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Biomedical subjects

P Gedigk

Publications and source records attributed to P Gedigk.

At least 37 records · Page 2Linked to original sources

[Ultrastructure and morphogenesis of ceroid pigment. I. Phagocytosis and formation of lipid-containing lysosomes in Kupffer Cells after intravenous injection of unsaturated lipids (author's transl)].

Wistar rats were injected intravenously with cod liver oil emulsion. The phagocytosis of these lipids by the Kupffer cells as well as the formation of lipid-containing lysosomes were studied electron microscopically within a period of 5 min to 12 hrs. The emulsified lipids are incorporated into the cytoplasm by membrane-vesiculation. The lipid-containing phagocytic vacuoles (lipophagosomes) were transformed into secondary lysosomes (lipophagolysosomes). This change occurs in two phases. Immediately after phagocytosis the lipophagosomes are provided with lysosomal enzymes by fusion with pre-existent lysosomes (dense bodies) of the Kupffer cells. These are mainly the so-called small homogenous dense bodies which are probably primary lysosomes of the type of "storage granules". In the second phase which begins 15-30 min after the injection; the fusion of lipophagosomes with newly produced primary lysosomes within the Golgi apparatus is predominant. Therefore, the enzyme supply of the phagocytic vacuoles does not occur at once but in small amounts during a longer period. The lipids slowly change into an amorphous electron-dense mass 12 hrs after the injection. Obviously, these changes are the first step to the formation of ceroid pigment.

Acid Phosphatase↗

[Liver disease in polyvinyl chloride production workers - Clinical and peritoneoscopic aspects (author's transl)].

Peculiar clinical symptoms observed in polyvinyl chloride production workers of a nearby chemical plant arose the suspicion of liver and spleen disease in these workers before first reports on vinyl chloride-induced angiosarcoma of the liver became known. Starting at the end of 1972, 44 workers were followed up by biochemical investigations, peritoneoscopy and liver biopsy. As early as 1973 it could be ascertained, that advanced vinyl chloride-induced liver damage presents as hepatic fibrosis with splenomegaly, portal hypertension, and thrombocytopenia without conspicuous deterioration of hepatic parenchyma function. Similar symptoms have been observed after chronic intoxication by arsenic and thorium dioxide (thorotrast). The clinical and peritoneoscopic aspects of the disease are described.

Chemical Industry↗

[Morphological changes of the liver after chronic vinyl chloride intoxication (author's transl)].

The monomer vinyl chloride in its gaseous form is used as basic product for industrial synthesis of polyvinyl chloride; it does cause lesions of the liver depending on the dose and the time of exposure. Lesions found on histological examination are: 1. degenerative alterations of liver parenchyma; 2. focal adaptive changes in the cytoplasma of hepatocytes; 3. enlargement of liver cells and polymorphy of cell nuclei; 4. slowly progressive fibrotic and to a lesser degree cirrhotic changes of liver parenchyma, localized in part around the sinus, in part in the septal-periportal areas; 5. activation and proliferation of sinusoidal cells. Sarcoma of the liver due to a probable oncogenic effect of vinyl chloride could be diagnosed in three patients exposed to the toxic agent.

Adult↗