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Biomedical subjects

S O Thier

Publications and source records attributed to S O Thier.

At least 19 recordsLinked to original sources
PubMed1992

Preventing the decline of academic medicine.

Academic medicine in North America has been highly successful in many ways in the last 50 years, including being able to resist change while unprecedented and fundamental changes are taking place in the practice, technology, and financing of medicine. This stance places academic medicine at risk of being bypassed by events. To prevent this, what balance between rigidity and flexibility should be sought? The author addresses this question by first reviewing the history of academic medicine and then defining in detail three current problems in medical education and two in biomedical research, two of academic medicine's domains. All these problems have in common some form of harmful dissociation of endeavors: for example, in education, there is a dissociation between both the teaching and academic clinical practice of medicine and the health care needs of the public. The author then proposes solutions to the problems, based on his examination of three major principles that motivate academic medicine. For example, he maintains that the teaching of all the medical sciences should be part of, and equal in quality to, the overall program of sciences in a university, and that the interdependence of medical schools and universities should be nurtured. He also maintains that the narrow conceptual framework of medicine that focuses on mechanisms of disease must be expanded to include rigorous attention to such areas as prevention, technology assessment, and organization of care.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Medicine↗
PubMed1991

Health care reform: who will lead?

The United States is almost alone among industrialized nations in failing to assure access to at least some health care for all of its citizens. Three major obstacles impede the provision of universal access. First is the deeply embedded sense among our citizens and in our health care system that some persons are more deserving than others of care. Second is a focus on costs and reimbursement mechanisms rather than on defining effective and appropriate care. Third and most serious is an absence of leadership in addressing the problems of access and of reform in the U.S. health care system. In choosing among the possible leaders, which include the federal government, the states, the business sector, unions, and physicians, a compelling argument can be made that physicians should lead, particularly in defining effective and appropriate care. Physicians may also lead in redesigning the health care system, but they are likely to be only one interested voice in the debates about financing health care.

Attitude to Health↗
PubMed1986

Anticystinuric effects of glutamine and of dietary sodium restriction.

We studied four patients with cystinuria to assess the effects of glutamine and dietary sodium on the urinary excretion of dibasic amino acids. In Patient 1, at an ad libitum dietary sodium intake of about 300 mmol per day, oral administration of glutamine led to reproducible and marked anticystinuria and antiornithinuria, whereas the excretion of lysine and arginine was not significantly affected. In Patient 2, at an ad libitum dietary sodium intake of about 150 mmol per day, no effect of glutamine could be demonstrated in studies lasting up to three weeks. Since the principal difference between Patients 1 and 2 was their dietary intake of sodium, Patient 3 was studied during dietary sodium intakes of 150 and 300 mmol per day. His cystine excretion was found to be higher at 300 than at 150 mmol per day. Glutamine suppressed his cystine excretion at a sodium intake of 300 mmol per day but had no effect at 150 mmol per day. When the effect of a further reduction in sodium intake alone was studied in a fourth patient, a decrease of 150 to 50 mmol per day was found to reduce cystine excretion markedly within 17 days. The low-sodium diet alone also reduced the excretion of lysine, arginine, and ornithine. We conclude that glutamine may reduce the excretion of dibasic amino acids at a high sodium intake but not at an intake of about 150 mmol per day. However, since a sodium-dependent excretion of the dibasic amino acids occurs at an intake down to about 50 mmol of sodium per day, dietary restriction of sodium can provide a safe approach to the treatment of cystinuria.

Administration, Oral↗
PubMed1986

Potassium physiology.

Potassium is the most abundant exchangeable cation in the body. It exists predominantly in the intracellular fluid at concentrations of 140 to 150 meq/liter and in the extracellular fluid at concentrations of 3.5 to 5 meq/liter. The maintenance of the serum potassium concentration is a complex bodily function and results from the balance between intake, excretion, and distribution between intracellular and extracellular space. Ingested potassium is virtually completely absorbed from and minimally excreted through the intestine under nonpathologic circumstances. Renal excretion of potassium, which is the major chronic protective mechanism against abnormalities in potassium balance, depends on filtration, reabsorption, and a highly regulated distal nephron secretory process. Factors regulating potassium secretion include prior potassium intake, intracellular potassium, delivery of sodium chloride and poorly reabsorbable anions to the distal nephron, the urine flow rate, hormones such as aldosterone and beta-catecholamines, and the integrity of the renal tubular cell. The maintenance of distribution between the inside and outside of cells depends on the integrity of the cell membrane and its pumps, osmolality, pH, and the hormones insulin, aldosterone, beta 2-catecholamines, alpha-catecholamines, and prostaglandins. Both distribution across cell membranes and/or renal excretion of potassium may be altered by pharmacologic agents such as diuretics, alpha- and beta-catechol antagonists and agonists, depolarizing agents, and digitalis. Problems with hypokalemia and hyperkalemia can be analyzed on the basis of potassium physiology and pharmacology; proper treatment depends on an accurate analysis.

Aldosterone↗
PubMed1979

Effect of acute metabolic acidemia on renal electrolyte transport in man.

The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p less than 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 +/- 16 mueq/min (mean +/- SEM) to 310 +/- 49 mueq/min (p less than 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O/(CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV. UKV fell acutely from 91 +/- 13 to 45 +/- 5 mueq/min (p less than 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 +/- 15 to 143 +/- 18 microgram/min and fractional excretion of calcium increased from 0.55 +/- 0.13 to 1.24 +/- 0.21% (p less than 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 +/- 0.05 to 4.30 +/- 0.03 mg/dl (p less than 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independetn of changes in parathyroid hormone (as reflected by urinary cAMP).

Acidosis↗