Titlebook: Regulation of Cell Proliferation and Differentiation; Warren W. Nichols,Donald G. Murphy Book 1977 Springer Science+Business Media New Yor

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ey explained today? This volume investigates relationships between forces of nature and human culture in a multidisciplinary context bridging science and the humanities..Forces of nature and cultural responses. is divided into four sections: (1) ball lightnings, (2) earthquakes and tsunamis, (3) vol

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Book 1977, New Jersey. Within this program there is a yearly workshop to promote theory and concept develop- ment in aging research with the specific purpose of addressing the use of genetically marked cells for aging research and to stimulate interest in aging research by workers in a variety of disciplines

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Delayed Mutation as a Cause of Genetic Disease in Man: Achondroplasia and the Wiedemann-Beckwith Syndigree of human extrodactyly when she suggested the possibility also in man.. Here we should like to describe some general aspects of the model of delayed mutation, using achondroplasia and the Wiedemann-Beckwith syndrome as specific examples.

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A Review of Controversial Issues in Myogenesismyotubes before they can transcribe and translate the mRNAs for the definitive contractile proteins. The central issue, in brief, involves delineating how relatively non-specific extracellular cues can activate rigidly circumscribed endogenous programs in cells in different compartments of the myogenic lineage.

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Adrenal-Glands

Application of Clonal Assay Methods to the Analysis of Tissue Development and Diseased Statess lacking the capacity for extensive proliferation when cultured under low density conditions will not be detected by the assay. The possibility of using high density culture techniques to study other aspects of the myogenic cell lineage have been discussed by Holtzer (1970), Holtzer and Bischoff (1970), and Holtzer .. (1972).

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Delayed Mutation as a Cause of Genetic Disease in Man: Achondroplasia and the Wiedemann-Beckwith Synal relatives. Auerbach postulated that the “connecting” unaffected ancestors of the affected individuals transmitted a labile premutated allele which, by delayed mutation, gave rise to the (fully) mutant allele. In unaffected offspring of such carriers the premutated allele could either have remaine

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Fusion, Phospholipase C, and Myogenesisis fusion related to other events of terminal differentiation. Elsewhere (Leung .., 1973; Leung .., 1975) we have reported that PLC releases a number of proteins from the surfaces of myogenic cells and we have suggested that at least one of these proteins is involved in the fusion process. Since the