid secretion was observed either in the basal condition (BAO 0.8 +/- 0.7 mEq/h) or following tetragastrin stimulation (MAO 9.0 +/- 6.9 mEq/h). Our results were inconsistent with the previous reports that high frequencies of peptic ulcers and increased gastric acid secretion were observed in patients with chronic renal failure. Our data suggest that the defensive factors rather than the aggressive factors of the gastroduodenal mucosa may be involved in chronic renal failure.

Adolescent↗
PubMedDate not supplied

[Lipid contents in blood of healthy subjects and patients with peptic ulcer during regular motor activity of the gastrointestinal tract].

The concentrations of total cholesterol, beta-lipoproteins, and triglycerides were measured three times in 20 to 65 min in venous blood of 45 men (8 normal and 37 patients with peptic ulcer). Lipid concentration in the blood was shown to vary within a wide range in just few minutes, particularly so in normal subjects. In some cases the maximal values surpassed the minimal ones twofold and even more. The chi 2 test helped detect a correlation between the content of cholesterol and triglycerides in the blood and the phase of regular motor activity of the gastrointestinal tract, which was registered by tensotransmitters located in the stomach and small intestine. Soon after the beginning of a new cycle of this motor activity cholesterol concentration in the blood increased and triglyceride level reduced. The phase of the motor activity of the gastrointestinal tract should be taken into consideration when measuring the concentrations of lipids in human blood serum.

Adolescent↗
PubMed2004

[The effects of chronic alcohol abuse on morphology and function of the gastrointestinal tract].

In this review we described the effects of chronic alcohol consumption upon the morphology and function of the gastrointestinal tract. Especially the attention was paid to the motility disorders, their pathogenesis and influence on symptoms occurrence and systemic consequences of alcoholism. Some recent publications, concerning the role of neuroendocrine small intestine system and ileum as an extrahepatic source of cytokine production in alcoholics, were reviewed.

Alcoholism↗
PubMed1992

Multiple granular cell tumors of the gastrointestinal tract with subsequent development of esophageal squamous carcinoma.

A 52-year-old woman initially presented to our medical center with synchronous, submucosal tumors of the esophagus, stomach, and transverse colon. The gastric and colonic tumors were resected, and both displayed infiltrating sheets of polygonal cells with coarsely granular cytoplasm and small vesicular nuclei. The neoplastic cells of both tumors were immunoreactive for S-100 protein. Ultrastructural studies revealed the lysosomal nature of the cytoplasmic granules. Although the esophageal mass was not resected, it was felt that this represented another focus of granular cell tumor of the gastrointestinal tract. Two years later, she presented with disseminated squamous carcinoma of the esophagus. At autopsy, a submucosal granular cell tumor was found adjacent to the squamous carcinoma of the esophagus. To our knowledge, this is the first reported case of synchronous granular cell tumors that involved multiple segments of the gastrointestinal tract, one of which was later associated with a squamous carcinoma of the esophagus.

Carcinoma, Squamous Cell↗
PubMed1963

TUMOUR CELLS IN THE CIRCULATING BLOOD OF PATIENTS WITH CARCINOMA OF THE BREAST AND OF THE GASTROINTESTINAL TRACT.

In view of the differences in the frequency of tumour cells in various reported series and the difficulty in reconciling the presence of these cells with survival, three groups of patients were studied in the following manner. In one group of 20 patients with breast cancer, multiple 20-ml. blood samples were studied. In another group of 18 patients, a single 100-ml. sample was used. Using this technique, tumour cells were found in 82.5% of patients in Group 1 and in 89% in Group 2. Similarly, in 44 patients with cancer of the gastrointestinal tract, tumour cells were identified in 70% of the patients, using the multiple-sampling technique. It seems therefore that if a sufficient volume of blood is studied, tumour cells are present in every patient with cancer of the breast and gastrointestinal tract. The presence of tumour cells in the peripheral blood does not mean that hematogenous metastases will invariably develop, and the presence of these cells is only one of many factors responsible for the development of such metastases.

Blood↗
PubMed1984

[Neurotensin--what is known about its role as a hormone in the gastrointestinal tract?].

Neurotensin is a tridecapeptide originally isolated and characterized from bovine hypothalamus and later, in identical form, from bovine and human intestine. In the rat about 85% of immunoreactive neurotensin is found in the gut and about 10% in the brain. When an antibody specific for the amino terminal region of neurotensin was used the highest concentrations were found in the mucosa of the ileum, while an antibody specific for the biologically active region, the carboxyl terminus, also detected large amounts in the mucosa of the upper gastrointestinal tract. After a meal neurotensin - as measured by carboxyl terminal antibodies - rises after 5 min, a time in which the chymus has not yet reached the ileum, the main source of whole neurotensin. It is therefore possible that the carboxyl terminal molecules of neurotensin, found in the upper gastrointestinal tract, play an important physiological role. In plasma, neurotensin is rapidly degraded into smaller amino terminal and therefore biologically inactive molecules. Increases of carboxyl terminal neurotensin have been found in plasma in only a very few studies. The nature of this immunoreactive material has not yet been established. Therefore, the physiological role of neurotensin as a circulating hormone is unknown. Potential actions of neurotensin include thermoregulation, regulation of hormone release from brain (pituitary hormones) and gut (glucagon, insulin, somatostatin, pancreatic polypeptide), increase of vascular permeability, vasodilatation, inhibition of gastric acid secretion, stimulation of pancreatic secretion and changes of gut motility from the fasting to the fed type.

Animals↗
PubMed1984

Tissue pO2 and pCO2 in the gastrointestinal tract and liver during intravenous vasopressin infusion. An experimental study in pigs.

Tissue pO2 and pCO2 were measured in the oesophagus, stomach, small and large bowel and liver of piglets before, during and after a 30-min infusion of vasopressin (2.75 mU/kg/min). For registration of the tissue gas tensions a silicone elastomer tube was used as a tonometer. Systemic arterial and portal blood gas analyses were performed. Plasma lactate was estimated. Cardiac output and portal vein and hepatic artery blood flow were registered. Vasopressin infusion caused significant fall in the tissue pO2 and increase in the pCO2 throughout the gastrointestinal tract. The liver pO2 also decreased, but no change in the liver pCO2 was found. Serum lactic acid increased. There seems to be risk of hypoxic lesion in all parts of the gastrointestinal tract during vasopressin infusion.

Animals↗
PubMed1995

Inhibitory effect of glycine on ethanol absorption from gastrointestinal tract.

The oral administration of glycine remarkably decreased the blood ethanol level in mice which had ingested ethanol, and a large amount of ethanol was retained in their stomachs. These effects were observed by the oral administration of glycine previous to the ethanol ingestion, and depended on the dose of glycine. An intravenous injection of glycine did not affect the ethanol absorption at all. These findings indicate that glycine suppresses the rate of ethanol absorption from the gastrointestinal tract. Glycylglycine, glycylglycylglycine and alanine showed the same effects, but glucose did not. However, ethanol absorption from the ligated stomach of mouse was inhibited not only by glycine but also by glucose. On the other hand, the rate of ejecting a pigment from the stomach to the small intestine was lowered by glycine, but not by glucose. Thus, glycine lowers the gastric emptying rate, resulting in the suppression of ethanol absorption from the gastrointestinal tract.

Administration, Oral↗
PubMed1991

Bacteremia following operative endoscopy of the upper gastrointestinal tract.

The rate of bactaeremia following surgical endoscopy of the upper gastrointestinal tract is reported with up to 50% depending on the therapeutic measure performed. In a prospective study we examined 160 patients treated by surgical endoscopy of the upper digestive tract. The rate of bactaeremia showed a significant difference with 12.5% after diagnostic and 28.96% after surgical endoscopy. Our results recommend a single shot antibiotic prophylaxis depending on the endoscopic measure performed and the patient's individual risk.

Anti-Bacterial Agents↗
PubMed2004

Angiosarcoma involving the gastrointestinal tract: a series of primary and metastatic cases.

Angiosarcoma occurs very rarely in the intestinal tract as either a primary or metastatic malignancy and can present great diagnostic difficulty, especially when it displays epithelioid cytomorphology. Since only isolated case reports have been published, the purpose of this study is to more fully delineate the histopathological and clinical features from a series of 8 angiosarcomas involving the gastrointestinal tract. There were 5 male and 3 female patients whose ages ranged from 25-85 years (median 57). Presenting symptoms included intestinal bleeding, anemia and pain. Five cases involved the small bowel and 3 involved the colon/rectum. Four cases were primary to the intestinal tract, 2 patients initially presented with secondary involvement of the large bowel from occult retroperitoneal primaries, 1 patient presented with disseminated disease including small bowel involvement, and 1 case was metastatic from a breast primary. Seven cases were composed predominantly of sheets of malignant appearing epithelioid cells with subtle areas forming cleft-like spaces suggestive of vascular differentiation. Immunohistochemical studies revealed the lesional cells to be immunoreactive for CD31 (8/8), CD34 (8/8), Factor VIII (8/8), cytokeratins AE1/AE3 (7/8), cytokeratin 7 (2/8), Cam5.2/cytokeratin 8 (5/8), and cytokeratin 19 (5/8). Cytokeratin 20 was negative in all eight cases, which contrasts sharply with the characteristic positivity for cytokeratin 20 in virtually all intestinal carcinomas. One case was weakly and focally positive for EMA and all cases were negative for S-100 protein. Cytokeratin staining was variable and ranged from focal to extensive. Follow-up was available in eight cases and ranged from 1-33 months (median 12.5). Five patients died of disease, between 1 and 33 months (median 6) after diagnosis. One recently diagnosed patient is alive with disease 18 months after diagnosis, and one patient is free of disease 27 months after original diagnosis. Angiosarcomas of the gastrointestinal tract commonly display epithelioid cytomorphology, may be diffusely and strongly positive for cytokeratins and only show subtle signs of vascular differentiation, creating potential diagnostic confusion with primary or metastatic carcinoma. Given the clinically aggressive behavior of angiosarcoma, proper classification and treatment is important. Immunohistochemistry with vascular markers, CK20, and S-100 protein may be helpful in differentiating angiosarcoma from carcinoma and melanoma.

Adult↗
PubMed1999

Viral infections of the gastrointestinal tract.

Acute gastroenteritis is common in adults. It can occur in institutional epidemics or epidemics of food-borne illness; in these cases, caliciviruses are the major cause of the condition. When acute gastroenteritis occurs in nonepidemic form, its causes are less clear. It may be due to caliciviruses or to the less common serotypes of childhood gastroenteritis viruses, such as rotavirus, astrovirus, and adenovirus. The pathogenesis of acute viral gastroenteritis is not completely understood. Old evidence suggests that mild villus damage is responsible, but new evidence indicates that active secretion and motility disturbance may be involved in the production of symptoms. Five common viruses can remain latent in gastrointestinal tissues and produce disease many years after initial infection. Two major herpesviruses, cytomegalovirus and herpes simplex virus, cause ulcerative disease of the gastrointestinal tract. This disease occurs in healthy persons but is more common and more severe in immunocompromised patients. Three other viruses--Epstein-Barr virus, human papilloma virus, and human herpesvirus-8--are implicated in benign and malignant proliferative diseases of the gastrointestinal tract. Epstein-Barr virus has been associated with immunoproliferative disease after transplantation and may also cause small-bowel and colonic lymphoma in healthy adults. It causes most AIDS-related lymphomas. Human papillomaviruses cause anorectal condyloma and anal cancer. Human herpesvirus-8 causes gastrointestinal Kaposi sarcoma.

Adult↗
PubMed1996

Inhibition of bacterial translocation from the gastrointestinal tract of mice injected with cyclophosphamide.

Effects of intraperitoneal injection of cyclophosphamide, an immunosuppressant, on the degree of bacterial translocation and morphological changes of Peyer's patches (PP) in the intestine were investigated with antibiotic-decontaminated SPF mice and germfree mice monoassociated with Escherichia coli C25. It has been reported that treatment with cyclophosphamide induces bacterial translocation. Cyclophosphamide treatment in this study, however, significantly decreased E. coli C25 translocation from the gastrointestinal tract to the mesenteric lymph nodes (MLN), although the numbers of lymphoid cells, especially B cells, in the PP, MLN, and spleen were remarkably reduced. Four injections of cyclophosphamide at a dose of 100 mg/kg inhibited bacterial translocation more than one injection at a dose of 200 mg/kg in SPF mice. Germfree mice, however, treated with one dose of 200 mg/kg showed the same inhibition of bacterial translocation as those given 100 mg/kg four times. In cyclophosphamide-treated mice, lymph follicles in the PP were obviously smaller than those in control mice, M-cells were similar in appearance to absorption epithelial cells except for short microvilli, and immune cells among the M-cells had disappeared. These data suggested that inhibition of bacterial translocation in mice treated with cyclophosphamide may be the result of morphological and physiological changes of epithelial cells in the gastrointestinal tract, especially M-cells, as a point of entry of invading bacteria, independent of the changes in immunological function.

Animals↗