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| Author(s): |
Nazareno Getter Ferreira de Medeiros
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Carlos. |
| Institution: | Universidade de São Paulo (USP). Instituto de Física de São Carlos (IFSC/BT) |
| Defense date: | 2001-03-02 |
| Examining board members: |
Roberto Nicolau Onody;
Jose Fernando Fontanari;
Richard Charles Garratt;
Suzana Moss de Oliveira;
Carmen Pimentel Cintra do Prado
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| Advisor: | Roberto Nicolau Onody |
| Abstract | |
There are two kinds of aging theories: biochemical and evolutionary. Biochemical theories invoke damage to cells, tissues, and organs and connect senescence with imperfections of the biochemical processes responsible for the maintenance of life. The evolutionary theories, on the other hand, explain senescence without any especific biochemical mechanisms. Aging evolutionary theories are hypothetico-dedutive and assume that senescence is a consequence of na optimal life history, controlled by natural selection, which guarantees perpetuation of the species. Such characteristics make the evolutionary theories more suited for the application of Physics methods. In our work, we will consider only this kind of theory. In the first part of this thesis, we present a brief discussion on the difficulties to obtain rigorously biological properties which can be efficiently used in the quantificaion of the aging process. One way to measure senescence is through an analysis of the so called table of life. These tables indicate the existence of a mortality Law which is responsible for a specific mortality pattern. We explain the main ideas on which the biochemical and evolutionary theories are based. We propose a simple age-structured population model containing all the relevant features of the evolutionary aging theories: beneficial and deleterious mutations, reproductive rates, and natural selection. An exact solution for this model is found and, to our surprise, it does not exhibit senescence. Average survival probabilities and Malthusian growth exponents are calculated and they indicate that the system may have a mutational meltdown. We believe that this model is a good candidate to appropriately describe some coelenterate and prokaryote groups. In the presence of the pleiotropic constraint and deleterious somatic mutations, the time evolution of the Partridge-Barton model is exactly solved for na arbitrary fecundity using a matricial formalism. The steady state values for the mean survival probabilities and the Malthusian growth exponent are obtained. The mean age of the population shows a Power Law decay. Finally, we study the aging model proposed by Heumann and Hötzel. By introducing a minor change in this model, we show that it is able to keep many age intervals in disagreement with previous ideas. Moreover, our numerical simulations show a plethora of new interesting features, namely catastrophic senescence, the Gompertz Law and the effects that different reproductive strategies may have on life expectancy. (AU) | |