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Biomedical subjects

J Oates

Publications and source records attributed to J Oates.

80 records · Page 5Linked to original sources
PubMed1980

Effects of dietary variation in linoleic acid content on the major urinary metabolites of the E prostaglandins (PGE-M) in infants.

1. EFA deficiency is associated with the impairment of prostaglandin E synthesis, which is reflected by the decrease of the urinary excretion of PGE-M. 2. Excessive administration of Intralipid results in increase of the relative concentrations of linoleic acid content in plasma, RBC, and tissues with a concomitant decrease of its higher homologue, arachidonic acid. These changes are associated with diminished PGE-M excretion similar to that seen in EFA deficiency. Further investigation is needed into the pathophysiologic consequences of EFA deficiency and the excessive administration of linoleic acid since both are associated with altered prostaglandin biosynthesis and turnover in the new-born infant, particularly among those stressed low birth weight infants whose nutritional status and management are an indication for these modes of therapy.

Dietary Fats↗
PubMed1978

Decreased prostaglandin E turnover in infants with essential fatty acid deficiency.

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. There was no significant difference in PGE-M excretion between the sexes among thriving infants nor did PGE-M excretion appear to be affected by postconceptual age. However, a significant difference between the PGE-M excretion in the group of infants with EFA deficiency before and after treatment is apparent (P less than 0.05). Significant differences in PGE-M excretion were also found between the control group and the EFA-deficient infants. The severity of the EFA deficiency correlates directly with the degree of PGs excretion. The biochemical evidences of EFA deficiency and the decreased levels of PGE-M excretion are rapidly corrected when patients resume a diet containing EFA.

Fatty Acids, Essential↗
PubMed1977

Changes in bone and bone marrow of rabbits bearing the VX-2 carcinoma. A comparison of local and distant effects.

The VX-2 carcinoma in 32 New Zealand white rabbits was studied morphologically with respect to the osseous effects induced by the innoculation and subsequent growth of tumour in the soft tissues over periods ranging from 1 to 5 weeks. Although more severe changes were noted in bones of tumor-bearing than in non-tumor-bearing limbs, effects could be seen in both experimental situations. Severe bone marrow hyperplasia was noted consistently in tumor-bearing animals. A marked increase in numbers of osteoclasts over control rabbit bones was observed along the surface of bones near and distant from the tumor. Resorptive changes were also noted in the cortex of tumor-bearing rabbits. The increase in osteoclast numbers was related chronologically to the development of hypercalcemia and was proportional to the degree of hypercalcemia at the time the animals died. The number of osteoclasts was inversely proportional to the serum creatinine. A diminution of osteoclast numbers was noted in the latter stages of the disease. These changes may be the morphologic expression of humoral hypercalcemia accompanying the VX-2 carcinoma.

Animals↗
PubMed1973

Effects of a false neurotransmitter, p-hydroxynorephedrine, on the function of adrenergic neurons in hypertensive patients.

Previous studies have shown that amphetamine and p-hydroxyamphetamine impair adrenergic transmission, and it has been suggested that this effect is mediated by an active metabolite, p-hydroxynorephedrine (PHN). Studies in experimental animals have shown that PHN can deplete and substitute for norepinephrine (NE) in the transmitter pool, thus meeting the criteria of a false neurotransmitter. The pharmacologic effects of PHN on adrenergic function and NE synthesis were studied in eight hypertensive patients and compared with placebo. Mean erect and supine blood pressure (BP) decreased 22/14 and 9/6 mm Hg, respectively, during PHN 600 mg daily. The post-Valsalva diastolic overshoot was abolished. The pressor sensitivity to tyramine decreased whereas the pressor response to NE was enhanced. A mild natriuresis occurred. The 24 h urinary excretion of catecholamines and catecholamine metabolites during the administration of PHN compared with placebo changed as follows: vanillylmandelic acid (VMA), 42% decrease; NE. 42% decrease; normetanephrine (NM), 400% increase: metanephrine, unchanged; dopamine, 40% decrease; while homovanillic acid was unchanged. The sum of VMA, NE, and NM decreased 23%. The posttreatment urinary excretion of PHN was biexponential with first and second phase half-lives of 13 and 55 h. respectively. The time of the second phase closely approximated the recovery of the changes in BP and excretion of VMA. No effects of PHN on the central nervous system were observed. These studies show that PHN acts peripherally to interfere with adrenergic function and NE synthesis in hypertensive patients with a resultant decrease in BP.

Adult↗
PubMedDate not supplied

Effects of ischaemic heart disease, Crohn's disease and antimicrobial therapy on the pharmacokinetics of sulphinpyrazone.

The renewed interest in sulphinpyrazone in recent years has arisen from its potential to inhibit platelet aggregation. In vivo much of the activity is probably due to the thioether or sulphide metabolite which has a greater potency and a longer half-life than the parent compound. The sulphide metabolite is formed exclusively by the gut microflora in man. The pharmacokinetics of sulphinpyrazone (200 mg orally) have been studied, with particular attention to the formation of the sulphide metabolite, in groups of patients who might be expected to show abnormal formation of this active metabolite due to altered delivery of the drug to the lower gut or altered gut flora. Five patients studied 1 month after a myocardial infarction did not differ markedly from young, normal volunteers with respect to either sulphinpyrazone or its metabolite. Crohn's disease in the quiescent phase did not significantly alter the pharmacokinetics or metabolism of the drug, but 1 patient who had undergone a hemicolectomy formed negligible concentrations of the active metabolite. Antimicrobial therapy produced highly variable results with almost complete suppression of sulphide formation in some subjects but no apparent effect in others.

Adult↗