Publications by authors named "Oates J"

The effect of tartrazine on prostaglandin production was evaluated in several in vitro systems in order to elucidate the interrelationship between aspirin-sensitive asthma and tartrazine. Unlike the nonsteroidal anti-inflammatory drugs, tartrazine did not inhibit cyclooxygenase activity in sheep seminal vesicles, guinea pig lung microsomes, and human platelets. Tartrazine had no effect on the activation of acyl hydrolase, which is the rate-limiting step in prostaglandin production.

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We assessed the release of neuronal and adrenomedullary catecholamines in response to various stimuli of the sympathetic nervous system in normal subjects. Plasma catecholamines and their urinary metabolites, normetanephrine and metanephrine, were measured. Sodium restriction increased supine plasma norepinephrine by 37% and ambulatory plasma norepinephrine by 22%, with urinary normetanephrine excretion increased 29%.

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Renal pappillae from rats were incubated in vitro. The release of prostaglandin by this tissue was found to be inversely related to the glucose concentration of the buffer. Estimates of prostaglandin release were determined by a rat stomach strip bioassay, and in some instances, gas-chromatography and mass spectrometry.

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We investigated the effect of stimuli activate the sympathetic nervous system on plasma catecholamines, renin activity, urinary metanephrine and normetanephrine, and various hemodynamic parameters in normal subjects (NIs) and borderline hypertensive (BH) subjects. No differences were observed in sympathetic nervous system activity or renin activity when the subjects were in the resting state on a 150 mEq sodium diet. However, the BH group exhibited greater responses in terms of plasma catecholamines and plasma renin activity in response to sodium deprivation and treadmill exercise.

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Urethral specimens from 726 patients with nongonococcal urethritis (NGU) were examined for Chlamydia trachomatis, Ureaplasma urealyticum, and Mycoplasma hominis. Chlamydiae were isolated from 35.9% of ureaplasma-positive patients and from 36.

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Although prostaglandins E(2) and F(2alpha) have been suggested as mediators of the pulmonary hypertension seen after endotoxin infusion or during alveolar hypoxia, their precursors, the endoperoxides (prostaglandins G(2) and H(2)) are much more potent vasoconstrictors in vitro. In this study we compared the effects of prostaglandin (PG)H(2), a stable 9-methylene ether analogue of PGH(2) (PGH(2)-A), PGE(2), and PGF(2alpha) on pulmonary hemodynamics in awake sheep. The animals were prepared to allow for measurement of (a) lung lymph flow; (b) plasma and lymph protein concentration; (c) systemic and pulmonary vascular pressures; and (d) cardiac output.

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1 A rapid, accurate and convenient technique for determination of acetylator phenotype of patients or subjects has not been available for routine clinical application. 2 An improved method for rapid and convenient determination of acetylator phenotype is described. 3 The plasma concentrations of dapsone (DDS) and monoacetyldapsone (MAD) were measured 3 h after a single oral 100 mg dose of dapsone using a specific and sensitive high performance liquid chromatographic assay.

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Feeding the ethyl ester of dihomo-gamma-linolenic acid for 25 days to rabbits resulted in increased PGE1 (20 to 30-fold) and PGE2 (1.5-fold) output by a hormone responsive, in vitro, renal papilla preparation. The relative amount of PGE1 increased from less than 5% of PGE2 in controls to 25-35% of PGE2 in the papillae of 20 : 3 omega 6-supplemented animals.

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A controlled pulsating-force system for the orthodontic movement of teeth was designed and its biologic effects were examined, with the dog serving as an experimental model. This system was applied to the maxillary right second premolar while a continuous force was delivered to the maxillary left second premolar. After a 12-day experimental period in which pulsating forces were used, the amount of tooth movement and the radiographic and histologic changes were comparable to those produced by continuous force.

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The effect of prostaglandin I2 (prostacyclin) on renal and intrarenal hemodynamics and function was studied in mongrel dogs to elucidate the role of this novel prostaglandin in renal physiology. Starting at a dose of 10(-8) g/kg/min, PGI2 decreased renal vascular resistance and redistributed the blood flow away from the outer cortex (zone 1) and towards the juxtamedullary cortex (zone 4). At 3 X 10(-8) g/kg/min, the renal vascular resistance decreased even further, but at this dose the mean arterial blood pressure also declined 13% indicating recirculation of this prostaglandin.

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[3H8]Thromboxane B2 was biosynthesized and infused into an unanesthetized monkey. Several urinary metabolites were isolated and their structures elucidated using gas chromatography-mass spectrometry. In addition to the major urinary metabolite, dinor-thromboxane B2, a series of metabolites resulting from dehydrogenetion of the alcohol group at C-11 were identified: 11-dehydro-thromboxane B2, 11-dehydro-15-keto-13,14-dihydro-2,3-dinor-thromboxane B2, and 11-dehydro-15-keto-13,14-dihydro-19-carboxyl-2,3,4,5-tetranor-thromboxane B2.

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We studied the effects of inhibiting prostaglandin synthesis on the renal blood flow and glomerular filtration rate of four conscious dogs with chronic unilateral renal artery stenosis. Dogs were prepared by exteriorizing the bladder trigone to allow repeated split renal function studies. Renal artery stenosis was produced with a Goldblatt clamp on one renal artery.

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Sick low birth weight infants (LBWI) are prone to develop rapid onset of essential fatty acid (EFA) deficiency. EFAs serve as precursors for prostaglandins (PGs). We measured the excretion of the major urinary metabolite of prostaglandins E1 and E2, 7alpha-hydroxy-5,11-diketotetranorprostane-1,16-dionic acid (PGE-M), in three EFA-deficient and in nine thriving neonates.

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The dose and plasma levels of indomethacin correlated with inhibition of prostaglandin synthesis as measured both by urinary excretion of the major metabolite of prostaglandin E2 (PGE-M) and by the release of prostaglandin E2 from thrombin-stimulated platelets. Considerable intersubject variability was observed in the suppression of PGE-M excretion. In some patients 37.

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To investigate the relation between acetvlator phenotype and the development of procainamide-induced lupus, we determined the rate of development of antinuclear antibodies in 20 patients of known acetylator phenotype receiving chronic procainamide therapy. The duration of therapy required to induce antibodies in 50 per cent of slow (11) and rapid (nine) acetylators was 2.9 and 7.

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Whole cell preparations of rat stomach corpus, jejunum, and colon were incubated and the released prostaglandin E2 (PGE2), PGF2alpha, PGD2, 15 keto-13,14 dihydro PGE2, and 15 keto-13, 14 dihydro PGF2alpha were measured by combined gas chromatography-mass spectrometry. All regions made PGD2 and possessed a high capacity for production 15 keto-13,14 dihydro derivatives of both PGE2 and PGF2alpha. Hypertonic sucrose solutions resulted in concentration-dependent increases in prostaglandin release, particularly of PGE2 and its metabolite.

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Microsomes prepared from rabbit renal cortex were found to synthesize substantial amounts of 6-ketoprostaglandin F1alpha from prostaglandin G2 or arachidonic acid during an incubation. In contrast, no 6-ketoprostaglandin F1alpha was formed by renal medullary microsomes which synthesize predominantly prostaglandin E2. Mass spectral confirmation of the structure of 6-ketoprostaglandin F1alpha from these incubations demonstrates the ability of the renal cortex to synthesize prostacyclin.

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In 17 patients, 15 women and 2 men, acute retention of urine developed in association with an attack of anogenital herpes. Constipation, blunting of sensation over the 2nd and 3rd sacral dermatomes, and neuralgic pains in the same area (with absence of the bulbocavernosus reflex in some individuals) suggested localised lumbosacral meningomyelitis with involvement of mainly sacral-nerve roots. The urinary dysfunction persisted on average for ten days and in 4 patients was severe enough to warrant catheterisation.

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