Donath julius (6 Ergebnisse)
Verlag: Zeitschrift f. klinische Medizin XXXVII. 1899, pp 169-182, 1899
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In den WarenkorbSC. Zustand: Gut. Obr, 13s., in gutem Zustand, [AZB12,3] (Samml.), Deu 400g.
Verlag: Wien, Braumüller, 1899., 1899
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In den Warenkorb4°. 5 SS. OBr. (gefaltet, tls. etw. fleckig und angestaubt). Separatabdruck aus der "Wiener klinischen Wochenschrift" 1899, Nr. 24.- Mit eigenh. Widmung von Julius Donath (geb. am 11. Nov. 1870 in Wien: gest. am 9. Jänner 1950). Er war Privatdozent (ao. Prof.) für Innere Medizin an der Medizinischen Fakultät der Universität Wien….Er wurde im Nationalsozialismus aus rassistischen Gründen verfolgt und am 22. April 1938 seines Amtes enthoben und von der Universität Wien vertrieben.- Ernst Czyhlarz, Internist (geb. am 1. Okt. 1873 in Prag, gest. am 3. Jänner 1950 in Wien 14) studierte in Prag und Wien (Dr. med. univ. 1897).1898-1905 war er Assistent an der I. Medizinischen Universitätsklinik in Wien unter Hermann Nothnagel, bei dem er sich 1903 habilitierte. 1904 mußte Czyhlarz - schwer an Tuberkulose erkrankt - für ein Jahr seine Assistentenstelle aufgeben. 1908 wurde er Primararzt der III. Medizinischen Abteilung des Kaiser-Franz-Joseph-Spitals in Wien, 1917 außerordentlicher Professor, 1927 Hofrat. Bis 1937 leitete er die I. Medizinische Abteilung des Allgemeinen Krankenhauses.
Verlag: Leipzig JABarth -1913, 1911
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In den Warenkorb0. 8°. S: 691-791. Broschur. [Samml. klin. Vortr., Innere Medizin, Nr. 225]. Sprache: Deutschu.
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In den WarenkorbNeurol. Zbl., 12/14. - Leipzig, Veit & Comp., 15. Juli 1893, 8°, pp.473-504, Rückenbroschur.
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In den WarenkorbZ. Immunit.forsch. Orig., 18/6. - Jena, Verlag von Gustav Fischer, 1913, 8°, pp.591-704, Broschur. Erstdruck.
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In den WarenkorbMMW, 51/36. - München, Verlag J.F. Lehmann, 6. September, 1904, 4°, pp.1585-1632, feiner Halbleinenband. First Print of the "first description of an auto-antibody, and of an auto-immune disease, paraoxysmal cold hemoglobinuria" by Julius Donath (1870-1950) and Carl Landsteiner (pp.1868-1943) Paroxysmal cold hemoglobinuria - "Thi…s fairly rare disease is characterized by the acute intravascular destruction of red cells with a resulting hemoglobinuria, after exposure of the patient to the cold. The pathogenesis of the disease was unknown until 1904, when Viennese clinician Julius Donath suggested that the cause of the disease is due to the formation of autoantibodies against the patient's own erythrocytes12. To further support his thesis, Donath enlisted the aid of Karl Landsteiner, with whom he had previously collaborated on other studies. Landsteiner was already a well-established investigator, who had earlier discovered the ABO blood group system of man13 (for which he received the 1930 Nobel Prize in Physiology or Medicine). With Donath providing the patients and Landsteiner the laboratory know-how, they attacked the problem together. The investigations proved to be both simple and conclusive because the principle feature of the disease could be reproduced in vitro. Blood from the affected patients was collected in oxalate, the plasma was separated and the red cells washed. Mixing the two at room temperature had no effect, but mixing them in the cold and then rewarming the mixture resulted in massive hemolysis. When the washed cells alone were subjected to the same temperature change, nothing happened, which indicated that it was something in the plasma that was responsible for the hemolytic event. When the plasma alone was cooled, rewarmed and then added to the patient's washed erythrocytes, again nothing transpired, which suggested that the two reagents must interact in the cold before rewarming. However, when the plasma was heated to 56 °C before use in the above tests, no hemolysis occurred, which indicated that some plasma participant in the reaction is thermolabile. This labile activity, however, could be replaced by any active (that is, unheated) serum or plasma from normal individuals, which suggested that whatever the thermolabile factor is, it is not peculiar to this disease. These experiments were followed up by testing patients' plasma against the red cells of normal controls, and patients' red cells against the serum or plasma of normal controls, using the same protocol as before. The result was clear: some thermostable substance in the plasma of the patient could lyse any human erythrocytes, whereas the red cells of the patient could not be destroyed by the plasma of control individuals. The only interpretation possible was that three components are involved in the process: red cells, a thermolabile factor and a thermostable factor. Only the thermostable factor appeared to be abnormal and to exist only in the patients' blood because the other two factors (red cells and unheated serum) could be furnished by normal controls. This finding was elegantly confirmed as follows: the patient's plasma was cooled in the presence of a large amount of washed, normal human red cells, which were then centrifuged and set aside. New cells were then added and the mixture warmed. No hemolysis resulted, which indicated that the active substance had been removed specifically by the initial treatment. However, the cells used for the absorption could then be lysed in the warm on the addition of an unheated serum, which showed that they had indeed interacted with (absorbed) the active substance. When a control was run under the condition where the initial mixture was maintained in the warm, it was found that no absorption of the active substance had taken place. Here was an interaction of active substance with erythrocyte that could occur only in the cold! It was clear to the investigators that the hemolysis .
