Titlebook: Werner’s Syndrome and Human Aging; Darrell Salk,Yoshisada Fujiwara,George M. Martin Book 1985 The Editor(s) (if applicable) and The Author

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Studies of SV40-Infected Werner Syndrome Fibroblasts of a temperature-sensitive mutant strain (tsA900). The infected WS cells and the infected normal cells proliferated at permissive temperatures, and then entered into “crisis” in which state they ceased proliferation. In their proliferative phase, both WS and normal cells infected with tsA900 prolif

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Experimental Studies on Werner’s Syndrome Fibroblastsmportant role in the maintenance of several types of body tissue. The mutation is pleiotropic in that it appears to accelerate changes related to ageing in these tissues. It would therefore be surprising if the identification of the nature of the biochemical defect in Werner’s syndrome did not yield

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Cell Fusion Studies in the Werner Syndrome et al. 1966). Skin fibroblast cells from patients with Werner syndrome (WS cells) have a greatly reduced lifespan . and showed marked retarded DNA synthesis even at early ages in culture (Goldstein, 1969; Martin et al., 1970; Danes, 1971; Fujiwara et al., 1977). One approach for the study of senesc

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Clinical and Metabolic Studies on Werner’s Syndrome: With Special Reference to Disorders of Lipid anre, but some of them are either incomplete or occasionally overlap. Only by cautious selection from among the publications in the medical literature, excluding incorrect cases, is it possible to reveal the clear-cut clinical features of this syndrome.

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