Environmentally enriched classrooms and the cognitive and perceptual development of Negro preschool children.
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Biomedical subjects
Publications and source records attributed to T Alexander.
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The purpose of this study was to evaluate the extent of cellular adhesion (density and morphological maturation), cellular membrane damage, and cellular viability after an electrostatic transplantation of human umbilical vein endothelial cells (HUVECs) onto 6-cm segments of 4-mm I.D. e-PTFE (GORE-TEX) vascular prostheses using a prototype electrostatic endothelial cell transplantation device (EECTD). The electrostatic transplantation parameters evaluated were the apparatus-applied voltage and transplantation time. By our definition, the combination of applied voltage and transplantation time that met the a priori criteria of: 1) maximum transplanted cellular viability, 2) maximum transplantation density, 3) maximum morphological maturation (degree of cellular flattening), and 4) minimal cellular membrane damage would be the prime transplantation procedure. The results of the experimentation indicated that the prime conditions for HUVEC transplantation were obtained when +1.0 V was applied for a transplantation time of 16 min. These conditions achieved an average viable graft surface coverage of 97.4+/-1.6% with an average transplantation density of 73,540+/-8.514 HUVECs/cm2. Furthermore, the transplanted HUVECs were morphologically mature (flattened) with minimal apparent cellular membrane damage (lysis or pitting). The overall clinical significance of this study is that viable endothelial cell transplantation to synthetic vascular grafts can be accomplished at high cellular densities and morphological maturation in 16 min using the EECTD. With the promising in vitro transplantation results, the next logical investigations will include additional in vitro evaluations (cellular retention upon shear stress exposure and biochemical assays) followed by in vivo evaluations to examine thromboresistance and influence on intimal/anastomotic hyperplasia.
Levodopa is the most efficacious and widely used symptomatic drug for Parkinson's disease (PD). There is currently, however, a great deal of interest focused on the possibility that levodopa-induced increases in dopamine (DA) turnover may increase oxidative damage derived from the breakdown of DA. Increased oxidative damage following levodopa may contribute to the progressive degeneration of remaining host nigral neurons as well as interfere with development and function of embryonic nigral neurons in neural grafting trials. There is abundant evidence that levodopa is toxic to embryonic nigral DA neurons in both cell culture and neural grafting models. These findings have prompted a number of studies on mechanisms of levodopa toxicity to identify effective means of ameliorating potential oxidative stress related to levodopa in PD. In the current study we have utilized cultures of embryonic nigral DA neurons to address the fundamental question of whether levodopa-induced toxicity is related to DA production or whether dopa itself contributes to cell death. We compared the degree of nigral DA cell death following chronic administration of: 1) levodopa (e.g.: l-dopa); 2) its less active stereoisomer d-dopa; and 3) DA. We examined the rank order of toxicity of these compounds in two species of rats, Fisher 344 (F344) and Sprague-Dawley (SD). Results indicate a toxicity profile of: DA > l-dopa >> d-dopa. In addition, although there was no difference in response of F344 and SD cultures to l-dopa, the SD cultures were significantly more susceptible to the neurotoxic effects of DA. Taken collectively, these results suggest that levodopa-induced toxicity is related primarily to DA production rather than oxidation of dopa to toxic metabolites, and that some strain related differences do exist.
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In a double blind crossover trial, acute effects of 8 mg intravenous oxyfedrine were compared with those of placebo in 18 patients with stable effort angina assessed by treadmill exercise testing. In the resting state, oxyfedrine caused an increase in heart rate (84 +/- 23 to 103 +/- 19 bpm, p less than 0.01), systolic blood pressure (123 +/- 16 to 133 +/- 20 mmHg, p less than 0.01) and double product (11 x 10(3) +/- 2 x 10(3) to 13.7 x 10(3) +/- 3.1 x 10(3), p less than 0.01) as compared to placebo. However, these parameters were not significantly different at the end of first or second stage of the treadmill test (p = NS). Time to one mm ST segment depression was increased with oxyfedrine as compared to placebo (1.5 +/- 1.5 to 1.9 +/- 1.5 minutes, p less than 0.05). Oxyfedrine did not increase the total duration of exercise (4.1 +/- 1.0 to 4.7 +/- 2.2 minutes, p = NS) or time to ischaemic symptoms (2.7 +/- 1.3 to 2.9 +/- 1.9 minutes, p = NS). The total work done was significantly more on oxyfedrine 312 +/- 189 joules/kg to 370 +/- 209 joules/kg, p less than 0.01) as also the double product achieved (20.6 x 10(3) +/- 6.1 x 10(3) to 22.5 x 10(3) +/- 6.4 x 10(3), p less than 0.01). It is concluded that intravenous oxyfedrine improves exercise capacity in patients with stable effort angina presumably by reducing myocardial ischaemia.
Nineteen consecutive patients who had coronary arteriography underwent dipyridamole stress testing with 0.14 mg/kg/min infusion over 4 minutes during computer assisted radionuclide ventriculography. Global ejection fraction, diastolic function and regional ejection fraction were calculated by a semiautomatic method. There were 17 patients with severe left anterior descending disease of which 12 involved the proximal segment of the LAD, 15 patients with left circumflex disease and 13 patients with right coronary artery disease. Abnormalities in resting or stress induced regional ejection fraction was used for localisation of severe coronary artery disease. The overall sensitivity was 75 per cent with a specificity of 75 per cent, a positive predictive value of 90 per cent and a negative predictive value of 45 per cent. For LAD disease the sensitivity was 94 per cent with a 100 per cent specificity while proximal segment of LAD had a sensitivity of 100 per cent and a specificity of 57 per cent. Identification of left circumflex disease had a sensitivity of 47 per cent and a 100 per cent specificity and right coronary artery had a 85 per cent sensitivity and a 50 per cent specificity. Four patients developed ST changes, 6 developed chest discomfort and 1 patient developed giddiness. All 7 were promptly reversed with intravenous aminophylline. Thus dipyridamole radionuclide ventriculography is a highly sensitive and specific method for localisation of CAD.
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