The sibling comments are very relevant, but I wanted to provide a marginally different perspective. You have to take not only what is being said, but _who is saying it_ into perspective.
In this case, this is a government official speaking to the press (i.e. in an official capacity). If they were to say "this was sabotage," that is a definite declaration that the government believes - again, officially and on the record - that an outside party has deliberately done material damage to their country. Given the general situation, it is not a huge leap to come to the interpretation that "this was an attack against our country, and possibly an act of war."
No government official would want to be within miles (or kilometers) of that sort of statement unless they have pretty much already internally decided from the top-down to escalate the situation. Almost no single government agent has the authority to escalate the situation in that manner. So what we end up with is "appears to be." This overtly says 'all available evidence points to this being the case, however something else cannot be ruled out.' (As a sibling comment suggests, it can also act as a type of propaganda). So it is not an official government declaration that another nation has damaged them, but they have reasons (probably both apparent and not) to believe what they are saying publicly.
>>"We don't say negative things about the art or the artist. Our stated goal is to collect, exhibit, and celebrate this art that would be appreciated nowhere else."
Perhaps this is a 'whoosh' moment for me, but it seems that by simply housing the art in the Museum of /Bad/ Art, you are certainly saying something quite negative about the art and the artist.
So I actually shave my beard every time I get a haircut (so, let's say every 8 weeks).
What does 'recent' mean, since you have already acknowledged that temporal recency is irrelevant? When am I traveling? What's accurate to my current appearance? What if I started a cancer treatment that renders me unable to grow a beard?
Your flippant reply ignores reality, and these aren't even edge cases.
If you are applying for a new passport where you are needing these photos, the common sense logic from the person accepting/rejecting them would be do the photos look like the person in front of them. No? Reject. Yes? Accept. The flow chart is pretty simple.
The frequency of your grooming habits AFTER receiving a passport are irrelevant to the actual approval of a passport. This doesn't need to be hard.
> do the photos look like the person in front of them
To what ridiculous extent do you take that, though? You must be wearing the same clothes? You must be made-up in the exact same way? I think it's pretty clear that the test should be "is it obvious that the person in the photo is the same as the person in front of you" and somebody with a beard does look like themself, even when they shave that beard.
Of course, this raises other interesting questions: is it OK for you to use a photo of your identical twin?
I'm not a cuber or a puzzle guy or a math guy, but I am curious: how do you know when it's solved? Or is this a 'whoosh' moment and I'm missing the obvious?
when it's solved you look at all blocks on a face from the same angle, so they all have the same color. the problem is, while you are solving you don't know from which angle you need look at one block. you see a red one on one face, and another red one on another, and when you bring them together you realize that you looked at one of them from the wrong angle and they don't actually match. so effectively you need more moves until you find the right block.
>>I wonder though what things look like with super high dimensions.
You need only look to healthcare in the USA. Many, many professionals (some of which you never interact with) handing off patient cases to each other in a very carefully choreographed dance designed to meet legal and regulatory requirements; quality, safety, and care standards; financial responsibilities; and each individual's own personal standards for the quality of care they believe they provide.
In healthcare, we often view risks using the Swiss Cheese Model [1]. Everyone makes mistakes sometimes, but the system of checks and balances catches most of them before they reach the patient. Prescriber ordered the wrong dose of medicine in the inpatient setting? Pharmacy intercepts and starts making calls or sending messages to verify. Pharmacy approves the order because "that's what they ordered?" Nursing lays hands and eyes to every medicine administered and can 'stop the line' if they deem appropriate. Not to mention the technical safeguards and guardrails (e.g., clinical decision support systems) that are also supporting everyone involved.
But still, failures happen, and they can be catastrophic.
This was just my understanding from seeing my grand-father 40 years ago having to drop his pants to use insulin syringe + needle, to the use today where you can lift your shirt and use a insulin pen in a couple of seconds.
The infection risk is real. What's the relative risk increase regarding death with (with, not from) Hepatitis B infection (not diagnosis, infection) between people who've never injected themselves with anything and injection drug users?
GLP-1 => weight loss => decreased obesity, improved cholesterol, improved blood pressure, improved glucose control, etc. etc. => better survival rates (all causes)
There is no presumed clinically relevant mechanism for GLP-1s to be protective specifically against COVID death. It is simply protective against all death, of which COVID is a type. Healthier people are less likely to die, statistically. The same benefit can be (and is being) said about GLP-1s and heart attacks, heart failure, stroke, kidney failure, etc.
Rather arrogant of you to spew forth unfounded conjecture without even bothering to skim the high-level details of a six paragraph article.
> the protective effect occurred immediately — before participants had lost significant amounts of weight.
> the participants taking the drug were not healthier than the others, said Dr. Harlan Krumholz, a cardiologist at Yale and the editor in chief of the journal.
I understand how you came to your conclusion, however what you are quoting is journalism (and it is factually incorrect). I read the actual peer reviewed article.
The patients in the COVID group, _when they got COVID_ had already begun losing significant amounts of weight. The NYT article is 100% incorrect on this matter. See:
>>The change in weight between randomization and reported COVID-19 in patients who died of COVID-19 according to treatment was −6.4 kg in the semaglutide group vs −0.9 kg in the placebo (P < 0.001) group and −8.4 kg vs −1.25 kg (P < 0.001), respectively, in patients who did not die.
They go on to say that there is a correlation between obesity and adverse COVID outcomes:
>>There was an associated increased risk of respiratory decompensation and mortality in patients with COVID-19 and obesity16,17 and plausible biologic hypotheses associating obesity with adverse COVID outcomes, including impaired respiratory status, lower cardiometabolic reserve, or immune hyperreactivity or dysregulation.18
And they double down on the fact that the patients absolutely had weight loss at time of COVID.
>>Accordingly, it is plausible that the decreased risk of infectious deaths is caused by weight loss, which was 5 kg greater in patients assigned to semaglutide compared to placebo by 1 year, the average time to COVID-19 diagnosis after randomization.
I will leave you with the note that nowhere in the journal article do they make any claims whatsoever about semaglutide's effect on COVID outcomes. They exclusively discuss outcomes as related to metabolic health. Semaglutide is a means to an end. The means is weight loss. The end is better health.
I read the JACC article too, and thought the NYT claims were decently supported:
> The second unexpected observation was the lower rate of non-CV death with semaglutide vs placebo, particularly infectious deaths, including in patients with reported cases of COVID-19. The mechanism by which semaglutide is associated with lower CV or non-CV mortality is unknown. Weight loss improves traditional cardiometabolic and kidney risk factors,3 such as hypertension, dyslipidemia, renal function,26 and dysglycemia. However, the blood pressure and lipid reductions in SELECT with semaglutide were relatively small compared with those in dedicated risk factor–lowering trials, and the observed reduction in major adverse cardiovascular events is more than would be expected based on those changes.
You could absolutely be right that body weight is a lagging indicator, and these patients are getting a bigger improvement in systemic inflammation/their hematologic profile than weight loss alone would suggest… but running immediately to that conclusion is major hubris in my book. I don’t think it’s remotely implausible that there are one or more yet-unknown metabolic pathways tweaked by GPL1 agonists that could explain the effect.
You're absolutely right. CEOs (and other execs) need measurable workload, just like the rest of their staff. If you're not measuring it, is the CEO landing deals, or are they just playing golf with other members of the managerial class? The inquiring mind wants to know.
Get over it. Until you earn yourself a seat on the board, your inquiring mind will likely remain inquiring. Not sure why you expect that the CEO needs to justify his/her schedule to rank-and-file employees.
My only commentary would be that these results do not read like clinical success, but rather something suggesting they should move on to phase III clinical trials.
This is the only publication I found in a quick search:
Objectives: Nerve growth factor β (β-NGF) is a protein which is important to the development of neurons particularly those involved in the transmission of pain and is central to the experience of pain in osteoarthritis (OA). Direct NGF antagonism has been shown to reduce OA pain but is associated with rapidly progressive OA. The aim of the study is to investigate the ability of soluble neurotrophin receptors in the NGF pathway to modulate pain in OA.
Methods: Synovial fluid (SF) was obtained from the knee joints of 43 subjects who underwent total knee arthroplasty. Visual analogue scale (VAS) pain scores were obtained prior to surgery. Customised-automated-ELISAs and commercial-ELISAs and LEGENDplex™ were used to measure soluble low-affinity nerve growth factor (LNGFR), soluble tropomyosin receptor kinase (TrkA), proNGF, β-NGF, other neurotrophins (NT) and cytokines including inflammatory marker TNF-α.
Results: The VAS score positively correlated with β-NGF (r=0.34) and there was positive association trend with neurotrophin-3 (NT-3), BDNF and negative association trend with ProNGF. sLNGFR positively correlated with VAS (r=0.33). The β-NGF/soluble TrkA ratio showed a strong positive correlation with VAS (r=0.80). In contrast, there was no correlation between pain and the β-NGF/sLNGFR ratio (r=-0.08). TNF-α positively correlated with β-NGF (r=0.83), NT-3 (r=0.66), and brain-derived neurotrophic factor (BDNF) (r=0.50) and negatively with ProNGF (r= -0.74) and positively correlated with both soluble TrkA (r=0.62), sLNGFR (r=0.26).
Conclusions: This study suggests that endogenous or cleaved sLNGFR, but not soluble TrkA may participate in OA pain modulation thus supporting further research into soluble LNGFR as a therapeutic target in OA.
Sounds significant. Phase II is typically not enough to tell if a drug is good because most drugs aren’t that effective compared to current standard of care- you need the large numbers of phase iii to see the real difference. But looks like this drug shows a marked improvement in phase ii itself so it’s actually quite impressive. Last time I read such a story was for imatinib. Expecting good things from this.
The thing with chronic pain is that often it is garbage data being sent by pain receptors. Or more accurately our muddled processing of the nerve impulses leads to poorly established thresholds that lead to a constant presence of perceived pain. So preventing this pathology based on my experience is a cure. Physical regeneration is a separate target in my opinion.
A cure for much arthritis is possibly a Nutritarian Diet promoted by Dr. Joel Fuhrman which reduces inflammation and helps the body rebuild:
https://www.drfuhrman.com/blog/119/a-progressive-approach-to...
"The traditional treatment of rheumatoid arthritis revolves around medications which typically include steroids and chemotherapeutic agents such as methotrexate, Imuran®, Gold®, Plaquenil®, Arava® and Remicade®. These medications are considerably toxic and can result in serious disability.
My approach to treating rheumatoid arthritis differs in that it incorporates dietary modifications and nutritional supplements, avoiding the use of toxic drugs in the vast majority of cases. The recommendations are customized to the needs and response of each patient to treatment and involve more than just putting them on a special diet. However, in most cases, dramatic improvements and even complete recoveries occur.
In spite of well-conducted scientific investigations and the clinical experience of many physicians, this effective nutritional treatment of autoimmune disease is generally ignored. I have seen scores of patients with rheumatoid arthritis as well as lupus, fibromyalgia and connective tissue disease obtain complete recoveries through these natural interventions. Also, I have many patients who have made complete recoveries from allergies and asthma. Not every patient obtains a complete remission, but the majority is able to avoid the use of medication."
The big problem in our current society is that there is no substantial money to be made by big companies in promoting these sorts of cures.
Methotrexate is the most vile substance (made one day per week about as useful as a full day hangover) It did help but honestly only as much as the effort I put into a diet change. I completely agree with parent comment.
Anyone with an autoimmune disorder or chronic inflammation who has not experienced an elimination diet is doing themselves a huge disservice.
> It sounds like, even in the best case scenario, the drug doesn't really cure arthritis but just blunts the pain.
> I was thinking it would be something that helps the worn ligament grow back. That I would consider a real cure.
As far as I can tell, that is what it does:
> The drug is based on a molecule he discovered while working at Pfizer, and can be delivered via a once-a-month EpiPen-style injection, where it restores protective processes to diseased joints and enables the regeneration of affected tissues. It works by blocking a compound that supports the nerve cells involved in transmitting pain signals to the brain.
This doesn't say it just blocks the pain, it says it directly affects the nerve cells involved in transmitting pain. Those nerve cells could also be responsible for other unpleasant things, like generally complaining and always being inflamed and inhibiting proper healing.
It is hoped the drug — which is not a cure but will make the condition much less painful for sufferers — could also be used to treat rheumatoid arthritis and chemotherapy-induced pain in the future.
As a writer myself who has watched journalism dying, crap articles being written by underpaid freelancers, the enshitification of the internet while everyone objects to any means used to monetize content creation, etc ad nauseum, I don't really feel like trying to figure out just how much this "really does" for patients.
The medical industry in the US tends to be about profit and I think people should, in fact, profit for their work but in medicine sometimes profit motive tosses the baby out with the bathwater. And I'm super burned out on trying to have any kind of meaningful discussion of that issue online.
"not a cure" means that if you stop taking the drug, the condition comes back, at least as far as I can tell. Which checks out given the other information given by the article.
I thought tissue degeneration was part of the issue here? Having regenerated tissue doesn't necessarily help if you stop taking the drug and the tissue just goes away again.
(It sounds weird to me that tissue can just disappear from that area so I think this might be wrong?)
If tissue gets regenerated, it shouldn't "just go away again" once you stop the drug unless perhaps there is an unidentified pathological process involved.
yeah, I too find it weird to imagine that tissue can just disappear from the inside of a joint. where would it even go? does it melt into the bloodstream or something? lmao
Interesting - this looks like Beransa[1] (Librela) which is a monthly injection for canines that have osteoarthritis. My dog did not have any noticeable changes to pain after using this for 2 months so I've decided to take him off of it.
My cat has been in the feline equivalent (Solensia/frunevetmab) for about two years, and although it had a huge positive impact for the first 12 to 18 months, it seems to have suddenly completely stopped working in the last little while.
One theory is that the immune system eventually starts attacking the monoclonal antibody med itself, another is that as in humans, the OA progression might accelerate under the drug.
I also have mine on Pentosan which did have a noticeable difference for him so that's great. You could possibly talk to your vet about this, it's significantly cheaper than Beransa (110AUD/month) and for my dog it's biannual with a booster shot in between
I actually (anecdotally) heard a similar issue with Pentosan that it stops working after 12-24 months due to the immune system so you have to "time it" at an appropriate time in a dog's life. To be blunt, by appropriate I mean you'd want to start using it 12-24 before the dog is expected to pass and not at the first sign of osteoarthritis.
Perhaps, but the original paper (harsher sentences before lunch) does not defy "common sense." Common sense tells people that when they are hungry, they are irritable. Many people are familiar with the concept of feeling "hangry."
Sure that’s why it’s plausible but it defies common sense to assume that judges are not managing their own hunger to the extent that it’s affecting their job performance.
Why wouldn’t surgeons or pilots have the same problem?
The paper is sensational because of the implications it has for the social justice causes certain people are obsessed about.
>to assume that judges are not managing their own hunger to the extent that it’s affecting their job performance.
>Why wouldn’t surgeons or pilots have the same problem?
Firstly, this is such an incredibly naive view of the world, especially in regards to the type of professionals that proliferate the legal system.
Past that, surgeons and pilots DO have these issues. The airline industry has religious standards and procedures for how pilots prepare and "rate" themselves before a flight mainly due to how visible egregious pilot errors typically are; in the case of surgeons the insurance company does it best to sweep things under the rug.
Pilots are supposed to be well rested, but then you have incidents like Northwest Airlines Flight 188[1], and pilots admitting they fall asleep more than you would imagine[2].
It's hard to gather data on surgeon-specific incidents since the medical industry does its very best to sweep things under the rug, but it's estimated that 400,000 deaths occur unnecessarily while in the hospital due to medical malpractice [3].
None of these systems or data are made available in the legal system, because it's all "scratch my back" etc. So no, you really shouldn't trust judges (or anyone else in the legal system) since there are no systems of accountability.
Parole judges are not accountable for their work in the same way surgeons or pilots are. If a judge makes a bad call on a parole hearing, a person stays in prison and it's effectively impossible to challenge the decision. Parole hearings are extremely subjective, so it's vanishingly unlikely that a judge will face any repercussions for making a ruling which people would consider unfair.
This means that there's no pressure for them to manage the influence of factors like hunger on their decision.
So it is impacting those highly empirical disciplines and they have managed to develop no standards and practices? But they have around food poisoning?
I don't think this is totally unreasonable, nor unique to judges.
For example, the developed world rolled out school lunch programs as a way to improve academic performance, which at the time of implementation was controversial.
Skipping lunch is bad for school performance, but judges aren't skipping lunch. Judges eat their lunch at a regular scheduled time and so they can naturally adjust their eating habits to get them through the day without experiencing discomforting hunger.
that's exactly what the original study was proposing as an effect:
> They found that the probability of a favorable decision drops from about 65% to almost 0% from the first ruling to the last ruling within each session and that the rate of favorable rulings returns to 65% in a session following a food break.
it's not unreasonable as an original hypothesis; and it's good that we're testing it and finding out later that it's wrong. but the base hypothesis is not particularly egregious.
It's unusual for people to experience mentally distracting hunger pangs before lunch on a regular basis, because people tend to eat larger dinners and/or breakfasts to get them to lunch without significant discomfort. Debilitating hunger is an unusual experience that comes from skipping meals for some unusual reason, a break in somebody's normal routine.
In this case, this is a government official speaking to the press (i.e. in an official capacity). If they were to say "this was sabotage," that is a definite declaration that the government believes - again, officially and on the record - that an outside party has deliberately done material damage to their country. Given the general situation, it is not a huge leap to come to the interpretation that "this was an attack against our country, and possibly an act of war."
No government official would want to be within miles (or kilometers) of that sort of statement unless they have pretty much already internally decided from the top-down to escalate the situation. Almost no single government agent has the authority to escalate the situation in that manner. So what we end up with is "appears to be." This overtly says 'all available evidence points to this being the case, however something else cannot be ruled out.' (As a sibling comment suggests, it can also act as a type of propaganda). So it is not an official government declaration that another nation has damaged them, but they have reasons (probably both apparent and not) to believe what they are saying publicly.
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