Sentence examples for robust lifespan from inspiring English sources
Consistent with these findings, pharmacological inhibition of the mTORC1 signaling pathway with rapamycin confers a robust lifespan extension in genetically heterogeneous mice (Harrison et al., 2009), yeast (Bonawitz et al., 2007), and fruit flies (Kapahi et al., 2004).
In conclusion, we replicate and validate our previous finding [12] that global deletion of Irs1 induces a robust lifespan extension in female mice.
BDR represents a DR method that gives robust lifespan extension and avoids many of the pitfalls associated with other worm DR protocols, as discussed above.
This robust lifespan extension across genders in Irs1−/− mice is consistent with findings reported for other manipulations including dietary restriction [24], [25], rapamycin treatment [6] and GH/GH-receptor deficiency [8], [23], but is not seen in other sufficiently powered longevity studies (e.g. [26]).
The ablation of germline stem cells has recently been shown to cause robust lifespan extension in Drosophila[ 21], suggesting that the effects of ubiquitous over-expression of p53 might in part be mediated by p53 function in this tissue.
One of the first exciting findings from the ITP was the report that treatment with rapamycin, an inhibitor of the mTOR kinase, produced robust lifespan in both male and female mice, albeit skewed in favor of females (Harrison et al., 2009).
The mNSCs are neurosecretory cells, genetic ablation of which decreases the levels of mNSC-expressed dilps and leads to a robust lifespan-extension, presumably by suppression of the insulin-signalling pathway (Broughton et al., 2005).
Moreover, the reduction in food availability needed for robust DR lifespan extension (≥6-fold, Fig. 5A,B) was greater than would be expected to arise from the proportion of time that rict-1 mutants spent off their food in plate culture.
However, it is also worth noting that the control mice in our study had robust median lifespan of over 30 months, whereas the control mice in the Svensson et al. study had median lifespans of 22-23 months, which is shorter than expected for C57BL/6 strain.
In C. elegans, mutations in the conserved insulin/IGF-1 signaling (IIS) pathway lead to a robust extension in lifespan, improved late life health, and protection from age-related disease.
We focused on mir-71 which when mutant led to robust and significant lifespan phenotype, demonstrating its requirement for a normal long life.
