University of Oklahoma

About: University of Oklahoma is a education organization based out in Norman, Oklahoma, United States. It is known for research contribution in the topics: Population & Radar. The organization has 25269 authors who have published 52609 publications receiving 1821706 citations. The organization is also known as: OU & Oklahoma University.

Trichomonas vaginalis associated with low birth weight and preterm delivery. The Vaginal Infections and Prematurity Study Group.

Abstract: Background:Several studies have suggested that pregnant women infected withTrichomonas vaginalismay be at increased risk of an adverse outcome.Goal:To evaluate prospectively the association betweenT. vaginalisand risk of adverse pregnancy outcome in a large cohort of ethnically diverse women.Study D

From State to Market: A Survey of Empirical Studies on Privatization

Abstract: This study surveys the literature examining the privatization of state-owned enterprises(SOEs). We overview the history of privatization, the theoretical and empirical evidence on the relative performance of state owned and privately owned firms, the types of privatization, if and by how much has privatization improved the performance of former SOEs in both non-transition and transition countries, how investors in privatizations have fared, the impact of privatization on the development of capital markets and corporate governance. We concentrate on the empirical evidence on the effects of privatization on firm performance. In most setting privatization "works" in that the firms become more efficient, more profitable, financially healthier, and reward investors. While this holds in both transition and non-transition economies, there is more variation in transition economies. Especially in transition economies, the identity of the new owners and managers is important in determining post-privatization performance.

Comparative efficacy of cognitive therapy and pharmacotherapy in the treatment of depressed outpatients

Abstract: Forty-one unipolar depressed outpatients were randomly assigned to individual treatment with either cognitive therapy (N =19)or imipramine (N =22).As a group, the patients had been intermittently or chronically depressed with a mean period of 8.8 years since the onset of their first episode of depression, and 75%were suicidal. For the cognitive therapy patients, the treatment protocol specified a maximum of 20 interviews over a period of 12 weeks. The pharmacotherapy patients received up to 250 mg/day of imipramine for a maximum of 12 weeks. Patients who completed cognitive therapy averaged 10.90 weeks in treatment; those in pharmacotherapy averaged 10.86 weeks. Both treatment groups showed statistically significant decreases in depressive symptomatology. Cognitive therapy resulted in significantly greater improvement than did pharmacotherapy on both a self-administered measure of depression (Beck Depression Inventory)and clinical ratings (Hamilton Rating Scale for Depression and Raskin Scale).Moreover, 78.9%of the patients in cognitive therapy showed marked improvement or complete remission of symptoms as compared to 22.7%of the pharmacotherapy patients. In addition, both treatment groups showed substantial decrease in anxiety ratings. The dropout rate was significantly higher with pharmacotherapy (8 Ss)than with cognitive therapy (1 S).Even when these dropouts were excluded from data analysis, the cognitive therapy patients showed a significantly greater improvement than the pharmacotherapy patients. Follow-up contacts at three and six months indicate that treatment gains evident at termination were maintained over time. Moreover, while 68%of the pharmacotherapy group re-entered treatment for depression, only 16%of the psychotherapy patients did so.

Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction.

Abstract: The interest for the antifibrillatory effect of vagal stimulation has been largely limited by the fact that this concept seemed restricted to acute experiments in anesthetized animals. To explore the potentially protective role of vagal stimulation in conscious animals we developed a chronically implantable device to be placed around the cervical right vagus. An anterior myocardial infarction was produced in 161 dogs; 1 month later an exercise stress test was performed on the 105 survivors. Toward the end of the test the circumflex coronary artery was occluded for 2 minutes. Fifty-nine (56%) dogs developed ventricular fibrillation and, before this test was repeated, were assigned either to a control group (n = 24) or to be instrumented with the vagal device (n = 35). Five dogs were excluded because of electrode malfunction. Compared with the heart rate level attained after 30 seconds of occlusion during exercise in the control test, vagal stimulation led to a decrease of approximately 75 beats/min (from 255 +/- 33 to 170 +/- 36 beats/min, p less than 0.001). In the control group 22 (92%) of 24 dogs developed ventricular fibrillation during the second exercise and ischemia test. By contrast, during vagal stimulation ventricular fibrillation occurred in only 3 (10%) of the 30 dogs tested and recurred in 26 (87%) during an additional exercise and ischemia test in the control condition (p less than 0.001 versus the vagal stimulation test; internal control analysis). Combined analysis of the tests performed in the control condition showed that ventricular fibrillation was reproducible in 48 (89%) of the 54 dogs tested. The protective effect of vagal stimulation was also significant in the group comparison analysis and even after exclusion of those four dogs in which ventricular fibrillation was not reproducible (92% versus 11.5%, control versus vagal stimulation, p less than 0.001). When heart rate was kept constant by atrial pacing, the vagally mediated protection was still significant (p = 0.015) as five (55%) of nine dogs survived the test. This study shows that vagal stimulation, performed shortly after the onset of an acute ischemic episode in conscious animals with a healed myocardial infarction, can effectively prevent ventricular fibrillation. This striking result seems to depend on multiple mechanisms having a synergistic action. The decrease in heart rate is an important but not always essential protective mechanism. The electrophysiological effects secondary to the vagally mediated antagonism of the sympathetic activity on the heart are likely to play a major role.