The whole point of AI browser automation is mimicking human behaviour, fighting the anti-bot detection systems. If the point is interacting with systems, we'd be using APIs
No, it's to automate tasks that can't be done using an API, like RPA.
Readit Newsjlpom commented on Show HN: Blast – Fast, multi-threaded serving engine for web browsing AI agents github.com/stanford-mast/... · Posted by u/calebhwin
Are you aware of https://addons.mozilla.org/fr/firefox/addon/consent-o-matic/?
KDE still seems pretty bloated
I rather think the right word is clunky: one of the dev is attached to Server-Side Decoration/against CSD for some reason (none of his arguments make sense), so every stock app are difficult to read and taking unneeded screen space. It's just bad UX.
jlpom commented on Launch HN: Browser Use (YC W25) – open-source web agents github.com/browser-use/br... · Posted by u/MagMueller
Hi, great contribution! Can you highlight how does it compare to https://github.com/TaxyAI/browser-extension which also uses the DOM?
The main reason topography emerges in physical brains is because spatially distant connections are physically difficult and expensive in biological systems. Artificial neural nets have no such trade-off. So what's the motivation here? I can understand this might be a very good regularizer, so it could help with generalization error on small-data tasks. But hard to see why this should be on the critical path to AGI. As compute and data grows, you want less inductive bias. For example, CNN will beat ViT on small data tasks, but that flips with enough scale because ViT imposes less inductive bias. Or at least any inductive bias should be chosen because it models the structure of the data well, such as with causal transformers and language.
It increases modularity and small-worldness, which are in my book critical for AGI (surprised by the way that this publication doesn't cite https://www.nature.com/articles/s42256-023-00748-9).
There's a plausible hypothesis that sleep is the thing that evolved precisely to stop us doing things for any more time than is strictly necessary. That is, sleeping is safe.
I don’t think any serious biologists agree with it. There is a hard physiological need to repair cellular damage from metabolism, UV (this a big deal in unicellular species), etc. If this theory was correct, and it is possible to do it entirely while awake, there would be species (apex predators in particular) that would have evolved without the need for it, like everything that is not a hard requirement. But this is not the case.
For the afficionados, there's an excellent paper titled "The neurobiological basis of narcolepsy" published in Nature Reviews Neuroscience which examines the relationship between orexin and sleep as it relates to narcolepsy patients: https://pmc.ncbi.nlm.nih.gov/articles/PMC6492289/
In narcolepsy type 1 (NT1), patients have severely diminished orexin levels. This appears to cause them to inappropriately enter REM sleep.
OP notes that the mutation lowering the sleep requirement causes an increase in orexin. I wonder whether the increased orexin could be inhibiting REM and perhaps facilitating a more restful architecture of sleep. Alternatively, perhaps elevated orexin levels during the day cause wakefulness such that you just don't need as much sleep, regardless of how efficient the sleep is.
It would be interesting to compare sleep tracking data of people with and without this mutation to see if there are significant differences in time spent in different sleep stages.
> Alternatively, perhaps elevated orexin levels during the day cause wakefulness such that you just don't need as much sleep, regardless of how efficient the sleep is.
As noted elsewhere ITT, there is a strong biological need for sleep, and its main role is very likely to reduce reactive oxygen species (though the amount needed vary by genetics) Orexin levels increase the noradrenaline ones, which is one of the few antioxidants able to reach neurons (along with melatonin) and by this way also increase slow wave sleep, making it more efficient. So yes, this could be a way they would need less sleep.
Hey, discussion of orexin receptor stuff! As someone with clinically-diagnosed insomnia, I've been lucky enough to/unfortunate enough to have to try the orexin receptor antagonist sleep aids for a while. As recent, on-patent drugs, they are very, very expensive ($360/month was the number marked on the receipt slip, not that that means much in the US; I certainly wasn't paying that)... and they work. They really, really do work. I was prescribed them because I tried every single other class of sleep aid on the market and they were mostly ineffective, had massive side effects, or were benzos (temazepam: best sleep of my life, but better not use it for longer than a month!).
This stuff? Orexin receptor antagonists? They work. Holy crap, do they ever work. Sleep quality better than the Z-drugs, great tolerability, no massive disruption going off them... when these things go off-patent they're going to be massive. Sleep quality was not perfect (maybe 80% of "normal"? I don't know) but that is absolutely minor compared to the alternative.
(And for the record, I'm off them now due to other stuff clearing up such that I don't need this level of sleep assistance anymore. Not because I can't afford them.)
I guess that's a long-winded way to say that if you're going to do questionably-advised sleep biohacking, orexin receptors are probably the place to start.
For me they significantly increase REM, it seems at the cost of slow wave sleep. (this is logical as orexin agonism prevent REM sleep)