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Biomedical subjects

M B Tomaselli

Publications and source records attributed to M B Tomaselli.

5 recordsLinked to original sources
PubMed1996

Streamlining breast disease management.

New technology has been developed for performing percutaneous (non-surgical) breast biopsy and tracking the outcome of breast disease patients. The procedure, mammotomy, takes a biopsy of breast tissue lesions quickly during the same office visit at which the screening mammography discovers an abnormality. Because the procedure is non-invasive, it bypasses the extra time and expense of open surgical biopsies. In conjunction with mammotomy, Breast Cancer Manager (BCM) software is intended to streamline breast care data management. These technologies provide the cornerstone of a comprehensive breast health plan that can streamline patient care across specialties. This plan uses an organ-based, multispecialty coalition of practitioners related to the diagnosis and treatment of breast disease. The BCM software provides a central, complete record of all care given to a patient from the first screening mammogram through surgery and adjuvant therapy. All practitioners will have access to its information and at the same time be able to add to it, making it the repository of patient and practice data for management analysis and outcomes reporting. This article looks at the treatment paradigm of breast disease and details the potential cost savings made possible by mammotomy and the BCM software.

Biopsy, Needle↗
PubMed1981

Elliptical erythrocyte membrane skeletons and heat-sensitive spectrin in hereditary elliptocytosis.

Erythrocyte membranes (ghosts) and membrane skeletons (submembranous reticula of spectrin, actin, and protein 4.1 prepared by extracting ghosts with Triton X-100) from 15 patients with hereditary elliptocytosis (HE) were elliptical, which indicates that the primary defect responsible for the abnormal shape of these cells resides in the skeleton. The protein composition of HE skeletons was normal, but in three kindreds purified spectrin heterodimer from 7/7 HE patients was heat sensitive and denatured at 48.0 +/- 0.1 degrees C instead of 49.0 +/- 0.3 degrees C (P less than 0.0005). Heat sensitivity was detected by precipitation and, in the spectrin from one patient, by changes in circular dichroism. In one other kindred spectrin dimer from 3/3 patients denatured at the normal temperature. In two of the three kindreds with heat-sensitive spectrin, intact erythrocytes exhibited budding and fragmentation at the temperature at which spectrin denatured. In the third kindred spectrin was heat sensitive, but erythrocytes were not. The symptoms in the latter kindred were clinically more severe (hemolytic HE with spherocytosis) than in the other three (mild HE). We conclude that defects in the erythrocyte membrane skeleton may be a common feature of HE. As judged by heat denaturation of erythrocytes and purified spectrin dimer, three phenotypically distinct forms of HE exist, two of which are characterized by defective, heat-sensitive spectrin. It remains to be determined whether the molecular defect in spectrin responsible for heat sensitivity is the primary genetic defect responsible for HE.

Drug Stability↗
PubMed1979

Hemolytic anemias associated with deficient or dysfunctional spectrin.

Elliptocytes from patients with hereditary elliptocytosis (HE) form elliptical ghosts and membrane skeletons. The composition of HE skeletons is quantitatively normal; however, in some but not all kindreds the major membrane skeletal protein, spectrin, is abnormally heat-sensitive, presumably due to a molecular defect which diminishes its conformational stability. Red cells from four mutants of the common house mouse (Mus musculus) with severe, recessive hemolytic anemias show marked membrane budding, fragmentation, and spherocytosis, which suggest membrane instability. Ghosts spontaneously vesiculate and are spectrin-deficient. The amount of spectrin varies from none to one-half the normal amount and correlates with the clinical severity of the four mutations. The cause of this deficiency remains to be determined. These mutants prove that spectrin is a critical determinant of membrane structural integrity and provide a unique opportunity to test, in intact red cells, putative functions of spectrin. Spectrin extracted from ghosts at low ionic strength is heterogeneous. At physiologic ionic strengths part (46 +/- 5%) is polymerized (P-spectrin) and complexed with actin, and part remains as nonpolymerized spectrin dimers and tetramers (NP-spectrin). We postulate that these are native membrane species which exist in a metabolically controlled equilibrium in vivo and that the proportion of these species regulates membrane shape, strength, and flexibility.

Animals↗