Yeah, I just searched for “driver_register”, a call that would show upin a large number of Linux drivers in the open source Linux kernel, not to mention other public-facing repos, and it only returned two results, neither from the mainline Linux kernel repo.
It sounds like most commenters here have never had a rosin tater. When I was kid, a very popular, upscale restaurant called Planters Back Porch in seafood mecca Murrells Inlet, SC specialized in rosin taters. They were very good, enough for there to always be long lines to get in.
In case it’s not clear from the description, after removing the potato from the rosin, and wrapping in paper, the thin layer of remaining rosin quickly solidifies into a hard shell, so you can then cut through it to get access to the flesh of the potato without accidentally eating rosin.
Yes. This comments section is peak HN. A lot of speculation by people with absolutely zero experience or data.
The article is admittedly tare on the _differences in outcome_, over and against more conventional methods, which I think drives a lot of the speculation here, but approached with curiosity, this becomes, "hmm, I wonder what, if any, the benefits might be?" instead of, "you could definitely replicate this with canola and also btw I solder with rosin"
it sounds like the authors are suggesting that additional energy usage caused by stress can, in isolation from other causes, be a mechanism for disease. But that doesn’t make much sense:
- our metabolisms are adaptable, so why wouldn’t this increase in energy use simply be offset by an increase in energy production? It can’t be that people who are stressed in general aren’t getting enough energy, because that would correlate stress with weight loss, but I would argue that there are plenty of overweight people with stress.
- if the argument is that an increased metabolism by itself is the culprit, then why wouldn’t people with higher metabolisms in general — like anyone who exercises regularly, but certainly athletes — not also experience more disease? If your answer is “that’s different for some reason”, then that means that increased energy usage and metabolism is not by itself the cause, which suggests it may not be the cause at all.
Furthermore, even granting the supposition that stress requires increased energy usage, their abstract doesn’t make much sense:
- “Living organisms have a limited capacity to consume energy.” Okay, so that means that no matter how stressed we get, there’s a cap to the energy we can use. But how is that relevant, since it also applies to exercise or other energy utilization by the body? Why does a limited capacity to consume energy only apply to stress?
- “Overconsumption of energy by [stress handling] brain-body processes leads to … excess energy expenditure above the organism’s optimum”. Thats basically a tautology, but more importantly, it doesn’t tell us that energy consumption above “optimal” — which seems extremely vague — is a bad thing.
- “In turn, [excess energy consumption above the optimal] accelerates physiological decline in cells, laboratory animals, and humans, and may drive biological aging”. So that “may” is a pretty good reason to dismiss this, since again why wouldn’t this lead to increased disease among athletes or anyone with higher metabolism?
- “Mechanistically, the energetic restriction of growth, maintenance and repair processes leads to the progressive wear-and-tear of molecular and organ systems” Maybe, but why are they energetically restricted if metabolism has increased to provide more energy? And again, why don’t we then see increased disease and aging in anyone who exercises regularly, since that exercise not only uses energy that restricts growth, maintenance and repair, but exercise causes more need for repair.
I think the core problem is that it’s all going to boil down to how you define “optimum”, which the authors conveniently don’t. The authors are going to be left with defining “optimum” as meaning “that energy usage which does not cause disease”. But that’s no different than simply claiming “stress causes disease”, so this model describes nothing, since it tells us nothing about how to identify non-optimum energy usage or how non-optimum energy usage causes disease.
Humans have a massive capacity to vary energy use. Highly trained endurance athletes like professional road cyclists and triathletes can average 3x or more the typical daily energy expenditure of a non-athlete on a long term basis. The idea that psychological stress can overwhelm the body's ability to produce energy does not seem credible to me.
Those people have trained very deliberately over years to reach that level of performance, on top of an innate genetic disposition.
Undoubtedly, in absolute terms they have a higher capacity to withstand the negative physical effects of psychosocial stress as described in the paper, precisely because of these physiological adaptations.
If regular people trained themselves to deal with stress then they would have a higher capacity too.
The paper is referring to the maximum capacity of a particular organism at a particular moment in time. It doesn't assert that the capacity is uniform across a species or doesn't change over time.
>Okay, so that means that no matter how stressed we get, there’s a cap to the energy we can use. But how is that relevant, since it also applies to exercise or other energy utilization by the body? Why does a limited capacity to consume energy only apply to stress?
It doesn't. That limited capacity to consume energy applies to exercise, brain activity, thermogenesis, digestion, and every other biological process as well. It is a fundamental aspect of cellular biology and a major focus in the field of exercise physiology.
Fitness training is the very slow and deliberate process of pushing these limits tiny percentages higher.
I suggest you build some practical and theoretical knowledge of the field before dismissing the paper.
I absolutely don't doubt you but can you provide some accessible education resources or some sports science/biochemistry papers for the claim around "That limited capacity to consume energy applies to exercise, brain activity, thermogenesis, digestion, and every other biological process as well. It is a fundamental aspect of cellular biology and a major focus in the field of exercise physiology." ?
What energy are we talking about here exactly? ATP?
Yes. Metabolism is rate limited by countless chemical reactions. Energy sources need to be broken down and moved around the body. Waste products need to be removed. Mitochondria only work at a certain rate. You can increase the number of mitochondria but that hits a practical ceiling as well.
You can start with the Wikipedia article for Metabolism or search for "metabolic scope" and "metabolic efficiency".
Ok, I understand some of this. I know that often the structure of proteins (especially e.g. with ATP Synthase) helps drive and time limits energy production or energy signalling. Just like how the plugging/unplugging of sodium channels naturally creates equal windows for sodium to enter Neurons during action potentials, the natural duration of ATP synthase and other processes establishes a sort of time unit, wherever the ATP is.
Please can you expand a little more. I am a novice so I'm sure there must be something here I have missed, and would love to know what that is:
What I am a little confused about is that the consumption of energy is not done at the same time as consumption, unless I am wrong?
For example when muscles are used or repair during hysteresis, the mitochondria produced the ATP used in that reaction long before the event.
I suppose you can argue any energy consumption via chronic stress effects that. However, because it is local, distributed and there are a few forms of stored energy in essence and uses of it (e.g. mitosis/DNA nucleotide production), it's not like having one singular energy total that goes down, is it?
It's feasible that each area of the body can upscale production and produce their different kinds of energy/energy store more efficiently over time, since most of the time the body is not producing ATP at peak rate. Is the argument that doing that would wear out parts of the cells we have faster or something, due to the chronic stress, compared to what they typically see?
I struggle to buy this argument because we know that heavily overweight people consume much more calories (and thus more ATP Synthase etc) for their number of cells but they don't necessarily die much younger until you reach severe levels of being obese.
A lot of people don’t remember that Intel was a huge early ARM licensee. If you were building a smart mobile device 25 years ago, you were probably seriously considering the Intel StongARM SoC. They then followed up on this with the more advanced ARM XScale family of SoCs, which you’d likely use if wanted to build a ARM battery-powered smart device in the early 2000s. Background per Wikipedia:
> The StrongARM is a family of computer microprocessors developed by Digital Equipment Corporation and manufactured in the late 1990s which implemented the ARM v4 instruction set architecture. It was later acquired by Intel in 1997 from DEC's own Digital Semiconductor division as part of a settlement of a lawsuit between the two companies over patent infringement. Intel then continued to manufacture it before replacing it with the StrongARM-derived ARM-based follow-up architecture called XScale in the early 2000s.
However, after developing and manufacturing these for nine years, Intel exited this business by selling their ARM unit to Marvell. Intel was developing its own “low power” x86 chip, the Atom, and decided to put all its mobile eggs in that basket, which unfortunately was never as low power as comparable ARM designs. I suspect Intel also saw that the number of licensees in the ARM market was growing and competition along with it, their value-add wasn’t that great, and their margins were necessarily smaller due to the ARM licensing fees.
I remember they, at some point, sold their perpetual license (was it with the Marvel deal?). Before that, IIRC, they didn’t need to pay volume-based licensing to make their ARM variants.
The oroduct description in the FAQ is entirely based on what it doesn’t or can’t do, but doesn’t say anything about what it will be able to do, except run an off-the-shelf window manager on an off-the-shelf OS. Are any apps going to be available, And how do customers install third-party apps without the dreaded Cloud?
They are aiming this at someone with:
> a high discretionary budget for personal electronics and willingness to pay a premium for novel ideas.
But what are those novel ideas that would justify the “quite high” price?
And if I wanted a BSD-based desktop computer with “No AI. No Cloud. No Distractions”, I would just buy a Mac Mini, not log into an Apple ID, disable Siri, out it into Do Not Disturb. And Mac OS has never been a “walled garden”. So from a customer’s perspective, why wouldn’t this be an easier, cheaper, and superior solution?
I don't see how that's an apt analogy. Geocentrism put the Earth at the center of the universe, around which the rest of the universe rotated. But saying life on Earth originated on Earth does not in any way put the Earth at the center of anything. Nor does it in any way mean that Earth is unique.
The bottom line is that -- because we don't know how abiogenesis occurred, whether here or somewhere else -- we have no way to judge how common it is. It could be that, given enough time, life spontaneously forms on any planet or moon that offers a certain set of conditions, and Earth just happens to be one of those planets, meaning it is still not "the center" of anything.
In fact, in the extreme case, panspermia is much more geocentric, saying that life formed in just one very special place -- maybe not the Earth, but somewhere, the "center of life in the universe" -- and then spread by diffusion to all the other locations in which life existed. But that seems like an unlikely and unnecessary model; if life can spontaneously begin somewhere, why should we assume it can't begin in many places, and if that's true, why not also on Earth?
The idea is that it puts Earth at the center of the biological universe.
Generally the idea is that abiogenesis is very rare. I don't think any panspermists are saying that it only happened in one spot. As you pointed out that's basically the same belief as thinking it happened just once on Earth. The two 'versions' (they're not mutually exclusive) I'm familiar with are spreading via waterbears on comets or whatever, and also seeding by intelligent life. I think we have evidence for both in our own solar system, although the life we've seeded probably didn't take hold for very long.
I think there’s a better example, but whether it applies it depends on one of two major divisions of C code: that designed to run on systems with a MMU (as typically used for Linux and other large OSes) — where virtual memory makes dynamic momory allocation practical — and those without — which today is primarily the very large world of embedded devices.
For the latter, the industry best practice is to avoid malloc(), except maybe at init time, and instead allocate memory statically. And in that use case, you break your code into modules, which can contain private data, public data, private functions, and public functions.
In other words, building an app out of C modules is a lot like building an app in a more modern language just using static classes, with no instantiation. And that design pattern — which is extremely common in the embedded world — we have a direct equivalent to the “private” qualifier, which is “static”, which restricts the rest of the app from accessing so-marked file-scope variables and functions.
Where this breaks down — as always with C — is when you need multiple instantiations of a module, which modern programming languages refer to as an object. The closest we can get in C is to pass the module’s public functions a struct with some sort of data structure containing the object’s n9n-static data. And the author explains, there are standard ways make that data structure opaque to calling code, but those are definitely workarounds to language shortcomings.
But the bottom line is that those language shortcomings — the lack of objects and a private qualifier for its members — are only shortcomings if you need those features, and in the embedded world, most applications don’t, they only require all the advantages offered by C. So as always, this is about picking the right language for the project, there’s no one size fits all.
The claim is that metformin greatly reduces viral load. If your long COVID is caused by the virus continuing to linger on 8n some tissues, as there is evidence might be the case for s9me patience, then it might. But if your long COVID is caused by microclots or lung scarring or other physiological damage caused by COVID, then no.
Makes sense. I found this too in a science journal:
> The exact pathophysiology of long COVID is unknown but is likely to be multifactorial, including the inflammatory cascade during acute infection and persistent viral replication. Mechanistic in-silico modelling predicts that translation of SARS-CoV-2 viral proteins is a particularly sensitive target for inhibition of viral replication, and previous studies have shown that metformin is capable of suppressing protein translation via mammalian target of rapamycin (mTOR) inhibition
