Management training in pathology.
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Biomedical subjects
Publications and source records attributed to E S Benson.
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Escalating health care costs constitute a public issue of paramount importance today, Among the leading growth factors in this rise is the cost of hospital services, notably laboratory services. With respect to the clinical laboratory, rising costs appear to be almost entirely attributable to expanding utilization and introduction of new services. The clinical laboratory has gone through a technological revolution in two decades that has changed it from a largely manual to a highly automated system of great speed and capacity. This change had produced a change in the style of providing services, a change that includes the provision of quantities of unsolicited data. A parallel change in the style of use of the laboratory has taken place on the part of patient care physicians from a relatively sparing, problem oriented use pattern to a relatively lavish, data oriented one. These reciprocal changes have transformed medicine, in the United States, at least, into a relatively high laboratory use culture. Abandonment of the new technology and return to a simpler, more primitive laboratory world would be a drastic and most inappropriate response to the new situation. Furthermore, arbitrary measures such as rationing, quotas, and tariffs are, if enacted, almost certain to fail. The most effective long term strategies, though more demanding of time and effort, lie through modification of physician behavior through the pathways of education and research. Education and research initiatives now in progress can in time influence laboratory use patterns of physicians at all career levels, improving the logic of test use and providing more strategic, prudent, and cost effective overall laboratory utilization practices. These approaches will require much improved communication between laboratory and bedside and a new intense involvement of laboratory physicians and scientists in the tasks of helping to improve the use of laboratory tests and laboratory data.
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Loss of cristae and matrix occur in the mitochondria of skeletal muscles prior to any observable changes in myofibrillar proteins during the development of rigor mortis. Care must be observed because ultrastructural changes in mitochondria in some studies may be attributed to a specific trauma, whereas the changes may be due to the lower pH in postmortem muscle.
The hydrogen exchange kinetics of human oxy-, deoxy-, and cyanomethemoglobin have been measured as a function of pH by the tritium tracer method. At 5 degrees C and in phosphate buffer both liganded and unliganded forms of ferrohemoglobin exhibit deviations from the regular pH dependence of exchange that is characteristic of cyanomethemoglobin. In oxyhemoglobin, the deviation from the normal exchange pattern is centered at pH 7.4 and is in the direction of increased exchange or solvent accessibility. The effect in deoxyhemogloin, while occurring at the same pH and being of the same order of magnitude, is in the opposite direction, thus suggesting a pH-induced conformational transition leading to a less accessible structure. The width of these pH-induced deviations in solvent accessibility is approximately 1 pH unit in both cases. We propose a model in which specific interactions between charged groups in both froms of ferrohemoglobin account for these deviations.
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Ultrastructural repair of the morphological damages produced in nutritional muscular dystrophy was studied by refeeding dystrophic rabbits with vitamin E. Weanling (1.2 kg body weight) rabbits were fed a vitamin E-deficient diet for 24 days. Half of this group was then sacrificed and the remainder was given an initial oral dose of 50 mg of DL-alpha-tocopherol acetate and a vitamin E supplemented diet for 28 days. Control animals were fed a vitamin E supplemented diet with 50 mg of DL-alpha-tocopherol acetate per kilogram of diet. Abnormalities of dystrophic muscles included streaming Z-disk, degenerated mitochondria, fragmented sacroplasmic reticulum and development and aggregation of myelin figures. The effect of vitamin E therapy resulted in significant repair of the dystrophic muscle. Small localized sections of rehabilitated muscle revealed abnormal mitochondria and residual myelin figures.
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