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Biomedical subjects

G Korn

Publications and source records attributed to G Korn.

At least 37 records · Page 2Linked to original sources

[Studies on the increase of weights of lymphatic glands, of lymph and peritoneal fluid and their contents of chymotrypsin and virus in pigs suffering hog cholera (author's transl)].

Swine fever is conceived as a disorder of the enzyme systems, that are controled by serine proteases. The virus is replicated in the cells of the lymphomycoid complex, whereby the production of a chymotrypsin is induced. In swine fever the lymphatic glands and the lymph flow are increased. Fifteen normal pigs had chymotrypsin contents in the lymph of the body lymphnodes of 0,4 U/l, nine pigs suffering hog cholera 1,5 U/l. In the intestinal lymphnodes the chymotrypsin concentration was normally 2,9 U/l and in swine fever 3,5 U/l. Chymotrypsin which is present may induce the production of further chymotrypsin. Fourteen pigs suffering from swine fever showed increased peritoneal fluids (50 to 120 ml), whereby chymotrypsin was found in 5 cases. The lymphflow was assumed to be five times higher, when compared to control animals. This entails a seven-fold increase of chymotrypsin which enters the blood stream. In some cases the virus titers are higher in the lymph specimen and peritoneal fluids than in the serum. Increase of chymotrypsin concentration reduces the resistance of the virus in the lymph. Obviously the virus is spread in the body migrating with the lymph flow. However, the increasing chymotrypsin concentration seems to inactivate the virus and lymph retains its defense character. Detection of the fluorescent antigen is correlated with the evidence of the proteolytic precipitating antigen. After infection with the virus of swine vesicular disease increase of chymotrypsin is also evidenced in the lymph but to a lower degree. Therefore in swine fever the lymphnodes cause chymotrypsin formation to an extent which may explain the pathophysiological disorders in those physiological systems, that are controled by serine proteases.

Animals↗

[The propagation of swine fever virus in cultures of macrophages and lymphocytes of normal and immune pigs (author's transl)].

Swine fever virus is replicated in the cells of the lymphoid complex. During the course of the disease cell-destruction, leucopenia and a disturbance of globulin and transferrin production is described. In the case of recovering firstly the leucocyte population, specially the lymphocytes, later on antibody titer increase. The production of virus neutralizing antibodies is not recognizable to be the cause of a recovery, the latter seems to be initiated by the production of a newly formed cell population. Therefore macrophages and lymphocytes of normal and of swine fever immune pigs are compared respecting the virus replication in vitro. Hereby macrophage cultures did not show any differences. In contrast to these findings in the tissue cultures consisting of predominantly lymphocytes of normal animals the virus replication exceeded that of immune pigs. Further on in the lymphatic organs of pigs killed in the recovering state newly formed clones of lymphoid cells were detected, which did not show swine fever specific but a globulin specific fluorescence. Obviously during the reconvalescent state a population of immune relevant lymphocytes is being created, which is different of these of non-immune pigs, since swine fever virus is not propagated by them anymore.

Animals↗

[Leukomalacia and subsequent brain status in relation to intensive neonatal care].

Leucomalacia or white matter necrosis is one of the major aspects of neonatal encephalopathies, especially in the premature baby. These necroses are found mainly in the deep periventricular white matter of the "semi-oval centre". Characteristically, they are ischaemic and their anatomical and histological progress is rapid: coagulation necrosis with rapid axonal fragmentation followed by polymorphic cellular reaction with glial cells and macrophages. Regeneration in the minor forms consists of glyosis process in severe forms; multiple cavities appear in a few weeks. Physiopathogenic hypotheses put forward are related to: 1 -- the very anatomic aite: special tissue and terminal arteries, 2 -- onset of myelinization process, 3 -- associated clinical and biological lesions such as hypoxia, acidosis and hypotention. These lesions are symptom-free during the neonatal period. One of us suggested in 1962 that these could be the anatomical basis of spastic monoplegia or diplegia (LITTLE's disease). All motor cerebral sequelae have disappeared since 10 years. This is particularly significant mainly in the case of spastic diplegia of the former premature baby under 2500 g. This decrease coincides with improvement in neonatal care, especially correction of hypoxia, acidosis and cardiovascular collapse. These findings seem to support the pathogenic hypotheses.

Brain Diseases↗