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Biomedical subjects

J D Martin

Publications and source records attributed to J D Martin.

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

Effects of bromocriptine mesylate on the composition of the mammary secretion in non-breast-feeding women.

A double-blind trial was performed on 26 women, who had elected not to breast-feed their infants, to determine the effect of bromocriptine mesylate (2.5 mg twice daily for 14 days postpartum) on the composition of the mammary secretion during lactogenesis. Mammary secretion (less than 5.0 ml) was collected from each breast of each woman at daily intervals during the 14-day treatment period and the progressive changes in the concentration of the milk constituents, lactose, alpha-lactalbumin, serum albumin, total protein, lactoferin, IgA, IgG, sodium and potassium were determined. The degree of milk leakage and breast engorgement were also assessed. Both the subjective assessments and the changes in the concentration of the milk constituents demonstrated that lactogenesis occurred between about Day 2 and Day 5 postpartum in the placebo group (in the absence of the suckling stimulus) but was suppressed in the bromocriptine-treated group.

Breast↗
PubMed1976

Dapsone motor neuropathy--an axonal disease.

Dapsone produces a potentially reversible toxic neuropathy, with its primary effect on the soma and axons of motor neurons as opposed to myelin. There is very little evidence to suggest involvement of sensory axons in most cases; if present, it would appear minimal. A "dying back" of motor axons is postulated to produce the clinical features of primarily distal weakness and wasting. Recovery appears to occur via axon regeneration and peripheral sprouting. The sporadic occurrence of this neuropathy may be due to slow acetylation of dapsone in some patients.

Action Potentials↗
PubMed1975

Arterial stationary wave phenomenon in Tolosa-Hunt syndrome.

In a patient with Tolosa-Hunt syndrome, serial cerebral angiograms showed arterial stationary wave phenomenon and persistent deformity of the carotid siphon. Stationary arterial waves are noted in only 0.3 percent of cerebral angiograms and have not been reported in Tolosa-Hunt syndrome. In accordance with theories proposed by Theander and New, we felt that the intense stenosis of the carotid siphon produced by the periarteritis in our patient caused relative obstruction and high resistance, giving rise to resonance of arterial pressure waves and creation of the arterial stationary waves.

Adolescent↗
PubMed1975

Highlights in the development of arterial surgery.

It is concluded that progress in medicine has been maintained at such a rapid pace that the delivery system has had difficulty in keeping up. This has been excellently demonstrated by the progress in the category of vascular surgery. Achievements have placed added demands on available trained personnel, materiel, and most importantly, the financial resources of every community and the government fulfilled, the problem will continue to be a vexing one and will not be easy to solve. The success of our scientific efforts will continue to be costly.

Arteries↗
PubMed1974

Effect of calcium and vasopressin on the response of frog skin to prostaglandin E1.

1. Prostaglandin E(1) increases sodium transport as measured by short circuit current (SCC) across isolated frog skin whereas calcium, added to the external Ringer fluid, decreases sodium transport. To help establish the site of action of prostaglandin the possible interaction of these two agents on sodium transport has been examined.2. The effect of a standard dose of prostaglandin (0.5 x 10(-6)M) on the short circuit current was tested on paired skins with either zero or high calcium (22.4 mM) in the external Ringer fluid. In ten experiments the responses to prostaglandin (expressed in muA/cm(2)) were not significantly affected by external calcium.3. In another series of experiments the chelating agent, EGTA, was included in calcium-free external Ringer in order to promote greater depletion of skin calcium. The response of these skins to the standard dose of prostaglandin was of the same order of magnitude as that of control skins. The response was not sustained in contrast to that of normal skins and skins in high-calcium fluids.4. In a further series of experiments the reverse procedure was adopted whereby the response of the skin to low and high doses of calcium in the external Ringer was recorded in control conditions and when the skin had responded fully to twice the standard dose of prostaglandin. In addition, the calcium-sensitive current was calculated for each skin in both circumstances. The latter was unchanged on addition of prostaglandin, and graded doses of calcium caused the same degree of inhibition of the short circuit current.5. The results show no interaction between external calcium and prostaglandin and also no need for external calcium in prostaglandin stimulation of sodium transport.6. The findings do not support the concept of chelation by prostaglandin of calcium from critical sites on the skin as the primary mechanism of its action on sodium transport. The results closely parallel those of a similar type of study into the relationship between vasopressin and external calcium on frog skin also.7. When frog skin has responded fully to either prostaglandin E(1) or vasopressin, it shows no response to the other, although removal of calcium from the external Ringer fluid causes a further increase in short circuit current.8. Vasopressin causes a further increase in short circuit current in skins treated with prostaglandin F(1alpha). Prostaglandin F(1alpha) may be a weaker agonist on frog skin than either vasopressin or prostaglandin E(1).

Animals↗