This is an uncharitable take on the original comment which literally said:
> the fact this is how hot it will be from now on
That sounds to me like an acknowledgement that, in fact, the climate has changed.
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> the fact this is how hot it will be from now on
That sounds to me like an acknowledgement that, in fact, the climate has changed.
A fun but off-topic note: "behave the same chemically" is only approximately true. For heavy atoms like the ones discussed in the article, it's basically true. But for hydrogen, adding one neutron doubles its mass and you can get real effects on chemical reaction rates.
https://en.wikipedia.org/wiki/Kinetic_isotope_effect
And of course, an obligatory "In The Pipeline" link on how it's used in drug discovery: https://www.science.org/content/blog-post/isotopes-get-your-...
A great example of this in relatively recent history is the treatment of hepatitis C. The treatments pre-circa-2011 were pretty crappy: interferon/ribavirin had poor cure rates and bad side effects. But it was still better than hepatitis destroying your liver, so people dealt with it.
Then, in 2011, as the culmination of years of trials, telaprevir (from Vertex/J&J) [1] and boceprevir (Schering-Plough/Merck) [2] were approved and were DRAMATICALLY BETTER than interferon/ribavirin.
...and then just two years later both of these drugs got nuked by the approval of sofosbuvir (aka Sovaldi, from Pharmasset/Gilead) [3], which has _cure_ rates in excess of 90%. Telaprevir and boceprevir were pulled from the market because there was simply no more market for them once sofosbuvir hit. Scientific competition at its finest.
There is absolutely a dark side to pharmaceutical pricing and licensing, but please don't let the existence of that dark side cloud your vision of the transformative impact that those of us in biotech R&D want to have (and in many cases, have had). I was at Vertex when the early trial data on telaprevir started coming out and it became clear that we might be able to offer patients real hope who did not have it before.
[1] https://en.wikipedia.org/wiki/Telaprevir [2] https://en.wikipedia.org/wiki/Boceprevir [3] https://en.wikipedia.org/wiki/Sofosbuvir
Those typically have a "stem" which indicate the mechanism by which the drug works. In this case, it's "-glipron", which you can parse as "glipr" -- GLP-1 receptor -- and "on" -- it's an "agonist", or something that turns "on" the receptor. So "-glipron"s are drugs which agonize, or activate, the GLP-1 receptor. There are other gliprons in trials, including danuglipron (https://en.wikipedia.org/wiki/Danuglipron) from Pfizer, and many others that don't have assigned INNs.
Semaglutide and liraglutide also agonize GLP-1, so why aren't they gliprons? Because chemically they are analogs of the naturally occurring GLP-1 peptide, so they get the -glutide (GLUcagon-like pepTIDE) stem.
I don't know why tirzepatide got that name. It's a peptide, so "-tide" makes sense, but it's actually listed as a "various" exception in the master document of INNs: https://iris.who.int/bitstream/handle/10665/379226/978924009....
The Wikipedia pages are decent -- the picture makes it fairly obvious how much smaller orforglipron is than tirzepatide even if you don't know how to read chemical structures; just count atoms!
Note that "video" is a little different here than the way we all usually think of it - think "minutes or hours between frames" not "frames per second".
But the biggest challenge for these tests is that this "tumor fraction" can be very very low in early stage cancers, which is why stage I sensitivity tends to be quite poor.
*"Below" meaning "on the opposite side from the objective" - you illuminate _through_ the sample.
1. How does your technology or product offering distinguish itself from prior attempts like NeoPrep (née Advanced Liquid Logic) from Illumina or Voltrax from ONT?
2. How "hackable" is the offering for power users to implement custom protocols on the instrument and consumables?
A relevant quotation for much of the discussion here:
> And, relevant to the question of whether Intuit controls U.S. tax policy: it can’t, because that would imply they have wrested control from Norquist. Norquist considers a public filing option a tax increase by stealth and opposes it automatically.
A typical L2 charger will provide in the range of 6-10kW (AC, marginally less ends up going to the battery after conversion losses). 10kW is only 13hp; forget acceleration - the car draws more than that at highway speeds.
(You can come at this result another way too - an L2 charge may take 6-10hr to refill the battery from empty. But the car would not be able to drive 6-10hr at highway speed starting at 100% charge! So the L2 must be delivering less power than the car consumes at cruising speed.)
It won't alter the underlying genetic condition, but there has been at least one case report that taking these CFTR modulators during pregnancy can improve the condition of the fetus/newborn:
https://www.sciencedirect.com/science/article/pii/S156919932...
https://med.stanford.edu/news/all-news/2023/07/cystic-fibros...
(The 3C-2E bonds in diborane are not linear, so that doesn't seem like what could be happening here.)
> To unlock the secret via Shamir's secret sharing, a minimum number of shares are needed. This is called the threshold, and is used to denote the minimum number of shares needed to unlock the secret. An adversary who discovers any number of shares less than the threshold will not have any additional information about the secured secret-- this is called perfect secrecy. In this sense, SSS is a generalisation of the one-time pad (which is effectively SSS with a two-share threshold and two shares in total).
It is interesting, but not for the reasons you may be imagining. And not a mysterious electrical mechanism.
It's well-known in the field that (e.g., in humans), chromosomes fold in on themselves in structured ways [1,2]. The functional consequence is not precisely mechanical or electrical -- rather, these folds bring regulatory domains close in 3D space to the sequences which they regulate (which may be far in 1-D sequence distance). These can be elements like "enhancers", which increase the level of transcription (DNA->RNA copying, the first step of gene expression); "insulators", which break up coherent blocks of gene regulation, etc. One of the mediating mechanisms is that regulatory proteins bind to these particular sequences; bringing them together in 3D space allows the assembly of a protein complex that actually carries out the relevant process (eg, transcription).
So, what's interesting here? There is extensive evidence of these contacts within mammalian chromosomes, but limited evidence _between_ different chromosomes. Insofar as the paper shows that mammalian macrochromosomes have homology to multiple reptile/avian microchromosomes (really, to their most recent common ancestor), it may be (speculation alert) that intra-chromosome contacts recapitulate contacts and organization seen in the ancestral microchromosomes.
(There are also "simple" interactions like wrapping of DNA on protein complexes called nucleosomes, like string on beads, but that's less interesting in this context.)
[1] https://en.wikipedia.org/wiki/Nuclear_organization#DNA_loopi... [2] https://en.wikipedia.org/wiki/Nuclear_organization#Chromosom...
You may be interested in the work of Jean-Louis Reymond's group, who have done more or less exactly what you suggest: https://gdb.unibe.ch/downloads/
GDB-11, with 11 heavy atoms, has 26.4M structures (110.9M stereoisomers -- molecules aren't 2D). Going up to 13 gives you 970M molecules. Going up to 17 (still mostly below 250Da) is 166,400M.
There's a lot of space up there below 500Da.
My point was that _if_ one's primary goal is to get the highest comp possible, it's probably better to go into finance than biotech. No bones about that; we don't pay as well. But that does not mean that biotech universally pays _badly_ for technical skills, as casual readers might assume based on reading this thread. My point was that if someone is both technically-minded and interested in the mission in biotech, it's worth taking a closer look, especially at the wave of companies from the last ten years bringing tech and biotech together.
* Not everything, I'm sure, but neither is everything in biotech!
The biotech industry (which is made up of at least three rather different verticals: tools, diagnostics, and therapeutics) is changing quite a bit today. There are certainly companies that have less of a technology or data emphasis or who are still trying to figure out the value those could bring, and those companies are far less likely to pay well in SW/DS roles. There are others that either from their inception or more recently realize the value these approaches can deliver and compensate accordingly. I personally find the new wave of biotech startups that are focused on being hybrids of experimental and computational capabilities extremely exciting (which is why I'm at one) and these are the firms where software and mathematical skill sets are most likely to be valued.
You'll probably still make more on Wall Street than you would in biotech. But you don't have to be _badly_ paid in order to work on a meaningful mission. OP is, IMO, correct that biology is entering a phase in which computational skills are a rate-limiting factor in our ability to make advances (note: not _the_ limit -- experiment is still absolutely critical), and it's a super exciting and impactful field to be in.
Shameless plug: Recursion is hiring a TON of positions in data science and machine learning, engineering, and elsewhere. Check us out: https://www.recursion.com/careers. (Contact info is in my bio.)