Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the influence of prolonged administration of the 5-HT1A receptor agonists (8-OH-DPAT or buspirone) or its antagonist, NAN-190 to rat pups on development of their cortical barrel field. Pups were injected daily with the drugs starting from the day of birth till either the 5th postnatal day or the 22-25th postnatal day and were perfused one day later. Square areas of their whisker barrel fields were measured on tangential sections of the cortex stained for cytochrome oxidase. Injections of 8-OH-DPAT or buspirone till the 5th postnatal day did not change any of the investigated parameters, while injections of NAN-190 resulted in 15% reduction of the pups' body and brain weight and proportional reduction of the square area of their barrel fields. Groups treated till the 22-25th postnatal day showed similar results. Some of these pups were injected with [C(14)]2-deoxyglucose to investigate the strength of responses of their cortical barrels to stimulation of corresponding vibrissae. The cortical area labeled with 2-deoxyglucose after stimulation of vibrissae of the row C was narrower in the NAN-190 injected rats. This functional deficit was more pronounced than the anatomical one, which resembled the effects of neonatal serotonin depletion (Neuroreport, 1997). Therefore, the results of injecting NAN-190 to the rat pups point to a deficit of trophic developmental influences of serotonin, adding new arguments for the hypothesis of a trophic role of 5-HT1A receptors in the brain development.
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PMID:Postnatal treatment with NAN-190 but not with 5-HT1A receptor agonists retards growth of the rat brain. 1602 84

This review argues that knowledge of microbial physiology and metabolism is a prerequisite to understanding mechanisms of pathogenicity. The ability of Neisseria gonorrhoeae to cope with stresses such as those found during infection requires a sialyltransferase to sialylate its lipopolysaccharide using host-derived CMP-NANA in the human bloodstream, the ability to oxidize lactate that is abundant in the human body, outer-membrane lipoproteins that provide the first line of protection against oxidative and nitrosative stress, regulation of NO reduction independently from the nitrite reductase that forms NO, an extra haem group on the C-terminal extension of a cytochrome oxidase subunit, and a respiratory capacity far in excess of metabolic requirements. These properties are all normal components of neisserial physiology; they would all fail rigid definitions of a pathogenicity determinant. In anaerobic cultures of enteric bacteria, duplicate pathways for nitrate reduction to ammonia provide a selective advantage when nitrate is either abundant or scarce. Selection of these alternative pathways is in part regulated by two parallel two-component regulatory systems. NarX-NarL primarily ensures that nitrate is reduced in preference to thermodynamically less favourable terminal electron acceptors, but NarQ-NarP facilitates reduction of limited quantities of nitrate or other, less favourable, terminal electron acceptors in preference to fermentative growth. How enteric bacteria repair damage caused by nitrosative and oxidative damage inflicted by host defences is less well understood. In both N. gonorrhoeae and Escherichia coli, parallel pathways that duplicate particular biochemical functions are far from redundant, but fulfil specific physiological roles.
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PMID:Legless pathogens: how bacterial physiology provides the key to understanding pathogenicity. 2249