Development of logical problem solving: a one-year retest.
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Biomedical subjects
Publications and source records attributed to N Lewis.
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Serum angiotensin-converting enzyme (ACE) activity, plasma renin activity (PRA), and serum aldosterone levels were measured up to four weeks in a population of adults exposed to thermal injury, with or without concomitant exposure to smoke inhalation. In 10 patients, plasma levels of angiotensin-2 and ACE activity in bronchial lavage were also evaluated. Patients with severe burn injury had a significant decline of serum ACE activity while the concentrations of aldosterone and PRA were markedly elevated. Smoke inhalation seemed to counterbalance the decline of serum ACE activity, and, in the last group of patients, ACE concentrations were higher than those recorded in patients suffering only from cutaneous burn. The ACE activity was evidenced in bronchial lavage of patients exposed to smoke inhalation with the highest values present in the first day after the injury. The same patients had also very elevated levels of plasma angiotensin 2. In conclusion, serum ACE activity decreases in burn patients according to the severity of the cutaneous burn; smoke inhalation influences serum levels of the enzyme with concentration values opposite to the low ones present in cutaneous burn. Finally, the enzyme activity has an independent pattern from that of the other components of the renin angiotensin aldosterone system. The evaluation of ACE activity may be a marker of pulmonary damage in smoke inhalation.
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A signal-averaging technique was used to minimize acoustic reflex measurement system noise while preserving temporal fidelity. In normal listeners, the interaction of signal intensity and signal duration was explored at visual detection threshold (VDT) and at varying suprathreshold signal levels. Reflex amplitude increases, with signal intensity, at a rate which changes as a function of signal duration, a finding which complicates the interpretation of temporal summation data based on VDT. A theoretical model is proposed to explain the complex interactions of signal intensity, duration, and band width on the amplitude of the acoustic reflex.