By A. V. S. de & Julie Knight. Reuck
Chapter 1 mobile harm and Alkylation of telephone elements (pages 1–29): P. N. Magee
Chapter 2 The Cytotoxic impact of Leucocidin (pages 30–52): A. M. Woodin and A. A. Wieneke
Chapter three Mechanism of motion of yes Exogenous poisonous brokers in Liver Cells (pages 53–73): ok. R. Rees
Chapter four Endogenous Mechanisms of harm relating to irritation (pages 74–86): W. G. Spector and D. A. Willoughby
Chapter five Interactions among useless Cells and residing Tissue (pages 87–105): G. Majno
Chapter 6 mobilephone harm within the baby Animal (pages 106–122): M. J. R. Dawkins
Chapter 7 Microsomal Peroxidation of Lipids and its attainable function in mobile harm (pages 123–135): P. Hochstein and L. Ernster
Chapter eight mobile accidents attributable to Folic Acid Antagonists and Somec Orticosteroids (pages 136–166): W. Jacobson
Chapter nine Interactions generating harm or fix of mobile Membranes (pages 167–186): A. D. Bangham
Chapter 10 attainable position of Ion Shifts in Liver damage (pages 187–208): J. D. Judah, okay. Ahmed and A. E. M. Mclean
Chapter eleven superb Structural Lesions precipitated by way of Viruses (pages 209–247): W. Bernhard
Chapter 12 Electron Microscopy of Liver and Kidney Cells in nutritional Deficiencies (pages 248–286): W. S. Hartroft
Chapter thirteen reports on mobile discomfort and loss of life: An try at class (pages 287–328): M. Bessis
Chapter 14 The dying of Cells in basic Multicellular Organisms (pages 329–351): J. D. Biggers
Chapter 15 managed Degeneration in the course of improvement (pages 352–386): E. Zwilling
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Additional resources for Ciba Foundation Symposium - Cellular Injury
A further consequeiice of the accumulation of calcium by the leucocidm-treated cell is that the cell acquires mechanical rigidity; normal cells suspended in sucrose can be disintegrated in a Potter-Elvjhem tube in a few seconds, but leucocidin-treated cells prepared in media containing calcium require at least I 5 minutes homogenization. Leucocidin-treated cells prepared in the absence of calcium behave like normal cells in this respect. This is taken as evidence that some of the calcium bound in the leucocidin-treated cells is present in the cell surface (Woodin and Wieneke, 19636).
1963). , 89, 32. , and MOHR,U. (1961). Z . , 64,305. , and MULLER, M. (1961~). Naturivissensch~tefierz,48,I 34. , and MULLER, M. (19616). Naturruissenschafien, 48,165. , and STEINHOFF, D. (1962). Naturivisscrisc~~aftc~ri, 49,497. DUNN,D. B. (1961). Biochim. biophys. Acta 46,198. DUNN,D. B. (1963). , 86, 14P. DUNN,D. , and SMITH,J. D. (1955). ), 175. 336. DUNN,D. , and SMITH, J. D. (1958). , 68,627. DUSTIN, P. (1947). ), 159,794. DUTTON, A. , and HEATH, D. F. (1956). ), 178,644. FARBER, E. (1963).
Each coniponeiit is adsorbed separately by thc cell surface and there is no competition for binding sites. Eithcr component adsorbed on the surface can be neutrahzed by antibody and so it is probable that penetration into the cytoplasni does not occur. There is no degradation of structural material in the first 10 minutes of intoxication. There is inhibition of glycolysis in the cell but this is not a direct effect of leucocidin. The permeability changes of the leucocidin-treated leucocytc are very specific.
Ciba Foundation Symposium - Cellular Injury by A. V. S. de & Julie Knight. Reuck