Horatio
22.1K posts
Individual aging is caused by the aging of the cells that make up the organism. However, there is currently no definitive conclusion on why cells age, with various theories proposed. The most prominent theory of cellular aging is the telomere theory. This is because telomere elongation can eliminate cellular aging markers, significantly increase the number of cell divisions, and enable some cells to divide indefinitely. No other theories can achieve this, indicating that they are incorrect. Nevertheless, the telomeres of many cell types do not shorten, yet their replication capacity remains limited. This suggests that, in addition to telomeres, another factor drives cellular aging. Based on this, I proposed the Telomere DNA and ribosomal DNA Co-regulation Model for Cell Senescence [1]. The paper titled rDNA array length is a major determinant of replicative lifespan in budding yeast (published April 8, 2022) states that the replicative lifespan of yeast cells is related to rDNA copy number. This supports the plausibility of my Telomere DNA and Ribosomal DNA Co-regulation Hypothesis for Cellular Aging. It will fundamentally unravel the mystery of mammalian cellular aging and identify a viable path for human rejuvenation: pnas.org/doi/10.1073/pn… I believe the mechanism of cellular aging is actually straightforward. First, as cells age, the level of the tumor suppressor protein p53 gradually increases. Moreover, sustained inhibition of p53 enables fibroblasts to proliferate indefinitely [2], and knockout of the p53 gene allows hepatocytes to do the same [3]. This demonstrates that p53 is the master regulator of cellular aging. p53 is primarily localized in the nucleolus (the site of rDNA concentration) and also binds to telomere-binding proteins, storing itself at telomeres. Therefore, the gradual reduction in telomere DNA and/or ribosomal DNA (rDNA) copy numbers leads to a progressive increase in p53 levels, driving cells from a youthful state to senescence. Thus, the fundamental mechanism of aging lies in the loss of telomere DNA and/or rDNA copy numbers. The ultimate strategy to reverse aging is to elongate telomeres and increase rDNA copy numbers. Both telomere DNA and rDNA are highly unstable multi-copy tandem repeat DNAs, prone to copy number loss and capable of binding p53. This implies that their shared characteristics represent two biological clocks designed by nature to govern development and aging. Reference: [1] Huang, B. Telomere DNA and Ribosomal DNA Co-regulation Model for Cell Senescence. Negative 2021, 12, 9–15. doi.org/10.13276/j.iss… (in Chinese) [2] Aksoy O, Chicas A, Zeng T, et al. The atypical E2F family member E2F7 couples the p53 and RB pathways during cellular senescence[J]. Genes Dev, 2012, 26(14):1546–1557. [3] Ma Di, Yan Xinqi, Peng Chenghong. Advances in hepatocyte immortalization research [J]. Journal of Tissue Engineering and Reconstructive Surgery, 2012, 8(1):46–48. (in Chinese)
ロボコンで披露された「紙飛行機大量生産ロボット」がかっこ良すぎる
The philosopher Michel Serres, who taught at Stanford for many years and was close to Rene Girard, noted in a number of books that the doubling of lifespans, as occurred in the twentieth century, had seismic social consequences: marriage vows designed for a decade or two become 65-year contracts; inheritance arrives in your old age instead of your prime; the willingness to die for a nation becomes less prevalent when you have six decades of life ahead. The radical slowdown of aging that some say is on the horizon would invert every institution built on the assumption that the old will soon yield to the young.
The U.S. Dollar has lost 30% of its purchasing power over the last six years
