When a link doesn't work, try googling a unique-looking prefix. In this case, 'acel.12344' looks like a unique ID. If I google "http://onlinelibrary.wiley.com/doi/10.1111/acel.12344/", the first hit is http://onlinelibrary.wiley.com/doi/10.1111/acel.12344/abstract which is the paper "The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs", Zhu & Tchkonia et al 2015 in Aging Cell; note that the journal sounds relevant, both Zhu and Tchkonia were mentioned by Darwin, the keyword 'senolytic' is present in the title, and the abstract reads:

The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous impact on quality of life and the burden of age-related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs termed senolytics, which selectively kill senescent cells. By transcript analysis, we discovered increased expression of pro-survival networks in senescent cells, consistent with their established resistance to apoptosis. Using siRNA to silence expression of key nodes of this network, including ephrins (EFNB1 or 3), PI3Kδ, p21, BCL-xL, or plasminogen-activated inhibitor-2, killed senescent cells, but not proliferating or quiescent, differentiated cells. Drugs targeting these same factors selectively killed senescent cells. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse BM-MSCs. The combination of dasatinib and quercetin was effective in eliminating senescent MEFs. In vivo, this combination reduced senescent cell burden in chronologically aged, radiation-exposed, and progeroid Ercc1−/Δ mice. In old mice, cardiac function and carotid vascular reactivity were improved 5 days after a single dose. Following irradiation of one limb in mice, a single dose led to improved exercise capacity for at least 7 months following drug treatment. Periodic drug administration extended healthspan in Ercc1−/∆ mice, delaying age-related symptoms and pathology, osteoporosis, and loss of intervertebral disk proteoglycans. These results demonstrate the feasibility of selectively ablating senescent cells and the efficacy of senolytics for alleviating symptoms of frailty and extending healthspan.

Hence you can be immediately confident that this must be the paper Darwin was linking. (Or if the link heuristic didn't occur to you, you could have tried googling the buzzwords in Google Scholar; "senolytics senescent cells in vivo in rodents, and in human cell culture cells" would have turned up that paper as #5, and the preceding papers all look relevant too. And if that didn't work, you could have searched "author:Tchkonia", since it's a highly unusual surname, and it would be #9 in Google Scholar.)

The paper can be downloaded from Wiley right now, but if it couldn't, you could have still gotten a copy from Libgen.

I would be VERY interested in reading that http://onlinelibrary.wiley.com/doi/10.1111/acel.12344/pdf paper. Unfortunately the link does not work for me (page not found).

Most of my childhood notes and cryo-memrobilia were lost when my house burned down in September, of last year. So, regrettably, I can't consult my notes from those experiments. However, as best I recall, the mortality rate in yeast frozen in distilled water was ~90%. No special treatment was required beyond removing them from the incubating medium and resuspending them in distilled water prior to freezing. Viability was determined indirectly by adding the frozen-thawed yeast in water to culture medium in an Erlenmeyer flask connected to a water displacement set-up very much like this:

http://herbarium.usu.edu/fungi/funfacts/respiration.jpg

I later repeated this experiment with red cells (my own) which is much more sensitive and directly quantative of cell survival. You do, however, need a centrifuge and related equiupment to measure microhematocrit - things I could easily acquire back in the day (and in fact, still have).

If people did hands-on biology in the same way and to the same extent they do hands-onelectronics and programming, we'd all likely be either "immortal," or dead, by now.

Here is an experiment I am currently struggling to tool to do which may serve as an example. Recently, a very simple way was discovered to induce apoptosis in a significant fraction of senescent cells in vivo in rodents, and in human cell culture cells, as well: http://onlinelibrary.wiley.com/doi/10.1111/acel.12344/pdf. This results in partial rejuvenation of the animals because senescent cells release myriad toxic cytokines, chemokines and other pro-inflammatory and probably telomere shortening species. While there is as yet no evidence that eliminating senescent cells - or reducing their number - will increase lifespan, there is ample evidence that it will greatly increase healthspan. This new class of drugs has been dubbed the "senolytics" by their discoverers, Zu and Tchkonia. The nice things about these two drugs is that they are both small molecules which are readily available, FDA approved/GRAS and have very low toxicity. One is the OTC nutrient quercetin, and the other is the relatively exotic molecularly targeted antineoplastic agent dasitinib, marketed under the name of Sprycell by Bristol-Meyers-Squibb.

In mice, one dose of these agents in combination was effective at reducing the senescent cell burden dramatically, with benefits lasting for 7 months. The cost of a dose of dasitinib for an adult human is about $400 - eminently affordable (the cost of the quercetin required is a few cents). So, what's the problem? Well, if you are over 30, odds are that you have a significant burden of senesacent cells, and by the time you are 50, somewhere between 15 to 30% of your body mass may be senescent cells. In my days in ICU doing hemodialysis, I saw more than a few patients critically ill and in renal failure from something called "acute cell death syndrome" (ACDS) which most often resulted from chemotherapy given to lymphoma or leukemia patients too rapidly, resulting in a massive die-off of cancer cells. Large scale cell death is toxic and can be, and often is, lethal.

Animals treated with dasitinib+quercetin do not show signs of ACDS. However, careful monitoring of blood chemistrires during the treatment phase was not done and the animals so far studied were middle aged rodehts - not humans, and certainly not older, or elderly humans. Thus, additiional data are needed. In my opinion, dogs are ideal for such a study because they are available in abundance as old and very old (senile) animals, have large blood volumes which allow for harmless routine clinical laboratory evaluations, and have neurobehavioral faculties which are easily and reliably assessed by untrained humans. They also stand to benefit from the treatment if it does not prove lethal, or can be adjusted so that it is easily tolerated.

You have to "make" your own aged rodents and that takes years. And years are something many of us no longer have... Research begun now (or soon) will very likly yeild results that will be immediately clinically applicable to humans. Unfortunately, this research cannot practically be done anywhere in the West legally.

(Habryka here. My account still appears to be broken)

I want to outline my thinking a bit, about why I decided to organize all of this with so much reliance on Facebook:

The attendance at these events heavily relies on networking effects and reducing trivial inconveniences. I did consider organizing it on LessWrong, but it's just less integrated into most peoples life as Facebook is. This was the easiest way for people to invite their friends, get notified of new parties, spread information and, most importantly, get interested in the event if you so far haven't been completely hooked on the book.

This is the last obvious big opportunity to get more people to read the book. Sending people to LessWrong, a website they've never been to and often only tangentially heard off, to then send an email to the current organizer, not really knowing who else of their friends will be there, if any, and then add that event manually in their own calendar, just seemed like a path that too many people would not bother to go.

I don't like Facebook. I don't like their stance on privacy, and I don't like the social pressure that drives everyone to sign up for it. But I think the stakes on this are high, and the potential positive impact on the world is large. And I think the number of people who are shied away from this because of its reliance on Facebook is smaller than the number of people who would not otherwise come.

This is the reason why I made all information available outside of Facebook and spent multiple hours copying details from the Facebook events into the spreadsheet. Because I want to make sure that if someone doesn't have Facebook, and wants to attend, that they will be able to. But the need to reduce trivial inconveniences for that category is a lot lower, as I think most would be willing to jump through a lot of hoops to be able to attend these.

I don't think the decision was completely clear, but I did make the decision consciously and tried my best at weighing the benefits and drawbacks. I am interested in anyone's thoughts on this.

I'd like to request that when the date and time of a meetup is finalized, that somebody post as much on LW. I don't have a facebook and would prefer to keep it that way, but I also don't want to miss the London party. Please and thank you.

Google scholar has the paywalled link on the left but the open link on the right.