91–100 of 133 posts
I'm starting to doubt the prion hypothesis now that we know amyloid-beta encapsulates viral particles in the brain. I think its more likely that viral infections are the transmitted agent.
You may find this interesting.
What’s preventing someone from testing 20 optometrists’ tools for prions and settling this?
An increase in amyloids will be observed any time cells are malfunctioning for whatever reason. They are the most thermodynamically stable structure that polypeptides can form, and require constant housekeeping to prevent. Accumulation of amyloids is like failing to taking out the trash in your house. Afaik, there has never been a disease state checked for amyloids that failed to be associated with them (heart diseas…
That's fascinating! I wonder if we could ever get to a point where people regularly can check their amyloid levels to see if they are becoming ill
In practice you have to figure out a way to detect them non-destructively (eg via light interacting with it in the tissue or some metabolite in excretions).
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Those are all one time use though, right?
Apparently lots of diabetics reuse lancets (thread on another HN story a day or two ago). But I can't imagine anyone sharing used lancets (or needles... except for desperate addicts).
Dumb question (Wikipedia was of no help), if amyloid beta looks and acts like a prion, why isn't it classified as a prion?
There is a huge misconception about what is meant by the word "prion". Get this... there is only one (1) prion protein! All mammalian prion diseases are directly related to the PRNP gene. People talk about Mad Cow, Kuru, Creutzfeldt-Jacobs, Chronic Wasting Disease, Scrapie, and a dozen other diseases like they are not all manifestations of the same underlying problem with PRNP gene variants. People talk about "prions…
Is it really the case that PRNP (https://en.wikipedia.org/wiki/PRNP) is the only known amyloid to be infectious?
An increase in amyloids will be observed any time cells are malfunctioning for whatever reason. They are the most thermodynamically stable structure that polypeptides can form, and require constant housekeeping to prevent. Accumulation of amyloids is like failing to taking out the trash in your house. Afaik, there has never been a disease state checked for amyloids that failed to be associated with them (heart diseas…
Is it fair to infer based on this that they are a symptom and not a cause? Or at least, not a primary cause, though their presence may crate a feedback loop?
Just like sneezing/coughing does occur normally, but is also a symptom of many different health issues, and in the worst cases could lead to broken ribs, etc.
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My guy uses a machine that does a puff of air. I've never had my eyeball physically touched by anything at an ophthalmologists office.
Lucky you. I've had injections into my eyeball every few years due to a retina issue. Imagine a metal clip holding your eyelid open, and watching the tip of a hypodermic needle approaching your eyeball, held by an older ophthalmologist with shaky hands.
Does this line of inquiry mesh at all with the idea that "Gum disease–causing bacteria could spur Alzheimer’s" Or are they competing hypotheses? reported here in January: https://news.ycombinator.com/item?id=18987015
My wife‘s grandmother had all her teeth pulled and replaced with implants (probably a hint towards lifelong gum issues, and PERHAPS stirring/aggravating infections), and 2 years later developed aggressive Alzheimer’s, dying about 3 years later. She was only 64 when she died. To my knowledge, she never had any neuro or eye surgery. It’s just n=1 of course, but to me the gum disease hypothesis looks way more promising.
Age when teeth are pulled probably correlates well with age when Alzheimer's is first noticed.
It's like "newspapers cause cigarette addiction, people always buy cigarettes in stores where they sell newspapers" [apparent correlation; insufficient observation].
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Or perhaps infection by prions by metal dental equipment.
Unlikely because only eye and neuro tissue would carry prions for contamination of equipment, right? Dental equipment should never come in contact with such tissue.
There was another HN thread about the "indestructibility" of prions, and I believe there is a growing consensus that they are not removed by existing techniques within dentistry.
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What a great idea, to have sleep deprived surgeons. Really, the legal limit should be much less than that for safety reasons alone (patient safety, not surgeon safety).
Somewhere I read tired health workers are better than fresh workers who need to take over patients (losing context and details in the hand offs). Not sure if that explains it though.
However, IMO you can do things to mitigate this but it involves paying workers who aren't working at full capacity; basically doubling staffing costs I think. If you have a large shift handover period, a staff member doesn't take on a new patient unless they can finish their active input within the shift, it goes to the people sitting idle waiting on the next shift - people are never under a single worker for less than a half-shift; so you can't start with one nurse for half-an-hour at handover and then get passed on, you'd start with that nurse and get half-shift + ½hour. At the back end of the shift the nurse -- and other personnel -- would not be taking on new patients who couldn't be signed-off within their shift, meaning they have fewer patients, meaning they can focus more on handover of the patients for whom it's necessary.
There's probably holes in that, it's like reverse pipelining.
You might get enough effect by having a smaller overlap and having workers shadow the worker who is going off-shift but that's not really reducing handovers so much.