The interplay between the circadian clock, intestinal stem cell niche, and epithelial cell fate is shaping our understanding of how gut homeostasis and cellular regeneration are regulated. Recent insights reveal that the circadian rhythm, a fundamental 24-hour cycle regulating numerous physiological functions, plays a crucial role in maintaining intestinal health by coordinating the proliferation and differentiation of intestinal epithelial cells.

Botulism outbreaks highlight the need for detection of food contamination at point of use. Printed on the inside of a jar lid, for example, a biosensing ink can tell the consumer if the product they are about to consume is sterile or contaminated by a simple change in color.

A research team explores how tea plants absorb, transport, and tolerate fluoride, shedding light on the mechanisms behind fluoride accumulation.

Neutralizing antibodies that merely block receptor binding are losing ground against heavily mutated SARS-CoV-2 Omicron sub-variants. A new approach now exploits a llama-derived nanobody—VHH21—that does not just bind the spike (S) protein but actively tears the trimer apart within seconds. Bactrian camels were immunized with a cocktail of recombinant S proteins from ancestral and VOC strains, yielding a high-diversity VHH phage library. Multi-round biopanning and BLI screening singled out six nanomolar-affinity binders; VHH21, which spontaneously dimerizes, stood out by destroying 68 % of surface-immobilized S-trimers in 20 min, far outperforming ACE2 or conventional nanobodies.

The Korea Research Institute of Standards and Science (KRISS, President Lee Ho Seong) has developed a diagnostic platform that amplifies the unique optical signals of molecules by more than a hundred million times, enabling the precise detection and quantification of trace amounts of Alzheimer’s disease biomarkers in body fluids.

The rise of large-scale artificial intelligence (AI) models, such as ChatGPT, DeepSeek, and autonomous vehicle systems, has significantly advanced the boundaries of AI, enabling highly complex tasks in natural language processing, image recognition, and real-time decision-making. However, these models demand immense computational power and are often centralized, relying on cloud-based architectures with inherent limitations in latency, privacy, and energy efficiency. To address these challenges and bring AI closer to real-world applications, such as wearable health monitoring, robotics, and immersive virtual environments, innovative hardware solutions are urgently needed. This work introduces a near-sensor edge computing (NSEC) system, built on a bilayer AlN/Si waveguide platform, to provide real-time, energy-efficient AI capabilities at the edge. Leveraging the electro-optic properties of AlN microring resonators for photonic feature extraction, coupled with Si-based thermo-optic Mach–Zehnder interferometers for neural network computations, the system represents a transformative approach to AI hardware design. Demonstrated through multimodal gesture and gait analysis, the NSEC system achieves high classification accuracies of 96.77% for gestures and 98.31% for gaits, ultra-low latency (< 10 ns), and minimal energy consumption (< 0.34 pJ). This groundbreaking system bridges the gap between AI models and real-world applications, enabling efficient, privacy-preserving AI solutions for healthcare, robotics, and next-generation human–machine interfaces, marking a pivotal advancement in edge computing and AI deployment.

Vascular aging is a silent but powerful driver of many age-related diseases, from heart attacks to dementia. Over time, our arteries lose elasticity, accumulate damage, and struggle to deliver oxygen and nutrients where they are needed most. This review reveals how a network of biological processes—endothelial dysfunction, oxidative stress, chronic inflammation, and cellular senescence—converge to weaken blood vessels. By mapping the key biomarkers that flag early vascular decline and exploring strategies to counteract it, the findings offer a blueprint for interventions that could slow, halt, or even reverse this decline. Such advances may help extend not just lifespan, but the number of years lived in good health.

For decades, Alzheimer’s disease (AD) research has focused on its visible villains—amyloid plaques and tau tangles. But beneath the surface, another player may be quietly steering the disease’s course: lipid metabolism. Lipids, the essential substances that build and fuel the brain, are proving to be powerful influencers of disease progression. When their balance falters, harmful proteins accumulate, synapses weaken, and inflammation spreads. This new review pulls together cutting-edge findings that link genetic risk factors, like APOE4, to disrupted cholesterol transport, faulty fat storage, and poor lipid clearance—unveiling a hidden layer of AD biology and pointing toward untapped therapeutic strategies.