After a few rounds of AI generating AI content from AI content, I'm sure it could eventually become slop...like the model collapse lol idk.

"AI models collapse when trained on recursively generated data" - https://www.nature.com/articles/s41586-024-07566-y

"The effects of parental occupational exposures on autism spectrum disorder severity and skills in cognitive and adaptive domains in children with autism spectrum disorder" https://www.sciencedirect.com/science/article/pii/S143846392...

The person leading this study, Erin C. McCanlies, was forced out of the CDC, her division eliminated and she went into early retirement from the CDC. https://www.psypost.org/scientist-who-linked-autism-to-chemi...

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"The findings suggest that workplace exposures to several specific chemical classes were associated with worse outcomes in children with ASD. One of the strongest and most consistent patterns involved plastics and polymer chemicals. Fathers’ exposure to plastics was associated with lower scores across all cognitive and adaptive skill domains, including language, motor coordination, daily living skills, and overall functioning. When both parents were exposed, the deficits appeared to compound.

“I was surprised how strongly and consistently plastics and polymers stood out as being linked with multiple developmental and behavioral outcomes including irritability, hyperactivity, and daily living,” McCanlies told PsyPost.

Exposure to ethylene oxide—commonly used in hospital sterilization—was also linked to more severe autism symptoms, lower expressive language abilities, and poorer adaptive functioning. Similarly, parental exposure to phenol (used in construction, automotive, and some consumer products) and pharmaceuticals was associated with increased ASD severity and more pronounced behavioral challenges, especially hyperactivity and stereotyped behavior.

While the results do not imply that all children exposed to these chemicals will develop more severe symptoms, the patterns suggest that early life exposure to workplace toxicants may amplify certain developmental difficulties in children who already meet criteria for ASD. The study provides one of the most detailed looks to date at how parental occupation may relate not just to diagnosis, but to variation in how autism is expressed.

“Our findings suggest that certain parental workplace exposures may be related not just to autism, but to worse symptoms and autism behaviors,” McCanlies explained."

Link for the 120B version: https://huggingface.co/lmstudio-community/gpt-oss-120b-MLX-8...

Its taking 21 gb of memory on my 64 gb mbp, still tuning it and settling on context size, temp, and other settings.

My comment from yesterday:

"thanks openai for being open ;) Surprised there are no official MLX versions and only one mention of MLX in this thread. MLX basically converst the models to take advntage of mac unified memory for 2-5x increase in power, enabling macs to run what would otherwise take expensive gpus (within limits). So FYI to any one on mac, the easiest way to run these models right now is using LM Studio (https://lmstudio.ai/), its free. You just search for the model, usually 3rd party groups mlx-community or lmstudio-community have mlx versions within a day or 2 of releases. I go for the 8-bit quantizations (4-bit faster, but quality drops). You can also convert to mlx yourself...

Once you have it running on LM studio, you can chat there in their chat interface, or you can run it through api that defaults to http://127.0.0.1:1234

You can run multiple models that hot swap and load instantly and switch between them etc.

Its surpassingly easy, and fun.There are actually a lot of cool niche models comings out, like this tiny high-quality search model released today as well (and who released official mlx version) https://huggingface.co/Intelligent-Internet/II-Search-4B

Other fun ones are gemma 3n which is model multi-modal, larger one that is actually solid model but takes more memory is the new Qwen3 30b A3B (coder and instruct), Pixtral (mixtral vision with full resolution images), etc. Look forward to playing with this model and see how it compares."

Comments URL: https://news.ycombinator.com/item?id=44818181

Points: 1

# Comments: 1

LM Studio community: 20b: bhttps://huggingface.co/lmstudio-community/gpt-oss-20b-MLX-8b... 120b: https://huggingface.co/lmstudio-community/gpt-oss-120b-MLX-8...

So FYI to any one on mac, the easiest way to run these models right now is using LM Studio (https://lmstudio.ai/), its free. You just search for the model, usually 3rd party groups mlx-community or lmstudio-community have mlx versions within a day or 2 of releases. I go for the 8-bit quantizations (4-bit faster, but quality drops). You can also convert to mlx yourself...

Once you have it running on LM studio, you can chat there in their chat interface, or you can run it through api that defaults to http://127.0.0.1:1234

You can run multiple models that hot swap and load instantly and switch between them etc.

Its surpassingly easy, and fun.There are actually a lot of cool niche models comings out, like this tiny high-quality search model released today as well (and who released official mlx version) https://huggingface.co/Intelligent-Internet/II-Search-4B

Other fun ones are gemma 3n which is model multi-modal, larger one that is actually solid model but takes more memory is the new Qwen3 30b A3B (coder and instruct), Pixtral (mixtral vision with full resolution images), etc. Look forward to playing with this model and see how it compares.

For simple tasks it can quickly respond and then understand to use MCP servers for tasks and other things, but offloading all the heavy lifting to claude code via sdk and cli, then bringing the results back in a summary or with clarifying questions as text to speech (TTS). I'm playing with Kyutai TTs b/c have great models that sound real and can do conversational streaming with VAD (though my mbp is too slow with it for now but see https://unmute.sh/ for demo).

I am looking for an orchestrator model that runs on 10-15 gb of ram and can do really good tool calling and model routing. I'm will likely move to something even smaller designed specifically for this, like Jan Nano and then spin up an intermediate model like Qwen if needed, or try a smaller Qwen. https://github.com/menloresearch/jan?tab=readme-ov-file

Ultimately, I want something that can see my screen and know what is going on and have full context and be live, so I was excited about Gemma 3N multi-modal, but its not really available yet fully with vision at least for MLX. https://deepmind.google/models/gemma/gemma-3n/

Next 6 months in this area is going to be pretty wild though.

edit: Fixed links below, thanks

https://huggingface.co/lmstudio-community/Qwen3-Coder-30B-A3... https://huggingface.co/mlx-community/Qwen3-Coder-30B-A3B-Ins...

follow these instructions https://youtu.be/q7dnkGdndNo?t=220

then load extension in developer mode

"Your eyes transform light into electrical impulses that coalesce into an image in your visual field, and your ears transform air-pressure waves into electrical pulses that you eventually perceive as sounds. Likewise, mitochondria transform dozens of hormonal, metabolic, chemical, and other information streams into their electrical membrane potential. This “bioenergetic” state then leads to the production of secondary messenger molecules that are intelligible to the nucleus. So in the same way you read messages on your phone, which receives signals, transforms them and projects decipherable information onto its screen, the nucleus of your cells can “read” the environment through the MIPS that surrounds it. Rather than having supplementary roles like those of battery chargers, mitochondria are more like the motherboard of the cell. Genes sit inert in the nucleus until energy and the right message come along to turn some of them on and some others off. Mitochondria provide these messages, speaking the language of the epigenome—the malleable layer of regulation that sits on top of the genome to regulate its expression.

My colleague Timothy Shutt of the University of Calgary likes to call mitochondria the “CEO of the cell”: the chief executive organelle. This metaphor captures how mitochondria not only are involved in integrating information but also give orders. They dictate whether the cell divides, differentiates or dies. Indeed, mitochondria have a veto on cell life or death. If the MIPS deems it necessary, it triggers programmed cell death, or apoptosis—a form of self-sacrifice for the greater good of the organism.

So vital are mitochondria that in difficult times cells may donate entire mitochondria to other cells. “In cellular emergencies, newly arrived mitochondria might kick-start tissue repair, fire up the immune system or rescue distressed cells from death,” journalist Gemma Conroy noted in a Nature news story last April. Inside tumors, cancer cells and immune cells appear to compete for mitochondria, using them as a kind of bioweapon. An international effort I participated in, led by Jonathan R. Brestoff of the Washington University School of Medicine in St. Louis, recently created an entirely new lexicon to guide the emerging field of mitochondria transfer and transplantation. All well and good, you may think. What does all this mean for my health or how long I’m going to live?

The short answer is that it may have everything to do with human health. Diabetes, neurodegenerative conditions, cancer and even mental health illnesses are all emerging as metabolic disorders involving malfunctioning mitochondria. And these findings are indicating new routes for intervention.

Mitochondria drive health—or disease—in several ways. One route derives from their role as energy processors. In an electrical circuit, if we crank up the input voltage too much, we can blow it out. Similarly, if our cells are exposed to too much glucose or fat—or, worse, both together, causing what doctors refer to as glucolipotoxicity—the mitochondria undergo fission and fragment into little bits, accumulate mtDNA defects, and produce signals that end up prematurely aging or killing the cell. Experiments in cells and in mice have shown that pharmacologically or genetically preventing mitochondrial fission induced by excessive glucose and fats may protect against insulin resistance. Cancer, too, may be a disorder of cellular metabolism. Cancer cells can burn glucose without oxygen, which suggests either that something is wrong with their mitochondria or that they prefer to reserve mitochondria for use in cell division—and proliferation.

A second pathway is through mitochondria’s influence on gene expression. Mitochondrial signals alter the expression of more than 66 percent of genes in the nuclear chromosomes. By changing which genes are expressed and to what extent, mutations in mtDNA may completely alter the nature, behavior and stress resilience of cells and ultimately of the whole organism."

"Gene duplications drive the recruitment of genes for secondary metabolism. Gene copies are gradually modified to create genes with specificities and expression patterns adapted to the needs of the new pathway in which they are involved. Duplicated genes are often in tandem repeats, forming clusters within the plant genome. However, in some cases, clusters of nonhomologous genes have also been identified as forming a functional unit. The selective forces that have caused the establishment of new pathways are far from understood and might have changed repeatedly during evolution owing to the continuously changing environment. Recent data show that the way several classes of secondary compounds are scattered among species is attributable to independent recruitment and the inactivation of biosynthetic enzymes."

https://www.cell.com/trends/plant-science/abstract/S1360-138...

If you want to understand secondary metabolites, which is not the "how" do they work part of plant-derived molecules, but the "why" do they work?

You can follow this line of research:

"Over recent years, the consensus as to the mechanisms responsible for these effects in humans has shifted away from polyphenols having direct antioxidant effects and toward their modulation of cellular signal transduction pathways. To date, little consideration has been given to the question of why, rather than how, these plant-derived chemicals might exert these effects. Therefore, this review summarizes the evidence suggesting that polyphenols beneficially affect human brain function and describes the current mechanistic hypotheses explaining these effects. It then goes on to describe the ecologic roles and potential endogenous signaling functions that these ubiquitous phytochemicals play within their home plant and discusses whether these functions drive their beneficial effects in humans via a process of “cross-kingdom” signaling predicated on the many conserved similarities in plant, microbial, and human cellular signal transduction pathways."

https://www.sciencedirect.com/science/article/pii/S216183132...

The functional aspect of the duplicated DNA goes back to the point that humans, insects, and plants are all eukaryotes...