Biomedical subjects

J C Falcone

Publications and source records attributed to J C Falcone.

21 records · Page 2Linked to original sources

PubMed1984

A comparison of students' clinical experience in family medicine and traditional clerkships.

The clinical experience of 40 Duke University medical students during their required two-month clinical clerkships is analyzed to compare experience on the traditional internal medicine, surgery, pediatrics, obstetrics-gynecology, and psychiatry clerkships with experience on a new family medicine clerkship. On the traditional clerkships, the students saw mostly hospital inpatients for an average of 36 different patients for 142 encounters and 300 problem contacts during a two-month rotation. On the family medicine clerkship, they saw mostly office ambulatory patients for an average of 184 patients for 236 encounters and 416 problem contacts. Traditional clerkships provided the most experience with neoplasms, blood problems, mental illness, obstetrical, perinatal, and congenital problems. The family medicine clerkship offered the most experience with circulatory, respiratory, digestive, neurological, musculoskeletal, and skin problems and with injuries. The family medicine clerkship contributed a substantive and important dimension to the clinical curriculum beyond that offered by the traditional five clerkships.

Clinical Clerkship↗

PubMed1982

A genetic defect in the binding of protein 4.1 to spectrin in a kindred with hereditary spherocytosis.

Indirect evidence suggests that the genetic defect in hereditary spherocytosis lies in the erythrocyte membrane skeleton, a submembranous meshwork of proteins (principally spectrin, actin, and protein 4.1) responsible for membrane shape and structural stability. To test this premise we systematically assayed the interactions of spectrin, the major skeletal protein, in six kindreds with autosomal dominant hereditary spherocytosis. In one these kindreds, enhancement of spectrin-actin binding by protein 4.1 was reduced, owing to a 39 +/- 4 per cent decrease (mean +/- S.D) in the binding of normal protein 4.1 by spectrin, in all of four members with the disorder. The defective spectrin was separated into two populations by affinity chromatography on immobilized normal protein 4.1. One population (41 +/- 2 per cent) lacked the ability to bind 4.1, but the other functioned normally. Presumable, the nonfunctional spectrin was the product of the autosomal dominant gene responsible for the hereditary spherocytosis in this kindred.

Actins↗

PubMedDate not supplied

Hemolytic anemia in the mouse. Report of a new mutation and clarification of its genetics.

A new mutation causing spherocytic, hemolytic anemia has been discovered in the house mouse. It is inherited as a single autosomal recessive gene, allelic with both sph and ha, which, in turn, were shown to be allelic with each other. A revised nomenclature for the three apparent alleles is proposed: sph (formerly sph), sphha (formerly ha), and sph2Bc (the new mutation). Like the other murine hemolytic anemias, sph2Bc involves a defect in the red blood cell membrane protein, spectrin.

Alleles↗