Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transfer factor (T.F.) prepared from 5 x 10(8) lymphoid cells from 500 ml of a parent's blood was given to 40 Australian aboriginal children aged 2-46 months who had been in hospital with acute infection. Many had protein-calorie malnutrition. These and a control group of 35 similar children were assessed blind for at least 12 months. In T.F.-treated children there were significantly fewer episodes of diarrhoeal disease for periods in excess of 26 weeks. Recurrent moderate diarrhoeal disease was particularly reduced, and the onset of severe gastroenteritis may have been delayed. There was no protection against chest, middle-ear, or skin infection.
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PMID:Therapy with parent's lymphocyte transfer factor in children with infection and malnutrition. 5 83

The primary gastrointestinal lymphomas in Shiraz, Iran, and Richmond, Virginia, USA were compared. Upper duodenojejunal lymphoma is always associated with atrophy of the surrounding nonlymphomatous mucosa, plasma cell infiltration and formation of lymph follicles. This is frequently linked to repeated gastroenteritis leading to mucosal atrophy, mutation of plasma cell precursors and secretion of alpha-heavy-chain. Gastrointestinal lymphoma in the USA and other industrialized countries is found in the stomach, where it is accompanied by superficial perifoveolar plasma cell gastritis of the surrounding mucosa, or in the performed lymphoid tissue of the ileocolon, surrounded usually by normal mucosa. A hypothesis for the pathogenesis of the different types of primary gastrointestinal lymphoma, considering the geographic distribution, and mucosal and immunologic antecedents, is presented.
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PMID:Gastrointestinal mucosa and primary gastrointestinal lymphoma. 10 21

Chlorozotocin was studied for toxic effects in beagle dogs and rhesus monkeys. The results are the subject of this report. The compound was administered i.v. as single and 5 daily doses in dogs and monkeys; and, in dogs, as 10 consecutive daily doses, once weekly for 6 weeks and for 5 daily doses followed by 9 days rest repeated 3 times. The most prominent toxicities in both species were dose-related renal tubular lesions. These appeared as a necrosis at the most toxic levels and a nephrosis at lower doses. The latter change was also seen in animals surviving higher doses but only after a 6-week posttreatment period. Bone marrow hypoplasia and lymphoid atrophy were other common findings at the highest doses in both species. The same general pattern of toxicity appeared in extended treatment studies in dogs, but also included aspermatogenesis. Signs of hepatotoxicity were seen in dogs at the highest dose levels, while monkeys receiving lethal doses also evidenced a toxic gastroenteritis. A single monkey had a diabetic response following 1 treatment with a high non-lethal dose. Renal lesions found in mice following acute, single dose administration were similar to those described for the larger laboratory animals.
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PMID:Toxicology studies in mice, beagle dogs and rhesus monkeys given chlorozotocin (NSC 178, 248). 15 61

We have investigated small intestinal biopsies from children with coeliac disease, acute gastroenteritis, failure to thrive and giardiasis, to find out if a high intraepithelial lymphocyte count is a feature specific to coeliac disease, or whether it is always associated with partial or subtotal villous atrophy. The results indicate that the normal range for childrens' intraepithelial lymphocyte counts is similar to that for adults (around 6-40 lymphocytes per 100 epithelial cells); that counts are high in coeliac disease, but also in some children with giardiasis or with failure to thrive in whom the jejunal biopsy appears otherwise normal; and that intraepithelial lymphocyte counts are normal in acute gastroenteritis even when there is partial villous atrophy with increased lamina propria lymphoid cell infiltrate. Thus, this measurement of small intestinal lymphocyte infiltration may be of diagnostic value is differentiating the diarrhoea of food intolerance from infectious diarrhoeas in young children.
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PMID:Intraepithelial lymphocyte counts in small intestinal biopsies from children with diarrhoea. 96 7

Leukocytes were harvested from the peripheral blood, mesenteric lymph node and small intestinal lamina propria from groups of three piglets before, and 1, 2 and 3 weeks after infection with virulent transmissible gastroenteritis virus (TGEV) at 2 weeks of age. The donor piglets developed clinical signs of transmissible gastroenteritis which persisted for up to 3 days, and they developed peak serum titres of TGEV-neutralizing antibodies 2 weeks post-infection. The leukocytes were cultured in the presence of pokeweed mitogen (PWM), various dilutions of purified TGEV, or control media for 3 or 5 days, and the culture supernatants were tested for antiviral activity in MDBK cells challenged with vesicular stomatitis virus. The antiviral activity was characterized as porcine interferon (IFN)-alpha or porcine IFN-tau on the basis of its stability at pH 2.0 and neutralization by anti-human IFN-alpha antibodies. Viability of the leukocytes in culture, determined by trypan blue exclusion, was highest for the peripheral blood leukocytes and lowest for the mesenteric lymph node leukocytes. There were no consistent differences in antiviral activity between cultures incubated for 3 or 5 days. Porcine IFN-alpha was found in the supernatants of the leukocyte cultures stimulated with TGEV antigen, harvested before or after infection of the donor piglets with TGEV. Porcine IFN-tau was demonstrated in the supernatants of the leukocyte cultures stimulated with PWM, more frequently when the leukocytes were harvested post-infection. This was the first demonstration of IFN induction in vitro in leukocytes from porcine gut-associated lymphoid tissue.
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PMID:Interferon induction in porcine leukocytes with transmissible gastroenteritis virus. 134 91

A variant of simian immunodeficiency virus (SIVSMM/PBj), isolated from a chronically infected pig-tailed macaque has been shown in previous studies to produce acutely fatal disease uniformly in pig-tailed macaques and in some rhesus macaques. The present study extends investigation of SIVSMM/PBj pathogenesis in rhesus and cynomolgus monkeys. Cynomolgus and rhesus macaques were found to be uniformly susceptible to infection, but as previously reported, the rhesus were found to not be uniform in their response during the acute disease. Homogenized tissues from a rhesus that died acutely from SIVSMM/PBj were passaged to 6 rhesus monkeys in an attempt to increase lethality. Five of 6 rhesus monkeys receiving intravenous inoculation of either spleen (10(3) TCID50) or lymph node (10(5) TCID50) homogenate developed acute disease; 4 died (days 8-10), 1 recovered, and one rhesus remained asymptomatic. Three of 3 cynomolgus macaques and 4 of 4 pig-tailed macaques receiving the same inoculum died acutely within 9 days. Clinical disease in macaques that died was characterized by diffuse lymphadenopathy within 5 days of inoculation and severe diarrhea beginning 1 to 3 days before death. Anorexia, lymphopenia (< 1000 cells/mm3), and mild hypoalbuminemia preceded onset of diarrhea by 24 h. Viral p27 was detected in circulation by day 6 postinfection, with all animals dying acutely having detectable serum p27 and no detectable humoral response. Acute lethality was attributed to severe metabolic acidosis (pH < 7.20) which was observed 24-48 h prior to death in the pig-tailed and cynomolgus macaques. Immunohistochemistry revealed numerous SIV antigen-positive lymphocytes and macrophages in the lymph nodes, spleen, gut-associated lymphoid tissues and gastrointestinal lamina propria. Histopathologic lesions included marked to severe hyperplasia of the T-cell-dependent areas in lymphoid tissues and diffuse nonulcerative lymphohistiocytic gastroenteritis. Surviving rhesus developed strong humoral immune responses to the major SIV proteins.
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PMID:Infection of rhesus and cynomolgus macaques with a rapidly fatal SIV (SIVSMM/PBj) isolate from sooty mangabeys. 145 9

A method is described for in vitro studies of viral humoral immune responses in the pig. After oral immunization with transmissible gastroenteritis (TGE) coronavirus, antibody production from primed mesenteric lymph node cells was revealed by an in vitro boost with viral antigen. For the latter the leukocytes were co-cultured with UV-inactivated virus using a variety of different methods of antigenic stimulation. Enumeration of specific antibody-secreting cells (ASC) and titration of secreted anti-virus antibodies were performed with ELISASPOT (using 3-amino 9-ethyl carbazole as the peroxidase chromogen) and ELISA tests respectively, according to the Ig isotype. The results showed a close relationship between ASC numbers and secreted antibody titres. The best in vitro antibody synthesis was observed when the sensitized cells were maintained in contact with virus during the whole culture period. Antibody responses were defined by a kinetic profile characterized by a narrow peak, with a maximum occurring after 4 and 6 days of culture and with the IgA response appearing earlier than the IgG. This methodology, which analyses specific antibody responses at the cellular level, may permit studies on the mechanisms of Ig isotype regulation. Extended to leukocytes from other organs of the immune system, it may also constitute an in vitro model to study antibody responses expressed in different lymphoid tissues of the pig.
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PMID:Kinetics of the in vitro antibody response to transmissible gastroenteritis (TGE) virus from pig mesenteric lymph node cells, using the ELISASPOT and ELISA tests. 216 14

The nature of antigens in enteropathogenic animal viruses--coronavirus--an agent of transmissive gastroenteritis of pigs (TGE) and pig enterovirus of serotype VI was studied. Basing on the results of the histomorphometric study of the white spleen pulp under the individual introduction of viruses and in combination with the lymphoid chalone it was established that the developing immune response has a thymus-dependent induction mechanism. The pharmacological stimulation of the T-system of animals suffering from virus gastroenteritis provides a positive therapeutic effect. The selective stimulation of the animal T-system may be considered as a promising trend in therapy of intestinal infections and as one of the possible ways to increase the immune response to the antigens of viral vaccines.
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PMID:[Thymus-dependent nature of the antigens of enteropathogenic viruses]. 254 35

Rabbits were treated with a single oral dose (1, 2, 4, 6, 8, 10 or 15 mg/kg body mass) of T-2 fusariotoxin. Doses of 4 mg or higher killed the animals in 24 to 48 h. As opposed to the controls, in the treated rabbits gross pathological and histopathological examinations revealed acute catarrhal gastroenteritis, necrosis of lymphoid cells of the gastrointestinal mucosa, centrolobular dystrophy of the liver, necrosis of cells of the mononuclear phagocyte system (MPS) in the liver, tubulonephrosis, focal dystrophy of the adrenal cortex, lymphocyte depletion involving both T- and B-cell-dependent zones of the lymphoid organs (spleen, lymph, ampulla ilei), and depletion and necrosis of the myelopoietic cell colonies of the bone marrow. Similar but milder changes were observed in surviving rabbits exsanguinated 48 h after treatment. In addition to the direct damage done to the digestive tract mucosa and liver, the toxin severely damaged the cells participating in humoral and cell-mediated immunity and in the local defence of the intestinal mucosa, and markedly impaired phagocytosis and granulocytopoiesis. In another experiment rabbits were given oral doses of 2 mg/kg body mass T-2 toxin daily for several days. One rabbit was killed by bleeding every day. In rabbits killed beyond day 7 there was subacute catarrhal gastritis, emaciation, and hypertrophy of the adrenal cortex.
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PMID:Acute toxicological experiment of T-2 toxin in rabbits. 262 5

After allogeneic bone marrow transplantation certain patterns of infectious complications emerge that follow the clinical course, are correlated to the immunobiology of transplantation and are almost predictable in their character and expression. The preparative regimen, designed to generate complete aplasia, will be associated with severe and sometimes life-threatening bacterial infections, predominantly with Gram-negative organisms derived from bowel flora, but also Gram-positive skin saprophytes. In this early aplastic phase, life-threatening viral infections are less common, consisting mainly of herpes simplex and possibly Epstein-Barr stomatitis and BK papovavirus cystitis. Systemic infections with invasive filamentous fungi are rare and are seen only when the induced aplasia is markedly prolonged. Once early marrow recovery has been achieved, systemic infections will generally disappear unless acute graft-vs.-host disease develops. This complication, which will lead to the breakdown of natural barriers such as skin and gastrointestinal epithelium and the marked impairment of all systemic defense mechanisms, can cause polymicrobial infections as well as set the stage for life-threatening viral infections. Such opportunistic viral infections, leading to either interstitial pneumonia or hemorrhagic gastroenteritis, are the major threat in the early recovery phase after engraftment has taken place. Usually caused by cytomegalovirus and rotavirus, respectively, these infections are the primary expression of the severe combined immunodeficiency post transplant, statistically associated with the presence of acute graft-vs.-host disease and amenable to immunologic manipulations. With the recovery of cellular and humoral immune function derived from transplanted donor lymphoid cells, the third phase of infectious complications is reached, covering 3 months to 2 years post grafting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infections and immunodeficiency in bone marrow transplantation. 304 57


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