温度对生命体寿命的影响

综述了温度对生命体寿命的作用,包括温度参与调节特定基因表达和细胞信号传导通路,温度对能量代谢、氧化还原水平、免疫功能和热量限制的影响。介绍了一种将温度系数引入死亡率定律的假设,以此计算温度与寿命之间的关系,为探究温度对寿命的直接影响提供参考和依据。     

无菌松材线虫的获得及培养方法研究

采用不同浓度的H2O2和抗菌素处理松材线虫虫卵和松材线虫虫体,筛选松材线虫无菌化处理有效途径.多种方法的比较表明,采用高浓度抗菌素和低浓度H2O2交替并反复处理松材线虫虫体,获得无菌线虫的比例高,线虫生命力强.将获得的无菌松材线虫与带菌线虫分别用PSA和玉米粒上培养的灰葡萄孢进行人工培养,发现线虫生长繁殖情况无明显差异.     

Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila

Overexpression of sirtuins (NAD(+)-dependent protein deacetylases) has been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae), Caenorhabditis elegans and Drosophila melanogaster. Studies of the effects of genes on ageing are vulnerable to confounding effects of genetic background. Here we re-examined the reported effects of sirtuin overexpression on ageing and found that standardization of genetic background and the use of appropriate controls abolished the apparent effects in both C. elegans and Drosophila. In C. elegans, outcrossing of a line with high-level sir-2.1 overexpression abrogated the longevity increase, but did not abrogate sir-2.1 overexpression. Instead, longevity co-segregated with a second-site mutation affecting sensory neurons. Outcrossing of a line with low-copy-number sir-2.1 overexpression also abrogated longevity. A Drosophila strain with ubiquitous overexpression of dSir2 using the UAS-GAL4 system was long-lived relative to wild-type controls, as previously reported, but was not long-lived relative to the appropriate transgenic controls, and nor was a new line with stronger overexpression of dSir2. These findings underscore the importance of controlling for genetic background and for the mutagenic effects of transgene insertions in studies of genetic effects on lifespan. The life-extending effect of dietary restriction on ageing in Drosophila has also been reported to be dSir2 dependent. We found that dietary restriction increased fly lifespan independently of dSir2. Our findings do not rule out a role for sirtuins in determination of metazoan lifespan, but they do cast doubt on the robustness of the previously reported effects of sirtuins on lifespan in C. elegans and Drosophila.     

黑洞温度修正与黑洞寿命

讨论了在黑洞熵具有量子修正的情况下黑洞温度的修正,以及由此而引起的黑洞寿命的变化.研究发现,黑洞蒸发到普朗克质量时,温度降出现无限大,再减小质量时将出现负温,此时黑洞熵也将出现极小值.     

Fitness benefits of prolonged post-reproductive lifespan in women

Most animals reproduce until they die, but in humans, females can survive long after ceasing reproduction. In theory, a prolonged post-reproductive lifespan will evolve when females can gain greater fitness by increasing the success of their offspring than by continuing to breed themselves. Although reproductive success is known to decline in old age, it is unknown whether women gain fitness by prolonging lifespan post-reproduction. Using complete multi-generational demographic records, we show that women with a prolonged post-reproductive lifespan have more grandchildren, and hence greater fitness, in pre-modern populations of both Finns and Canadians. This fitness benefit arises because post-reproductive mothers enhance the lifetime reproductive success of their offspring by allowing them to breed earlier, more frequently and more successfully. Finally, the fitness benefits of prolonged lifespan diminish as the reproductive output of offspring declines. This suggests that in female humans, selection for deferred ageing should wane when one's own offspring become post-reproductive and, correspondingly, we show that rates of female mortality accelerate as their offspring terminate reproduction.     

Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan

In diverse organisms, calorie restriction slows the pace of ageing and increases maximum lifespan. In the budding yeast Saccharomyces cerevisiae, calorie restriction extends lifespan by increasing the activity of Sir2 (ref. 1), a member of the conserved sirtuin family of NAD(+)-dependent protein deacetylases. Included in this family are SIR-2.1, a Caenorhabditis elegans enzyme that regulates lifespan, and SIRT1, a human deacetylase that promotes cell survival by negatively regulating the p53 tumour suppressor. Here we report the discovery of three classes of small molecules that activate sirtuins. We show that the potent activator resveratrol, a polyphenol found in red wine, lowers the Michaelis constant of SIRT1 for both the acetylated substrate and NAD(+), and increases cell survival by stimulating SIRT1-dependent deacetylation of p53. In yeast, resveratrol mimics calorie restriction by stimulating Sir2, increasing DNA stability and extending lifespan by 70%. We discuss possible evolutionary origins of this phenomenon and suggest new lines of research into the therapeutic use of sirtuin activators.     

PFOS暴露对秀丽线虫寿长的影响及其与IIS相关基因的关联

以秀丽隐杆线虫(C.elegans)为模型,本文研究了全氟辛烷磺酸(PFOS)对机体寿长的影响及初步机理.结果显示0.2~200μmol/L的PFOS暴露50 h导致野生型秀丽线虫寿长呈剂量依赖性缩短.在4类转基因线虫上,观察到Insulin/IGF-l.1信号通路(IIS)相关的daf-16、daf-2和age-1基因突变或敲除能影响线虫的寿长.进一步观察PFOS暴露导致4类转基因线虫的寿长变化率,并与野生型线虫比较.在CF1139和CF1580突变种上daf-16或daf-2的突变均未改变PFOS的缩短寿长效应.而在CF1295和TJ1052转基因型上发现daf-16b的基因敲除或age-1基因突变阻断PFOS的减寿效应.结果表明PFOS慢性暴露能加速动物衰老,缩短寿长.PFOS作用与IIS信号通路关系密切,daf-16b和age-1基因在其中起重要作用.     

Regulation of lifespan by sensory perception in Caenorhabditis elegans

Caenorhabditis elegans senses environmental signals through ciliated sensory neurons located primarily in sensory organs in the head and tail. Cilia function as sensory receptors, and mutants with defective sensory cilia have impaired sensory perception. Cilia are membrane-bound microtubule-based structures and in C. elegans are only found at the dendritic endings of sensory neurons. Here we show that mutations that cause defects in sensory cilia or their support cells, or in sensory signal transduction, extend lifespan. Our findings imply that sensory perception regulates the lifespan of this animal, and suggest that in nature, its lifespan may be regulated by environmental cues.