Physicists working on the LHCb experiment have spotted an elusive and fleeting particle, a heavier and more charming cousin to the proton, that has been sought for decades
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Striped or checkered? Magnetic field influences competing electronic patterns in a graphene-like quantum material
In most everyday materials, such as copper, silver and silicon, the behavior of electrons is relatively predictable. In quantum materials, however, electrons can interact in complex ways, giving rise to collective electronic states with remarkable properties. Understanding how these states emerge—and, ultimately, how to control them—is one of the central challenges in quantum materials research.
Now, researchers from the Okinawa Institute of Science and Technology (OIST) and Hiroshima University have discovered that a small magnetic field switches the layered quantum material CeTe₃ between competing electronic states that appear as striped or checkerboard patterns.
Published in Nature Communications, the work reveals how magnetism can reorganize a quantum material’s entire electronic state.
Obesity-derived metabolites modulate anti-tumor immunity in the tumor microenvironment: from mechanisms to clinical applications
The tumor microenvironment (TME) is increasingly understood as a metabolically dynamic ecosystem in which local metabolite availability, composition, and trafficking shape immune cell fitness and therapeutic responsiveness. Against the backdrop of the global obesity epidemic, obesity-associated systemic metabolic dysregulation has been implicated in tumor initiation and progression and may also influence the immune contexture and treatment responsiveness of tumors. This Review examines how obesity-derived systemic metabolites may modulate anti-tumor immunity and influence cancer immunotherapy, with particular emphasis on pathways involved in metabolic reprogramming and TME remodeling. We further discuss intervention strategies spanning (i) upstream metabolite generation, (ii) systemic-to-local trafficking into the TME, and (iii) direct functional antagonism within the TME.
This is one of the biggest stars in the Universe. Scientists say it looks like it’s about to explode
Star WOH G64 could be about to explode, and its extreme transition offers a rare opportunity to witness stellar transformations in real time.
The Surprising Evidence our Universe is INSIDE a Black Hole
What if everything we know — every galaxy, every star, every atom — is actually inside a black hole? In this video, we explore the fascinating possibility that our entire universe could exist within a black hole embedded in a larger “parent” universe. This idea isn’t science fiction; it arises from real solutions to Einstein’s equations in general relativity and from modern efforts to connect gravity with quantum mechanics. We examine what physics predicts happens inside a black hole, how space and time behave at an event horizon, and why the Big Bang might resemble the birth of a black hole from the outside.
We also explore the deeper implications of this theory: whether a collapsing star in another universe could create a new expanding universe on the inside, how spin and entropy might relate to cosmic expansion, and what this could mean for the concept of a multiverse. Could every black hole be the seed of a new universe? And if so, what does that say about where we came from and the true structure of reality? This is one of the most mind-bending ideas in cosmology — and it challenges our very notion of what “inside” and “outside” even mean.
Three genetic modifiers may alter inherited Alzheimer’s onset and progression
Autosomal dominant Alzheimer’s disease (ADAD) is a genetically inherited form of Alzheimer’s disease that accounts for only about 1% of Alzheimer’s disease cases. However, because individuals with the gene mutations are extremely likely to develop Alzheimer’s disease at an early age, and because the mutation is highly heritable, ADAD is widely studied by Alzheimer’s disease researchers.
A new study by WashU Medicine researchers and collaborators, published in The Lancet Neurology, identified variants in three other genes that seem to change how Alzheimer’s disease presents in people with ADAD mutations. Pinpointing these and other genetic factors that affect Alzheimer’s disease development and progression may allow investigators to provide more effective genetic counseling for families, design clinical trials and develop new treatments to prevent or slow Alzheimer’s disease in the larger population.
Previous studies had already identified three key genes—amyloid precursor protein (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2)—that are associated with ADAD, as well as 279 variants in those genes that lead to Alzheimer’s disease. What remains unclear, however, is what leads to differences in disease onset and progression among individuals who have a disease-causing variant. For instance, even if a person carries an APP, PSEN1 or PSEN2 mutation and is therefore very likely to develop early-onset Alzheimer’s, there is variability in when symptoms of cognitive decline might begin, even among individuals who have the same disease-causing mutation.
Creating a healthspan digital twin: A new era for humanity to better living — Jul 30
Zahi A. Fayad, PhD, is the Lucy G. Moses Professor of Medical Imaging and Bioengineering at the Icahn School of Medicine at Mount Sinai, where he also serves as Vice Chair for Research in Radiology and holds professorships in Medicine (Cardiology) and AI & Human Health. He is the founding Director of the BioMedical Engineering and Imaging Institute (BMEII), home to one of the nation’s top NIH-funded radiology programs (#2 in 2025 per Blue Ridge rankings). Dr. Fayad also co-leads Mount Sinai’s system-wide Healthspan initiative, coordinating research, clinical, and digital infrastructure to advance precision prevention across the enterprise.
Dr. Fayad is Principal Investigator on multiple major grants, including five NIH-funded projects (3 R01s, 2 P01s) supported by the National Heart, Lung, and Blood Institute, NIAID, and NIDA. A leader in biomedical engineering, his interdisciplinary work integrates advanced imaging, AI, and nanomedicine to drive precision medicine, with research interests focused on how lifestyle stressors — chronic stress, diet, exercise, and sleep — affect long-term cardiovascular and whole-person health.
A Clarivate Highly Cited Researcher since 2018 (~190,000 citations; h-index 142), Dr. Fayad’s seminal contributions include MRI vessel wall imaging (leading to Carotid Plaque-RADS), FDG PET imaging of vascular inflammation, and defining the link between amygdala activity, systemic inflammation, and cardiovascular risk. His research on HDL-based nanoparticles for immune modulation is progressing toward clinical translation for cancer, autoimmune diseases, and transplant rejection — work he is advancing commercially as co-founder of Trained Therapeutix Discovery (TTxD), an early-stage biotech company. He is also a recipient of the Jean Paul II Award for Medicine and Research.
His current projects span cardiovascular, neuroimmune, and transplant-focused research, including stress-induced immune dysregulation; mitral valve prolapse and arrhythmia risk; cocaine use–related carotid atherosclerosis and cognitive impairment; cardiac sarcoidosis therapy monitoring; and immune tracking in organ rejection using nanobiologics — together shifting care upstream toward risk prediction and intervention before clinical events.
He also leads the Mount Sinai DigiTwin Project, an AI-driven platform designed to personalize health optimization by integrating imaging, multi-omics, and real-time physiologic data — initially focused on cardiovascular health and now expanding to whole-person healthspan modeling. Dr. Fayad and colleagues at Mount Sinai are finalists in the $80m XPRIZE Healthspan competition, where they are evaluating a multimodal strategy to meaningfully extend human healthspan.