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Biomedical subjects

F Davidoff

Publications and source records attributed to F Davidoff.

At least 19 recordsLinked to original sources
PubMed1992

What is a curriculum?

Dissatisfaction with the current internal medicine residency experience has led to proposals for various new curricula. Unfortunately, the more basic question of "What is a curriculum?" or more accurately, "What curriculum model is most appropriate for clinical training?" has remained largely unexamined. The dominant curriculum model, although valuable, may not be adequate for the task. In its place we propose an experimental model that is more congruent with the realities of graduate medical education.

Curriculum↗
PubMed1989

Changing test ordering behavior. A randomized controlled trial comparing probabilistic reasoning with cost-containment education.

A controlled trial of a probabilistic reasoning curriculum to change test ordering behavior was conducted. Twenty-four medical interns in university, veterans, and community hospitals were randomly assigned to "probabilities" or "placebo" groups. Four months after the curriculum sessions, interns in the probabilities group wrote 16% fewer orders for "little ticket" laboratory tests than placebo group interns (P = 0.032). The probabilities group ordered fewer tests than the placebo group at all hospitals, but differences were greatest in the community hospital. Probabilities interns ordered ten of 97 tests significantly less often in the postcurriculum period than at baseline; multitest panels were particularly affected. Placebo curriculum interns ordered three of 97 tests less often in the postcurriculum period. Differences in test ordering were not explained by differences in case mix. Testing rates correlated slightly with case mix and length of stay at baseline; all three measures correlated strongly in the postcurriculum period. Teaching about probabilistic reasoning improves the efficiency of test ordering.

Clinical Laboratory Techniques↗
PubMed1978

Enhancement of the mitochondrial Ca2+ uptake rate by phenethylbiguanide and other organic cations with hypoglycemic activity.

At concentrations below 50 micronM, phenethylbiguanide enhanced the initial rate of enertized Ca2+ uptake into energized guinea pig liver mitochondria by as much as 45 per cent; Ca2+-stimulated O2 uptake increased in parallel. The biguanide concentration that enhanced Ca2+ uptake maximally was at least 15 times lower than that required for 50 per cent inhibition of respiration. Kinetic studies indicated that the enhanced rate of Ca2+ transport resulted from an increase in Vmax, while Km for Ca2+ was unaffected by the biguanide. Several other organic cations known to lower blood sugar in intact animals or to block the hepatic gluconeogenic response to glucagon also enhanced the mitochondrial Ca2+ uptake rate; three of these compounds did not inhibit respiration even at high concentrations. One organic cation, triethyltin, which is a potent respiratory inhibitor that does not affect blood sugar, had no effect on Ca2+ uptake. We concluded that enhancement of the mitochondrial Ca2+ uptake rate is related to the mechanism of therapeutic blood sugar lowering by these drugs, probably by impairing the gluconeogenic response of the liver to glucagon.

Animals↗
PubMed1976

(+)-alpha-(N-1-phenethyl) urea stereospecifically inhibits Ca2+ - but not ADP-stimulated mitochondrial respiration.

The (+) isomer of alpha-(N-1-phenethyl) urea is a moderately potent inhibitor of Ca2+ -stimulated mitochondrial respiration of 45Ca2+ uptake (50 percent inhibition at 0.18 mM) while having no effect on adenosine diphosphate-stimulated respiration; the (-) isomer is without effect up to 4 mM. beta-Phenethylurea does not inhibit with either stimulus. The data support the involvement of a Ca2+ -specific protein in energized mitochondrial Ca2+ uptake.

Adenosine Diphosphate↗
PubMed1976

Quantitative aspects of the metabolic response to pancreatic islet transplantation in rats with severe ketotic diabetes.

Injection of 100-140 mg/Kg of streptozotocin produced severe, ketotic diabetes in 12 pairs of adult rats. Transplantation of intact islets of Langerhans from syngeneic adult donors into a muscle pocket or a pouch created from pancreatic tissue of one animal from each pair eliminated ketonemia in the immediate postoperative period, while ketonemia persisted in the sham-operated controls. Mean survival of transplanted animals was 145 days, versus 70 days for controls. Mean body weight increased and blood sugar decreased in transplanted animals compared with controls; the differences were greatest in those animals which received the largest number of islets per unit body weight. In one animal, all metabolic indices returned to normal for a period of 8 wk following transplantation of 650 islets. After gaining to 300% of initial body weight, diabetes reappeared in this transplanted animal and was again reversed by a second transplantation. The metabolic data indicate that: (1) islet tissue from adult donors survives and functions in severely diabetic, ketotic hosts; and (2) metabolic response to transplantation is a function of the ratio of islet tissue to body mass, a minimum ratio of about 2-3 islets/gm body weight being required to maintain normal homeostasis.

Animals↗