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Biomedical subjects

S Wallach

Publications and source records attributed to S Wallach.

103 records · Page 6Linked to original sources
PubMed1966

The cellular transport of calcium in rat liver.

The bidirectional transport of calcium in rat liver was studied using slices labeled with Ca(47) in a closed two compartment system. Steady-state conditions were observed with influx and efflux transfer coefficients of 0.070 and 0.018 per minute, respectively. The rapidly exchanging cell fraction of calcium existed at a concentration three times higher than the average cell concentration of calcium and occupied cell loci comprising less than 25% of the cell mass, suggesting that calcium associated with the cell membranes, nuclei, and mitochondria participated in the rapidly exchanging fraction. At pH 7.4 and 377deg;C, the influx transfer coefficient was 25% above the steady-state condition and accumulation of calcium by the slices occurred. Studies of the effects of varied physical and chemical conditions revealed that the influx transfer coefficient was increased by elevated pH, strontium, certain metabolic inhibitors, and 2 mM concentrations of cyclic adenosinemonophosphate and adenosinetriphosphate. The influx transfer coefficient was decreased by reduced temperature, decreased pH, magnesium, and 10 mM adenosinetriphosphate. The efflux transfer coefficient was increased by elevated pH, strontium, iodoacetate, and adenosinetriphosphate, and was decreased by reduced temperature and by N-ethylmaleimide. These data support the thesis that cell transport of calcium is accomplished by the attachment of calcium atoms to the cell surface and transport through the plasma membrane bound to either specific carriers or to membrane constituents. Conditions which change the affinities, capacities, and mobilities of plasma membrane ligands that bind calcium or cause extracellular chelation of calcium are capable of altering the rate of calcium transport.

Adenine Nucleotides↗
PubMedDate not supplied

Furosemide vasodilates the canine gastrointestinal tract.

The ability of furosemide to induce vasodilation in the canine gastrointestinal system was studied by quantitative flowmetry. Blood flow and conductance increased maximally by 60 per cent in the stomach and duodenum and by 80 per cent in the small and large intestine. Vasodilation was evident at 2.4 mg/kg furosemide and higher. The onset of vasodilation occurred at 24 to 30 seconds and was maximal at 36 seconds in the stomach, at 66 seconds in the duodenum, at 78 to 84 seconds in the small intestine, and at 90 seconds in the large intestine. Hepatic arterial, splenic, and renal blood flows were unchanged. Simultaneous arteriovenous sampling from the small intestine indicated that the increased blood flow was not associated with increased O2 consumption. However, CO2 addition to the venous effluent decreased by 70 per cent. These data indicate that furosemide has a vasodilatory action on the gastrointestinal tract due either to a delayed effect on the vascular smooth muscle cell or on anaerobic bowel wall metabolism. The CO2 data are compatible with, but do not prove, stimulation of secretion of HCO3- by the intestinal mucosa.

Animals↗
PubMedDate not supplied

Osteoporosis: the need for comprehensive treatment guidelines.

Osteoporosis is a debilitating disease that results in nearly 1.3 million fractures per year in the United States. The cost of treating these fractures has been estimated to be as high as $10 billion per year. These costs are expected to more than double during the next 50 years unless comprehensive programs of prevention and treatment are initiated. Both pharmacologic and nonpharmacologic interventions (eg, diet and exercise) have been shown to have a significant impact on the incidence of osteoporosis, depending on the time of their application. Unfortunately, osteoporosis is often not diagnosed until after fractures have occurred, when it may be too late for treatment to have a major impact. To be most effective, therapy should be started early, before serious bone loss has occurred. Because of its efficacy and relatively low acquisition cost, long-term hormone replacement therapy (HRT) is considered first-line pharmacologic therapy for the prevention of osteoporosis. However, for various reasons, less than 25% of US women who might benefit from HRT are receiving it. Aside from HRT, the only other products approved by the US Food and Drug Administration for the treatment of osteoporosis are salmon calcitonin and alendronate. Several other agents are under development, including sustained-release fluoride and other products in the bisphosphonate class. The development and adoption of early detection programs and treatment guidelines are crucial to help ease the economic burden of osteoporosis. These guidelines should incorporate preventive measures such as diet and exercise, risk assessment through proper screening programs, and the appropriate use of pharmaceutical products. The purpose of this paper is to discuss relevant economic issues associated with osteoporosis and discuss the need for a management algorithm that could be used to more efficiently prevent and treat this disease. We conclude that further modeling is needed to determine which programs and treatments are most cost-effective within each at-risk subgroup. As clinicians better understand the need for preventive care and the advantages of the various pharmacologic therapies, patients with osteoporosis will receive higher-quality and more efficient medical care.

Calcitonin↗
PubMedDate not supplied

Relation of magnesium to osteoporosis and calcium urolithiasis.

Magnesium influences mineral metabolism in hard and soft tissues indirectly through hormonal and other modulating factors, and by direct effects on the processes of bone formation and resorption and of crystallization (mineralization). Its causative and therapeutic relationships to calcium urolithiasis (CaUr) are controversial despite an association between low urinary Mg and CaUr. Recent studies have also found a tendency to low serum and/or lymphocyte Mg levels in CaUr. Despite earlier studies demonstrating an inhibitory effect of Mg supplementation on experimental CaUr in animals and in spontaneous CaUr in humans, at least two properly controlled clinical trials of Mg supplementation have failed to demonstrate a beneficial effect on CaUr frequency. With regard to the skeleton, experimental studies have shown that Mg depletion causes a decrease in both osteoblast and osteoclast activity with the development of a form of 'aplastic bone disease'. At the same time, bone salt crystallization is enhanced by Mg deficiency. Conversely, Mg excess impairs mineralization with the development of an osteomalacia-like picture, and may also stimulate bone resorption independently of parathyroid hormone. Whether or not Mg depletion may be a causal factor in human osteoporosis is also controversial, and there are conflicting reports as to the Mg content of osteoporotic bone. Small decreases in serum and/or erythrocyte Mg in osteoporotic patients have been reported, and one author has noted improved bone mineral density with a multinutrient supplement rich in Mg. The extant data are sparse and indicate a clear need for more rigorous study.

Animals↗