Deficits in temporal processing correlate with clinical progression in Huntington's disease.

OBJECTIVES: Precise temporal performance is crucial for several complex tasks. Time estimation in the second-to-minutes range-known as interval timing-involves the interaction of the basal ganglia and the prefrontal cortex via dopaminergic-glutamatergic pathways. Patients with Huntington's disease (HD) present deficits in cognitive and motor functions that require fine control of temporal processing. The objective of the present work was to assess temporal cognition through a peak-interval time (PI) production task in patients with HD and its potential correlation with the Unified Huntington's Disease Rating Scale (UHDRS). MATERIALS AND METHODS: Patients with molecular diagnosis of HD and controls matched by age, sex and educational level (n=18/group) were tested for interval timing in short- (3 seconds), medium- (6 seconds) and long (12 seconds)-duration stimuli. RESULTS: Significant differences were observed in the PI task, with worse performance in HD compared to controls. Patients underestimated real time (left-shifted Peak location) for 6- and 12-second intervals (P<.05) and presented decreased temporal precision for all the intervals evaluated (P<.01). Importantly, a significant correlation was found between time performance and the UHDRS (P<.01). Patients' responses also deviated from the scalar property. CONCLUSIONS: Our results contribute to support that timing functions are impaired in HD in correlation with clinical deterioration. Recordings of cognitive performance related to timing could be a potential useful tool to measure the neurodegenerative progression of movement disorder-related pathologies.

Kaliuretic response to potassium loading in amiloride-treated dogs.

To assess whether an intact mechanism of sodium transport in the distal nephron is a prerequisite for the development of a kaliuresis in response to an acute potassium load (0.4 M KCl, 1 ml/min), the effects of a simultaneous infusion of KCl and amiloride (1 mg/kg/h) were evaluated in anesthetized dogs. A major reduction in potassium excretion mainly due to a sharp decrease in urine K+ concentration to one tenth of control levels was found after amiloride. The simultaneous infusion of KCl and amiloride resulted in a rapid and major increase in kaliuresis that was accounted for mostly by the rise in urine K+ concentration. The increased kaliuresis after the acute potassium infusion was of similar magnitude when expressed as percent value of control to that previously reported in dogs not receiving amiloride; the absolute rates of K+ excretion, however, were only 2.7 and 7.3% (before and after KCl infusion, respectively) of the values in dogs not receiving amiloride. Our observations suggest that potassium infusion in the intact dog increases kaliuresis primarily as a result of a more favorable chemical gradient of this cation between blood and/or distal tubular cells and urine. Yet, when a chemical gradient is the only driving force of potassium secretion, as was the case in our amiloride-treated dogs, the absolute rate of kaliuresis is very modest. The presence of an unimpaired electrical profile and sodium transport mechanisms in the distal nephron, although not critical for the development of kaliuresis in response to a K+ load, accounts for a severalfold rise in renal potassium excretion above basal levels.

Cefoperazone en el tratamiento de infecciones respiratorias graves del tracto respiratorio inferior. / Cefoperazone in the treatment of lower respiratory tract infections

Se trataron con cefoperazone sodico 20 pacientes (promedio 45.7 anos) portadores de una infeccion grave del tracto respiratorio inferior (8 bronquitis, 5 bronconeumonias, 3 abscesos de pulmon, 2 neumonias lobares, 1 empiema y 1 bronquiolitis). De los 20 pacientes, 18 presentaban una enfermedad predisponente a la infeccion y 12 de ellos requirieron intubacion endotraqueal y/o traqueostomia con asistencia respiratoria mecanica. El germen mas frecuentemente aislado (90% de las veces por puncion transtraqueal) fue la Pseudomonas aeruginosa, siendo en todos los casos sensible a la prueba por difusion de disco.El cefoperazone se administro por vias endovenosa o intramuscular a una dosis de dos a tres gramos cada 12 horas y el tratamiento duro, en promedio, 12.1 dias (rango entre 6 y 19 dias). La respuesta global fue entre excelente y buena en 85% de los pacientes,con una cura bacteriologica de 70%. No hubo efectos colaterales ni alteraciones de laboratorio atribuibles a la droga en ninguno de los 20 pacientes. El cefoperazone sodico resulto ser un antibiotico eficaz y seguro para el tratamiento de las infecciones graves del tracto respiratorio inferior

Correction of severe metabolic acidosis: a physiological approach.

1 - Five patients with severe metabolic acidosis secondary to methanol poisoning were studied before and after receiving 6.7 to 10 mEq NaHCO3/kg body weight. 2 - Two thirds of the infused HCO3- left the extracellular space and, since its apparent volume of distribution was much larger than under normal conditions, it largely overestimated HCO3- needs. On the contrary, the volume of distribution of the buffer base excess was found to be more stable and little affected by the acid-base status. 3 - Based on these observations, a simple method for estimating HCO3- needs in severe metabolic acidosis is proposed, requiring only the initial excess buffer base space which is calculated from body weight and blood buffer base excess values obtained before and after a first dose of bicarbonate.

Correction of severe metabolic acidosis: a physiological approach.

1 - Five patients with severe metabolic acidosis secondary to methanol poisoning were studied before and after receiving 6.7 to 10 mEq NaHCO3/kg body weight. 2 - Two thirds of the infused HCO3- left the extracellular space and, since its apparent volume of distribution was much larger than under normal conditions, it largely overestimated HCO3- needs. On the contrary, the volume of distribution of the buffer base excess was found to be more stable and little affected by the acid-base status. 3 - Based on these observations, a simple method for estimating HCO3- needs in severe metabolic acidosis is proposed, requiring only the initial excess buffer base space which is calculated from body weight and blood buffer base excess values obtained before and after a first dose of bicarbonate.

Correction of severe metabolic acidosis: a physiological approach

1 - Five patients with severe metabolic acidosis secondary to methanol poisoning were studied before and after receiving 6.7 to 10 mEq NaHCO3/kg body weight. 2 - Two thirds of the infused HCO3- left the extracellular space and, since its apparent volume of distribution was much larger than under normal conditions, it largely overestimated HCO3- needs. On the contrary, the volume of distribution of the buffer base excess was found to be more stable and little affected by the acid-base status. 3 - Based on these observations, a simple method for estimating HCO3- needs in severe metabolic acidosis is proposed, requiring only the initial excess buffer base space which is calculated from body weight and blood buffer base excess values obtained before and after a first dose of bicarbonate.