Titlebook: Mechanisms in the Pathogenesis of Enteric Diseases 2; Prem S. Paul,David H. Francis Book 1999 The Editor(s) (if applicable) and The Author

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Comparative Pathogenesis of Enteric Viral Infections of Swine,eriod. Most infect the small intestinal enterocytes, inducing various degrees of villous atrophy and subsequently a malabsorptive, maldigestive diarrhea. In addition rotaviruses possess an enterotoxin (NSP4) which induces a secretory diarrhea in mice. These viruses have distinct predilections for di

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Molecular Evolution of Corona-And Toroviruses,positive-stranded RNA viruses infecting mammals and birds. The order consists of the bigeneric family ., to which the genera . and . have been assigned, and the monogeneric family . (Murphy et al., 1995).

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A Viral Enterotoxin, Rotavirus is recognized as the most important etiologic agent of infantile gastroenteritis, and studies of rotavirus serve as models to understand the complex interactions between enteric viruses and the multifunctional cells of the gastrointestinal tract. Understanding such interactions is signifi

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Comparative Pathology of Bacterial Enteric Diseases of Swine,hese infections include diarrhea, reduced growth rate, weight loss, and death of preweaned, weanling, grower-finisher, young and adult age breeding animals. The most common etiological agents include ., and . (.) spp. With the exception of ., the cause of swine dysentery, and ., the cause of prolife

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Mechanisms and Impact of Enteric Infections,ctive interventions. While the overwhelming mortality (>3 million children per year) due to diarrheal diseases is well-recognized, the potential long-term impacts of enteric infections and early childhood diarrhea morbidity are just beginning to be appreciated. Furthermore, several enteric infection

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Insulin Modulates Intestinal Response of Suckling Mice to the , Heat-Stable Enterotoxin,) of two day old Swiss Webster suckling mice were used. Five, 10,25, and 50μg of insulin were given orally to half the mice in each group respectively. The rest of the mice in each group were given normal saline as intra-litter controls. After 7 days, the suckling mouse assay for STa was performed o

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Reproduction of Lesions and Clinical Signs with a CNF2-Producing , in Neonatal Calves,ain in order to reproduce clinical signs and lesions. We observed diarrhoea in each inoculated calf, bacteraemia (80%), the presence of CNF2+ bacteria in the lungs (80%) and in the liver (20%). The observed lesions were inflammation of the entire gut, hypertrophy of the mesenteric lymph nodes and he

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