Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P00790 (
PGA
)
2,475
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Testicular interstitial cells were utilized to study the effects of prostaglandins (PG) on in vitro testosterone production and to examine the role of cyclic adenosine-3',5'-monophosphate (cAMP) in this process. Testosterone production was assessed after 3 hour incubations while cAMP accumulation was examined after a 0.5 hour incubation period. Testosterone and cAMP were measured by radioimmunoassay. None of the PGs tested (
PGA
, PGA2, PGB1, PGE1, PGE2, PGF1alpha PGF2alpha) altered basal testosterone production when present in incubates at concentrations of 1.3 X 10(-8) M to 1.3 X 10(-4). However, at concentrations of 1.3 X 10(-4) M all of these PGs were capable of decreasing Luteinizing Hormone (LH; 100ng)-induced testosterone production. The inhibition of LH-induced testosterone production by the B, E and F series PGs was less pronounced than that for the A series. PGA1 and PGA2 exhibited 80% and 95% inhibition, respectively, at 1.3 X 10(4) M. The inhibitory action of 4 X 10(5) M PGA1 or PGA2 was evident within 30 minutes. Preincubation of interstitial cells with indomethacin (10(-5) or 10(-6) M) for 30 minutes did not alter subsequent basal or LH (100ng)-induced testosterone production. Accumulation of cAMP was stimulated by LH (10 microgram) or by PGs (1.3 X 10(-4) M PGA1, PGA2, PGB1, PGE1 or PGF2alpha). The PG-induced cAMP accumulation thus occurred at concentrations where LH-stimulated testosterone production was inhibited. Furthermore, PGA1 and PGA2 (1.3 X 10(-4) M) inhibited testosterone production induced by either 3-isobutyl-1-methyl xanthine (MIX; 10(-4) M or 10(-3) M) or dibutyryl cAMP (dbcAMP; 10(-4) M or 10(-3) M). These results indicate that PGs can block testosterone production by a direct effect on testicular interstitial cells and suggest that PGs exert their inhibitory action distal to stimulation of cAMP formation. PGs do not appear to play a role in the mechanism of LH action.
Steroids
1978 Oct
PMID:Prostaglandin inhibition of testosterone production induced by luteinizing hormone, dibutyryl cyclic AMP or 3-isobutyl-1-methyl xanthine in dispersed rat testicular interstitial cells. 8 81
The efficacy, safety and health-economic outcomes were compared between corticosteroid and non-corticosteroid treatments in acute gout patients. All electronic literatures comparing the curative effects or full economic evaluations of corticosteroids versus non-corticosteroids on acute pain in acute gout patients and published until June 30, 2017 in any language were searched through PubMed, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. Pooled odds ratios with 95% confidence intervals and standard(or weighted) mean difference were calculated using random-or fixed-effects models according to the I
2
statistic test of heterogeneity. Economic elevations were combined through qualitative narrative synthesis. Finally, seven randomized controlled trials(RCTs) involving 929 patients were included here and suggested corticosteroids had comparable analgesic efficacy to non-corticosteroids on day 5. As for inflammation and
PGA
, corticosteroids might outperform non-corticosteroids in reducing tenderness and swelling. Corticosteroids versus non-corticosteroids could significantly reduce incidence of only serious adverse advents, but not total adverse advents, with substantial heterogeneity. Qualitative narrative synthesis of economic elevation involving only one study shows corticosteroids are more cost-effective than indomethacin. The existing RCTs do not provide sufficient or precise evidence that corticosteroids are superior to non-corticosteroids in pain relief of acute gout patients. Therefore, studies on chronic use of corticosteroids or comparative studies with colchicine, tramadol and/or opiates may be needed in the future, as is patient satisfaction with analgesic control.
Steroids
2017 12
PMID:Benefit-risk of corticosteroids in acute gout patients: An updated meta-analysis and economic evaluation. 2889 26