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Scientists capture superconductivity’s ‘dancing pairs’ for first time, revealing missing pieces in a decades-old theory

For the first time, scientists have directly imaged the quantum process underlying superconductivity, a phenomenon in which paired electrons cause electric current to flow without resistance at sufficiently low temperatures. The results weren’t quite what they expected.

In the study, published April 15 in Physical Review Letters, the scientists directly imaged individual atoms pairing up in a special gas cooled nearly to absolute zero—the unreachable limit to how cold things can get. The type of gas, called a Fermi gas, allows scientists to substitute electrons with atoms and probe the physics of superconductors in a controlled way.

Surprisingly, the scientists found that after pairing up, the atoms moved in a synchronized dance, with their positions dependent on those of other pairs—a phenomenon not predicted by the 70-year-old, Nobel-prize-winning theory of superconductivity.

Multitasking quantum sensors can measure several properties at once

A special class of sensors leverages quantum properties to measure tiny signals at levels that would be impossible using classical sensors alone. Such quantum sensors are currently being used to study the inner workings of cells and the outer depths of our universe.

Particularly promising are solid-state quantum sensors, which can operate at room temperature. Unfortunately, most solid-state quantum sensors today only measure one physical quantity at a time—such as the magnetic field, temperature, or strain in a material. Trying to measure both the magnetic field and temperature of a material at the same time causes their signals to get mixed up and measurements to become unreliable.

Now, MIT researchers have created a way to simultaneously measure multiple physical quantities with a solid-state quantum sensor. They achieved this by exploiting entanglement, where particles become correlated into a single quantum state. In a new paper, the team demonstrated its approach in a commonly used quantum sensor at room temperature, measuring the amplitude, frequency, and phase of a microwave field in a single measurement. They also showed the approach works better than sequentially measuring each property or using traditional sensors.

AI chatbot teaches AI ‘student’ to love owls, even after data is scrubbed

Large language models (LLMs) can teach other algorithms unwanted traits, which can persist even when training data has been scrubbed of the original trait, according to new research published in Nature. In one example, a model seems to transmit a preference for owls to other models via hidden signals in data. The findings demonstrate that more thorough safety checks are needed when producing LLMs.

LLMs can generate datasets to train other models through a process called distillation, in which a “student” model is taught to mimic the outputs of a “teacher” model. While this process can be used to produce cheaper versions of an LLM, it is unclear which properties of the teacher model are transferred to the student.

Alex Cloud and colleagues used GPT-4.1, which was prompted to have traits unrelated to a core task (a preference for owls or certain trees, for instance), to train a student model with output consisting only of numerical data, with no references to the trait. When the resulting student was subsequently prompted, it mentioned the teacher’s favorite animal or tree over 60% of the time, compared to 12% for a student trained by a teacher with no favorite animal or tree. This effect was also observed when the student was trained on a teacher’s output that contained code instead of numbers.

Abstract: Immune signaling and function in neurodegeneration:

Yvonne L. Latour & Dorian B. McGavern contribute a Review to the JCI Series on Neurodegeneration, discussing signaling pathways, cellular players, and immune responses shared across multiple neurodegenerative diseases, while considering external factors that may influence CNS disease progression. Neurodegeneration.

Viral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.

Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus

Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older.

Until now.

A landmark study from researchers at the Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

Led by Dr. Ashok Shetty, university distinguished professor and associate director of the Institute for Regenerative Medicine, along with senior research scientists Dr. Madhu Leelavathi Narayana and Dr. Maheedhar Kodali, the team developed a nasal spray that, with just two doses, dramatically reduced brain inflammation, restored the brain’s cellular power plants and significantly improved memory.

The most surprising part? It all happened within weeks and lasted for months.

The findings, published in the Journal of Extracellular Vesicles, could reshape the future of neurodegenerative therapies and may even change how scientists think about brain aging itself.

Continue reading “Intranasal Human NSC‐Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS‐STING Signalling, in Aged Hippocampus” | >

Scientists Just Took A Major Step Towards One Of Sci-Fi’s Biggest Tropes

Major milestone in the viability of cryonic suspension in the form of revival of cells after vitrification. Vitrification is basically the use of chemical fixation at ultra cold temperatures, kinda like antifreeze. It prevents ice crystals forming in your cells, preventing them from being torn apart.

It’s INSANELY toxic, so solving that problem would mean we can really revive people in suspension who underwent vitrification (which is standard practice at ALCOR for a long time now).

That said, we still will need ways to repair whatever disease or injury that the patient actually died from. 😁👍

Researchers in Germany have developed a technique to vitrify mouse brain tissue and then thaw it out, all without significant loss of function.

Human Gene Editing Has Begun | George Church

We are already gene editing humans. You just haven’t noticed.

George Church, Harvard geneticist and Human Genome Project pioneer, explains why CRISPR wasn’t the real breakthrough, how multiplex gene editing unlocked organ transplants and de-extinction, and why aging will likely require rewriting many genes at once.

Hosted by Mgoes → https://twitter.com/m_goes_distance
Brought to you by SuperHuman Fund → https://superhuman.fund/

0:00 — Gene Editing Mammals → Humans
8:36 — Germline vs Somatic
14:56 — Modified Humans Are Already Here
18:50 — Enhancing Healthy Humans
25:00 — Aging Therapies vs Cognitive Enhancement
30:20 — Embryo Selection
38:10 — Is US Losing To UAE?
42:33 — Biotech Failures
49:31 — Next Dire Wolf Moment
54:21 — AI x Science
1:02:07 — Synthetizing Entire Genomes.

The Accelerate Bio Podcast explores the future of humanity in the age of Artificial Intelligence. Subscribe for deep-dive conversations with founders, scientists, and investors shaping AI, biotechnology, and human progress.

This episode discusses George Church, gene editing, CRISPR, human enhancement, longevity, aging, embryo selection, synthetic biology, multiplex editing, AI biotech.

Continue reading “Human Gene Editing Has Begun | George Church” | >

Genetic atlas reveals how human liver cells divide their labor

If scientists could shrink themselves to microscopic size and take a journey through the human body—like the submarine crew in the 1966 science fiction classic “Fantastic Voyage”—one of their first stops would no doubt be the liver. The unique structure of our largest internal organ comprises small, hexagonal functional units called lobules, each carrying out more than 500 functions simultaneously. Studies from the 1970s and 1980s revealed that liver cells divide these many tasks among themselves according to their location within each subunit; however, the technology available at the time provided only a blurred picture of this division of labor.

In a new study published in Nature, scientists from the Weizmann Institute of Science, together with colleagues at Sheba Medical Center and the Mayo Clinic, present the first genetic atlas of a healthy human liver at a resolution of 2 microns. The findings show that the division of labor in the human liver differs from that of other mammals and is more extensive than previously recognized, helping explain why certain regions of the liver are particularly vulnerable to fatty liver disease.

In recent years, technological advances have made it possible to identify which genes are active in each individual cell while also mapping the cells’ precise spatial positions within the tissue. Still, a comprehensive map of functional division in the human liver remained elusive, largely due to the difficulty of obtaining tissue samples from healthy donors.

AARS1-mediated lactylation of STAT1 drives immune evasion

Du et al. demonstrate that AARS1-mediated STAT1 K193 lactylation blocks JAK2 binding and STAT1 phosphorylation, which impairs IFN-γ signaling, reducing chemokine expression and promoting immune escape. Inhibition of this modification with the cell-penetrating peptide K193-pe restores IFN-γ responsiveness, enhances CD8+ T cell recruitment, and improves immune checkpoint therapy efficacy.

By cutting selected synapses, brain circuit ‘editing’ could make memory stronger and rewire how learning works

Every thought, memory, and feeling we experience depends on trillions of tiny connection points in the brain called synapses. These are the junctions where one neuron passes signals to another, forming the vast communication network known as the connectome—the brain’s wiring diagram. Although scientists have developed powerful tools to increase or decrease neural activity, directly redesigning the brain’s physical wiring has remained far more difficult.

A research team led by Dr. Sangkyu Lee and Director C. Justin Lee at the Center for Memory and Glioscience within the Institute for Basic Science (IBS), in collaboration with Dr. Kea Joo Lee of the Korea Brain Research Institute (KBRI), has now developed a molecular tool that makes such structural editing possible. The new platform, called SynTrogo (Synthetic Trogocytosis), enables researchers to induce astrocytes to selectively remodel synaptic connections in a targeted brain circuit. The paper is published in the journal Nature Communications.

The brain already has a natural mechanism for refining its wiring. During development and throughout life, unneeded or weak connections are removed in a process known as synaptic pruning, much like trimming unnecessary branches from a tree. This pruning is partly carried out by astrocytes—star-shaped glial cells that closely surround synapses and help maintain the neural environment. When this process becomes dysregulated, either through too much or too little pruning, it has been linked to disorders such as schizophrenia, autism spectrum disorder, and Alzheimer’s disease.

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