This is good news. In general, since all forms of existential risk seem underfunded as a whole, funding more to any one of them is a good thing. But a donation of this size for AI specifically makes me now start to wonder if people should identify other existential risks which are now more underfunded. In general, it takes a very large amount of money to change what has the highest marginal return, but this is a pretty large donation.

Do we know why he chose to donate in this way: donating to FLI (rather than FHI, MIRI, CSER, some university, or a new organization), and setting up a grant fund (rather than directly to researchers or other grantees)?

"You guys" has absolutely none of the hostile/contemptuous feeling that "you people" has (at least for me). It's distinctly informal and (as you surmise) some people may interpret it as sexist.

I think I'd generally just say "you" and, if necessary, make it explicit what particular group I had in mind.

It hadn't occurred to me that you might not be a native English speaker; sorry about that. I guess it's one of the perils of speaking the language very well :-).

A question I've been curious about: to those of you who have taken modafinil regularly/semi-regularly (as opposed to a once off) but have since stopped: why did you stop? Did it stop being effective? Was it no longer useful for your lifestyle? Any other reasons? Thanks!

I take fish oil (generic) capsules most days, for the usual reasons they're recommended. Zinc tablets when I'm feeling run down.

Perhaps not what you mean by supplements (in which case, apologies!), but If we're including nootropics, I take various things to try to extend my productive working day. I take modafinil twice a week (100mg in mornings), and try to limit my caffeine on those days. I take phenylpiracetam about twice a week too (100mg in afternoons on different days to modafinil), and nicotine lozenges (1mg) intermittently through the week (also not on modafinil days) - usually if I start getting sluggish in the evening. I also only take nicotine if I'm working, and usually on something I find hard or don't want to do - as I like the feeling, hoping this sets up a 'reward effect'. I drink coffee and green tea throughout the week, although I intend to start limiting my coffee intake more.

I regularly experiment with other supplements for mental focus and stamina - recently I've experimented with L-theaninine with caffeine, and rhodiola rosae for more general mental stamina. However I don't track much, and my lifestyle is so variable (travel, etc) that it can be hard to track what's effective for me, other than the really obvious ones (modafinil, caffeine, nicotine, phenylpiracetam). However, it can be helpful for placebo effect if nothing else!

Interesting. It really seems to be field thing - neither the maths nor the philosophy I did were much into figures.

Yes! Thanks for pointing me at that paper, I hadn't seen it before.

Enveloped viruses are in general much more fragile than non-enveloped viruses. They contain the genetic material of the virus and viral proteins surrounded by a lipid membrane derived from the membrane of a host cell, which they then fuse with the membrane of another host cell to get the genome in. Easier entry to the host cell at the expense of fragility. If the membrane is broken the virus is dead, and a bubble of membrane is a lot more fragile than a protein/RNA crystal (which is basically the entire structure of non-enveloped viruses which need to somehow pass through the cell membrane without killing the cell which is more difficult). In particular, dessication tends to kill enveloped viruses fairly quickly meaning they need to be wet from host to host. Ebola viruses are filamentous viruses, meaning their genome is stretched out in a long ribonucleoprotein fiber which is surrounded by a big tube of membrane (those long funny shapes we have all been seeing), so they have a lot more membrane per particle than most viruses and are particularly vulnerable.

One might note that the flu virus is also membrane-bound but goes through the air. Sort of. It empirically requires droplets of several microns in size to move through the air in natural conditions, which only make it so far (a few feet) before drying out or settling to the ground. In real-world conditions smaller droplets or dry particles don't seem to be important for its spread, though you can set up experiments where a few manage to make it through that way. Also, any flu virus that gets breathed in or on a mucous membrane is already in its perfect environment - epithelial cells - so a very small viral dose is required to make it in, whereas in living organisms ebolaviruses seem to have a much lower affinity for epithelial cells than blood vessel or connective tissue cells from research I've been able to look up, so you need more viruses to get into and infect a surface.

In the above-linked experiment, monkeys had their heads put in a sealed 8-liter box inches away from a nebulizer that produced aerosols from a liquid containing ebolaviruses, kicking up single-micron-sized droplets. They found that in this circumstance as few as 400 functional virus particles delivered this way to the respiratory tract/face was enough to cause a lethal infection (as compared to <10 functional virions via injection, though they did not try lower viral levels for inhalation), showing that a smallish number of freshly-aerosolized viruses landing on a respiratory surface can cause disease.

However, that you can set up an experiment in which you give enough viruses through the air to cause infection does not mean that under normal conditions that circumstance is likely to happen - the latter being the usual definition of 'airborne'. There's also a difference between 'airborne' and 'screwed if someone sneezes on your face' which is more akin to what's happening here.

They note this. Quotes from the paper:

"Epidemiology studies of human disease outbreaks in sub-Saharan Africa did not suggest that aerosol transmission of filoviruses was likely in that setting [emphasis mine]. Virus did not spread easily from person to person during the Ebola virus epidemics in Africa, and attack rates were highest in individuals who were in direct physical contact with a primary case... no cases occurred in children whose only known exposure to the virus was sleeping in the huts occupied by their fatally ill parents."

"It is possible that the quantity and distribution of virus within most patients' respiratory tracts may have been below the level needed to establish effective aerosol transmission."

The structural factors that make Ebola more fragile in the air are not ones that are likely to change much via mutation - that's things like cell affinity, how obvious it is to the immune system, replication speed, or toxicity to infected cells. There's reasons that viruses generally don't change their modes of spread during evolution.

On the other hand, there's this:

"Both elevated temperature and relative humidity (RH) have been shown to reduce the aerosol stability of viruses... Our experiments were conducted at 24C and < 40% RH, conditions which are known to favour the aerosol stability of at least two other African haemorrhagic fever viruses... If the same holds true for filoviruses, aerosol transmission is a greater threat in modern hospital or laboratory settings than it is in the natural climatic ranges of viruses... As previously stated, aerosol spread was implicated in the spread of disease among the monkeys at Reston [an accidental 1990s outbreak of ebolavirus among monkeys in a laboratory of a strain that could not infect/cause disease in humans, after work I may look up more about it to see what they mean about 'implicated']"

And this:

"While both parenteral [injected] and aerosol exposure to Ebola virus cause a systemic disease involving all organs, monkeys exposed to viral aerosols during our study developed strong immunoreactivity for Ebola virus antigen in airway epithelium, in oral and nasal secretions, and in bronchial and tracheobronchial lymphoid tissue. By electron microscopy, viral replication after aerosol exposure occurred in the lungs and tracheobronchial lymph nodes, and extracellular virus accumulated in alveoli of the lung." The monkeys exposed via fresh aerosol developed much more shedding virus in the lungs than their needle-exposed counterparts which you could imagine affecting infectivity.

You may find another paper making the rounds about aerosol transmission between monkeys and pigs; these were in a cage separated by bars and space and scientists make note that in that circumstance they can't necessarily tell the difference between respiratory aerosols, splashed liquid, and liquid kicked up during periodic cage cleaning.

My experience so far is that first time I tried to sign up, I entered a form field wrong and couldn't correct it without starting over. The second time, I got to the stage of entering my bank details and clicking confirm, and the website timed out. Then they took money from my account, and sent me physical mail asking for proof of identity. (I assume this is a legal requirement, but I don't remember seeing anything about it before signing up.) I've sent it to them, and they said they needed a week to review the documents, and that letter was dated the 17th and I haven't heard anything since.

I'll add to this - I'm in the process of setting one up. I couldn't find anything about Scottish Mutual online. I'm currently trying with M&G, but I anti-recommend them. I believe when I asked who people are currently using, the answers were Fidelity and Legal & General, so those are probably sensible places to try.

I don't have particular advise, but I would point out that UK and the rest of Europe differ. You want to invest in a fund in your own currency to avoid exchange rate risks. If the currency that you need in your life is Euro, invest in a Euro notated fund. If it's Pound Sterling, invest in a fund in that currency.