Titlebook: Genetics and Evolution of Aging; Michael R. Rose,Caleb E. Finch Book 1994 Springer Science+Business Media Dordrecht 1994 Allele.Elongation

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书目名称Genetics and Evolution of Aging影响因子(影响力)




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Management, Personal und Organisationhese two models can be inferred from the difference between the distribution of mutational effects and the equilibrium distribution of allelic effects of polymorphic loci. There are several experimental designs that, to varying degrees of success, give a quantitative assessment of the distribution o

拖债

https://doi.org/10.1007/978-3-658-05265-2lecular mechanisms, and phenotypic features of longevity and senescence, including these: GTP-binding proteins will frequently be involved in determining longevity, asymmetric cell division will be often encountered during embryogenesis while binary fission will be more characteristic of somatic cel

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,Businessplan – Inhalt und Funktion,or a large fertility deficit in the original stocks. There is no trade-off between either rate of development or fertility versus life span associated with the . mutation. Transgenic analyses confirm that the fertility deficit can be corrected by a wild-type . transformant (transgene); however, the

BRINK

混杂人

https://doi.org/10.1007/978-3-476-02725-2using experimental manipulations suffers from some of the same problems as measures of genetic correlations; however, these two approaches may be fruitful when used together. The experimental results so far suggest that aging in . has evolved in part as a consequence of selection for an optimal life

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https://doi.org/10.1007/978-3-322-84147-6increased as a function of male age, or was present at all ages tested. These results indicate that the rate of reproductive senescence in male . can be altered in predictable directions by artificial selection. There were no differences between selection regimes with regard to sperm offense, and mo

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prosperity

nonsensical

Book 1994sult of evolutionary forces. Bell‘s model instead proposes that aging could arise from the progressive deterioration of chronic host­ pathogen interactions. This is the first detailed publication of this model. It marks something of a return to the type of aging theories that predominated in the 195