Biomedical subjects
Publications and source records attributed to P P Tóth.
Splenic infarction is a clinical entity seldom encountered. The most frequent causes of splenic infarction include thromboembolic phenomena, hematologic malignant neoplasms, and vasculitides. We describe a patient who sustained splenic infarction secondary to diabetes-induced, small-vessel atherosclerotic disease.
Turner's syndrome is one of the most frequently occurring chromosomal defects and is associated with a well-characterized set of anatomic malformations. We studied clinical findings in an elderly woman who was diagnosed as having cytogenetically proved Turner's syndrome late in life. Because most patients with Turner's syndrome have normal intelligence and mild phenotypic abnormalities, the condition was never properly diagnosed in many affected women born earlier in this century. Given the range of clinical abnormalities and physiologic deficits to which these women are predisposed, it remains important to diagnose and treat them accurately irrespective of age.
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A comatose male newborn infant with congenital lactic acidosis caused by pyruvate decarboxylase deficiency was treated with dichloroacetate (DCA), which stimulated an 88% drop in serum lactate concentration and reversed his coma. The response to DCA was temporary and the lactic acidosis worsened until his death, but DCA may confer more lasting benefit in less severely affected infants.
1. In the absence of exogenous Ca(II), Pi induces a swelling change that is kinetically first order with k = 1.08 +/- 0.1 min-1. The first-order rate constant is independent of [Pi] over the range of 0.5-45 mM. 2. In the presence of exogenous substrate, the volume change induced by Pi is monophasic and can be reversed by ADP. 3. The swelling process and the approach to steady state is accompanied by controlled losses of both K+ and Mg(II) from within the mitochondria. 4. The loss of K+ is biphasic as a function of time with ki = 14.1 +/- 1.6 and k2 = 4.4 +/- 0.34 nmol min-1 mg mitochondria-1. 5. The loss of Mg(II) is monophasic and the rate at which this cation is released decreases as a function of time. Ca(II) fluxes are not involved in the volume occurring secondary to Pi uptake. 6. In the absence of exogenous substrate, Pi induces a triphasic change in mitochondrial volume. 7. The sequence of volume changes corresponds to an initial first-order swelling secondary to the addition of Pi, a contraction apparently triggered by the loss of approximately 85% of total intra-mitochondrial Mg(II), and a second larger swelling phase that cannot be reversed with ADP. 8. The Pi-induced swelling of chick heart mitochondria is not inhibited by EGTA and does not depend on the provision of exogenous Ca(II). 9. The Ca(II) and Mg(II) ions released from within the mitochondria are responsible for activating divalent cation-dependent ATPases which cosediment with isolated chick heart mitochondria.