Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Get the latest international news and world events from around the world.

Log in for authorized contributors

Feedback neurons based on perovskite memristor with nickel single-atom engineered reduced graphene oxide cathode

Scientists have long looked to the human brain as the ultimate blueprint for computing, seeking to build “neuromorphic” systems that process information with the same efficiency and flexibility as our own neurons. However, replicating the brain’s complex ability to both excite and inhibit signals—essentially “talking” and “listening” simultaneously—has proven difficult with standard hardware.

The problem? Perovskites are often too chaotic. Tiny charged particles called ions tend to zip around inside the material too quickly, making the device’s behavior hard to control. Additionally, the “bottlenecks” (barriers) where the electricity enters the device often cause lopsided performance, preventing the smooth, bidirectional communication required for advanced brain-like tasks.

Li et al. report feedback neurons based on perovskite memristors with a nickel single-atom modified reduced graphene oxide cathode. The device successfully implements an unsupervised learning network with over 50% clustering accuracy and cooperative learning for solving NP-hard combinatorial optimisation problem.

Nobel Prize in Physics 1903

The Nobel Prize in Physics 1903 was divided, one half awarded to Antoine Henri Becquerel “in recognition of the extraordinary services he has rendered by his discovery of spontaneous radioactivity”, the other half jointly to Pierre Curie and Marie Curie, née Skłodowska “in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel”

How dietary restriction rewires immunity to protect against infection

To understand the complex interactions involved in an immune response during scarcity, the team put mice on a 50% restricted-calorie diet and then exposed the animals to bacteria that infect the gut. The mice that were fed a standard diet experienced a metabolic crash— their blood glucose levels and body weight plummeted.

The researchers had expected this would happen to all the animals because mounting an immune response can consume up to 30% of the entire body’s fuel reserves. But in the calorie-restricted mice, the immune system appeared to be functioning perfectly well without using much glucose.

To unravel this enigma, the researchers inventoried the immune cells of the infected animals and discovered that T cells, which normally target invading microbes, were depleted in the calorie-restricted mice. Instead, short-lived neutrophils, which serve as the body’s first responders to infection, were ramped up to twice the normal amount and had measurably enhanced pathogen-killing abilities. The cells seemed to be operating in energy-saving mode, consuming much less glucose than neutrophils from well-fed animals.

The researchers are breaking new ground by outlining how a sudden fall in food intake triggers glucocorticoid levels to rise, resulting in two major shifts. First, the body repositions certain immune cells—especially naïve T cells—into the bone marrow, which becomes a kind of “safe house” for when the cells are needed. Second, during an infection, glucocorticoids tilt the immune response away from energy-intensive T cells toward neutrophils, abundant cells that act as immediate, short-lived defenders.

Beyond clearing a current infection, glucocorticoids prepare the immune system for repeat encounters with infectious agents. While the hormones direct killer T cells to stand down and neutrophils to step up, they also ensure memory T cells are preserved for future confrontations.

When food is scarce, stress hormones direct the immune system to operate in “low power” mode to preserve immune function while conserving energy, according to researchers. This reconfiguration is crucial to combating infections amid food insecurity.

Continue reading “How dietary restriction rewires immunity to protect against infection” | >

NAD+ sensing by PARP7 regulates the C/EBPβ-dependent transcription program during adipogenesis

Stokes et al. demonstrate that PARP7 “senses” the levels of nuclear NAD+ during early adipogenic differentiation via an ADP-ribosylation-ubiquitin-proteasome pathway to regulate C/EBPβ-dependent proadipogenic gene expression through p300-mediated H3K27 acetylation. Stabilized PARP7 promotes the binding of C/EBPβ to chromatin genome-wide, enhancing lipid synthesis and adipogenesis in vivo.

A neuron subtype-specific role of MEK-ERK signaling in axon survival via transcriptional regulation of Nmnat2

Yue et al. find the subtype-specific regulation of Nmnat2 transcription by Raf-MEK-ERK in DRG neurons, while cortical and spinal neurons use a MEK-independent mechanism. This context-dependent axon survival paradigm helps explain differential MEKi vulnerability of PNS and CNS neurons, indicating Nmnat2 as a potential target to counteract MEKi-induced neuropathy.

Genetic defect that weakens esophageal lining identified!

But the molecular factors responsible for the onset of Barrett’s esophagus remain poorly understood.

The findings, published in Nature Communications, combined family studies, laboratory experiments and genetically engineered mouse models to identify and understand how genetic defects contribute to disease development.

The team sequenced and analyzed genetic material of 684 people from 302 families where multiple members developed Barrett’s esophagus or esophageal cancer. They discovered that a subset of affected family members carry inherited mutations in a gene called VSIG10L.

“We found that this gene acts like a quality control system for the esophageal lining,” said the lead researcher. “When it’s defective, the cells do not mature properly and the protective barrier in the esophageal lining becomes weak, allowing stomach bile acid to cause tissue changes that enhances the risk of developing Barrett’s esophagus.”

When researchers genetically engineered mice with human-equivalent VSIG10L mutations, they found that the esophageal lining became disrupted structurally and molecularly, according to the author. The study found that when the mice were exposed to bile acid, they developed Barrett’s-like disease over time, effectively replicating the disease’s progression in humans.

These genetically engineered mice also represent the first animal model for Barrett’s esophagus based directly on human genetic predisposition to the disease, the author said.

With VSIG10L shown to be a key gene in maintaining esophageal health, family members can now be screened for genetic variants to identify those at a high-risk of developing Barrett’s esophagus or esophageal cancer. ScienceMission sciencenewshighlights.

Continue reading “Genetic defect that weakens esophageal lining identified!” | >

Hair-width LEDs could eventually replace lasers

LEDs no wider than a human hair could soon take on work traditionally handled by lasers, from moving data inside server racks to powering next-generation displays. New research co-authored by UC Santa Barbara doctoral student Roark Chao points to a practical path forward. The study is published in the journal Optics Express.

“We’re talking about devices that are literally the size of a hair follicle,” said Chao, who studies electrical engineering. “If you can engineer how the light comes out, those microLEDs can start to replace lasers in short-distance data communication.”

The work builds on UCSB’s longstanding strengths in gallium nitride research and optoelectronics. Chao is co-advised by Steven P. DenBaars and Jon A. Schuller, both co-authors on the study, which also includes Nobel laureate Shuji Nakamura, whose pioneering work on blue LEDs transformed global lighting and display technologies. The research was conducted in the laboratories of the DenBaars/Nakamura and Schuller groups, where teams focus on gallium nitride materials growth and nanoscale photonics.

A new form of aluminum unlocks sustainable and cheaper catalysts

A research team at King’s College London has isolated a new form of aluminum—a highly abundant metal, that could provide a far cheaper and more sustainable alternative to commonly used rare earth metals. Dr. Clare Bakewell, Senior Lecturer in the Department of Chemistry, and her lab developed highly reactive aluminum molecules able to break apart tough chemical bonds. Published in Nature Communications, their work has also unlocked molecular structures that have never been observed before, which creates the potential for new kinds of reactive behavior.

The team reported the first example of a cyclotrialumane, a compound comprising three aluminum atoms arranged in a trimeric—triangular—structure. The trimeric molecule carries unprecedented reactivity as the structure is retained when dissolved into different solutions, making it robust enough for use in a range of chemical reactions. These include splitting dihydrogen and the stepwise insertion and chain growth of the 2-carbon hydrocarbon, ethene.

Metals are vital for making a whole range of commodity and fine chemicals produced in industry. However, many processes, especially catalytic ones, use expensive precious materials like platinum, which are environmentally damaging to extract.

/* */