Basic life sciences 

Abstract: Aging is the progressive accumulation of changes with time that are associated with or responsible for the ever-increasing susceptibility to disease and death which accompanies advancing age. These time-related changes are attributed to the aging process. The nature of the aging process has been the subject of considerable speculation. Accumulating evidence now indicates that the sum of the deleterious free radical reactions going on continuously throughout the cells and tissues constitutes the aging process or is a major contributor to it. In mammalian systems the free radical reactions are largely those involving oxygen. Dietary manipulations expected to lower the rate of production of free radical reaction damage have been shown (i) to increase the life span of mice, rats, fruit flies, nematodes, and rotifers, as well as the "life span" of neurospora; (ii) to inhibit development of some forms of cancer; (iii) to enhance humoral and cell-mediated immune responses; and (iv) to slow development of amyloidosis and the autoimmune disorders of NZB and NZB/NZW mice. In addition, studies strongly suggest that free radical reactions play a significant role in the deterioration of the cardiovascular and central nervous systems with age. The free radical theory of aging provides reasonable explanations for age-associated phenomena, including (i) the relationship of the average life spans of mammalian species to their basal metabolic rates, (ii) the clustering of degenerative diseases in the terminal part of the life span, (iii) the beneficial effect of food restriction on life span, (iv) the greater longevity of females, and (v) the increase in autoimmune manifestations with age. It is not unreasonable to expect on the basis of present data that the healthy life span can be increased by 5-10 or more years by keeping body weight down, at a level compatible with a sense of well-being, while ingesting diets adequate in essential nutrients but designed to minimize random free radical reactions in the body.

Abstract: A hypothesis was proposed several years ago that Escherichia coli possesses an inducible DNA repair system (“SOS repair”) which is also responsible for induced mutagenesis. Some characteristics of the SOS repair are (1) it is induced or activated following damage to DNA, (2) it requires de novo protein synthesis, (3) it requires several genetic functions of which the best-studied are recA + and lex + of E. coli, and (4) the physiological and genetic requirements for the expression of SOS repair are suspiciously similar to those necessary for the prophage induction. The SOS repair hypothesis has already served as the working hypothesis for many experiments, some of which are briefly reviewed. Also, some speculations are presented to stimulate further discussions and experimental tests.

Abstract: Since Polyploidy has been recognized as a widespread and common phenomenon among eukaryotes, particularly higher plants, biologists have been interested in possible causal connections between Polyploidy and distribution, and have tried to present relevant generalizations and “rules.” A quick historical survey of this topic takes us back to the first relevant studies on angiosperms during the thirties: Hagerup (1) and Tischler (2) demonstrated a frequency increase of polyploids from southern to northern latitudes and interpreted it as the result of greater hardiness of polyploids under extreme ecological conditions. Manton (3), on the basis of her studies on Biscutella in glaciated and unglaciated areas in Europe, was the first to stress the better colonizing potential of polyploids. The further elaboration of this question in the forties and fifties can be exemplified by contributions from A. and D. Love (4,5), Stebbins (6,7), and many others. During the same time studies concerned with Polyploidy and distribution were extended to some animal and other plant groups (cf. contributions in this Conference), foremost to the pteridophytes, again by Manton (8). Her finding of very high chromosome base numbers in many fern plants paved the way to our understanding of paleoPolyploidy, a phenomenon to which publications by Favarger (9) and S. and G. Mangenot (10) have further contributed during the sixties.

Abstract: Polyploidy in populations of well-differentiated plant species is now widely recognized (1,2). Most reports, however, are limited to a few individuals from one or several populations and thereby illustrate only a fraction of the extant genomic diversity in most species. They rarely purport populational dynamics involving Polyploidy as an evolutionary process. Nevertheless, there are recent notable exceptions and these will be utilized freely in this review of Polyploidy within species populations.

Abstract: Several different estimates of polyploid frequency in angio-sperms have been made, including G.L. Stebbins’ (1,2) figure, first published in 1950, of 30–35%, and suggestions by M.J.D. White in 1942 (3) of at least 40%, and by Grant in 1963 (4) of 47%. These figures represent different ways of calculating Polyploidy and different interpretations of the meaning of the word in the context of plant systematics. Stebbins’ estimate includes as polyploid those species which have gametic chromosome numbers that are multiples of the basic diploid number found in their genus, in other words, intrageneric Polyploidy. White’s figure is based on the simple observation that even haploid numbers exceed odd by about 40% and he thus assumed this 40% to be largely attributable to a polyploid origin. Grant postulated that species with haploid numbers in excess of n=13 would mainly be polyploid and those with n=13 or less, predominantly diploid. Grant’s study also included the only estimate I have encountered of Polyploidy in each of the two subclasses of angiosperms. He calculated a frequency of 43% in Dicotyledonae and a much higher 58% in Monocotyledonae. These figures were based on chromosome data accumulated by 1955 for some 17,138 species.