I stumbled upon this tweet on a great free opportunity to move the field forward by giving a suggestion on a longevity cocktail to test in the wormbot!
Source: https://twitter.com/OraBiomedical/status/1781331548274647431?s=19
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I had missed out this great wormbot longevity prize contest. Just submit a proposal and have a possibility to win 25k. If I win any money from this contest then I will invest all of it in more experiments in the wormbot. Now I just need to think out some good proposal 
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It’s $2.5k for first place.
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Ah, I missed the dot there. Thanks for highlighting that. But 2.5k is ok.
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Watching the Campisi/foundmyfitness video about senescence I was pointed to the following
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC693382/
Adult activity: C. elegans germline stem cells divide in the adult animal. No other cells divide in the adult.
and
The extent to which the primary causes of aging in C. elegans are the same or different to those in humans will only become clear once both are fully understood. However, it is already evident that C. elegans and mammals share some but not all senescent etiologies. For example, in mammals stem cell exhaustion (Shaw et al., 2010; Conboy and Rando, 2012) and accumulation of senescent cells (van Deursen, 2014) (sensu Hayflick; note that there are two distinct meanings of the word senescence ) contribute to senescence in the broad sense. By contrast, in adult C. elegans somatic cells are post-mitotic, and cellular senescence (sensu Hayflick) does not seem to occur. By contrast, interventions reducing insulin/IGF-1 or mTOR (mechanistic target of rapamycin) signaling or supporting protein folding homeostasis protect against aging in C. elegans and mammals (Zhang and Cuervo, 2008; Kenyon, 2010; Labbadia and Morimoto, 2014). Moreover, interventions causing loss of antioxidant defense or mitochondrial impairment which cause death in mammals can increase lifespan in C. elegans (Rea, 2005; Van Raamsdonk and Hekimi, 2009).
particularly:
By contrast, in adult C. elegans somatic cells are post-mitotic, and cellular senescence (sensu Hayflick) does not seem to occur.
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Looking at this retrospectively given the information about adult somatic cells being mitotic and not dividing you would not necessarily expect any HDAC inhibitors such as baicalin to have that much effect.
The molecules that should have an effect are ones which operate to make mitochondria more efficient rather than those that operate on the genome (which will have a small effect, but cannot do much given the limits on the mitochondria).
What would you test John?
I was talking to them about citrate, but as one of its key effects is on senescence I don’t think testing it on C Elegans is that good an idea.
It might be worth them trying Urolithin A to see how it compares to rapamycin.
Sorry, but it looks to me as an attempt to make you register on twitter. Fishing!