This study presents a prefusion-stabilized vaccine candidate against Hantaan virus. The DNA and mRNA-LNP formats induce lasting neutralizing immunity in female mice, highlighting a promising advance in vaccine development.
Category: biotech/medical
Stelarc on Transhumanism: We Are in a Time of Circulating Flesh!
“We are in a time of circulating flesh.”
Stelarc said that to me 13 years ago. In 2026, it reads less like art criticism and more like a status report.
He had grown an ear on his arm. He had hung himself from hooks 25 times. He had let strangers on the internet choreograph his muscles through electrical stimulation, his body remote-controlled across continents.
Most people called it spectacle. I think it was inquiry.
Because long before deepfakes, before voice cloning, before AI agents wearing our faces, was already asking the question we now cannot avoid:
Where does the body end and the network begin?
This ‘living plastic’ activates and self-care destructs on command
Many plastic products are designed to be used only once, yet the material itself lasts for years. But a new strategy is addressing this problem by creating products that self-destruct on command, known as living plastics. These materials incorporate activatable, plastic-degrading microbes alongside the polymers. One team reporting in ACS Applied Polymer Materials used two bacterial strains that worked together and completely broke down the material within just six days, without making microplastics.
Why scientists are rethinking plastics Zhuojun Dai, a corresponding author on the paper, explains that “the realization that traditional plastics persist for centuries, while many applications, like packaging, are short-lived, led us to ask: Could we build degradation directly into the material’s life cycle?”
Many microbes can break long polymeric chains into smaller pieces using enzymes. Because plastics are polymers, these enzymes or the microbes that make them could be incorporated into living plastics.
Glucose nanoparticles help CBD cross the blood-brain barrier
Breakthrough in brain medicine: a new way to deliver CBD!
Cannabidiol (CBD) has incredible potential to fight brain inflammation, but it has always faced a major roadblock: it struggles to dissolve and cross the blood-brain barrier. Researchers have just developed an ingenious solution using glucose-coated nanoparticles to get CBD exactly where it needs to go.
Here’s why it’s a game-changer: 🔬 Sneaky Delivery: The glucose coating helps the particles “hitch a ride” on the brain’s natural glucose transporters, successfully smuggling the CBD across the blood-brain barrier. 🎯 Smart Release: Once inside the brain, the nanoparticles target immune cells (microglia) and only release the CBD when they detect the chemical stress of active inflammation. 🐁 Promising Results: In mouse models of Parkinson’s disease and depression, this new delivery method drastically reduced inflammation, protected neurons, and improved behavioral recovery compared to standard CBD.
This targeted approach could be a massive step forward in treating chronic neuroinflammatory diseases! 🧬✨
Studty.
Glucose-coated nanoparticles carry CBD across the blood-brain barrier, trigger release in inflamed tissue, and reduce neuroinflammatory signs in mice.
The Many Faces of Nonthrombotic Pulmonary Artery Embolism
Not all pulmonary emboli are thrombotic. NTPE spans septic, tumor, fat, air, and iatrogenic causes, often mimicking PE but requiring different management. Recognizing key imaging clues + clinical context is critical for timely, lifesaving diagnosis.
Nonthrombotic pulmonary artery embolism (NTPE) involves occlusion of pulmonary arteries by nonthrombotic material, such as septic emboli, tumor cells, fat, air, or foreign substances. NTPE is less common than thrombotic pulmonary embolism (PE) and may be misdiagnosed as PE. Although the clinical manifestation mimics that of PE, NTPE has distinct pathophysiologic mechanisms that necessitate different management. Diagnosis requires a high index of clinical suspicion and knowledge of imaging findings. The authors provide an overview of the various causes of NTPE, including infectious, neoplastic, iatrogenic or exogenous, and miscellaneous entities, and highlight their key imaging findings. Early and accurate diagnosis is essential for appropriate management.
©RSNA, 2026
AI is starting to beat doctors at making correct diagnoses
Researchers show that a type of AI known as a large language model often outperformed physicians at diagnosing complex and potentially life-threatening conditions, including decreased blood flow to the heart, even in the fast-moving stages of real ER care when information is limited.
In early ER cases, the model identified the correct or a very close diagnosis in about 67% of cases, compared with roughly 50% to 55% for physicians. And the technology is only getting better.
If you walk into an emergency room (ER) in 10 years, you’ll encounter a new type of caregiver: an artificial intelligence (AI) system designed to get you a diagnosis faster and help your care team make more informed decisions. While you sit in the waiting room, you’ll be hooked up to a blood pressure cuff that’s constantly and autonomously monitored. All the while, an AI agent will be listening in while you and your doctor talk about your symptoms, ready to flag any mistakes your physician makes or suggest next steps.
This vision of AI-assisted emergency health care may soon be reality. In a new study, researchers show that a type of AI known as a large language model (LLM) often outperformed physicians at diagnosing complex and potentially life-threatening conditions, including decreased blood flow to the heart, even in the fast-moving stages of real ER care when information is limited, they report today in Science. In early ER cases, the model identified the correct or a very close diagnosis in about 67% of cases, compared with roughly 50% to 55% for physicians. And the technology is only getting better.
“Evaluating AI in medicine demands both depth and breadth across different clinical tasks and settings,” and these authors were able to incorporate both in this study, says Shreya Johri, a computer scientist at the Dana-Farber Cancer Institute who was uninvolved with the new research. Still, she notes, wide adoption of these AI systems in health care will hinge on knowing the contexts in which they’re most reliable.
Biomimetic Microfibers for Myelin-Enhancer Screening and Neural Regeneration
Roles of lysosomal small-molecule transporters in metabolism and signaling
Small-molecule transporters of the lysosomal membrane export lysosomal catabolites for reuse in cell metabolism.
These transporters often show substrate promiscuity and, conversely, a given metabolite is often exported through distinct transport routes and sometimes in different states (e.g., single amino acids versus dipeptides).
Some lysosomal transporters import metabolites into the lumen. The combination of importers and exporters can create small-molecule shuttles across the lysosomal membrane, which regulate the lumen state.
Some lysosomal transporters participate in intracellular signaling cascades. sciencenewshighlights ScienceMission https://www.cell.com/trends/cell-biology/fulltext/S0962-8924(25)00222-3 https://sciencemission.com/lysosomal-small-molecule-transporters
Remyelination requires the precise wrapping of axons by oligodendrocyte processes, a critical step for restoring neural circuit function. However, a lack of quantitative systems that recapitulate axonal geometry and chemistry has limited mechanistic and pharmacological insights into myelin wrapping. Here, we present a bioengineered microfiber platform that mimics neurite architecture and surface chemistry, enabling high-content quantification of oligodendrocyte wrapping. Through compound screening, we identified dimemorfan, a clinically used sigma-1 receptor agonist, as a potent enhancer of myelin wrapping. Dimemorfan treatment accelerated remyelination and functional recovery in demyelinated mice and promoted myelin wrapping by human induced pluripotent stem cell (iPSC)-derived oligodendrocytes.
How an HIV/AIDS tragedy spurred human evolution
Researchers show that a type of AI known as a large language model often outperformed physicians at diagnosing complex and potentially life-threatening conditions, including decreased blood flow to the heart, even in the fast-moving stages of real ER care when information is limited.
In early ER cases, the model identified the correct or a very close diagnosis in about 67% of cases, compared with roughly 50% to 55% for physicians. And the technology is only getting better.
Before antiretroviral (ARV) drugs started to become widely available in KwaZulu-Natal in 2005, there was “kind of the perfect storm,” with several unusual factors coalescing to drive a devastating epidemic, says Philip Goulder, an immunologist at the University of Oxford who led the study, which appears today in the Proceedings of the National Academy of Sciences. HIV had made few inroads into South Africa until the early 1990s, when an epidemic exploded in the heterosexual population, infecting about 40% of pregnant women in KwaZulu-Natal. (That astonishingly high prevalence persists today.) Because of a mix of genetics, limited health care, and possibly the viral subtype in circulation, infected people developed AIDS—when the destruction of the immune system threatens survival—exceptionally quickly, within about 4.5 years versus 10 years in North America.
Other studies have shown how infectious diseases, including malaria and tuberculosis, have altered the human genome. But those changes took thousands of years. “That’s what is quite exciting about this: You can see how rapidly evolution actually can occur,” Goulder says.
Similar evolutionary forces may have been at work in North America and Europe, but they are more difficult to see—and less likely to affect future generations. HIV prevalence in those regions is below 1%, and the hardest-hit group is men who have sex with men. “They are generally not a population that’s leaving behind as many offspring,” Worobey notes.
Neutrophils manufacture schizophrenia-linked protein, according to new research
The most common white blood cells in your body—immune cells called neutrophils—can make a protein nobody knew they were making, Stanford Medicine investigators have discovered. That unexpected sighting joins a growing list of hints tying schizophrenia, a disorder of the brain, to events occurring elsewhere in our bodies. The findings are summarized in a paper published in Proceedings of the National Academy of Science.
The newly noticed neutrophil nexus, as a source of the protein called C4A, links a long list of other observations that are somewhat puzzling when looked at in isolation: For example, large-scale population-genetic studies have identified C4A, already known to be produced mainly in the liver, as a pronounced risk factor in schizophrenia. People with schizophrenia tend to have increased numbers of neutrophils in their blood. And the most effective medication for schizophrenia inhibits neutrophils.
Schizophrenia affects one in every 100 persons globally almost without variation by geography or ethnicity. Its most noticeable symptoms are hallucinations, delusions and fixations. A fundamental feature of the disease is cognitive impairment: inability to think clearly, reduced working memory, disorganized thinking and behavior.
SIRT6 protein could protect against age-related breakdown in chromatin, possibly help reverse aging
Researchers at Bar-Ilan University have successfully restored youthful patterns of DNA organization in the livers of old mice, reversing key molecular features associated with aging. The study, published in Nature Communications, identifies the protein SIRT6 as a powerful protector against age-related breakdown in chromatin, the complex system that packages DNA and controls how genes are switched on and off.
The findings suggest that aging is not simply a passive process of wear and tear, but may be driven in part by reversible changes in the way DNA is organized inside cells.
DNA inside cells is tightly folded and packaged into chromatin, a structure that acts like a biological control system for gene activity. Using advanced tools to study DNA organization and gene activity, the researchers examined multiple molecular changes in the livers of young and old mice. What they discovered was dramatic: aging disrupts chromatin architecture in the liver, causing inflammatory pathways to become overactive while weakening the metabolic programs that define healthy liver tissue.