Japan is investing a lot into Longevity Research in hopes of keeping us young forever. And recently, they managed to bring about a new kind of vaccine which…
Category: life extension – Page 186
Senescent macrophages are in fact also found to express senescence-related markers p16(Ink4a) and β-galactosidase (β-gal), and promote inflammation in diseased tissues [25, 26]. Our previous work has indicated increased cellular senescence in dystrophic muscles of mdx/utr(−/−) mice [3], however, whether or not macrophages in particular develop cellular senescence and promote senescence associated phenotypes was still unknown. To this end, here we further examined mdx/utr(−/−) mice and solved these puzzles.
Immune cells in the skeletal muscle are activated during muscle injury and promote the process of muscle regeneration by coordinating with muscle stem cells. However, studies with severely diseased muscles further demonstrate that immune cells can become dominantly activated and is inductive of increased fatty infiltration and fibrosis formation, while at the same time potently repress the proliferation and function of muscle stem cells [27]. Our current results in severely dystrophic muscle reveal a similar situation of interaction between macrophages and MPCs, showing that the function of MPCs is repressed by the senescent macrophages. As senescent cells accumulate in the aged or diseased tissues, it can exert profound effects on the growth and function of normal cells by releasing SASPs [9, 10].
Axolotls Can Regenerate Their Own Brains: New research maps out the different cell types hoping to pave the way to regenerative medicine!
O.o!!!
According to recent research, the protein CHIP can control the insulin receptor more effectively while acting alone than when in a paired state. In cellular stress situations, CHIP often appears as a homodimer – an association of two identical proteins – and mainly functions to destroy misfolded and defective proteins. CHIP thus cleanses the cell. In order to do this, CHIP works with helper proteins to bind a chain of the small protein ubiquitin to misfolded proteins.
As a result, the cell detects and gets rid of defective proteins. Furthermore, CHIP controls insulin receptor signal transduction. CHIP binds to the receptor and degrades it, preventing the activation of life-extending gene products.
Researchers from the University of Cologne have now shown via tests using human cells and the nematode Caenorhabditis elegans that CHIP can also label itself with ubiquitin, preventing the formation of its dimer. The CHIP monomer regulates insulin signaling more effectively than the CHIP dimer. The research was conducted by the University of Cologne’s Cluster of Excellence for Cellular Stress Responses in Aging-Associated Diseases (CECAD) and was recently published in the journal Molecular Cell.
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Article originally published on LINKtoLEADERS under the Portuguese title “Sem saber ler nem escrever!”
In the 80s, “with no knowledge, only intuition”, I discovered the world of computing. I believed computers could do everything, as if it were an electronic God. But when I asked the TIMEX Sinclair 1000 to draw the planet Saturn — I am fascinated by this planet, maybe because it has rings —, I only glimpse a strange message on the black and white TV:
SINGAPORE — A new longevity clinic where the doctor will diagnose a healthy person’s biological age and then provide a customised plan to slow ageing is being set up at Alexandra Hospital and is expected to open by early next year.
It will be the first publicly funded outpatient clinic in longevity medicine in Singapore and possibly in the world, Professor Andrea Maier, the co-director of the National University Health System (NUHS) Centre for Healthy Longevity told The Straits Times at the sidelines of the centre’s opening on Wednesday.
The clinic will be manned by internal medicine specialists like Prof Maier, who is also the founding president of the International Longevity Medicine Society that was set up last month.
Water is a key ingredient to all life on Earth, yet tardigrades with their near immortal-like powers can somehow endure being sapped of almost all their H2O.
Now, researchers have discovered another trick these chubby microscopic anomalies use to survive years of extreme dehydration.
“Although water is essential to all life we know of, some tardigrades can live without it potentially for decades,” says University of Tokyo biologist Takekazu Kunieda.
Excerpt from an interview by Rich Roll to Peter Diamandis, founder and executive officer of XPrize Foundation, co-founder of Singularity University in Silicon Valley, CA., three-time best selling author, public speaker, philanthropist, and prolific investor.
Peter Diamandis has started over 20 companies in the areas of longevity, space, venture capital and education.
The interview took place in March 14, 2022.
To watch the entire interview clic here: https://youtu.be/gbpzdlib2us
Ageing, defined as the decline in survival probability and fecundity with advancing adult age, is often viewed as the evolutionary outcome of the declining force of natural selection at older age (17 ; 22). Ageing can be due to the accumulation of late acting deleterious mutations (17 ; 12 ; 4), and/or due to pleiotropy, as the result of constrained life-history optimization (36 ; 4 ; 22 ; 38). For instance, increased allocation of limited resources to reproduction can be an important cause of senescence and later mortality (17 ; 35 ; 14 ; 15 ; 31). Most of the evidence for this phenomenon comes from experiments showing the deleterious consequences of an increase in reproductive effort on life span (21 ; 32 ; 3 ; 10 ; 24 ; 28). Artificial selection on age at reproduction showed the reverse effect that selection regime favouring individuals that retained fecundity at a later age resulted in populations with increased life spans (7 ; 39 ; 22). Data for higher organisms, e.g. mammals, have until now been mostly lacking.
The hypothesis that investment in reproduction reduces the resources available for somatic maintenance has recently been tested in Homo sapiens by 33 ). Using 1,200 years of genealogical data on British aristocracy, they showed that the number of progeny was small for women who died at an early age, increased with the age of death, reached a plateau through the sixth, seventh and eighth decades of life, and was lower again for women who died at an age of 80 years or over. This relationship supported the expectation that heavy investments in reproduction diverts resources away from the maintenance and repair of cells, with ageing and earlier death as results (33). For unknown reasons, the authors found a virtually identical pattern among men.
As manipulative experiments on humans are unethical, the statistical search for congruent patterns offers an alternative to understand variation in life-history parameters among human populations. Fortunately, there are considerable statistics on humans and their activities, and other ways of detecting similar patterns and of testing relevant hypotheses are possible. The aim of the present paper is to assess the generality of this trade-off among humans. We test whether the variation of life-history parameters found in the study of British aristocrats is also present across different human populations worldwide. After controlling longevity and fecundity for possible effects exerted by historical, spatial, economical and population patterns, we determined the relationship between longevity and fecundity, using data from 153 countries located all over the world.