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“All that takes is just the right incentive.” Reliably identifying the mutations that matter for disease risk, drug response, and personalized medicine remains one of the hard problems in genomics. On the latest Novelty Search, Minos explained how SN107 uses Bittensor to improve variant calling, the step that turns...

23,157 次观看 • 2 个月前 •via X (Twitter)

12 条评论

Openτensor Foundaτion 的头像
Openτensor Foundaτion2 个月前

Watch the full episode with @theminos_ai here:

On Chain Fox 🦊 的头像
On Chain Fox 🦊2 个月前

@theminos_ai 🚀🚀

ThisisYeesus 的头像
ThisisYeesus2 个月前

@theminos_ai 🔥 🔥 🔥

Alex 的头像
Alex2 个月前

@theminos_ai bittensor:native 💎

🇺🇸 DOUBLE-INFINITI-88 🇺🇸 的头像
🇺🇸 DOUBLE-INFINITI-88 🇺🇸2 个月前

@theminos_ai This is massive! 🔥 Bittensor powering real breakthroughs in genomics with Minos SN107 – right incentives unlocking better mutation detection and faster validation. Game changer for precision medicine! 🚀🙌 #Bittensor #TAO #MinosSN107 #DI88

khay 的头像
khay2 个月前

@theminos_ai const at it again

Zaki fathurrobani 的头像
Zaki fathurrobani2 个月前

@theminos_ai dump Tao 🤣🤣

Dr/ Ahmed Eljarhy 的头像
Dr/ Ahmed Eljarhy2 个月前

@theminos_ai i sold this trach called tao not moving and it died

Lamida 的头像
Lamida2 个月前

@theminos_ai Minos turns genome research into a fast live global experiment.

Maciej 'Mack' Stachowiak 的头像
Maciej 'Mack' Stachowiak2 个月前

computational reproducibility is not yet a clinical validation, plus there is a problem of overfit the models to standard benchmarking datasets (like Genome in a Bottle). This might/will also fail on generate edge cases or different sequencing platforms (like shifting from Illumina to PacBio)

Trung Duong 的头像
Trung Duong2 个月前

@theminos_ai Totally agree! Genomics is wild rn, so much potential 🔬

Jason傑森 🇭🇰 | 🛠️ 的头像
Jason傑森 🇭🇰 | 🛠️2 个月前

@theminos_ai 嘿基因组要來扭轉變速球了嗎

相关视频

Demis Hassabis, the Nobel Prize winner who runs Google DeepMind just described the most consequential project on earth, and most people have no idea it exists. The project is called Isomorphic Labs and the goal is to end the way drugs have been developed for the last century. Here is the problem it is trying to solve. Developing a single drug today takes an average of 10 years, costs billions of dollars, and fails 90 percent of the time before it ever reaches a patient. Of every 10 drugs that enter clinical trials, only one makes it through. The other nine years of work, the other billions of dollars, the other scientific careers, gone. Hassabis believes AI can collapse that entire process from identifying a disease target to designing a compound that binds to it, predicts how it behaves in the body, and minimizes side effects , end to end, on a computer, before a single experiment is run. The foundation is AlphaFold, the AI system that solved one of biology's hardest problems predicting the 3D structure of every protein in the human body and won him the Nobel Prize in Chemistry in 2024. But knowing a protein's shape is only one part of designing a drug. Isomorphic is building what Hassabis describes as adjacent systems , AlphaFold 3, AlphaFold 4, and now a unified model called IsoDDE , that take the next steps. From designing the actual chemical compound that binds to the protein, predicting its binding strength, identifying new pockets to target that no one has ever found before. IsoDDE more than doubles the accuracy of AlphaFold 3 on the hardest protein-ligand prediction benchmarks that exist. Isomorphic is already running 18 to 19 live drug programs, cardiovascular disease, cancer, immunology in partnership with Eli Lilly, Novartis, and Johnson and Johnson. The first human clinical trial of a fully AI-designed drug is expected by the end of 2026. If that trial succeeds, it will be the first time in history that a drug put into a human body was designed not by a team of chemists working for a decade but by an AI working for months. Hassabis's long-term vision is even more direct, one day you describe a disease, click a button, and a drug blueprint comes out the other side. AI will solve almost all diseases within 10 years.

Milk Road AI

36,062 次观看 • 5 个月前

Demis Hassabis just described the moment medicine stops treating disease and starts deleting it from the source code. For all of human history, doctors have fought symptoms. The tumor. The organ failure. The collapse. Always downstream. Always after the damage has already started. The cause sits upstream. Written into the DNA. Ninety-eight percent of the human genome sits in non-coding regions. For decades, science understood the genes but couldn’t read the vast dark territory between them. That’s where most disease hides. Hassabis: “It takes the big, long genetic sequences and then it tries to predict, if you made a mutation to this particular single letter, single position in the genetic sequence, will that be a harmful mutation that might cause disease, or is it benign?” AlphaGenome reads your entire genetic sequence and identifies the exact letter that’s corrupted. Not a region. Not a probability range. A single position in a three-billion-letter sequence. That alone would be a generational breakthrough. But most diseases aren’t that clean. Hassabis: “What if they’re multigenic diseases where there’s cascades of mutations causing the problem? Those are even harder to detect, but actually perfect for sort of AI.” One mutation is hard enough to find. A cascade of mutations interacting across the genome is a problem no human researcher can hold in their head at once. Three billion data points. Compounding errors across all of them. The human brain cannot solve that. AI doesn’t solve it either. It maps it. All of it. At once. The most devastating diseases on Earth. The ones medicine has called untreatable for generations. They are not mysteries to the algorithm. They’re compute problems. But finding the error was only ever half the equation. You also need the ability to fix it. That tool already exists. CRISPR is a molecular scalpel. It cuts DNA at exact positions. The limitation was never the editing. It was knowing exactly where to cut. Hassabis: “A kind of combination of things like AlphaGenome and CRISPR could be incredibly powerful.” AI reads the code. CRISPR rewrites it. One finds the mutation. The other corrects it at the source. Not managing symptoms. Not slowing progression. Deleting the error from the genome. The implications go beyond treatment. A disease corrected at the genetic level doesn’t just disappear from one patient. It disappears from their bloodline. The read access is here. The write access exists. The merge is inevitable. The era of accepting a broken genetic hand is ending. We stopped being passengers in our own biology.

Dustin

197,790 次观看 • 5 个月前

🚨Here's what a lot of people misunderstand about cancer treatment, says drpaulmarik: "Cancer is not homogeneous. The somatic mutation theory—which is the current theory in which treatment is based—posits that you have a mutation in a single cell, and that gives rise to a whole population of cells that look the same and have the same mutation. But the Cancer Genome Atlas has shown that that theory is completely wrong. The cancer cells are very heterogeneous, so they're made up of very different populations of cells with different mutations, and one of the populations is the cancer stem cell. It's a sub-population of the cancer. These are generally slow-growing, but they're distinct in that they have the ability to divide indefinitely and grow indefinitely, and can change their characteristics. Basically, if you get rid of the fast-dividing cells, which is the cancer, you're left with the stem cells, which then become the roots, which grow back to form the tumor" sometimes years later. Conventional chemotherapy gets rid of the fast-dividing regular cancer cells but *NOT* the stem cells. So the key question is: how do you get rid of the stem cells? “There are a number of repurposed drugs that do it, and this has been well-established in scientific medical literature. One of the most effective treatments to knock out the stem cell is the famous horse deworming medicine," says drpaulmarik. Yes, ivermectin. Independent Medical Alliance

Jan Jekielek

96,002 次观看 • 1 年前

Experiments in progress. The one on the right has been learning for ~3 hours, the one in the middle for ~1 hour, and the one on the left just started a few minutes ago. The initial motivation for making the physical Atari was just to commit ourselves to a subset of algorithms that can make progress in this setup. This commitment rules out algorithms that require billions of samples to learn (or worse, require multiple environments running in parallel). Atari games are simple enough that we should be able to show learning on them in a short amount of time with no prior knowledge. Since then, I've realized that this setup is also a good way to compare different paradigms in robotics in a principled way. These paradigms are sim2real, learning from tele-operated data, and learning directly on the robots. So far, I have observed that getting sim2real to work reliably is hard. It requires tweaks that don't scale. Policies that can play perfectly in simulation fall apart because of latencies and the messiness of the real world. These aspects could be modeled to improve the simulation, but not without sinking significant human engineering hours. I have higher hopes for learning from tele-operated data, but that requires a human to learn the task first. These experiments are on my to-do list. I have to learn to play some of the games well through the robot. I’m half-decent at playing Pong and Ms Pacman now. Learning directly on robots is looking like the most promising approach. This approach takes away pesky distribution shifts and makes it possible to have algorithms that continually improve with more data and time without any human intervention. It feels great to let experiments run overnight and wake up to find improved policies. With learning on robots, I should, in principle, be able to go on a long vacation and come back to find better policies for complex tasks beyond Atari games. Whether that is possible with current learning algorithms is a different question.

Khurram Javed

52,110 次观看 • 9 个月前