A small molecule inhibitor of 15-hydroxy prostaglandin dehydrogenase causes cartilage regeneration. I hope they fast-track it to human trials.
So this is one of those standard poor estrogen signaling downstream things and simply improving the estrogen signaling and you get improved cartilage. Anyone can do this today along with getting all of the other positive effects. Those with EDS who have say variants on their TNXA/B have poor production ability to start and so we do everything we can to improve their cartilage production as they can only make so much which include doing stuff like this.
Please explain
It is being trialed to prevent muscle weakness and some of those patients will have arthritis and they can be assessed for statistical improvement.
Same thing happened with GLP1
It's discouraging to see these on HN and then realize that most never go anywhere, or are so far out you may not see it in your lifetime.
Maybe we should flag anything not already in a phase 3 trial :)
The researchers also tested cartilage taken from patients undergoing total knee replacement for osteoarthritis. After one week of treatment with the 15-PGDH inhibitor, the tissue showed fewer 15-PGDH-producing chondrocytes, reduced expression of cartilage degradation and fibrocartilage genes, and early signs of articular cartilage regeneration.
Cartilage Regrowth
Room Temperature Semiconductors
Quantum Computing
def generate(topic, year):
return f"Scientists have made a major breakthrough in {topic}"
Heard.
But if even one of their interests panned out it would be paradigm changing for millions and they’re doing it to save your lives not get a updoot on hacker news. They’re all pretty anonymous and understated Imo but i am a great fan and i would love for it to be the “year of” anything they’re studying. I listed a few and I’m sure there’s dozens I’m unaware of.
I’ve been thinking that this stuff is all more closely related than we think and that as they go down one of these paths they’re finding all this other stuff along the way, it’s genuinely fascinating.
Heart disease and failure is one of the biggest ways we meet our ends right now. There’s so much interplay between aging processes, ceasing t-cell production, shortening telomeres , that ties in together with this and im glad they see a bigger picture than me having another 20 years , too winded to stand up and piss or strapped to a bed hooked to tubes and groaning!
Notably absent:
The fat pill HIV fix Cystic fibrosis
We make fun of the stuff that hasn't been solved yet ("It's always ten years away!") while ignoring the things that were previously always ten years away until scientists cracked it.
After Win11 Microsoft really did all they could to get us there this year.
I've had Windows as my main personal computer for practically forever, because of games. Before that it was DOS. That changed a couple months ago.
Literally just now--in preparation for this comment--I decided to try something I never tried before: I mounted my Win10 drive, picked an arbitrary old Windows game EXE (2006 "Prey" game demo), and launched it as a "non-Steam game" with just one little drop-down menu tweak... and it launched! I may get 10 FPS instead of 200, but that's more than I expected off the bat.
In the the "years of the Linux desktop" of my youth, I wasn't nearly as optimistic. In terms of more-recent games, I have little reason to keep my old drive for dual-boot purposes except for specific games that go out of their way to interfere with clumsy anti-cheat rootkits.
It involved removing the poor mouses existing eye, so there was no net gain (still had a mouse with only 1 working eye), but I was hopeful progress would be made so I could get myself a working optic nerve.
Nope. No progress in 20+ years. Someone got a paper published and went on and did something else.
It is a relatively uncommon problem, for ~98% of children with a problem with their optic nerve, patching the opposite eye works to force the optic nerve to grow. I'm in the (un)lucky 2%!
Admittedly not the worst rare health problem to have.
Bingo!
:-D
Reduce arthritis, get cancer?
A study led by Stanford Medicine researchers has found that an injection blocking a protein linked to aging can reverse the natural loss of knee cartilage in older mice.Especially when it comes to pregnancies we know more about a lot of animals than about humans. Why? Well pregnancies is how you multiply meat in animals, which is what farmers are interested in (and pay for). Which ironically also means animal pregnancies can be treated in case of trouble much more effectively.
Why pregnancies? Pregnancy changes a LOT of chemical processes in the body and so quite a bit of "normal" medical knowledge doesn't apply to pregnant women. Which has caused the medical establishment to declare anything that isn't explicitly tested on pregnant women as a no-go zone. So even problems and medications that we do know about, doctors won't apply them to pregnant women.
By analogy, "A drug is something that cures cancer in lab mice."
Are there areas of medicine where mouse models have a much higher or lower success rate in human trials?
This is not being a contrarian, but a realist.
Not if pharma execs and shareholders have anything to say about that
That would be quiet something to feel that again.
So they are using hyaluronic acid injections for patella tendonitis. Taking hyaluronic acid orally would probably take longer for effects compared to injections. Most people would prefer the injections because they feel safer for a doctor to do all the work. I prefer the tablets. If you have the money, I guess go for the injections. I would use the H.A. tablets. (With a tall glass of water, and do not take at the same time as blood-thinning medication, like pain killers or drugs.)
Once again, not in humans, in mice. We don't know if the same result happens in humans. At all. We need to proceed to clinical trials to determine if a result is indeed positive.