Aging, Cancer and Cell Membranes [antikvár]

In recent years biologic research in the field of aging has greatly profited from new knowledge and technics contributed by rapidly expanding areas such as cellular and molecular biology. Consequently, studies in aging consist now of a wide variety of approaches both theoretical and experi- mental, evaluating genetic and epigenetic mechanisms in the process of senescence. These studies utilize biologic systems which include human sub- jects, animal models, cultured cells, and cellular macromolecules and attempt to correlate Aging with a variety of structural and functional endpoints. Both cellular and extracellular regulatory mechanisms are being explored, with some attempts to modulate the process of senescence. The aim of the present symposium has been to try to focus on some of the key problems and approaches currently prevailing in the area of the biology of aging and to bring together investigators from diverse yet related fields. The life-spans of multicellular organisms vary widely and can be modified by numerous genetic and environmental factors (see Sacher, Hart, Martin, Shock, Cutler). These include diseases (see Yunis, Makinodan, Finch, Brody, Martin, Hayflick), changes in the immune system (see Yunis, Makinodan, Harrison), diet (see Andres, Yunis), genetic instabilities and cumulative damage to cellular DNA and proteins (see Strehler, Hart, Martin, Sacher, Hayflick, Hirsch), neuroanatomic and neurochemical modifications (see Brody, Finch) and responsiveness to homeostatic regula- tors such as hormones (see Roth, Finch, Cristofalo, Yunis, Makinodan). Clearly, the initiation, expression and modulation of aging are attributable to multiple events and no single genetic or environmental factor will uni- formly accelerate all facets of aging. From a biologic point of view, the process of aging is associated with structural and functional impairments which occur in a living organism and are expressed in gradual deterioration and decline in performance. The functional manifestation of this loss is multiple, occurring at all levels of biologic organization and in all processes, with different rates in species of different life forms but not markedly different when species maximum lifespan is normalized (see Sacher, Hart). Longevity has evolved as a posi- tive trait with the increase in body and brain sizes, lower reproductive rates, and longer maturation periods (see Sacher). Differences in longevity between individuals or between genotypes within a species are not due to differences in rates of aging (see Sacher) or to differences in amount of exposure, damage or in targets exposed (see Hart), but rather to variation in resistance to stress and capacity to cope with it (see Sacher, Hart) or to pre-