Biomedical subjects

V Travis

Publications and source records attributed to V Travis.

3 recordsLinked to original sources

PubMed2001

Kaiser Permanente's "metadata-driven" national clinical intranet.

This paper describes the approach taken to build Kaiser Permanente's national clinical intranet. A primary objective for the site is to facilitate resource discovery, which is enabled by the use of "metadata", or data (fields and field values) that describe the various resources available. Users can perform full text queries and/or fielded searching against the metadata. Metadata serves as the organizing principle of the site--it is used to index documents, sort search results, and structure the site's table of contents. The site's use of metadata--what it is, how it is created, how it is applied to documents, how it is indexed, how it is presented to the user in the search and the search results interface, and how it is used to construct the table of contents for the web site--will be discussed in detail. The result is that KP's national clinical intranet has coupled the power of Internet-like full text search engines with the power of MedLine-like fielded searching in order to maximize search precision and recall. Organizing content on the site in accordance with the metadata promotes overall consistency. Issues currently under investigation include how to better exploit the power of the controlled terminology within the metadata; whether the value gained is worth the cost of collecting metadata; and how automatic classification algorithms might obviate the need for manual document indexing.

Computer Communication Networks↗

PubMed1990

Plasma catecholamine responses to exercise after training with beta-adrenergic blockade.

Exercise training has been shown to decrease plasma norepinephrine (NE) and epinephrine (EPI) levels during absolute levels of submaximal exercise, which may reflect alterations in sympathetic tone as a result of training. To determine if beta-adrenergic blockade altered these changes in the plasma concentration of catecholamines with exercise conditioning, we studied the effects of beta-adrenergic blockade on NE and EPI at rest and during exercise in 24 healthy, male subjects after a 6-wk exercise training program. The subjects were randomized to placebo (P), atenolol 50 mg twice daily (A), and nadolol 40 mg twice daily (N). There were no changes in resting NE and EPI compared with pretraining values in any subject group. During the same absolute level of submaximal exercise NE decreased in P and A but was unchanged in N, whereas EPI decreased only in P. At maximal exercise all three groups developed significant increases in NE after training that paralleled increases in systolic blood pressure. EPI at maximal exercise increased after training with N but was unchanged with P or A. These training-induced changes in plasma catecholamine levels were masked or blunted when the A and N groups were studied while still on medication after training. Thus beta-adrenergic blockade has important effects on adaptations of the sympathetic nervous system to training, especially during submaximal exercise.

Adrenergic beta-Antagonists↗

PubMed1986

Effects of selective and nonselective beta-adrenergic blockade on mechanisms of exercise conditioning.

Exercise conditioning involves adaptations in the heart, peripheral circulation, and trained skeletal muscle that result in improved exercise capacity. Since the specific influence of beta-adrenergic stimulation on these various adaptations has not been clear, we studied the effect of beta 1-selective and nonselective beta-adrenergic blockade on the exercise conditioning response of 24 healthy, sedentary men after an intensive 6 week aerobic training program. Subjects randomly assigned to receive placebo, 50 mg bid atenolol, or 40 mg bid nadolol were tested before and after training both on and off drugs. Comparable reductions in maximal exercise heart rate occurred with atenolol and nadolol, indicating equivalent beta 1-adrenergic blockade. Vascular beta 2-adrenergic selectivity was maintained with atenolol as determined by calf plethysmography during intravenous infusion of epinephrine. All subjects trained at greater than 85% of maximal heart rate and 80% of VO2 max determined on drug. VO2 max increased after training 16 +/- 2% (p less than .05) in the placebo group and 6 +/- 2% (p less than .05) in the atenolol group, while there was no change in the nadolol group. At maximal exercise, subjects receiving placebo increased their exercise duration and oxygen pulse significantly greater than those receiving atenolol or nadolol. During submaximal exercise there were reductions in heart rate and heart rate-blood pressure product in all three groups, but these reductions were greater with placebo than with either drug. Leg blood flow during submaximal exercise decreased 24 +/- 2% (p less than .01) in the placebo group but was unchanged in the atenolol and nadolol groups. Lactates in arterialized blood during submaximal exercise were reduced equivalently in all three groups after training. Capillary/fiber ratio in vastus lateralis muscle biopsy specimens increased 31 +/- 6% in the placebo group and 21 +/- 6% in the atenolol group (both p less than .05) and tended to increase in the nadolol group. Succinic dehydrogenase and cytochrome oxidase activities in muscle biopsy specimens increased equivalently in all three groups, especially during submaximal exercise, these changes were less marked than that with placebo. While beta-adrenergic blockade attenuated the exercise conditioning response, skeletal muscle adaptations including increases in oxidative enzymes, capillary supply, and decreases in exercise blood lactates were unaffected. Cardiac and peripheral vascular adaptations do appear to be affected by beta-adrenergic blockade during training. Cardioselectivity does not seem to be important in modifying these effects.

Adrenergic beta-Antagonists↗