A single-atom platinum catalyst lights ammonia at 200 °C and keeps it burning steadily at 1,100 °C with low NOx, generating high-grade, carbon-free heat for steel, cement and chemicals.
What if the tools for sustainable space exploration could be found in cellular life on Earth? A NASA astrobiologist explains
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Geoff Marcy (UC Berkeley)KITPFeb 28, 2015’Prospects for Intelligent Life in the Universe’ lecture given by Geoff Marcy at the KITP Teachers’ Conference: Worl…
Immunotherapy resistance remains a significant clinical challenge in the treatment of colorectal cancer. A recent study by Mount Sinai researchers, published in Cell Reports Medicine, reveals that overcoming this resistance requires more than just activating cancer-fighting T cells; it depends on restoring crucial communication between T cells and myeloid cells, specifically macrophages. Using advanced preclinical models and single-cell analyses, the research team identified exhausted T cells and immunosuppressive macrophages as key drivers of treatment failure. To counter this, they tested a novel combination therapy that targets multiple immune checkpoint proteins (PD-1, CTLA-4, and LAG3) alongside TREM2, a marker found on suppressive macrophages. By successfully reprogramming the tumor microenvironment to simultaneously reinvigorate T cells and neutralize suppressive macrophages, this combination strategy achieved up to 100% tumor clearance in mismatch repair-deficient cancer models and over 70% clearance in typically resistant mismatch repair-proficient models. Furthermore, the approach established long-lasting immune memory against cancer recurrence, highlighting the profound clinical potential of rationally designed combination immunotherapies that address both T cell dysfunction and the suppressive tumor environment.
Mestrallet et al. show that T cell-myeloid interactions determine response to PD-1 blockade in colorectal cancer. Targeting TREM2 macrophages together with LAG3, CTLA4, and PD-1 reprograms the tumor microenvironment and drives antitumor immunity, achieving up to 100% tumor clearance in mismatch repair-deficient and 70% in mismatch repair-proficient models.
Become a Big Think member to unlock expert classes, premium print issues, exclusive events and more: https://bigthink.com/membership/?utm_… What do physicists actually mean when they talk about the Multiverse? Sean Carroll explains.
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The Multiverse is having a moment. From “Rick and Morty” to Marvel movies, the idea that our Universe is just one of many has inspired countless storylines in recent popular culture.
Why is the Multiverse so compelling? To theoretical physicist and philosopher Sean Carroll, one reason is that we’re drawn to wondering how things might have turned out differently. What if you had chosen a different career path? Married someone else? Moved to a different city?
Of course, there’s obviously no guarantee that you’re living out those alternate timelines in a different universe. But there are real scientific reasons to think that the Multiverse exists. And as Carroll explains, that possibility comes with some fascinating philosophical implications.
What’s changed in the year since he coined “vibe coding and explains why he’s never felt more behind as a programmer, why agentic engineering is the more serious discipline taking shape on top of vibe coding, and why we should think of LLMs not as animals but as ghosts: jagged, statistical, summoned entities that require a new kind of taste and judgment to direct. He also touches on Software 3.0, the limits of verifiability, and why you can outsource your thinking but never your understanding.
Cancer cells frequently develop the ability to expel anticancer drugs before they can work—a phenomenon called multidrug resistance (MDR)—which is one of the leading reasons why chemotherapy fails in patients. Research published in the Journal of Controlled Release addresses that problem with a fundamentally new strategy: instead of simply increasing drug doses or switching drugs, researchers engineered nanoparticles that first disable the cancer cell’s drug-expulsion mechanism, and only then release the anticancer drug.
By combining this sequential drug delivery approach with photothermal therapy (using near-infrared laser light to heat and destroy the tumor), complete tumor elimination and 100% survival in a mouse model of drug-resistant cancer were achieved, with no detectable toxicity to normal tissues.
This remarkable drug delivery system was developed by an international research team led by Professor Eijiro Miyako at Tohoku University, who is also a Visiting Professor at Japan Advanced Institute of Science and Technology, in collaboration with the group of Drs. Alberto Bianco and Cécilia Ménard-Moyon at the French National Center for Scientific Research (CNRS)/University of Strasbourg.
In a recently published review, researchers led by Prof. Wu Qingfeng at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences explored the ongoing process of neural cell competition (NCC), a fundamental mechanism that shapes the brain across the lifespan.
The review is published in National Science Review, and provides fresh insights into how brain cells continuously “compete” for survival and how this competition impacts brain development, wiring, function, and aging.
Although neural cell competition is widely recognized for its role during early brain development, Prof. Wu’s team demonstrated that this process continues to be vital throughout life. They revealed that NCC not only helps maintain healthy brain function but also contributes to age-related cognitive decline when disrupted.