Here, Johann de Bono, Luke Gaughan & team identify the protein TRA2B as being key for the synthesis of AR-Vs.
1Newcastle University Centre for Cancer, Paul O’Gorman Building, Framlington Place, Newcastle upon Tyne, United Kingdom.
2The Institute for Cancer Research, London, United Kingdom.
3The Royal Marsden NHS Foundation Trust, London, United Kingdom.
4Newcastle University Bioinformatics Service Unit, Medical School, Newcastle University, Newcastle, United Kingdom.
Scientists have developed a new way to fight gum disease without wiping out the mouth’s helpful bacteria—a major shift from traditional treatments. Instead of killing everything, this targeted approach blocks only the harmful microbes that drive periodontitis, allowing beneficial bacteria to thrive and restore balance naturally.
The debilitating, chronic loss of joint cartilage known as osteoarthritis causes pain and bone decay for hundreds of millions of people every day, but new help may be on the way – in the form of a simple, single shot.
Based on ongoing animal experiments, injecting a carefully engineered, slow-release drug-delivery system into the damaged joint can coax the body’s own cartilage and bone cells to carry out an effective repair job in just a few weeks.
“In two years, we were able to go from a moonshot idea to developing these therapies to demonstrating that they reverse osteoarthritis in animals,” says chemical and biological engineer Stephanie Bryant, from the University of Colorado (UC) Boulder.
In a paradigm-breaking study, researchers have discovered a novel way the immune system, specifically Tcells, attack their target cells, reshaping long-held assumptions in immunology and demonstrating direct implications for the field of cancer immunology and bone marrow transplantation. The team consists of Dr. Pavan Reddy, director of the Dan L Duncan Comprehensive Cancer Center at Baylor College of Medicine (BCM) and his team, in collaboration with Drs. Arul Chinnaiyan, S P Hicks Endowed Professor of Pathology, and Marcin Cieslik, assistant professor of pathology, both from University of Michigan Rogel Cancer Center. The study is published in Nature Immunology.
Rewriting the rules of T cell biology The immune system relies on molecules called major histocompatibility complexes (MHC) to detect external “threats” to the body, including from cancerous or foreign (allogeneic) cells. Historically, MHC class I molecules were believed to present signals only to CD8+ T cells (“killer” T cells), while MHC II activated CD4+ T cells (“helper” T cells). This division of MHC class roles guided decades of immunology and cancer research.
In an example of collaborative work, Reddy’s graduate students Emma Lauder and Meng-Chih Wu from BCM and Chinnaiyan and Cieslik’s student Mahnoor Gondal, from University of Michigan, worked with colleagues on various components of the work that spanned several years. The work challenges this foundational MHC class-restricted dichotomy and reveals a previously unrecognized role for the class I pathway in CD4+ T cell–mediated immune defense.
Malignant tumors are sneaky. They tend to fly under the immune system’s radar because, unlike invaders such as viruses or bacteria, cancer cells arise from normal cells, so they bear many of the same familiar molecules on their surface.
Once tumors are established, they become even more adept at hiding out from the immune system. They might cloak themselves in proteins to block immune cells from entering them or undergo genetic changes to further reduce the chance that disease-fighting cells will notice anything is amiss.
Great article. I should note that it actually has nothing to do with slow and boring research — it’s about the importance of scientists practicing good communication and public engagement to facilitate fundraising from non-governmental sources.
As federal research funding shrinks, scientists are looking to other sources of support. Can they learn to sell their work without selling out?
Since the middle of the twentieth century, the National Institutes of Health and the National Science Foundation have embodied an imperfect social contract: Federal agencies would fund basic research at scale, and in return, that research would serve the public good through medical advances, technological progress, and economic growth.
For scientists, this system created a reliable pathway: Do good work, write strong grants, and federal agencies would keep your lab running. It was never a perfectly fair system, but it was predictable enough that you could build a life around it. If your work was solid and your grants were strong, the system would fund you.
A new study shows that the overexpression of somatostatin (SST), a neuropeptide produced in neurons and acting mostly on microglia, lowers inflammation and amyloid β burden, improving cognitive abilities in a mouse model of Alzheimer’s. Drugs affecting this pathway are already available [1].
The unusual suspect
In Alzheimer’s disease, many signaling pathways in the brain become dysregulated. Since going after the main hallmarks of the disease (amyloid β and tau protein accumulation) has only yielded modest results so far, scientists are exploring various secondary targets whose levels correlate with the disease.
Why mammals cannot regenerate limbs like amphibians do presents a long-standing puzzle in biology. To uncover the underlying differences, we compared amputation responses of embryonic mouse (Mus musculus) and Xenopus laevis tadpole limbs. Lowering environmental oxygen or stabilizing the oxygen-sensitive hypoxia-inducible factor 1A (HIF1A) induced rapid wound healing in mouse limbs. This response was accompanied by altered cellular mechanics, metabolism, and a histone landscape that primed regenerative cell states. Conversely, Xenopus tadpole limbs retained these features even under high oxygen levels. Their reduced oxygen-sensing capacity was associated with decreased HIF1A-regulating gene expression. Our results thus identify species-specific oxygen-sensing capacity as a fundamental, targetable mechanism that can unlock latent regenerative programs in mammals.
【】 Full article: (Authored by Nader Butto, from Petah Tikva, Israel.)
This work presents a vortex-based geometric interpretation of atomic structure, in which electrons are described as localized vortex excitations embedded in a structured vacuum, offering a physically intuitive framework for understanding shells, subshells, orbitals, quantum numbers, and electron configurations without altering the formal structure of quantum mechanics. QUANTUM_NUMBERS vortex_geometry ElectronConfiguration.
The atomic structure of matter represents one of the foundational achievements of modern physics and chemistry. Early experimental investigations by Rutherford established the nuclear model of the atom [1], while Bohr introduced the concept of discrete electronic energy levels to explain atomic spectra [2]. Sommerfeld subsequently extended this picture by incorporating angular momentum quantization and relativistic corrections [3]. These developments paved the way for the formulation of quantum mechanics, which replaced classical electron orbits with a wave-based description of electronic states.
The quantum-mechanical framework, formalized through the work of Schrödinger, Pauli, Born, and Dirac, provides a mathematically rigorous and highly successful description of atomic behavior [4]-[7]. Within this formalism, electrons are described by wavefunctions whose squared modulus gives the probability density of finding an electron in a given region of space. Atomic orbitals arise as solutions of the Schrödinger equation and are characterized by a set of quantum numbers that determine their energy, angular momentum, spatial orientation, and spin. This approach accurately predicts atomic spectra, selection rules, and chemical periodicity.
Among patients with anterior myocardial infarction, adding low-dose rivaroxaban to dual antiplatelet therapy did not significantly reduce left ventricular thrombus formation at 1 month but increased minor bleeding.
Importance Anterior acute myocardial infarction is associated with increased risk of left ventricular (LV) thrombus. The benefit and risk of adding an oral anticoagulant to dual antiplatelet therapy (DAPT) in preventing LV thrombus remain uncertain.
Objective To determine whether the addition of low-dose rivaroxaban to DAPT reduces the incidence of LV thrombus at 1 month in patients with anterior ST-segment elevation myocardial infarction (STEMI).
Design, Setting, and Participants This multicenter, open-label, blinded–end point randomized clinical trial was performed in 29 centers in France. The trial was nested in the ongoing FRENCHIE (French Cohort of Myocardial Infarction Evaluation) registry. Between October 2021 and January 2023, patients with anterior STEMI were enrolled. The last date of participant follow-up was in March 2023. Data analysis was performed from September 2024 to July 2025.
(opens in new tab)