Author
Steven N. Austad
Other affiliations: University of Idaho, University of Texas Health Science Center at San Antonio, American Federation for Aging Research ...read more
Bio: Steven N. Austad is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Longevity & Oxidative stress. The author has an hindex of 61, co-authored 203 publications receiving 13800 citations. Previous affiliations of Steven N. Austad include University of Idaho & University of Texas Health Science Center at San Antonio.
Topics: Longevity, Oxidative stress, Senescence, Medicine, Population
Papers published on a yearly basis
Papers
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TL;DR: The evolutionary theory of ageing explains why ageing occurs and helps to clarify how the genome shapes the ageing process, thereby aiding the study of the genetic factors that influence longevity and age-associated diseases.
Abstract: The evolutionary theory of ageing explains why ageing occurs, giving valuable insight into the mechanisms underlying the complex cellular and molecular changes that contribute to senescence. Such understanding also helps to clarify how the genome shapes the ageing process, thereby aiding the study of the genetic factors that influence longevity and age-associated diseases.
1,624 citations
TL;DR: The goal here is to seek evidence for common mechanisms among diverse organisms amenable to genetic analysis and oxidative damage is a candidate for such a public mechanism of ageing.
Abstract: Evolutionary theory predicts substantial interspecific and intraspecific differences in the proximal mechanisms of ageing. Our goal here is to seek evidence for common (‘public’) mechanisms among diverse organisms amenable to genetic analysis. Oxidative damage is a candidate for such a public mechanism of ageing. Long-lived strains are relatively resistant to different environmental stresses. The extent to which these stresses produce oxidative damage remains to be established.
640 citations
TL;DR: It is argued that - with the fallacy that wild animals do not senesce finally dead and buried - collaborations between bio-gerontologists and field biologists can begin to test the ecological generality of purportedly 'public' mechanisms regulating aging in laboratory models.
529 citations
TL;DR: Several hypotheses have been proposed for sex differences in longevity, including more active female immune functioning, the protective effect of estrogen, compensatory effects of the second X chromosome, reduction in the activity of growth hormone and the insulin-like growth factor 1 signaling cascade, and the influence of oxidative stress on aging and disease.
403 citations
TL;DR: Bats have maximum life spans a minimum of 3 times those of nonflying eutherians--a trend resulting from neither low basal metabolic rate, the ability to enter torpor, nor large relative brain size, consistent with an evolutionary theory that posits exceptionally long life spans among mammals with reduced environmental vulnerability.
Abstract: This study compared trends in body size, life span, metabolic rate, and ecology of bats and marsupials with those from mammals generally, using a 580 species data base. The linear logarithmic relationship between mammalian body mass and maximum longevity, deleting bats and marsupials, is used as a standard against which to measure life spans of particular mammal groups. Bats have maximum life spans a minimum of 3 times those of nonflying eutherians--a trend resulting from neither low basal metabolic rate, the ability to enter torpor, nor large relative brain size. Marsupials live about 80% as long as nonflying eutherians despite averaging lower basal metabolic rates; similarly, there is no effect of heterothermy or relative brain size. These results directly conflict with predictions of both "rate of living" and brain-size mediated theories of aging. However, they are consistent with an evolutionary theory that posits exceptionally long life spans among mammals with reduced environmental vulnerability.
392 citations
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28 Jul 2005
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
TL;DR: Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols used xiii 1.
Abstract: Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols Used xiii 1. The Importance of Islands 3 2. Area and Number of Speicies 8 3. Further Explanations of the Area-Diversity Pattern 19 4. The Strategy of Colonization 68 5. Invasibility and the Variable Niche 94 6. Stepping Stones and Biotic Exchange 123 7. Evolutionary Changes Following Colonization 145 8. Prospect 181 Glossary 185 References 193 Index 201
14,171 citations
TL;DR: Evidence that the appropriate and inappropriate production of oxidants, together with the ability of organisms to respond to oxidative stress, is intricately connected to ageing and life span is reviewed.
Abstract: Living in an oxygenated environment has required the evolution of effective cellular strategies to detect and detoxify metabolites of molecular oxygen known as reactive oxygen species. Here we review evidence that the appropriate and inappropriate production of oxidants, together with the ability of organisms to respond to oxidative stress, is intricately connected to ageing and life span.
8,665 citations
TL;DR: The status of the free radical theory of aging is reviewed, by categorizing the literature in terms of the various types of experiments that have been performed, which include phenomenological measurements of age-associated oxidative stress, interspecies comparisons, dietary restriction, and the ongoing elucidation of the role of active oxygen in biology.
Abstract: Beckman, Kenneth B., and Bruce N. Ames. The Free Radical Theory of Aging Matures. Physiol. Rev. 78: 547–581, 1998. — The free radical theory of aging, conceived in 1956, has turned 40 and is rapidl...
3,812 citations
TL;DR: Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing.
Abstract: Cells continually experience stress and damage from exogenous and endogenous sources, and their responses range from complete recovery to cell death. Proliferating cells can initiate an additional response by adopting a state of permanent cell-cycle arrest that is termed cellular senescence. Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing.
3,677 citations