I’d certainly like to see more experiments automated, yet I wonder if widespread automation would result in less resources directed to novel experimental designs (or new tools) that fall outside of automated workflows. Hopefully a balance can be attained!
AI-driven autonomous robots are coming to biology laboratories, but researchers insist that human skills remain essential.
Sherlock et al. examine an IRES RNA that initiates translation of a small downstream coding region within a viral genome. The structure, function, and mechanism of this IRES are interrogated experimentally. Differential translation efficiencies between two IRESs within one viral genome exemplify RNA-structure-based tuning of gene expression.
This RedJournal article presents a first step towards continuous dosimetry in targeted radiopharmaceutical therapy by developing a sparse sensor system to reconstruct continuous time-activity curves in preclinical 177Lu-based therapies, demonstrating high accuracy with short scan times.
177Lu-based radiopharmaceutical therapy (RPT) has shown increasing promise in the treatment of neuroendocrine and metastatic prostate cancer. Delivering optimal radiation dose to tumors while minimizing dose to organs-at-risk (OAR) remains an unmet need due to significant patient-to-patient heterogeneity in treatment response, necessitating multiple snapshots of the in vivo activity distribution. Towards this goal, here we present a high temporal-resolution activity reconstruction method demonstrated on preclinical prostate cancer models.
Editor’s Note: Associate Editor Pablo Penaloza-MacMaster provides context for Long et al. on targeting the host factor HGS-viral membrane protein interaction: https://doi.org/10.1172/JCI200225
While current antivirals primarily target viral proteins, host-directed strategies remain underexplored. Here, we performed a genome-wide CRISPR inhibition (CRISPRi) screening to identify the host protein, hepatocyte growth factor-regulated tyrosine kinase substrate (HGS), facilitating the pan-coronavirus infection both in vitro and in vivo. Mechanistically, HGS interacts with the viral membrane (M) protein, facilitating its trafficking to the ER-Golgi intermediate compartment for virion assembly. Conversely, HGS deficiency caused M retention in the ER, blocking assembly. Leveraging this interaction, we designed M-derived peptides and screened over 5,000 FDA-approved or commonly used drugs, identifying riboflavin tetrabutyrate (RTB).
Our planet plunged into one of the most dramatic climate states in its long history, approximately 720–635 million years ago. During a period geologists call Snowball Earth, ice sheets crept from the poles all the way to the tropics, covering the oceans and continents in a nearly global freeze.
Evidence for this extreme climate comes from rock formations around the world that bear the signatures of ancient glaciers at low latitudes—signs that Earth’s surface was encased in ice far beyond what we see in today’s polar regions.
Scientists have long studied how a feedback process known as ice-albedo helped lock in and amplify this deep chill. Albedo is a measure of how much sunlight a surface reflects; snow and ice are bright and reflect most of the sun’s energy back into space, cooling the planet further as more of it spreads across the surface.
Researchers at Washington University in St. Louis have developed a novel cell therapy for Alzheimer’s disease using genetically modified astrocytes — the brain’s most abundant cells. By equipping these cells with a chimeric antigen receptor (CAR), scientists enabled them to specifically target and clear beta-amyloid plaques, the toxic protein deposits that accumulate in brain tissue and drive neurodegeneration. In mouse trials, a single injection prevented plaque formation in young healthy rodents and reduced existing plaque levels by half in older mice. While the approach is still being refined to minimize side effects and must be evaluated for human safety, it holds promise both as a preventive measure and as a treatment at various stages of Alzheimer’s. The same technology may eventually be adapted for cancer therapy by reprogramming the cells to target tumor markers.
Alzheimer’s disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. Despite advances in anti-amyloid immunotherapies, important limitations remain, highlighting the need for new therapeutic strategies. Here, we introduce anti-amyloid chimeric antigen receptors expressed in astrocytes (CAR-A) and validate their function in vitro. We show that two CAR-A designs reduce amyloid and associated pathology after plaque formation and prevent early plaque deposition in vivo. Single-nucleus RNA sequencing shows that CAR-A treatment induces a distinct glial response to amyloid pathology involving coordinated activity of astrocytes and microglia. Each construct additionally elicits distinctive, receptor-specific effects in astrocytes or microglia.
Think of a video game that doesn’t just run on code, but is “dreamed up” in real-time by an AI—much like how AI generates videos or images today. While this technology (known as a Diffusion Game Engine) is incredibly exciting, it has long faced two major hurdles: you couldn’t easily “edit” the world once it was generated, and you couldn’t play in that world with friends because the AI couldn’t keep the environment consistent for everyone at once.
Traditional AI game engines work like “next-frame predictors.” They look at what’s happening right now and guess what the very next split-second should look like. Because they have a short memory (a “context window”), the world often feels like a shifting dream—turn around, and the door you just walked through might have disappeared or changed color. This makes it impossible to design a specific “level” or play with others, as the AI can’t keep a steady map in its head.
We are living in the age of maximum AI hype: A superintelligence that surpasses humanity is going to emerge at any moment, according to the most breathless corners of the tech world.
There are basic technical grounds to be skeptical of that claim, but beyond that, a much deeper issue lies at the boundary between science and philosophy: What makes life different from non-life? Why is a rock inert and insensate, while even the simplest cell manifests open-ended activity in the relentless pursuit of staying alive? Since the only systems that indisputably display intelligence are alive, if we can’t understand life, we’re probably missing something essential about intelligence.
Sixty years ago, an influential but little-known philosopher named Hans Jonas gave a potent, creative, and radical answer to this question of what makes life different from non-life. In the decades since, the power and reach of his perspective have gained traction. Today, for a growing group of researchers — in fields ranging from neuroscience to the physics of complex systems — Jonas has become an incisive voice arguing forcefully that organisms are more than just machines, and minds are more than just computers.