Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II (AII) stimulates capacitation and fertilizing ability in mammalian spermatozoa, with the binding of AII to its receptors resulting in stimulation of cAMP production in both uncapacitated and capacitated cells. This study investigated possible mechanisms whereby AII affects cAMP availability. The first question was whether extracellular Ca2+ is required for responses in mouse spermatozoa and, using chlortetracycline fluorescence analysis, it was clear that cells responded to AII only when the medium contained CaCl2, with both 90 microM and 1.80 mM supporting a significant acceleration of capacitation. Consistent with those results, AII significantly stimulated cAMP production in both CaCl2-containing media tested, the response being greater in that containing 1.80 mM. Several different agents that might affect the signalling pathway stimulated by AII were then evaluated in uncapacitated suspensions. Chlortetracycline analysis revealed that pertussis toxin abolished responses to AII, suggesting the involvement of an inhibitory Galpha subunit; dideoxyadenosine, a specific membrane-associated adenylyl cyclase (mAC) P-site inhibitor, also blocked responses, suggesting involvement of an mAC. cAMP determinations confirmed that both reagents also abolished AII's stimulation of cAMP. In contrast, nifedipine, a Ca2+ channel blocker, did not inhibit AII's effects on spermatozoa. Finally, in capacitated suspensions, both pertussis toxin and dideoxyadenosine were again shown to block AII's stimulation of cAMP. These results suggest that responses to AII involve an inhibitory G protein and an mAC, but it is likely that AII-receptor coupling does not stimulate directly mAC but rather does so in an indirect manner, perhaps by altering the intracellular Ca2+ concentration.
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PMID:Mechanisms of action of angiotensin II on mammalian sperm function. 1569 15

Polymyxin is an effective antibiotic for the treatment of severe infections produced by Ps. aeruginosa, H. pertussis, H. influenzae, E. coli, and A. aerogenes. Its toxicity to date precludes its general use in infections susceptible to its therapeutic effects. Chloromycetin has been demonstrated to be an effective antibiotic agent for the treatment of rickettsial diseases and typhoid fever. It will undoubtedly prove effective in the treatment of other infections produced by certain Gram-negative micro-organisms and viral agents. Aureomycin has been shown to be an active antibiotic agent against rickettsial diseases, primary atypical pneumonia, acute brucellosis, pneumococcal, streptococcal, and staphylococcal infections, urinary tract infections produced by E. coli, A. aerogenes and Strept. fecalis, certain types of infections of the eye, and in subacute bacterial endocarditis when the infecting agent is Strept. fecalis. Its clinical use in forms of extrapulmonary tuberculosis is in a completely experimental stage. It is not recommended in typhoid fever or in infections due to Ps. aeruginosa or P. vulgaris, and it seems to be ineffective in whooping cough. To date, neither chloromycetin nor aureomycin has shown significant signs of systemic toxicity.
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PMID:The experimental and clinical use of polymyxin, chloromycetin, and aureomycin. 1811 50