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We examined arterial stiffness, baroreflex sensitivity (BRS), and systolic arterial pressure (SAP) variability after an acute bout of aerobic exercise compared to resistance exercise. We hypothesized that arterial stiffness would be reduced after aerobic exercise, while it would be increased after resistance exercise, and these alterations would be associated with differential changes in BRS and SAP variability. Arterial stiffness, BRS, and SAP variability were assessed before and 20 min after a bout of aerobic exercise and resistance exercise in 13 male participants. Pulse wave velocity (PWV) was used to measure central (carotid-femoral) and peripheral (femoral-dorsalis pedis) arterial stiffness. BRS was derived via the sequence technique. Spectral decomposition of beat-to-beat SAP variability was used as an estimate of sympathetic vasomotor tone. A mode-by-time interaction (p < 0.001) was detected for central PWV, due to an increase in PWV (p < 0.05) following resistance exercise and a decrease in PWV following aerobic exercise (p < 0.05). A mode-by-time interaction was also detected for peripheral PWV (p < 0.05), due to a decrease in peripheral PWV following aerobic exercise (p < 0.05) with no change following resistance exercise. BRS was significantly lower following resistance compared with aerobic exercise (p < 0.004). SAP variability increased following resistance exercise (p < 0.05) but there was no interaction. In conclusion, aerobic exercise decreased both central and peripheral arterial stiffness, while resistance exercise significantly increased central arterial stiffness only. BRS was reduced after both bouts of exercise, but significantly greater reductions were seen following resistance exercise.

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The objective was to determine whether factors could be identified in medical and legal records that are associated with the successful defense of obstetrical malpractice cases involving the death or neurological impairment of infants. Obstetrical claims (169) closed by PROMUTUAL between January 1, 1990, and December 31, 1994, were retrospectively abstracted and analyzed to identify associations between medical and legal factors, and the medicolegal outcome. Multivariable analysis identifies that the use of pitocin, diagnosis of asphyxia, a delay in delivery, and the use of multiple defense expert witnesses decreased the chances of a successful defense. Two statistical models explaining indemnity payment were developed. The first, based on medical outcome, showed an increased indemnity payment when a case involved major neurological deficits, diagnosis of asphyxia, newborn seizures, later year of delivery, and participation of a particular defense firm. Perinatal or childhood death and the use of pitocin were indicators of a decrease in payment. The second model was based on long-term care requirements. In this model, indicators of increased indemnity payment were: nonreassuring intrapartum fetal heart rate tracing, later year of delivery, intensity of long-term care required, and participation of a particular defense law firm. Perinatal or childhood death, the use of pitocin, and settlement date increasingly removed from the occurrence date were the determinants of decreased payments in this model. Finally, the presence of major neurological deficits, the prolongation of a case, and the involvement of multiple law firms and defense witnesses increased the expense charged to and paid by the insurance company. Using the medical, legal, and financial data relevant to 169 obstetrical cases closed by one malpractice insurance carrier between 1990 and 1994, statistical models with potential predictive values for future malpractice claims involving neurologically impaired infants were constructed. These models may help determine in advance the chance a future case has for successful defense and the likely amount of expense and indemnity dollars that will be paid out to settle and defend it.

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We studied the kinetics of testicular response to human chorionic gonadotropin (hCG) in oligoasthenospermic and asthenospermic patients (OAZ-AZ). The responses of testosterone (T), androstenedione (A), 17 OH-progesterone (17OHP), and estradiol (E2) were evaluated in 60 OAZ-AZ patients and compared to those of 10 normal men. The responses of T, A, and 17OHP to hCG in the control group displayed a biphasic pattern with an initial peak at 4 hours and a second peak after 24 hours. The E2 response showed a single peak between 24 and 48 hours after hCG administration. OAZ-AZ patients had two types of T responses: group 1 (n = 40) had no first peak and group 2 (n = 20) had a normal response pattern. The response of A was similar to that of T, and the E2 response was normal in both groups. There were three types of 17OHP responses in group 1 (low, high, or normal); however, the 17OHP response was normal in group 2. Treatment of group 1 with aromatase inhibitors (aminoglutethimide or testolactone) induced an improvement of the acute T response only in patients with high or normal 17OHP response to hCG, whereas no effects were observed in patients with low 17OHP response. In group 2, the aromatase inhibitors induced no changes in the T response. These results demonstrate that in some OAZ-AZ patients (group 1, blunted T response) testicular hormone production is altered. They also suggest the presence of two enzyme blocks: one at the 17,20 desmolase level, mediated by E2, and another at early biosynthetic steps, not mediated by E2.

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