Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E(2) (PGE(2)) and PGE(1) in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the alpha-adrenoceptor in this tissue was also studied.2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration-dependent flattening of the noradrenaline concentration-effect curve.3 A concentration-dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin-depressed responses to noradrenaline was: PGE(2), PGE(1), PGA(1), PGF(2alpha), PGA(2).4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE(2) and PGE(1) restored responses towards the control level whereas PGA(1), PGA(2) and PGF(2alpha) increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed.5 At concentrations equi-effective in restoring depressed responses to control levels PGA(1) but not PGE(2), caused a parallel shift of the noradrenaline concentration-effect curve to the left and a small, gradual rise in the basal perfusion pressure.6 The reason for the differing effects remains obscure but does not seem to involve a change in the alpha-adrenoceptor as indicated by the pA(2) of phentolamine. Furthermore, the restorative and potentiating effect of PGA(1) is not mediated by blockade of neuronal uptake of noradrenaline.7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug-receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.
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PMID:The influence of prostaglandins on noradrenaline-induced vasoconstriction isolated perfused mesenteric blood vessels of the rat. 20 65

Previous studies have reported indirect evidence for the mediation of folate antagonism in the induction of malformations by diphenylhydantion. We have demonstrated that a teratogenic regimen of folate-deficiency and antagonism using 9-methyl PGA in the rat produces significantly decreased rates of oxygen consumption in the maldeveloping embryos. The present study reports similar reductions in oxygen uptake by mouse embryos from mothers treated with teratogenic doses of diphenylhydantoin, and documents a significant depression of the actual folate levels in such embryos. The differences are less significant with lower doses of diphenylhydantoin, and do not occur with a nonteratogenic dose.
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PMID:Folate antagonism following teratogenic exposure to diphenylhydantoin. 45 36

In eight volunteers the effect of pentagastrin (0.15, 1.0 and 6.0 microgram/kg body weight/h), secretin (0.5 and 1.0 clinical units/kg b.w./h), and cholecystokinin (CCK) (0.5 and 1.0 Ivy dog units/kg b.w./h) on the gastric secretion of pepsin was investigated to ascertain whether interaction occurred. A high intraindividual variation was found, and also a significant washout of pepsin in the initial period after stimulation. Pepsin secretion was stimulated after pentagastrin (50% above basal level) and even more after secretin (75%-200% above basal level), whereas no stimulation but a tendency for depression was seen after CCK. With the doses of gastrointestinal hormones used in this investigation, no interaction between secretin and CCK on gastric secretion of pepsin in man was demonstrated.
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PMID:Effect of Pentagastrin, secretin, and cholecystokinin on gastric secretion of pepsin in man. 679 45

The gastric secretion and gastric mucosal blood flow (GMBF) under simultaneous action of M1-cholinergic antagonist gastrocepine (3 mg/kg i.v.) and L-Ca2+-channels blocker verapamile (1.25 mg/kg i.v.) were investigated in urethane-anaesthetized rats. The stomach was perfused with saline, and GMBF was measured by using hydrogen gas clearance technique. The acid production under combined action of both blockers was lower by 57.3% and 18.6%, than in case of separate action of gastrocepine and verapamile accordingly. Pepsin concentration decreased by 32%, which did not differ from verapamile action alone. The above changes of gastric secretion was accompanied by significant decrease of GMBF. Inhibition of M1-cholinergic receptors by gastrocepine did not show their key role in basal gastric secretion in rats, but they exacerbate L-Ca2+-channels blocker action. We conclude, that enhance of acid output inhibition is related to the simultaneous depression of nervous impulses in ganglionic neurons and acethylcholine release from parasympathetic postganglionic neurons. Synchronous block of M1-cholinergic receptors and L-Ca2+-channels of smooth muscles stomach vessels resulted in reducing of gastric mucosal blood flow.
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PMID:[Blood circulation and secretory function in the gastric mucosa during inhibition of M1-cholinergic receptors and L-Ca2+-channels]. 1580 Dec 5

The aim of this work was to develop two logistic regression models capable of predicting physical and mental health related quality of life (HRQOL) among rheumatoid arthritis (RA) patients. In this cross-sectional study which was conducted during 2006 in the outpatient rheumatology clinic of our university hospital, Short Form 36 (SF-36) was used for HRQOL measurements in 411 RA patients. A cutoff point to define poor versus good HRQOL was calculated using the first quartiles of SF-36 physical and mental component scores (33.4 and 36.8, respectively). Two distinct logistic regression models were used to derive predictive variables including demographic, clinical, and psychological factors. The sensitivity, specificity, and accuracy of each model were calculated. Poor physical HRQOL was positively associated with pain score, disease duration, monthly family income below 300 US$, comorbidity, patient global assessment of disease activity or PGA, and depression (odds ratios: 1.1; 1.004; 15.5; 1.1; 1.02; 2.08, respectively). The variables that entered into the poor mental HRQOL prediction model were monthly family income below 300 US$, comorbidity, PGA, and bodily pain (odds ratios: 6.7; 1.1; 1.01; 1.01, respectively). Optimal sensitivity and specificity were achieved at a cutoff point of 0.39 for the estimated probability of poor physical HRQOL and 0.18 for mental HRQOL. Sensitivity, specificity, and accuracy of the physical and mental models were 73.8, 87, 83.7% and 90.38, 70.36, 75.43%, respectively. The results show that the suggested models can be used to predict poor physical and mental HRQOL separately among RA patients using simple variables with acceptable accuracy. These models can be of use in the clinical decision-making of RA patients and to recognize patients with poor physical or mental HRQOL in advance, for better management.
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PMID:Logistic regression models for predicting physical and mental health-related quality of life in rheumatoid arthritis patients. 1856 85

Oxygen was taken up by both intact and broken chloroplasts when catalase was posioned. In confirmation of other work we found that oxygen enters the electron transport chain of isolated chloroplasts by oxidizing the primary photoreductant of system I. In isolated intact chloroplasts this reaction proceeds in addition to oxygen evolution by PGA reduction. The reductant produced by photosystem II does not react with oxygen at a significant rate.In normal leaves oxygen depresses chlorophyll fluorescence. However, this depression does not take place in DCMU poisoned leaves or in a mutant having a nonfunctional photosystem II; furthermore, another mutant with a weakly functioning photosystem I gave only a very small fluorescence depression with oxygen. This shows that the site of interaction of oxygen is at the reducing end of the electron transport chain. This view is supported by the extent of the fluorescence depression in leaves as a function of oxygen concentration which is very similar to the oxygen dependence of oxygen uptake by isolated chloroplasts.An oxygen requirement of isolated intact chloroplasts reducing PGA and nitrate was indicated by lower reaction rates and faster decay of activity under nitrogen than under air.
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PMID:Effects of oxygen on the electron transport chain of photosynthesis. 2452 48