[Results following canine pulmonary transplantation (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Radaszkiewicz.
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A primary retroperitoneal tumor is reported. Histologically the tumor consists of epithelial and mesenchymal compartments. By reason of the positive SRCA-reaction the tumor was classified as a mesodermal mixed-cell tumor.
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We have postulated that binding of the hydrophobic anticonvulsant drug diphenylhydantoin (DPH) to lymphoid cells might induce graft-versus-host (GVH)-like cell reactions by T lymphocytes and thus trigger autoimmunization and lymphoma development observed in patients treated with DPH. This hypothesis was studied in mice by means of the popliteal lymph node (PLN) assay. DPH, injected s.c. into the footpads of mice, induced a significant T cell-dependent PLN enlargement. The B cell-derived population comprised the majority of cells in the enlarged PLN. A T cell-dependent activation of Ig-secreting cells in the PLN was induced by DPH. Thymectomy of young adult mice significantly amplified the PLN reaction to DPH and facilitated the activation of Ig-secreting cells. Since injection of the hydantoin rings only completely failed to induce PLN reactions, it is assumed that the observed PLN reactions are caused by the phenyl groups and/or the highly reactive intermediates of DPH. In conclusion, DPH can induce a T cell-dependent proliferation and functional activation of B cells. Conceivably, if such a process persists, it might lead to the GVH-like lymphomagenesis and autoimmunization observed in patients treated with this drug.
Seven patients with primary non-Hodgkin lymphoma of the skeleton were examined with MRI. The results were compared to "small cell" primary malignant bone tumors. The latter showed marked hyperintensity on SE T2-weighted images; in contrast, the lymphomas appeared as inhomogeneous lesions of low signal intensity on T2-weighted images. Histologic examination with silver stains of specimens of these lesions revealed a high content of fibrous tissue, which could explain the signal behavior on MR. All seven lymphomas were located in the epiphysis or metaphysis of the appendicular skeleton; intraarticular tumor growth was demonstrated in five cases.
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The immunophenotype of 6 cases of Langerhans cell histiocytosis (LCH) of the hypothalamus and 3 cases of cranial bone manifestation of LCH was investigated by means of immunohistochemistry on paraffin sections. Antibodies against S 100 protein, lysozyme, CD68 (PG-M1), CD68 (KP1), HLA-DR, beta 2 microglobulin, placental alkaline phosphatase (PLAP), the monoclonal antibody MAC 387, and a monoclonal antibody against CD1a were used. All examined cases showed positive staining of lesional cells for S 100 protein, HLA-DR, beta 2 microglobulin, macrophage associated markers and CD1a. According to the "confidence levels" of the Writing Group of the Histiocyte Society [Chu et al. 1987], a "definite diagnosis" of LCH requires the demonstration either of Birbeck granules in lesional cells by electron microscopy, or of CD1a antigenic determinants on the surface of lesional cells. Since electron microscopy of these rare CNS lesions is not possible in many cases, we are now able to give a definite diagnosis of LCH of the hypothalamus by means of immunohistochemistry for CD1 a on routinely fixed and processed tissue.