Studies on the inhibiting factors to Yoshida sarcoma in several animals sensitized with organs of several strains of rats.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Five days following implantation of a Yoshida sarcoma, female rats developed an increase in plasma fibrinogen concentration and a decrease in the number of platelets. The endotoxin induced fibrinisation of the microcirculation, as measured in percent involvement of glomerula, was found to be five to ten times higher than in control animals. A single injection of endotoxin without infusion was sufficient in tumor bearing animals to induce glomerular capillary thrombosis. The Yoshida sarcoma induced pathophysiological changes with a "preparative" effect on the endotoxin-induced disseminated intravascular coagulation.
Extinctions in the sera of Yoshida-sarcoma-bearing and normal rats were determined by means of a photometric measurement after the reaction of the sera with Ehrlich's reagent. Thereby the increase of the extinctions of the tumor bearers could be confirmed, also being found in tumor patients. The difference in terms of normal animals was statistically significant. The supposed relations between the exitation of the extinctions and the level of glycoproteins could be supported by correlating calculations.
Explore the source record for details and available documents.
Inactivation of (Na+ + K+)-ATPase of Yoshida sarcoma cells and beef brain microsomes by phospholipase A2 and a cytotoxin P6 from snake venom has been examined in relation to their activity to degrade phospholipids. Cytotoxin P6 which was most basic and devoid of phospholipase activity was most effective in inhibiting the (Na+ + K+)-ATPase of Yoshida sarcoma cells. Phospholipase A2 from Naja naja which was most active in degrading phospholipids was least effective in inhibiting (Na+ + K+)-ATPase in Yoshida sarcoma cells or in beef brain microsomes. Addition of trace amounts of cytotoxin P6 to the phospholipase considerably enhanced the inactivation of (Na+ + K+)-ATPase. The evidence suggests that the charge of the inhibitor protein and its specific structure play an important role in the inactivation of (Na+ + K+)-ATPase.
Cells of the methylene dimethanesulphonate-(MDMS)-resistant Yoshida sarcoma cell line contain a low molecular weight "resistance factor" which is present in the culture medium of these cells and may be utilized by MDMS-sensitive Yoshida sarcoma cells either by co-culturing the two cell lines or by culturing the MDMS-sensitive Yoshida cells in a medium containing 20% used medium of MDMS-resistant Yoshida cells or in the presence of dialysed medium from resistant cells. The "resistance factor" does not inactivate the drug itself or its metabolites, and it has no influence on the sensitivity of the cells if added after MDMS treatment. Twenty-four hours seems to be enough time for the transfer of the resistance factor, but its effect on whole populations decreases within 24 hours of ceasing the supply. The relationship between these findings and the known phenomena of metabolic co-operation are discussed.