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Biomedical subjects

J Hood

Publications and source records attributed to J Hood.

At least 91 records · Page 5Linked to original sources
PubMed1978

Birth weight standards in a community of mixed racial origin.

A prospective study of approximately 2000 consecutive deliveries at a north London hospital, with a mixed population distribution of Caucasian, British and Irish, Indian and West Indian mothers was made between May 1975 and August 1976. Most of the results are based on 1322 births of known gestational age. Babies of Indian mothers were found to be approximately 300 g lighter than their Caucasian equivalents at term, and by United Kingdom birth weight standards, 15 per cent of the babies of Indian mothers were below the fifth centile. Birth weights of babies of West Indian mothers ranged between those of the Indian and the Caucasians.

Black or African American↗
PubMed1978

A multislice positron emission computed tomograph (PETT IV) yielding transverse and longitudinal images.

We designed, built, and tested a positron emission tomograph (PETT IV) capable of providing seven slices of the human body simultaneously. PETT IV utilizes a moving hexagonal array of 48 scintillation detectors placed around the subject. Each detector consists of a cylindrical activated sodium iodide crystal optically coupled to two photomultiplier tubes. The multislice capability is achieved by comparing the light outputs of the two photomultiplier tubes in each detector. The images are displayed either as transverse or as longitudinal tomographic sections. This system provides high sensitivity and resolution, and permits rapid and accurate three-dimensional imaging of the head and body.

Electrons↗
PubMed1976

SC 23992: radioreceptor assays for therapeutic and side effects.

1. A new spirolactone (SC 23992) has been assayed in vitro to determine its affinity for mineralocorticoid and androgen receptors. 2. Although two to eight times as potent as anti-aldosterone agent as Aldactone in vivo, SC 23992 has only approximately 10% the potency in vitro. 3. This discrepancy between potency in vivo and in vitro appears to be explained on radioreceptor assay of the principal metabolites of Aldactone SC 23992. 4. SC 23992 may represent an antimineralocorticoid with less antiandrogen side effects.

Animals↗
PubMed1970

Autonomic reflexes and vascular reactivity in experimental scurvy in man.

Ascorbic acid is a required cofactor in the conversion of dopamine to norepinephrine in vitro, and the deficiency of this vitamin in guinea pigs is associated with degeneration of autonomic ganglion cells and with cardiac supersensitivity to norepinephrine. Because of these findings, we tested the hypothesis that ascorbic acid deficiency in man alters autonomic cardiovascular reflexes and vasomotor responses to adrenergic stimuli. We studied five normal volunteers who had been deprived of ascorbic acid for a period of 3 months; they had developed symptoms and signs of scurvy and their plasma levels of ascorbic acid averaged 0.178 +/-SE 0.07 mg/100 ml. We repeated the studies after giving the subjects vitamin C for a period of 4 months; they had become asymptomatic and their plasma ascorbic acid had increased to an average of 1.68 +/-0.151 mg/100 ml. Blood flow to the left forearm (plethysmograph), arterial and central venous pressures, and heart rate were measured before and after exposure of the lower half of the body to subatmospheric levels of pressure and before and after intravenous and intra-arterial (left brachial artery) infusions of norepinephrine and tyramine. Average values of blood flow (7.9 +/-1.4 ml/min per 100 ml), arterial pressure (91.2 +/-4.6 mm Hg), heart rate (68 +/-4.4 beats/min), central venous pressure (6.1 +/-1.1 mm Hg), and plasma catecholamines (0.68 +/-0.20 mug/liter) obtained during ascorbic acid deficiency were not altered significantly after correction of the deficiency. Vasoconstrictor responses to intra-arterial norepinephrine and tyramine were augmented after vitamin repletion. During ascorbic acid deficiency, four subjects had reduced responsiveness of resistance vessels of the forearm to lower body negative pressure as compared to the responsiveness observed after vitamin repletion. Reflex tachycardia during lower body negative pressure and reflex bradycardia during the pressor responses to intravenous tyramine and norepinephrine were similar during the two studies. The results suggest that the decreased vascular responsiveness to intra-arterial norepinephrine and tyramine and to lower body negative pressure during ascorbic acid deficiency is caused by a defect in the ability of resistance vessels to constrict in response to adrenergic stimuli. Ascorbic acid deficiency in man does not interrupt autonomic reflexes and does not appear to cause significant depletion of endogenous norepinephrine.

Ascorbic Acid↗