AnthonBerg
I've later come to suspect that this glittering is sometimes useful as… fuel? Feeling-of-progress hands-on motivation-fuel.
It's extremely interesting, and I'll be frank here, that people who just can't tell the difference are usually judgy and kind of status- and comparison-oriented towards people. In my experience. Others may not notice that difference.
Or, jokes aside, I honestly think that you might just have beefier time-integrating sensory-processing circuits in your brain than I do. Really. I do profoundly notice the difference, and it's a gritty and distracting thing. A slight but persistently intrusive and distracting perceptual thing. I honestly wish I didn't notice, but I do. I basically ask this: believe us when we ask for higher framerates and lower end-to-end latency.
And I'm fairly certain that the hardware and software to do higher frame rates across the board is a baseline commodity in the Apple source hardware ecosystem the build and integrate from. And it's certainly a better fit to consider it a line drawn between "pro" and "not pro" for marketing and pricing purposes than any fundamental and meaningful price-of-equipment threshold.
If they INSIST that it MUST be 60 Hz, I'd accept the consolation/compromise of 60 Hz but 0ms-ish latency. (Maybe they already do it that way.)
As in waiiiiit until the 16.67ms between frames is almost up while sampling inputs, then bam!, render quicky, bam!, transfer it over a link that could carry more than 60 frames per second, bam!, fast OLED display. Each frame fresh and close to input.
To the why?-sayers: Because the difference is noticeable. We can get all philosophical and discuss whether it's a competitive advantage for someone to not notice the difference, or vice versa. Why the why?, why not just… take us difference-noticers on our word? Like… we're not taking your 60Hz 16.67ms crunchiness away from you?
SONG OF INDRA
Thus indeed, thus is my mind : kine and horses will I win. Have I not drunk of the Soma ?
Like the roaring winds the draughts of Soma have roused me up. Have I not drunk of the Soma ?
The draughts have roused me up, as swift horses a chariot. Have I not drunk of the Soma ?
The hymn has drawn nigh to me, as a lowing cow to her dear calf. Have I not drunk of the Soma ?
As a carpenter a seat for the chariot, round my heart I bend the hymn. Have I not drunk of the Soma ?
Haha, had to. This is such an absurdly beautiful translation of a Vedic hymn by Thomas. Source: page 50: https://archive.org/cors/vedichymns00unse/vedichymns00unse.p...
I remember the feeling of playing Baba is You. The wonder and the sense of… a sort of abyssal depth of the mechanics, once you start to get a feeling for how they expand. And then how that yields to intuition. Hadn't come to such a lovely crack in the metacognitive vessel!, to deliverately pry at. Thanks!
The perspective you offer here makes me want to find or bring about a venue for… this.
it's very funny to have written SO MUCH WORDS under the link "Why is every rationalist blog post way too long?", aaahahah
Hence the disclaimer that it's super guessy what I wrote.
So I come to this perspective having had reason to look into synucleopathic disorders like Parkinson's and Lewy body dementia. Read a ton of literature as best I could. (Regular people can read academic literature. To actionable insight. It just takes some care regarding certainty, and one must work with doctors with anything significant. It's a… help the doctor help you thing.)
And indeed: Pesticides. That New York times article mentions paraquat.
It's interesting to look at how pesticides might bring about Parkinson's. Cell death in the substantia nigra.
It's interesting with paraquat that it's especially and specifically destructive to the lung. As well as generally-yet-specifically inducing oxidative stress, which seems as far as I can tell to kind of be… the cause of death so to speak?, for the crucial substantia nigra cells. The Wikipedia page on paraquat underpins this pulmonary impact reasonably well I think, well enough for the sake of discussion: https://en.wikipedia.org/wiki/Paraquat
Then there's stuff like this: "Elevated PM2.5 concentrations were significantly correlated with an increased risk of PD among patients with COPD. Furthermore, exposure to high PM2.5 levels can further increase the risk of PD." – Association between PM2.5 exposure and risk of Parkinson’s disease in individuals with chronic obstructive pulmonary disease in Taiwan: a nested case-control study, https://www.e-epih.org/journal/view.php?doi=10.4178/epih.e20...
And this: "This nationwide retrospective cohort study demonstrates that [Parkinson's disease] risk is significantly increased in patients with [chronic obstructive pulmonary disease] compared with those of the general population." — The association between chronic obstructive pulmonary disease and Parkinson's disease: a nationwide population-based retrospective cohort study, https://academic.oup.com/qjmed/article-abstract/108/1/39/158...
Then I've been surprised and sort of amazed to read studies of the OTC compound ambroxol in Parkinson's. These seem to show that ambroxol has protective effects against Parkinson's, even seemingly curbing the progression of the full clinical manifestation of the disease. Ambroxol is an over-the-counter mucolytic and "cough syrup" thing. It also happens to have specific antioxidant properties – redox-adjusting properties? – and in general very complex and very interesting effects on neuronal signaling; "Ambroxol is a potent inhibitor of the neuronal Na+ channels, explaining its anaesthetic effect", as per Wikipedia: https://en.wikipedia.org/wiki/Ambroxol
Ambroxol has extensive effects on fine pulmonary function "through several mechanisms, including breaking up phlegm, stimulating mucus production, and stimulating synthesis and release of surfactant by type II pneumocytes."
And! Get this: "Ambroxol is also anti-inflammatory, reducing redness in a sore throat. It reduces the release of inflammatory cytokines and histamines in cell cultures. It also acts as an antioxidant, scavenging free radicals and hypochloric acid generated by neutrophils.[14] These two effects explain its effect in treating acute lung injury caused by paraquat.[7]"
At that point I was like whoa.
Here's a bunch of research stuff on ambroxol and Parkinson's:
Ambroxol-induced rescue of defective glucocerebrosidase is associated with increased LIMP-2 and saposin C levels in GBA1 mutant Parkinson's disease cells – https://pubmed.ncbi.nlm.nih.gov/26094596/
Ambroxol as a Treatment for Parkinson Disease Dementia – https://jamanetwork.com/journals/jamaneurology/fullarticle/2...
Protocol of ASPro-PD: a phase 3 trial of ambroxol to slow progression in genetically stratified Parkinson’s disease – https://link.springer.com/article/10.1007/s00415-026-13683-7
Ambroxol as a disease-modifying treatment to reduce the risk of cognitive impairment in GBA-associated Parkinson’s disease: a multicentre, randomised, double-blind, placebo-controlled, phase II trial. The AMBITIOUS study protocol – https://neurologyopen.bmj.com/content/5/2/e000535
Ambroxol for the Treatment of Patients With Parkinson Disease With and Without Glucocerebrosidase Gene Mutations – https://jamanetwork.com/journals/jamaneurology/fullarticle/2...
It's wildly interesting. I'm super curious.
So a thing with these studies is that it's looks like ambroxol doses for Parkinson's need to be substantially higher than the cough-syrup/OTC-mucolytic doses. Seemingly to get enough to cross the blood-brain barrier. So this doesn't pin down any pulmonary foundation for Parkinson's.
But it is very, very interesting that... practically all of the stuff that impacts Parkinson's for better or worse always has a pulmonary element. All of it, as far as I can tell. But I don't know! I'm just seeing a structure of evidence as leaning a certain way. Could just be my imagination. And I don't trust it. But I'ma keep reading for sure.
It is also readily apparent to me that nicotine is bad for us, generally and broadly.
The combination leaves wiggle room for nicotine to be a net-good lever on certain mechanisms. I do think it's best to avoid it; It's a challenging double-edged sword.
The molecular biology of how it's maybe-good and maybe-bad is probably the most useful aspect of it. It's a strange sort of bronchodilator and has weird and ambiguous antiinflammatory properties. (Which seem to tie in to how it is addictive: Short-term bronchodilation and oddly-shaped short-term antiinflammatory properties turn into bronchoconstriction and proinflammatory effects as time passes from taking nicotine, which feels like it would be rather inductive to generating a craving for more nicotine.)
Re. Parkinson's: Wild guess, addled brain hunching on nebulous perspectives, but I do think that nicotine's protective effects against Parkinson's are indeed related to the bronchodilation and antiinflammatory aspects, and more specifically it seems to me that Parkinson's has pulmonary basis. I think we're nuking our lungs in many subtle ways that in some of us cause the dam of cell death in the substantia nigra to break. How might we be nuking our lungs? Say… Air pollution, incl. microplastics and plasticizers, various disruptors of fine pulmonary epithelium and metabolic function and neuroendocrine autonomic control. And I'd think that once we start to lose fine autonomic control by way of loss of dopamine cells in the substantia nigra, we'd be poised to enter a vicious cycle of further loss of pulmonary foundations.
but idk, just sayin lol
For what it's worth, I could squeeze latency down to sub-millisecond buffers on Linux on an AMD AM4 machine. With random USB audio devices.
Spoiler warning: Starting in 2013, two mechanics graft a Celica GT-Four drivetrain into an Austin Mini. Now thirteen years later, Episode 43 came 12 days ago and they drove it. Project Binky drives!! it drives!!! In our lifetime!!
Deprival of insulin is torture.
Even setting aside the very real risk of life-ending ketoacidosis, high enough blood sugar is pure suffering in itself.
Many aspects to it. The nuances are horrific; For instance. the amygdala is wired with blood glucose sensing capability and processes blood sugar alterations as foundational threat markers. Directly.
It is known that elevated blood sugar nukes sensory nerves and capillaries.
This is torture. Literal. physical torture.
(Source: A loved one just barely escaped death due to a badly missed T1D diagnosis. It's torture.)
And I mean this in the best possible way. It's really interesting.
There's this feeling of an intrusive forcing of something. A feeling that things don't… breathe? Feels like one already sifts out this sort of semantic weight when reading and to me the highlighting adds strange janky emotional-processing noise to the text; Uncomfortable and somewhat… dissonant?
It's really, really interesting. I hate how disparaging to the project this comes out!! my apologies for that! I LOVE the project and what it reveals about text comprehension and perception of saliency and rhythm in written text!
(† footnote: feels like this to me)
Apropos of nothing.
My point was exactly the hope to indicate how much knowledge there exists. That's the truly wild thing. Or yeah, how unread most of it lays.
Lightly edited from Wikipedia:
"Menthol's [agonism of] the cold-sensitive Transient Receptor Potential cation channel subfamily M (melastatin) member 8 or TRPM8 receptors is responsible for the well-known cooling sensation it provokes.
Menthol's analgesic properties are mediated through a selective activation of κ-opioid receptors. Menthol blocks calcium channels and voltage-sensitive sodium channels, reducing neural activity that may stimulate muscles.
Some studies show that menthol acts as a GABAᴀ receptor positive allosteric modulator and increases GABAergic transmission in PAG neurons."
…and! Check this out:
"Menthol has anesthetic properties similar to though less potent than propofol, interacting with the same sites on the GABAᴀ receptor."
Propofol. PROPOFOL. The -ol in propofol is the -ol in menthol, haha.
"Menthol may also enhance the activity of glycine receptors and negatively modulate 5-HT3 receptors and nAChRs."
Aaaaand:
"Menthol also lowers blood pressure and antagonizes vasoconstriction through TRPM8 activation."
And wont accept clear straightforward plain language explanation of what others want, because in their heads they should not.
I find it extremely interesting that GLP-1 agonists and GLP-1 receptors are highly pulmonary.
(There seems to be a persistent correlation between detailed pulmonary mechanisms, biology, responses… and neuroinflammation. Which does make sense when we consider the metabolic demands of the brain, which can be highly localized and sensitive to fine variances in supporting system capacity.)
My from-the hip take – from the hip!, no judging pls; It's a hunch, working to falsify it – is that… everything that makes humans aggressive to someone. Every feature someone can present that increases the odds of aggression… is a heuristic for neuroinflammation.
It's a lot of things, but neuroinflammation is a pretty consistent good match as core heuristic.
As in: GLP-1 agonists do reduce neuroinflammation. And then the hunch: This generally and ubiquitously reduces the aggression-induced features thereof.
(This take is somewhere between riffing on concepts and a surprisingly earnest and mechanistic theoretical perspective. Started as jokey banter but it's kinda hard to unsee it. not sure where else to place it, haha.)
(I'm kidding when I say this, and it's also concretely true.)
Been working on realtime DSP and ad-hoc A/V integration and sync.
Audio DACs are a solved problem. Pristine D/A conversion is a ubiquitous low-cost commodity. It's fun to buy a bunch of cheap "chi-fi" DACs – quality is excellent – and ad-hoc merge them into one big audio interface and do per-channel DSP. Toss in some TPA3255 amplifiers. Bodge together a crossover and room correction monstrosity in Reaper or Logic. Run system audio through that. It's easy to get super arcane. My home stereo is frightening. The interesting part is thinking about how to get a human interface on top of it. How to get it to assemble and stay assembled and present human-comprehensible knobs – or not.
Also had an extended family health crisis. About 9 years non-stop of extremely unlikely convergences of life-threatening conditions. (My close family has dissolved due to trauma and stress. (It's okay.)) And I haven't been working a programming or computer-science job since 2020… but I have very serious and significant work experience in things that are… how to even put it. It's not immediately clear how to add the past few years to my resumé?
Did an invisible PhD in mitochondrial neuroimmunobiology at the School of Hard Knocks? Stint of off-piste biomedical engineering? Amateur placental biotechnologist? Independent researcher?, or just… faceplanted into some PDFs on Google Scholar and accidentally read some out-of-my-lane stuff and it turns out it's actionable. Results from molecular biology are actionable.
It is said that there's a 15 year gap before something reaches clinical practice. Between having in one hand some concrete scientific results. On how to treat something in the body. And on the other hand… to clinical practice. A 15 year gap.
What's that 15 year gap made out of?, and can we cross it earlier?
We can.
Trying to figure out how to get this into words, and what to do with it.
And then when I've got the realtime-DSP-ed-to-the-hilt home-computer workstation going, I'm going to work on Idris 2 because we need dependent types.