Now online! An unbiased niche-labeling method, SAMENT, maps cellular and molecular features of metastatic niches and highlights the role of ERα⁺ niche macrophages in preventing T cell infiltration, thereby promoting bone metastasis.
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How do you study something you can never step outside of?
Studying the thing you can never step outside of and look back at is the fundamental problem facing every cosmologist who has ever looked up at the night sky. The Universe is not a laboratory you can peer into from above, it’s the thing you are already inside. The only way to truly test your ideas about how it works is to build a copy of it, run the clock forward from the Big Bang, and see if what emerges matches what your telescopes are actually telling you.
That is exactly what the FLAMINGO project has been doing. And this week, its creators made the results available to the entire world.
An international team of astrophysicists, led by researchers at Leiden University in the Netherlands, has released one of the largest cosmological simulation datasets ever produced. The archive contains more than 2.5 petabytes of data (roughly equivalent to half a million high definition films) and is free to access for researchers anywhere on the planet.
MRI reveals cerebrospinal fluid shifts after mild brain injury
Researchers at University of Tsukuba have found that cerebrospinal fluid (CSF) microdynamic motion shows region-specific alterations after mild traumatic brain injury (TBI). Using a specialized magnetic resonance imaging (MRI) technique, the team noninvasively visualized these CSF changes, which have been difficult to quantify with conventional imaging. The approach is expected to advance the understanding of the relationship between post-traumatic brain conditions and cognitive function. The study is published in Frontiers in Neuroscience.
The brain contains cerebrospinal fluid (CSF), which protects neural tissue and helps clear metabolic waste. Rather than being static, CSF exhibits continuous subtle motion, and this motion is thought to be closely linked to brain health. However, little has been known about how CSF motion is altered after a mild head injury.
The researchers employed a specialized magnetic resonance imaging (MRI) technique known as intravoxel incoherent motion (IVIM) MRI to evaluate CSF microdynamic motion through the incoherent movement of water molecules. The results showed that, after mild traumatic brain injury (TBI), CSF motion increased in some brain regions and decreased in others.
T cells secrete DNA to boost the immune system’s cancer-fighting ability
Activated immune cells secrete tiny capsules bearing DNA that can enter other immune and tumor cells to stimulate the body’s defense systems, according to a study led by investigators at Weill Cornell Medicine. The discovery extends the scientific understanding of the immune system, identifies a new strategy for boosting immunity against cancers and potentially offers a new tool for delivering genetic payloads to other cells.
Most animal cells secrete tiny capsules known as extracellular vesicles—nanoscale, membrane-bound particles—whose cargo can include proteins, snippets of DNA and other molecules. In the new study, published April 30 in Cancer Cell, the researchers discovered that vesicles secreted by activated T cells —major weapons of the immune system—carry DNA that enters immune cells and nearby tumor cells to enhance the immune response against the tumor. Preclinical experiments showed that this vesicle-associated DNA could be useful therapeutically, boosting T cell attacks against tumors that otherwise evoke little or no immune response.
“These findings reveal a natural mechanism for treating immunologically silent tumors and other diseases that stem from insufficient immune surveillance,” said study co-senior author Dr. David Lyden, the Stavros S. Niarchos Professor in Pediatric Cardiology and a member of the Gale and Ira Drukier Institute for Children’s Health and the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.
Deciphering the Nanoscale Architecture of Presynaptic Actin Using a Micropatterned Presynapse-on-Glass Model
Prefrontal cortex encodes behavior states decoupled from motor execution.
By tracking the natural actions of freely moving rats, Välikangas et al. show that prefrontal cortex encodes abstract behavioral states rather than low-level physical aspects of movement. Prefrontal activity anticipates behaviors and operates on slow timescales, suggesting that it represents high-level goals rather than moment-to-moment motor output.
Rethinking robotics with physical intelligence
Today’s advances in robotics are often driven by breakthroughs in artificial intelligence, machine learning, and perception. But in complex and constrained environments, the limiting factor is often hardware, not software. Systems that rely on constant data processing, high-bandwidth communication, and centralized compute can face delays, power constraints, and vulnerabilities that limit performance or prevent mission success altogether.
DARPA is looking to tackle these challenges by embedding intelligence directly into the physical materials of robotic systems. A new Request for Information (RFI), calls on the research community to help define a new class of materials capable of intermixed sensing, adapting, and acting in real time without relying on continuous external computation or communication links.
While the RFI itself is exploratory, it is a first step toward a more immediate opportunity: an invite-only, in-person workshop planned for the summer 2026. Selected participants will have the chance to present their ideas, engage with DARPA, and inform future program directions.
Endocannabinoid modulation of a reciprocal fronto-coerulear connection in contextual discrimination
Locarno, Nava, Barsotti et al. define a fronto-coerulear anatomical-functional loop under endocannabinoid (eCB) negative feedback that regulates contextual discrimination. Prefrontal cortex (PFC) inputs drive locus coeruleus (LC) norepinephrine (NE) release to enhance cortical firing, while locally mobilized eCBs weaken PFC to LC synapses, constraining NE-dependent entrainment of PFC neuronal assemblies.
NO-independent inflammatory response by iNOS
The finding challenges a longstanding assumption in immunology: that iNOS controls immune cell behaviour primarily through nitric oxide production. The study shows that the physical shape of iNOS – stabilised by its cofactor, tetrahydrobiopterin (BH4) – is what drives the interaction with IRG1, independently of whether iNOS is producing nitric oxide at all.
The researchers used co-immunoprecipitation and mass spectrometry to confirm that iNOS is a direct binding partner of IRG1 in living cells, with computational modelling and molecular dynamics simulations used to predict and validate the structure of the interaction. Surface plasmon resonance confirmed that the binding is stable and high-affinity in both mouse and human models, and that it does not occur with the related protein eNOS – pointing to a specific, evolutionarily conserved function.
In cells lacking iNOS, IRG1 produced more than 15 times more itaconate compared with normal cells following immune stimulation. Critically, iNOS mutants unable to produce nitric oxide still suppressed IRG1 – what mattered was whether iNOS could adopt the correct shape, determined by BH4 binding. Disrupting that binding abolished the effect entirely.
The work also showed that in the absence of iNOS, IRG1 associated with a different set of partner proteins involved in glycolysis and cell metabolism – suggesting iNOS effectively sequesters IRG1 away from those roles, with wider consequences for how immune cells manage energy during inflammation.
A protein long understood to drive inflammation by producing nitric oxide has a second, previously unknown role – it physically binds to another key protein inside cells to directly modulate the immune response. The discovery, published in Nature Metabolism, could open new routes to treating conditions such as cardiovascular disease, arthritis, Crohn’s and other inflammatory diseases.
When the immune system detects infection or injury, it triggers inflammation to fight back. That response is essential, but it must be carefully controlled. If it runs too hard for too long, it causes the tissue damage that underlies many chronic diseases. Understanding the molecular switches that regulate inflammation – and finding new ways to target them – is one of the biggest challenges in modern medicine.