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Biomedical subjects

L Lewis

Publications and source records attributed to L Lewis.

At least 109 records · Page 6Linked to original sources
PubMed1979

Case note descriptions of the placenta: are they worthwhile?

In 429 placentae, measurements were made of weight, diameter, shape, eccentricity of the cord and weight and length of the cord, and the results were compared with Apgar score of the infant at birth and its standardized birth weight. There was no evidence that cord eccentricity, placental shape or "thickness", or the dimensions of the cord had any significant relation to the growth of the fetus or its condition at birth. The value of routine recording of crude measurements and qualitative assessments of the placenta in case notes is questioned.

Apgar Score↗
PubMed1976

A model for therapeutic interventins on established coronary atherosclerosis in a nonhuman primate.

The observations so far conducted in cynomologus monkeys on semipurified diets containing butter and cholesterol suggest that this nonhuman primate is an excellent model for studying the therapy of established coronary atherosclerosis. (1) This species is available at a reasonable cost and can be kept in captivity in good health for prolonged periods of time. (2) It readily accepts semipurified diets with a percentage composition similar to that of human diets in the U.S. (3) Ingestion of these diets leads quite rapidly (around 6 months) to moderate coronary atherosclerosis. More prolonged feeding leads to lesions which are histologically very similar to those in man. (4) The distribution of lesions in the main coronary arteries is similar to that in man. (5) Methods to quantify the coronary lesions are available. (6) The diets can be so modified that cholesterol levels closely resemble those in hypercholesterolemic man. (7) The monkeys are amenable to several therapeutic regimens which show promise of arresting the progress or inducing the regression of the coronary lesions.

Animals↗
PubMed1975

Kinetics of renin-antirenin reaction: micromethods for the assay of renin and antirenin.

Indirect micromethods were designed for the assay of human renin (lower limit 0.25 times 10-4 U and of antirenin to human renin (lower limit 3 times 10-4 U), with the rat used for the bioassay of the angiotensin produced by the action of renin on renin substrate. This made possible the assay of unusually small amounts (0.01 mu1) of serum for antirenin. The Michaelis-Menten concept of a dissociating complex can be applied to the antireninrenin reaction: the rate constants for the formation and for the breakdown of the complex were k1 equal to 1.65 (ml/U antirenin per min) and k3 equal to 1.97 times 10-3 (U inactivated renin/U antirenin per min), respectively; the apparent Michaelis constant was 12 times 10-4 (U renin/ml). A second method of analysis was also applied by assuming the formation of a rather tight complex, with antirenin functioning as an irreversible inactivator of renin. Both methods of analysis yielded practically the same rate constant (k1 equal to 1.65 and k1 equal to 1.71), but the treatment according to the Michaelis-Menten equation affords a slightly better fit of the experimental data (accuracy equal to plus or minus 15.5 percent) than the second method of calculation (accuracy equal to plus or minus 21.6 percent).

Angiotensin II↗
PubMed1975

Release of antirenin to human renin by anaphylactic shock or by antihypertensive agents.

In dogs that have had repeated intravascular injections of small doses of human renin, even for long periods, the development of antirenin to human renin in the blood has not been previously noted, and their pressor response (30 mmHg) to 1 U of human renin has remained unchanged for years. In such dogs, however, a profound, abrupt fall of the systemic blood pressure, due to an anaphylactic reaction to human renin, or to the infusion of depressor agents, such as Arfonad, histamine, or diazoxide, resulted in the appearance in the blood of an inhibitor specific for human renin. This inhibitor was suddenly released into the blood-stream from the tissues in which it presumably had been stored, and it persisted, in a relatively high concentration, in some animals for months. It did not occur in dogs that had not previously received many injections of human renin. This study has shown that the inhibitor has all of the properties of antirenin to human renin. It abolished the pressor response to hog, dog, and rat renin or to angiotensin and norepinephrine. It inactivated human renin, but not dog renin, duringits incubation with renin substrate to form angiotensin.

Anaphylaxis↗