1,889 karma · joined April 24, 2014
I wonder if Claude could go from NixOS spec to actual config without the Nixos provider. The provider becomes a natural language description and some links to the docs/source code and then a verifier is all you need.
Is that much different from the entire pypi ecosystem, and npm, and dockerhub (people disable Selinux, --privileged turns off seccomp and apparmour, sandbox escape CVES exist)?
edit: Bouncing around the room is one of their hit songs. Give it a listen.
But yet in some countries pediatricians will libreally prescribe it to toddlers
[1] https://www.bmj.com/content/368/bmj.m1086
Also from [2] "In this systematic review of NSAID use during acute lower respiratory tract infections in adults, we found that the existing evidence for mortality, pleuro-pulmonary complications and rates of mechanical ventilation or organ failure is of extremely poor quality, very low certainty and should be interpreted with caution."
https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bcp.1451...
Good lens.
The crux of the auto research repo is basically one file - program.md which is a system prompt that can be summarized as “do this in a loop: improve train.py, run the training, run evals, record result. Favor simplicity”. The other files are an arbitrary ML model that is being trained.
Gamma ray burst that kept going for seven hours, fired three distinct bursts spread across an entire day: July 2 2025
just saying
This complexity to understanding compression will be a big market going forward.
DRACO "is a chimeric protein with one domain that binds to viral double stranded RNA (dsRNA) and a second domain that induces apoptosis when two or more DRACOs crosslink on the same dsRNA." (Ridder et al 2011). This article is about packaging mRNA for a set of 10 interferon-stimulated genes that express multiple proteins that target various stages of viral replication.
My summary for programmers:
When you get a viral infection, immune cells make a signalling protein called a IFN-1 (Type I Interferon) cytokine, and this flips a boolean flag to True on a bunch of genes (interferon-stimulated genes or ISGs) that produce a bunch of proteins (hundreds) that control the infection. ISG15 is one of them and its role appears to be to downregulate and to limit the inflammation.
The paper title refers to a ISG15 deficiency, meaning if you are dificient in ISG15 that inflamation limitation goes away. But the paper is actually about how in people that naturally have a ISG15 deficiency, there is an always-on low level expression of some of these pro-inflamation genes. So they take that as a safe level.
The did RNA sequencing on experimental ISG15 deficient cells and from heatlhy individuals, identified the mutations, narrowed down to 10 genes (antiviral ones not inhibitors) that in combination significantly inhibited viral replication. They stuck the RNA for such genes in lipid nanoparticles such that they enter host cells, whose ribosomes happily read the RNA like a turing head reads a tape in base 20 and produce proteins encoded by these genes, similar to how the mRNA vaccine works.
So why not dose with the IFN-I directly? Three referenced papers show its "poorly tolerated with significant side effects" and all those downregulators that get expressed limit the inflammation response.
Disclaimer: IANAB (not a biologist) corrections might be due..