Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrointestinal degradation of urea might, according to a new hypothesis, have consequences for the regulation of acid-base balance as well as control of breathing during infancy. Thirteen infants were investigated from their first few days of life to the age of 6 months by collecting faecal samples at the age of 3 days, 2, 3, and 6 months, respectively. The faecal microflora was determined after aerobic and anaerobic cultivation and the faecal urease activity was assessed after 36 h aerobic and anaerobic preincubation. The infants were mostly breast fed and had a faecal microflora containing anaerobic bacteria such as Bifidobacteria, Bacterioides and Lactobacilli but also aerobics such as Escherichia coli, Enterococci and sometimes Klebsiella. The faecal pH increased from approximately 5.30 to 5.90, the pH after anaerobic preincubation being on an average 0.2 pH units lower than after aerobic preincubation. Simultaneously the nitric oxide production of the faecal specimens increased approximately 10-fold and the urease activity decreased by a factor of 3 to 5. We also found an inhibitory action of nitrate, nitrite (in mumolar concentration) and nitric oxide (in parts per million concentration) on the faecal urease activity. Hence, the present results warrant further research in order to determine more precisely the action of different concentrations of various nitrous oxides on individual bacterial species, and furthermore, to assay the faecal urease activity in victims of sudden infant death syndrome as well as in infants dead due to other causes.
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PMID:Faecal microflora and urease activity during the first six months of infancy. 905 88

Helicobacter pylori may be linked to sudden infant death syndrome (SIDS) through synthesis of inflammatory cytokines, particularly interleukin-1, which can produce fever, activation of the immune system, and increased deep sleep. A relatively minor respiratory or enteric infection, together with overwrapping and prone sleep position could then induce terminal hypoxemia. Alternatively, H. pylori produces large amounts of urease which, if aspirated in gastric juice, could reach the alveolae, react with plasma urea, and produce ammonia toxicity leading to respiratory arrest. Epidemiological similarities between H. pylori and SIDS are presented along with possible transmission mechanisms for H. pylori which support this hypothesis.
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PMID:Proposed link between Helicobacter pylori and sudden infant death syndrome. 942 99