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H Kotze

Publications and source records attributed to H Kotze.

7 recordsLinked to original sources

Emergent migration policy in a democratic South Africa.

This article sets recent debates on migration policy in South Africa against broader historical realities that have shaped patterns of population movement on the subcontinent since the end of the nineteenth century. During the course of the last century, most forms of population movement were the result of disjointed regional economic development which can be traced to two epochal events at the end of the nineteenth century: the creation of the modern African state system and the discovery of mineral wealth in Southern Africa. Although regulation of migrant labor was a fundamental feature of the colonial period, it was only after 1950, when independent states began to define specific migration priorities, that states began to restrict significantly the flow of transnational labor. From this point notions such as internally displaced person, refugee and illegal immigrant become increasingly appropriate to the study of regional migration. Particular attention is given to current debate on the definition of refugee which forms part of a broader international debate. A number of South African writers have argued that, given the structural imbalances contained in the regional economy, the term "refugee" should be redefined to included economic migrants. This position is not shared by the South African Government, and an analysis of current policy and legislation demonstrates a growing tendency to restrict the influx of undocumented migrants. This is due, in part, to the recent political transition and the institutional compromises that it produced as well as the growth of negative sentiment towards illegal immigrants at both mass and elite levels, as demonstrated by two recent research findings. The article concludes with a summation of recent trends in South African migration policy and an evaluation of the ambiguous position that South Africa occupies within Southern Africa.

Africa↗

Kinetics and sites of destruction of 111Indium-oxine-labeled platelets in idiopathic thrombocytopenic purpura: a quantitative study.

Kinetics and quantification of the sites of destruction of 111-Indium-oxine-labeled autologous platelets were investigated in eight patients with idiopathic thrombocytopenic purpura. The mean platelet count was 17 +/- 9 X 10(9)/liter; platelets were separated by differential centrifugation and labeled with 5.6 +/- 2.5 MBq 111In. Whole body and organ 111In-platelet distribution was quantitated with a scintillation camera and a computer-assisted imaging system acquisition matrix. Areas of interest were selected with the computer and organ 111In-radioactivity expressed as a percentage of whole body activity. Mean platelet survival was 49.5 +/- 29.6 hr and the survival curves were exponential. Equilibrium percentage organ 111In-radioactivity was (normal values in parentheses): spleen 33.7 +/- 8.8 (31.1 +/- 10.2); liver 16.1 +/- 9.5 (13.1 +/- 1.3); thorax 22.8 +/- 3.7 (28.2 +/- 5.6). Percentage organ 111In-activity at the time when labeled platelets had disappeared from the circulation was: spleen 44.5 +/- 16.4 (40 +/- 16); liver 16.0 +/- 11.5 (32.4 +/- 7.2); thorax 19.7 +/- 6.0 (17.7 +/- 10.3). Thorax activity corresponds to bone marrow radioactivity. Three patterns of platelet sequestration were evident. Three patients had mainly splenic sequestration, two mainly hepatic sequestration, and three diffuse reticuloendothelial system sequestration with a major component of platelets destroyed in the bone marrow. Splenectomy was performed in two patients. The pattern of 111In-platelet sequestration was not predictive of response of glucocorticoid therapy or indicative of the necessity for splenectomy. Quantitative 111In-labeled autologous platelet kinetic studies provide a new tool for the investigation of platelet disorders.U

Adolescent↗

Kinetics and sites of sequestration of indium 111-labeled human platelets during cardiopulmonary bypass.

A new approach for the study of the kinetics and quantification of the in vivo and ex vivo sites of sequestration of platelets during cardiopulmonary bypass (CPB) is described. Autologous platelets of four patients were labeled with 111In-oxine and reinfused on the day prior to CPB for coronary artery bypass grafting. Changes in blood 111In-labeled platelet radioactivity and blood platelet counts were monitored during the operation. In vivo 111In-labeled platelet redistribution was quantified with a scintillation camera and a computer-assisted imaging system before and after CPB. Sequestration of 111In-labeled platelets in the bubble oxygenator was measured. 111In-labeled platelet activity in the blood decreased by 46% +/- 5% within 5 minutes of CPB, but this decrease was mostly due to hemodilution; the true loss of platelets from the circulation was 13% +/- 4%. Intraoperatively, whole body 111In activity decreased by oxygenator 10.8% +/- 1.3% of administered platelets were sequestered, especially in the innermost active layers of the defoaming mesh of the bubble oxygenator. Mean survival time of circulating platelets was 58 +/- 8 hours and fitted an exponential function best. The bleeding time increased to 40 minutes during operation and returned to normal within 24 hours. During operation 111In-labeled platelets accumulated somewhat in the liver (10.7%) but not in the spleen, thorax, or head. In the 48 hours after operation, platelets were sequestered mainly in the liver. The scintillation camera with computer-assisted imaging allows in vivo quantitative studies of platelet kinetics of a type which has not been possible with previous techniques.

Blood Platelets↗

Kinetics and in vivo redistribution of (111)Indium-labelled human platelets after intravenous protamine sulphate.

The pathogenesis of thrombocytopenia induced by intravenous protamine sulphate was studied in six patients who underwent cardiopulmonary bypass surgery, and in three normal volunteers. Autologous platelets were labelled with (111)Indium-oxine. Platelet lifespan was determined. In vivo (111)In-platelet localization, organ redistribution and sites of destruction were quantitated with a scintillation camera and a computer-assisted imaging system. Protamine induced a transient thrombocytopenia, maximal 5-10 min after injection, and 30-40 min in duration. . The thrombocytopenia was accompanied by a transient accumulation of platelets in the liver. The splenic platelet pool remained unaltered and no platelets accumulated in the lungs. Platelet survival, measured in two volunteers, was slightly longer than normal and fitted a linear function best. There was a severe transient neutropenia during the period of thrombocytopenia. We conclude that protamine-induced thrombocytopenia is caused by hepatic accumulation of "activated" platelets or platelet aggregates, the process is reversible, and in the two normal volunteers studied, platelet survival was not affected.

Blood Platelets↗

Orthostatism and heat acclimation.

Three groups of subjects (6 subj in each group) underwent the following precedures: group A was given a 20-min head-up tilt at 21 degrees C followed by 4 h of exercise at 33.9 degrees C DB, 32.2 degrees C WB, and a repetition of tilting after exercise in heat; group B underwent the same procedure at 21 degrees C; group C was tilted at 21 degrees C, rested in heat for 4 h and was retilted in heat. The above procedures were repeated for 8 days, and on the last day groups B and C underwent the same treatment as group A. Group A showed the usual decreases in heart rate and rectal temperature and an increase in sweat rate on acclimation. This corresponded to marked improvements in heat-orthostatism. While five subjects in group A fainted during post-exposure tilting on the first exposure, none fainted on the last day. Resting in heat (group C) did not cause any acclimation to work in heat. This corresponded to poor heat-orthostatism after the work-heat procedure when five subjects fainted. Mild training at 21 degrees C (group B) resulted in minor improvements to work in heat as evident by some improvements in heart rate responses after the 1st and 2nd h of exposure. This corresponded to better heat-orthostatism and fewer men fainting than in group C. The results indicated that heat-orthostatism improves on acclimation to the same extent as exercise heart rate and rectal temperature.

Acclimatization↗