Stopping of heavy ions in a hydrogen plasma.
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Biomedical subjects
Publications and source records attributed to H Wahl.
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Skin biopsies of 26 patients with leukemia and seven patients with aplastic anemia were investigated before and at different stages after allogeneic bone marrow transplantation (BMT) to establish the immunological criteria which distinguish skin alterations during normal reconstitution from dermal lesions mediated by graft-versus-host disease (GvHD). Of the 33 patients studied 27 presented with clinically diagnosed acute and/or chronic GvHD, one patient died of bone marrow rejection. Immunohistological analysis of the respective skin biopsies with selected monoclonal antibodies against human leukocyte antigens (HLA) and differentiation antigens of the lympho-hematopoietic cells revealed low dermal mononuclear cell counts with phenotypically normal constituents in five cases with uncomplicated reconstitution post-grafting. In contrast, increased dermal cellular infiltrates predominantly consisting of Lyt 3+, OKT 8+ T-lymphocytes, as well as of a large number of Ia-like (immune response associated = HLA-D) determinant + monocytes/macrophages were observed in all patients with active acute/chronic GvH reactivity. As sign of activation simultaneous expression of HLA-D region products was also found on a subset of the invading OKT8+ T-lymphocytes. Progression of GvHD was associated with additional surface staining of keratinocytes for Ia-like determinants. Loss of Ia-like determinant+, OKT6+ dentritic epithelial cells in all leukemic patients, as well as in patients with aplastic anemia with or without GvHD suggested damage of Langerhans cells due to the previous radiotherapy and/or specific immunological destruction. In patients with fatal outcome of GvHD prolonged reduction of these dentritic epithelial cells seemed to be indicative of impaired immune reconstitution or bone marrow dysfunction. Thus immunopathological features of skin GvHR may enable early recognition and prognostic evaluation of this disease possibly allowing more effective therapy.
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The haemodynamic effects of portal ligation combined with mesocaval H-grafting were evaluated experimentally as follows: acute portal hypertension was induced in 20 mongrel dogs by ligation of the portal vein, in 15 of these a mesocaval shunt was constructed using an autogenous venous segment, the rest served as controls and were left without shunting. All animals with portal occlusion only died within 80 minutes, whereas nine dogs in the H-graft groups survived. The one-month patency rate was 78 per cent. Slight portal hypertension was observed only in the early post-shunt period, one month later the pressure was normal. By this time the flow through the shunt was significantly reduced and numerous but small portosystemic collaterals were visualized radiographically. Varices formation was not observed. The Xe-133 wash-out of the liver and liver pO2 were normal in the early post-shunt period. These findings were in marked contrast to those in the control group where both variables showed rapid deterioration. The pre-shunt spleen flow proved to be of prognostic significance: poor flow was associated with bad prognosis. After one month the liver flow was decreased whereas the spleen flow was increased, perhaps indicating increased splenocollateral flow. Portal ligation combined with mesocaval H-grafting thus seemed to induce slight and temporary portal hypertension in this model. This appeared to be caused by relatively narrow lumen of the shunt. Normotension was soon established by rapid opening up of portosystemic collaterals.
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Since recent reviews of the behavioural effects of septal lesions agree that more than one explanatory concept is required, a multivariate analysis of the septal syndrome has been made. A total of 127 rats have been tested 73 with septal lesions and 54 controls. The rats were tested in a standard test battery consisting of a residential maze, spontaneous alternation, spatial learning, approach/avoidance conflict and one-way active avoidance. Factor analyses reveal a complex change in the factor structure after septal lesions. None of the previous explanations of septal functions receives unequivocal support. The findings do not exclude the possibility that septal lesions interfere with a few general behaviour mechanisms or perhaps only one. However, if so, this factor does not explain as much of the variance as expected. Situational or test-dependent factors play a greater role in the variance. This is interpreted as an indication of insufficiency in the theoretical structure, or in conventional test designs.
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