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ABSTRACTCobas Amplicor MTB and later Cobas TaqMan MTB were used to test a very large series of consecutive specimens received for tuberculosis diagnosis. Performance parameters were estimated and compared overall and for separate specimen categories. Both systems showed excellent specificity, and that of TaqMan was the higher. The sensitivities were similar but satisfactory only with respiratory specimens and smear-positive samples.

Urinary kallikrein excretion was evaluated in 85 normal subjects and in 149 uncomplicated and recently diagnosed essential hypertensive patients. Moreover, the possible interrelationships between urinary kallikrein excretion and age, sex, electrolyte excretion, and plasma renin activity were examined. In patients with essential hypertension, urinary kallikrein excretion was similar to that of normal subjects. In these patients the enzyme was weakly and positively related to urinary potassium and plasma renin activity; no correlation was found with blood pressure, urinary sodium, age, or sex. In normal subjects and in patients with essential hypertension, the variables studied account for only 25% and 17%, respectively, of the variability of urinary kallikrein excretion. We conclude that the relatively short duration of hypertension in our patients may explain the unaltered values of urinary kal'ikrein excretion with respect to controls.

Objectives. We sought to study the dose dependence of in vivo suppression by aspirin of enhanced thromboxane biosynthesis in the setting of coronary angioplasty and to evaluate the effects of heparin and aspirin during cardiac catheterization.

We measured the renal and extrarenal synthesis of prostacyclin and thromboxane A2, as reflected by the urinary excretion of the stable hydration products 6-keto-prostaglandin F1αand thromboxane B2and the corresponding 2,3-dinor-derivatives, during chronic administration of sulindac (200, 400, 600, and 800 mg/day, each dose given for 7 days in successive weeks) in seven healthy subjects. Urinary eicosanoids were measured by negative ion, chemical ionization–GC/MS–validated RIA techniques. Both 2,3-dinor-thromboxane B2and 2,3-dinor-6-keto-prostaglandin F1αshowed a dose-dependent reduction, ranging between 45% and 85%. In contrast, the urinary excretion of 6-keto-prostaglandin F1αand thromboxane B2did not change significantly throughout the study. These results extend previous observations of a selective sparing of renal cyclooxygenase activity by sulindac in humans and demonstrate that this selectivity is not related to an overall weaker enzyme inhibition.