DNA 与衰老

衰老是生物体各种功能的普遍衰弱,以及抵抗环境伤害和恢复生理稳态的降低过程。衰老、衰老的原因、衰老的机理及衰老与疾病、衰老与死亡的关系,一直是生物及医学领域的科学家们积极探讨的问题。衰老这一极其复杂的生物学过程,涉及物理、化学、生物、医学诸领域。现已发展的近300种衰老学说分别从整体、器官、细胞、分子水平对生物衰老的机制进行了阐述。本文将从分子的角度阐述生物信息分子－DNA及其相关物质与生物衰老的关系。     

Aging in Perennials

Compared with our knowledge of senescence processes in annuals and biennials, relatively little is known about age-related changes in perennials. The study of aging in plants is very complex and there is no consensus in general concepts related to this topic. Furthermore, there is also a problem of scaling up, which makes us wonder whether cells, tissues/organs or whole organisms really age in plants. This is particularly interesting in the case of perennials, which have the ability to make new leaves every year and live for several years or even centuries or millennia. Recent studies indicate that physiological burdens, such as demands on water and nutrient supply, are responsible for reduced growth as plants age. Aside from the extrinsic factors, it is also possible that intrinsic changes in the shoot meristems could occur through repeated cell divisions and could be fixed during plant development, thereby affecting the physiology of leaves that originated from these cells. Additionally, the increased size associated with the aging of woody perennials (trees and shrubs) has also been proposed as a determining factor responsible for the age-related reductions in growth and photosynthetic rates in leaves. This review is aimed at compiling our current understanding of aging in perennials. After defining some fundamental questions and concepts, and introducing the model plants presently used in the study of aging in perennials, the major role meristems play in perenniality and how aging is manifested in the physiology of perennials (changes in phytohormones, water relations, photosynthesis and oxidative stress) are described. Finally, the causes underlying age-related changes in perennials are discussed in detail and a model based on plant plasticity to explain the aging phenomenon in perennials is presented.     

Mitochondria and Aging

Cover illustration: Mitochondria and Aging, a special issue edited by Professor Heinz D. Osiewacz (Frankfurt, Germany), devoted to aging research and the involvement of mitochondria “from models to humans”. Depicted are a 3D section of a human cell with mitochondria shown in red (© NIH, see http://ghr.nlm.nih.gov/handbook/illustrations/cellmitochondria) and from top to bottom: micrograph of mitochondria from the model organism Podospora anserina (© C. Scheckhuber, see p. 781), hand with pill (© Photodisc Inc.) and the worm Caenorhabditis elegans with typical senescent morphology (© B. Braeckman, see p. 803).     

Data on Aging

Federal payment for hospitalization and partial medical care of certain citizens 65 and over is proposed in H.R. 4222. There are several important aspects of this proposed legislation which merit consideration, notably (1) How great is the actual need? and (2) Who would actually be covered by the proposed measure?1. The need for subsidized hospitalization and medical care is believed to be distinctly limited. A national study of the total life situation of those 65 and over (by Wiggins and Schoeck) showed that 90 per cent of the respondents reported no unmet medical needs of which they were aware. About 96 per cent reported no medical debts. This would leave presumably 4 per cent with such debts.2. The proposed legislation would cover those eligible for benefits under the Social Security Act and the Railroad Retirement Act, but not other elderly persons.The Wiggins-Schoeck Report has been bitterly assailed by supporters of H.R. 4222 as being nonrepresentative and incomplete. Its authors (in a recent letter to Science) point out that it is indeed representative of the older population currently designated in H.R. 4222, and that it intentionally omitted those segments which would not be covered by H.R. 4222. In other words the data on needs of elderly persons as uncovered by Wiggins and Schoeck is pertinent to the legislation at hand. For this reason it is believed that physicians will be interested in reading the reply of these authors to the criticisms of their survey.With the permission of Science and of the authors, it is reprinted herewith.     

Paradoxes of Aging

Insightful articles by Kirkwood and other outstanding scientists reveal paradoxes of aging. The source of paradoxes is an assumption that aging is caused by random accumulation of molecular damage. Here I demonstrate that a concept of TOR-driven program-like aging almost automatically resolves eleven paradoxes of aging. This article discusses why the accumulation of molecular damage does not limit life span, why calorie restriction and inhibition of protein synthesis extend life span, why non-existing ‘program’ for aging is nevertheless robust, why a key gene for aging cannot be found by knocking it out, why low insulin is associated with good health but low insulin response with bad health, why aging is not a disease but can be treated as a disease, why ‘healthy’ aging is slow aging, and how do we know that calorie restriction actually slows aging in humans.     

Aging in birds

Rodents are the most commonly used model organisms in studies of aging in vertebrates. However, there are species that may suit this role much better. Most birds (Aves), having higher rate of metabolism, live two-to-three times longer than mammals of the same size. This mini-review briefly covers several evolutionary, ecological, and physiological aspects that may contribute to the phenomenon of birds’ longevity. The role of different molecular mechanisms known to take part in the process of aging according to various existing theories, e.g. telomere shortening, protection against reactive oxygen species, and formation of advanced glycation end-products is discussed. We also address some features of birds’ aging that make this group unique and perspective model organisms in longevity studies.