Exposure model analysis of streptococcal acquisitions.
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Biomedical subjects
Publications and source records attributed to P R Sheehe.
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The authors speculated that normal growth might cause the release of stored lead in children, providing an endogenous source of exposure for years after the acute toxic episode had resolved. The purpose of this study was to answer the following two questions (1) Is a chelation-responsive lead burden present 2 to 5 yr after therapy for acute poisoning? and (2) Does blood pressure or creatinine clearance correlate with body lead burden, as demonstrated by chelation? Thirty-eight children who had undergone ethylene diamine tetraacetic acid mobilization testing at least one time during the course of treatment in a lead clinic returned for follow-up care within 2-5 yr. all were asymptomatic. To determine the current level of body lead burden, a single-dose oral chelation with penicillamine was performed. Blood pressure and creatinine clearances were measured. From the data obtained for each child, we generated a geometric "area" representing the magnitude of lead burden integrated over the length of carriage of this burden. Multiple regression analysis indicated that after adjustment for the background variables of age, sex, height, and weight, none of the three parameters--mobilization ratio "area," blood lead level, or FEP level--was a significant contributor to the variation observed in the blood pressures or creatinine clearances of the 38 lead-exposed children (P greater than .05).
Using the 133-Xenon inhalation technique, cerebral blood flow (CBF) and hemispheric blood flow (HBF) were determined serially in 45 patients with acute stroke undergoing pharmacologic trials and in 8 transient ischemic attacks (TIA) schedules for superficial temporal-middle cerebral artery anastomoses. Both patient populations had lower blood flow than a control group of similar ages. Patients in both populations with lateralized clinical signs demonstrated an asymmetry in HBF which corresponded to their clinical signs. In the stroke population, the trend we expected over time toward development of asymmetrical HBF as the non-infarcted hemisphere recovered from diaschisis did not appear.