4,217 karma · joined September 1, 2008
It's not clear that we have the health infrastructure in place to know what to do with frequent, low resolution, whole body scans of the human body. How often do anomalies show up and then go away? How often are anomalies purely a scanning/data processing artifact? Who reads the scans and makes recommendations about follow-ups, if any? I think this is the kind of thing that sounds exciting and with low direct risk, but with all kinds of questions that are not only unanswered, but apparently unconsidered.
https://en.wikipedia.org/wiki/Historical_rankings_of_preside...
A radiotropic fungus that’s in TFA can’t meaningfully affect the rate at which nuclear decay is happening. What it can do, supposedly, is to harvest the energy that the nuclear decay is releasing; normally there’s too much energy for an organism to safely handle.
At the risk of vastly oversimplifying, you can’t plug your phone into high voltage transmission lines. These fungi are using melanin to moderate the extra energy, stepping it down into a range that’s useful (or at least minimally harmful).
Yes, some people have more money than they know what to do with (and, I would argue, than is good for them or us), but I've seen no reasonable suggestions that as many of us can have what we want without a reasonably open market economy. I don't think we're at a local optimum in the fine details of the rules for that economy, but I don't think moving to a whole different part of the possibility space is likely to be better than where we are now.
Transmission of cancer is rare in humans—if it were not, it would make someone’s career to find many cases of it. While we can’t say that all sheep are white, we’ve looked at enough of them to say that black sheep are not common. Furthermore, it’s very clear how the Tasmanian devil cancer is spread—it’s around the mouth while they are biting each others faces; it’s not as obvious how one would spread most human cancers.
It might still be useful to know you have weird protease activity that isn’t cancer derived, but the more of these tests we do, the more likely it is that for every person, there’ll be at least one non-cancer oddity that looks like cancer signal for at least some test.
Just to be clear, most drug trials for anything where we have an effective treatment are not “new drug vs placebo”, but instead “new drug vs standard of care”. Thus the goal being to prove it’s better than what already exists.
On the other hand, if the butterfly is eating the nectar and the pollination is an ancillary effect, then you have to start invoking more complicated mechanisms. Maybe successful pollination of the plants increases the food supply later? Maybe the flowers are not neutrally charged, but instead become oppositely charged when the pollen is ready to bias pollinators to come close at appropriate times? You can always construct some just-so story that fits the observed evidence, but where it becomes science is when you make predictions and test them.
My concern would be that the team would cut safety corners until the probability of success just barely rises above some threshold, rather than engineering everything to have as low a risk as is feasible. Is 0-1atm easier than 1-infinity atm? Yes, but that just means you can cut more corners.
https://en.m.wikipedia.org/wiki/1954_Guatemalan_coup_d%2527%...
Invitae has argued that (especially in certain under-represented populations), the 23andme approach is going to miss a lot of important variants [1].
_disclaimer: I’m a former Invitae employee and still holding the bag on what used to be a lot of stock . All opinions are my own. _
[0] Rare on the population scale. To a good approximation each person has only 0, 1, or 2 copies of any given polymorphism.
[1] https://www.biospace.com/article/invitae-challenges-accuracy...
1) one or several mutations in the protein FOXP4 affects susceptibility to long covid [edit: reading the paper more after my coffee, the affected region isn’t actually in the coding region of FOXP4. “ no variant in LD with the lead variant is coding”]
2) a variant in a region that controls expression of FOXP4 affects long covid.
3) variant(s) in a gene near FOXP4 is actually what’s causing long covid (though this is somewhat less likely given the locations of the snps that are associated).
To make this more complicated, genes starting with FOX are usually transcription factors, meaning they control the expression of many other genes. So it’s certainly plausible that it’s a hinge point that controls a large, amorphous downstream response. I don’t know much about the biology of this gene in particular.
What one could say with moderate confidence after a 23andMe style test (assuming they have one or more associated variants) is that you might be at elevated risk for long covid, but only about twice the likelihood as the general population, assuming I’m reading the figures right. Not insignificant risk, but not perfectly predictive either. Where this result is more useful is directing further studies on the mechanism of long covid and (once we understand that) potentially ways to treat the underlying cause.
> The difference between DCA and SI is that in DCA you have all the money available since the beginning, but in SI you have to wait until the next month to have access to the quantity to be invested.
I just asked DALLE for “A scientific illustration of a membrane bound protein being phosphorylated”, and while the results aren’t all that credible, I could imagine using them as a starting point.
Credentials: did my PhD and postdoc at R1 institutions, before going to greener pastures in industry.
The question is not “does the SAT provide some globally useful measure of college performance,“ to which the answer is “very probably yes”; instead, Columbia is asking “does requiring it help them identify top tier talent from underrepresented backgrounds rather than filter out top talent from those backgrounds”, to which the answer is “quite possibly not”. They aren’t banning it as a factor, they are just permitting those with a low score to omit it.
And lest I sound like I’m cheerleading elite universities here, I suspect there are enough people with >1500 SATs and family incomes <$50k that you could fill 2 whole Columbias. They’re obviously going to keep admitting legacies and other high donor value applicants because they’re mostly trying to maximize return on investment.
Depends on the college. A friend of mine who went to an “elite institution“ struggled to supervise themselves and got set up with a counselor to keep them on track. I’m not certain this was actually in their best interests, since they’ve spent most of their late 20s and early 30s struggling to apply to med school but missing deadlines.