Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two clearly defined types of E. coli infection are recognised and the factors predisposing and giving rise to pathogenicity are discussed. The mode of action of enterotoxins in the secretary mechanism is thought to be through stimulation of adenyl cyclase activity. Treatment and prevention of the disease is considered in relation to the pathogenesis of the infection.
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PMID:Pathogenesis and treatment of Escherichia coli infections in calves. 79 47

Infection is one of the leading causes of death in elderly humans, and the importance of the early diagnosis of severe infection is undisputed. In the elderly a delay in diagnosis is often due to a reduced or absent fever. To understand more fully the pathogenesis of fever in senescence, we assessed the febrile response to E. coli peritonitis in 3-, 12-, and 24-month-old rats. Baseline temperatures were unchanged with age. Following infection with 1 x 10(8) CFU E. coli, a fever was evident in 2.8 h in the young, 3.9 h in the 12-month-old rats, and delayed until 5.8 h in the senescent rats. The magnitude of the fever was quantitatively less in the older rats compared with the two younger age groups throughout the time course of the fever. Because beta-adrenergic-mediated thermogenesis in brown adipose tissue has been implicated in the genesis of fever, we also assessed adenylate cyclase activity in this tissue. There was a progressive age-related decrease in both receptor- and postreceptor-stimulated adenylate cyclase activity. Our findings indicate there is both a delay in the onset of the fever and a reduced febrile response in the senescent rats following E. coli infection.
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PMID:The association of E. coli peritonitis with an impaired and delayed fever response in senescent rats. 162 91

This first article of a 2-part series examined the epidemiology, therapy, and prospects for immunoprophylaxis of diarrheal infections in infants. 3 main strains of Escherichia coli can be identifiied with the etiology of infantile diarrhea: enterotoxigenic E. coli, invasive E. coli, and enteropathogenic E. coli. Viral agents may also be the etiological agents. Specific pathogens can be identified in 55-85% of cases of infantile diarrhea today; in the 1960s, only 25-34% of cases could be identified by specific etiology. Rotavirus, the usual viral etiological agent, and shigella, salmonella, campylobacter, and yersinia occur less commonly in summer diarrhea syndrome than does E. coli. Possible mechanisms of infection for each specific pathogen are discussed. For example, enterotoxigenic E. coli infection is thought to proceed by a mechanism similar to that of cholera, where a toxin is released by the organism and attaches to intestinal epithelial cells. Then, part of the toxin molecule migrates to the inner plasma membrane where, by stimulating the adenylate cyclase-cyclic adenosine monophosphate system, it evokes active fluid and electrolyte transport and blockade of sodium and chloride reabsorption, resulting in copius diarrhea. Studies showing the existence of antibody to rotavirus in exposed populations indicate that immunoprophylaxis is conceivable.
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PMID:Acute diarrheal infections in infants I. Bacterial and viral causes. 624 8