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Biomedical subjects

D Levenson

Publications and source records attributed to D Levenson.

8 recordsLinked to original sources
PubMed1991

Candida zeylanoides: another opportunistic yeast.

A patient with a long history of scleroderma and gastrointestinal malabsorption requiring total parenteral nutrition was admitted with Candida zeylanoides fungemia. The yeast responded to therapy, but on two subsequent admissions for episodes of fever the blood cultures yielded the same yeast. The identity of the Candida species was established biochemically by both the API (Analytab) and Vitek system approaches. C. zeylanoides ATCC 20356 and ATCC 7351 served as controls for these analyses and for antifungal susceptibility studies and restriction endonuclease analyses of chromosomal DNA. These investigations indicated that representative isolates of the yeasts from the three episodes were identical and differed in several respects from the ATCC strains, which did not share many of the characteristics bands with the DNA restriction fragment analysis. C. zeylanoides variants capable of tolerating 35 degrees C can complicate the recovery of patients, especially individuals compromised by their underlying disease.

Amphotericin B↗
PubMed1990

Electrophysiologic changes accompanying Wallerian degeneration in frog sciatic nerve.

The time course of the physiological changes accompanying Wallerian degeneration in the frog is markedly prolonged in comparison with that in mammals. Following transection of frog sciatic nerve, stimulation of the distal segment results in muscle contraction of normal amplitude through day 4, after which tension and EMG signals decline rapidly to levels that are undetectable by day 7. The compound action potential in the severed nerve continues for a much longer period of time, however, persisting as long as approximately 6 weeks. The amplitude remains at normal levels for nearly 3 weeks, after which it declines progressively, approaching zero at approximately 6 weeks. Conduction velocity remains normal in both alpha- and beta-fibers for approximately 3 weeks; thereafter, velocity in the alpha-fibers declines to approximately 71% of normal, and beta-fiber conduction is no longer detectable. Contraction could be elicited by direct stimulation of the muscle during the entire 6-week period of the study. The failure of nerve-mediated muscle activity in the face of persistent nerve conduction could be the result of either a defect in the most distal portions of the nerve fibers or a defect in neuromuscular transmission. These results suggest that EMG evaluation may be more sensitive than nerve conduction studies for clinical assessment of axonopathy at early stages.

Action Potentials↗
PubMed1986

A diamond jubilee.

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Architecture↗
PubMed1978

Cardiovascular responses to blockade of angiotensin and alpha-adrenergic receptors.

Both angiotensin and alpha-adrenergic blocking agents reduce arterial blood pressure in hypovolemic states. We have compared the effects of an angiotensin antagonist (saralasin) and an alpha-adrenergic blocking agent (phenoxybenzamine) in supramaximal dosage on cardiac output, total peripheral resistance, and venous tone in rabbits rendered hypovolemic by restriction of sodium intake, supplemented by a furosemide-induced diuresis 48 h prior to study. Saralasin (10 microgram/kg per min) reduced arterial blood pressure significantly (-15 +/- 1.2 mmHg) despite an unchanged cardiac output (P less than 0.025) due to a fall in total peripheral resistance. Phenoxybenzamine (5 mg/kg) induced a much larger fall in arterial blood pressure (-28 +/- 3.6 mmHg), despite an identical reduction in total peripheral resistance, because cardiac output also fell (+/- 9 ml/kg per min). The reduction in cardiac output was associated with a significant increase in hindlimb venous distensibility (P less than 0.001) after alpha-adrenergic blockade. Saralasin, conversely, had no influence on venous tone. Adrenergic mechanisms contribute to cardiovascular homeostasis through an influence on both arteriolar and venous tone, whereas the effect of angiotensin is directed entirely to the arteriolar side of the circulation.

Animals↗