Biomedical subjects
Publications and source records attributed to U Saxena.
This paper describes the cost-benefit analysis of a computerized medical record system for use in physicians' offices. Actual data for savings in physician time in paper work was collected. The qualitative benefits of the system were evaluated using a questionnaire. The cost-benefit ratios demonstrated that the use of a computerized medical system is justified.
A laboratory study was conducted (1) to evaluate the effects of lifting frequency and technique on maximum acceptable work loads using psychophysical measurement technique, and (2) to compare the physiological fatigue criteria of 5 Kcal/min with the psychophysical fatigue criteria by measuring the metabolic rates at maximum acceptable work loads determined by subjective estimates of physical fatigue. Six male college students were required to lift from the floor to a 0.5 m height for 40 minutes. Four levels of lifting frequency (3, 6, 9 and 12 lifts/min) and three different lifting techniques (free sytle, stooped back and straight-back, bent-knee) were employed. Oxygen consumption rates were measured at maximum acceptable work loads (and were reduced to STPD). Statistical analysis showed that the maximum work loads acceptable to the workers were significantly affected by both lifting frequency and technique. Maximum acceptable work loads increased with an increase in lifting frequency. Both the subjective estimates of physical fatigue and the metabolic energy expenditure rate favored the free style lifting technique. The measured metabolic rates were in agreement with the physiological fatigue criteria of 5 Kcal/min only for six of the twelve combinations of lifting frequency and technique. Use of the physiological fatigue criteria will result in more liberal standards of work load at low work paces, especially for the stooped back and the free style lifting techniques.
A comparative controlled study was carried out in 40 patients suffering from rheumatoid arthritis, osteoarthrosis or ankylosing spondylitis to assess the efficacy of ketoprofen and ibuprofen. Patients were allocated at random to receive either 100 mg ketoprofen twice daily or 400 mg ibuprofen 3-times daily over a period of 3 months. Subjective overall assessments of symptoms, based on rating scale scores for pain, duration of morning stiffness and inflammation, showed that there was a greater, more rapid and more sustained improvement in those patients treated with ketoprofen. Measurements of inflamed joint size and of grip strength also improved more with ketoprofen than with ibuprofen. Side-effects, notably nausea, epigastric discomfort and abdominal pain, were more frequent and severe with ketoprofen, leading to the withdrawal of 2 patients in the early stage of the trial, and were probably related to the high dosage used. Three patients receiving ibuprofen needed 7 injections of ACTH to control their symptoms.
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The major functional pool of lipoprotein lipase (LPL) that hydrolyzes triglycerides in circulating lipoproteins is located on the vascular endothelium. The macrophage-secreted cytokine tumor necrosis factor (TNF), a molecule known to affect endothelial cell functions, was used to test the hypothesis that alterations of endothelial cell metabolism regulate the binding of LPL to these cells. TNF addition induced rapid (maximum release at 45 minutes) dissociation of LPL protein and activity from its binding sites on cultured porcine aortic endothelial cells. LPL release by TNF required endothelial cell metabolic event(s) which involved cell secretion. In addition, LPL release was inhibited by pertussis toxin, suggesting the involvement of guanine nucleotide regulatory protein(s). Addition of arachidonic acid, a molecule known to be released by endothelial cells due to phospholipase A2 activation by TNF treatment, released LPL from the cell surface. Furthermore, direct modulation of cellular phospholipase A2 activity also led to changes in the release of LPL. Our studies demonstrate that alterations in the cellular metabolism of endothelial cells, for example, by TNF, may release functional pools of LPL from the vascular endothelium. This decrease in LPL on endothelial cell surfaces might be involved in the development of hypertriglyceridemia and redirection of energy flow during infections and inflammation.