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    Loss of NAD during aging inhibits nuclear-encoded genes for mitochondrial proteins. New work suggests it inhibits DNA repair, releasing pieces of nuclear DNA into the cytoplasm, causing SASP inflammation in aging & cancer

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  2. proslijedio/la je Tweet
    31. sij

    Senescent cells display cytoplasmic chromatin that activates cGAS-STING and inflammation. But what triggers cytoplasmic chromatin? Mitochondria play a role. From Peter Adams lab and our lab. Led by

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  3. proslijedio/la je Tweet
    22. sij

    A high‐fat diet reverses metabolic disorders and premature aging by modulating insulin and IGF1 signaling in SIRT6 knockout mice

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  4. proslijedio/la je Tweet
    30. sij

    Calorie restriction-mediated lifespan extension is independent of Nrf2 in mice

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  5. proslijedio/la je Tweet
    30. sij

    The list they came up with. Hopefully it will inspire further research along the same lines.

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  6. proslijedio/la je Tweet
    29. sij

    Final version of methods paper on workflow for quantifying calcium/bioelectricity tracking in frog embryos, by Patrick McMillen (from our lab) and Richard Novak, a great collaborator and scientist at :

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    Unlike more robust species, we mammals lose our hearing because we fail to regenerate damaged cochlear hair cells. New study shows long-term activation of Sirt1 with resveratrol increases mitochondria & reduces hair cell loss in old BL6 mice. Music to our👂

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  8. proslijedio/la je Tweet
    26. sij

    High insulin levels (like with ) activate inflammation and inhibit autopaghy in joint cells; may be a mechanism wherein IR links to .

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  9. proslijedio/la je Tweet
    26. sij

    Tissue specificity of cell accumulation during physiologic and accelerated aging of mice

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  10. proslijedio/la je Tweet
    24. sij

    Hyperactivation of TORC1 Drives Resistance to the Pan-HER Tyrosine Kinase Inhibitor Neratinib in HER2-Mutant Cancers:

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    23. sij

    Transplanting cells from old but not young donors causes physical dysfunction in older recipients

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  12. proslijedio/la je Tweet
    22. sij

    The Future is Now! In Vivo AAV-CRISPR/Cas9–Mediated Gene Editing Ameliorates Atherosclerosis in Familial Hypercholesterolemia

    , , i još njih 2
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  13. proslijedio/la je Tweet
    20. sij

    mTORC1 directly inhibits AMPK. Well it would, wouldn’t it. Discovery made in yeast by the wonderful Janni Petersen at Flinders Uni, my team confirmed in mammals. A simple story with 157 Westerns at the last count😁

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  14. proslijedio/la je Tweet
    21. sij

    Anyone interested in anti-aging / life extension should give a follow to

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  15. proslijedio/la je Tweet
    19. sij

    The hypothesis of aging is still alive but our work and others show that we need to find better ways of selectively inhibiting mTORC1, and avoid inhibiting mTORC2 or other kinases that are necessary for health and survival

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    8. sij

    Collaboration with on the link between vacuole/lysozomes, mitochondria, and aging in individual cells is starting clarify different trajectories of aging.

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    Complete removal of food (all adult life) prolongs life of the worm C elegans. So all adult life the aging worm is doing something that activates mTOR and shortens its life. Why? Aging is mTOR-driven quasi-program, a continuation of developmental growth

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  18. proslijedio/la je Tweet
    3. sij

    Probably best medical resources in the world. Yet, our country has the lowest longevity of developed countries & ⬇️. Also, highest expenditure by far..But the epidemic of cardiometabolic disease, Alzheimer’s and (maybe?) cancer hasn’t started yet...Economic collapse inevitable.

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  19. proslijedio/la je Tweet
    19. pro 2019.
    Odgovor korisnicima

    Couldn’t agree more!!! Yes!!! You are right as always!!! Please read and re-read this editorial (2010). Every word is worth it. Am J Cardiol 2010;106:1364–1366

    , , i još njih 5
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  20. proslijedio/la je Tweet
    17. pro 2019.

    One of the most important science debates of the decade. Gary Taubes versus Stephan Guyenet, March 19th, on the Joe Rogan Experience. Why this is so important.

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