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Genie 3: Creating dynamic worlds that you can navigate in real-time

Genie 3 is a world builder powered by generative AI. It appears that it could in principle be built into a game engine.

One thing I’d like to do is have procedural generation as the backbone, and have generative AI modify things further that regular proc-gen textures just are not able to accomplish.

Introducing Genie 3, a general purpose world model that can generate an unprecedented diversity of interactive environments. Given a text prompt, Genie 3 can generate dynamic worlds that you can navigate in real time at 24 frames per second, retaining consistency for a few minutes at a resolution of 720p.

Watch the Google DeepMind episode on Genie 3 with Hannah Fry here: • Genie 3: An infinite world model | Shlomi…

Our team has been pioneering research in simulated environments for over a decade, from training agents to master real-time strategy games to developing simulated environments for open-ended learning and robotics. This work motivated our development of world models, which are AI systems that can use their understanding of the world to simulate aspects of it, enabling agents to predict both how an environment will evolve and how their actions will affect it.

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A grad student’s wild idea triggers a major aging breakthrough

Senescent “zombie” cells are linked to aging and multiple diseases, but spotting them in living tissue has been notoriously difficult. Researchers at Mayo Clinic have now taken an inventive leap by using aptamers—tiny, shape-shifting DNA molecules—to selectively tag these elusive cells. The project began as an offbeat conversation between two graduate students and quickly evolved into a collaborative, cross-lab effort that uncovered aptamers capable of binding to unique surface proteins on senescent cells.

Abstract: Helping cancer lose its grip

Here, Pengda Liu & team show SPOP inhibitors act as molecular glue degraders, stabilizing and activating STING to enhance immunotherapy in melanoma mouse models:

The figure shows the SPOP inhibitor 6lc reduces CBX4 and BMI1 foci, while ectopic CBX4 restores BMI1 foci and H2AX interactions.

4Department of Pharmacology.

5Division of Oncology, Department of Medicine, and.

6UNC Metabolomics and Proteomics Core, Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

Role of brain’s immune system in social withdrawal during sickness

“I just can’t make it tonight. You have fun without me.” Across much of the animal kingdom, when infection strikes, social contact shuts down. A new study details how the immune and central nervous systems implement this sickness behavior.

It makes perfect sense that when we’re battling an infection, we lose our desire to be around others. That protects them from getting sick and lets us get much needed rest. What hasn’t been as clear is how this behavior change happens.

In the research published in Cell, scientists used multiple methods to demonstrate causally that when the immune system cytokine interleukin-1 beta (IL-1β) reaches the IL-1 receptor 1 (IL-1R1) on neurons in a brain region called the dorsal raphe nucleus, that activates connections with the intermediate lateral septum to shut down social behavior.

“Our findings show that social isolation following immune challenge is self-imposed and driven by an active neural process, rather than a secondary consequence of physiological symptoms of sickness, such as lethargy,” said study co-senior author.

Neurons use physical signals, not electricity, to stabilize communication

Every movement you make and every memory you form depends on precise communication between neurons. When that communication is disrupted, the brain must rapidly rebalance its internal signaling to keep circuits functioning properly. New research from the USC Dornsife College of Letters, Arts and Sciences shows that neurons can stabilize their signaling using a fast, physical mechanism—not the electrical activity scientists long assumed was required.

The discovery, published recently in Proceedings of the National Academy of Sciences, reveals a system that doesn’t depend on the flow of charged particles to maintain signaling when part of a synapse—the junction between neurons—suddenly stops working.

Maintaining this balance between neurons is essential for muscle control, learning and overall brain health. Failure to maintain this “homeostasis” has been linked to neurological conditions such as epilepsy and autism.

Real-time tracking of mRNP complex assembly reveals various mechanisms that synergistically enhance translation repression

Using single-molecule fluorescence microscopy, Payr et al. reveal how multiple RNA-binding proteins synergize to repress translation. One RNA-binding protein binds via facilitated diffusion, recruits other proteins with highly accelerated on rate, and gets stabilized by several co-factors. The findings highlight various mRNP assembly mechanism as key to efficient translational control.

‘Zombie’ cells spark inflammation in severe fatty liver disease, researchers find

Mayo Clinic researchers have uncovered how aging “zombie cells” trigger harmful inflammation that accelerates a severe and increasingly common form of fatty liver disease called metabolic dysfunction-associated steatohepatitis (MASH). As obesity rates rise worldwide, MASH is projected to increase and is already one of the leading causes of liver transplantation.

“Liver scarring and inflammation are hallmarks of MASH. If left untreated, it can progress to liver cancer. This is why it’s so important to understand the mechanisms driving the disease so that we can prevent it or develop more effective treatments,” says Stella Victorelli, Ph.D., who is the lead author of the study published in Nature Communications.

Dr. Victorelli and colleagues, who study aged or senescent “zombie” cells, identified a mechanism by which these cells drive liver scarring and inflammation. They found that small molecules called mitochondrial RNA, typically found within the cell’s energy-producing mitochondria, can leak into the main part of the cell, where they mistakenly activate antiviral sensors called RIG-I and MDA5—normally triggered when a virus infects a cell. In this case, the danger signal comes from the cell’s own mitochondria, prompting a wave of inflammation that can damage nearby healthy tissue.

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