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Objectively Measured Daytime Napping and All-Cause Mortality in Older Adults

Among older adults, longer and more frequent daytime napping, especially in the morning, was associated with higher AllCauseMortality, supporting wearable sleep assessment for risk evaluation.

Question Are objectively measured daytime nap characteristics, including duration, frequency, variability, and timing, associated with all-cause mortality among community-dwelling older adults?

Findings In this prospective cohort study of 1,338 adults aged 56 years or older, longer and more frequent daytime napping, as well as morning napping, were associated with higher all-cause mortality. Variability in nap duration was not associated with mortality.

Meaning The findings suggest longer and more frequent, particularly morning, napping may be a behavioral marker of increased mortality risk in late life, underscoring the potential clinical value of incorporating wearable device–based nap assessments into routine health monitoring.

Protein’s second role in inflammation could reshape treatment for Crohn’s, arthritis and heart disease

A protein long understood to drive inflammation by producing nitric oxide has a second, previously unknown role—it physically binds to another key protein inside cells to directly modulate the immune response. The discovery, published in Nature Metabolism, could open new routes to treating conditions such as cardiovascular disease, arthritis, Crohn’s and other inflammatory diseases.

When the immune system detects infection or injury, it triggers inflammation to fight back. That response is essential, but it must be carefully controlled. If it runs too hard for too long, it causes the tissue damage that underlies many chronic diseases. Understanding the molecular switches that regulate inflammation—and finding new ways to target them—is one of the biggest challenges in modern medicine.

Researchers from the University of Surrey and the University of Oxford have identified one such switch. They have shown that inducible nitric oxide synthase (iNOS)—a protein that produces nitric oxide during inflammation—can also bind directly to a second protein, IRG1, inside mitochondria. That physical interaction blocks IRG1 from producing itaconate, a metabolite that acts as a brake on the inflammatory response.

Abstract: Expanding clones, expanding aneurysms through macrophage-to-osteoclast differentiation:

Jessica A. Regan & Svati H. Shah Comment on Yonekawa et al.: https://doi.org/10.1172/JCI198708 aneurysm.

Address correspondence to: Jessica A. Regan, Duke Molecular Physiology Institute Duke University School of Medicine, 300 N. Duke Street, Carmichael Building, Durham, North Carolina, 27,701, USA. Email: [email protected].

Real-time impedance-based cell migration measurements with integrated electrodes on porous membranes for next generation microphysiological systems

A new laboratory technique for measuring how quickly cells penetrate and pass through a porous membrane and reach the opposite side could help identify cancer cells with the greatest potential to spread in the human body.

The method relies on tiny electrodes placed on either side of an artificial membrane. The electrodes measure changes in electrical resistance as cells pass through the material. The most aggressive cancer cells pass through the membrane more rapidly than other cells.

The illustration depicts cells (green and blue) moving through a membrane (grey) studded with microelectrodes (gold rings).

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We present a novel microfluidic device capable of electrically interrogating both surfaces of a porous membrane quantitatively and in real time using electrical impedance spectroscopy to monitor cell migration. This device holds patterned gold electrodes on both sides of the membrane, which enable independent impedance measurements on each side of the membrane. We introduce the term cross-over cell migration (CoCM) to describe this dual-sided approach, which allows precise monitoring of cells at their seeding location and as they move through a porous membrane. To ensure reliable tracking, we developed a normalization method, the CoCM index, that allows us to compare both membrane surfaces directly in real-time. Human renal carcinoma cells (786-O) were passively seeded in the device’s top microfluidic chamber, and we collected impedance data from both sides of the membrane surfaces simultaneously over a three-day period. These measurements successfully captured the onset and progression of cell migration across the membrane interface. We tracked the cells with fluorescence imaging in parallel to validate our impedance data. As cells appeared in focus on the bottom-side electrode surface, their numbers kept increasing over the course of our experiment. The CoCM index decreased by about 20% in the top chamber and increased by approximately 15% in the bottom chamber. Symmetrical CoCM index trends appeared after 40 h, consistent with the fluorescent images captured. Finally, we performed live-cell fluorescence assays to confirm post-experiment cell viability and to quantify migrated cells, further validating our CoCM platform measurements. This platform is a valuable tool not only for real-time and quantitative cell migration studies of cancer and other cells in bulk but also for future studies of single-cell migration processes.

This artificial retina doesn’t just aim to restore sight—it opens a hidden channel of vision

The retina, the thin layer of tissue at the back of the eye, is made up of photoreceptor cells that convert visible light into electrical signals, which is essential for human vision. Some diseases, such as retinal degeneration, cause these photoreceptor cells to stop working, which results in blindness. Researchers at Yonsei University, the Institute for Basic Science (IBS) and other institutes in the Republic of Korea have recently developed a new artificial retina that could partly restore vision in people with damaged retinas.

The new device, introduced in a paper published in Nature Electronics, works by detecting near-infrared light and converting it into electrical signals, which stimulate another type of cells in the retina that are undamaged.

“Many people suffer from blindness due to retinal diseases that cause photoreceptor degeneration,” wrote Won Gi Chung, Inhea Jeong and their colleagues in their paper. “Electrical stimulation of retinal neurons can recreate the action potentials associated with seeing that are generated by these cells. We report a thin artificial retina that can be adhered to the epiretinal surface and can convert near-infrared (NIR) light into electrical stimuli that selectively stimulate ganglion cells.”

Machine learning identifies catalyst ‘sweet spot’ for greener urea from waste gases

Urea is an extremely important chemical, especially for fertilizers. But, making urea is energy intensive and relies heavily on fossil fuels. However, new findings from Griffith University and the Queensland University of Technology have highlighted new ways to produce urea electrochemically, using electricity and waste gases such as carbon monoxide (CO) and nitrogen oxides (NO) instead.

The paper, “Machine Learning-Assisted Design Framework of Carbon Edge-Dominated Dual-Atom Catalysts for Urea Electrosynthesis,” has been published in ASC Nano.

“The challenge is that when CO and NO react on a catalyst, they usually don’t form urea,” said co-lead author Professor Qin Li from Griffith University.

Subversion of kynurenine-induced AHR activation in CD8 T cells by kynureninase-expressing antigen-presenting cells

Giacomantonio et al. demonstrate an immunomodulatory role for a metabolic enzyme kynureninase in antigen-presenting cells (APCs). Kynureninase-expressing APCs degrade kynurenine, including that generated by cancer cells, and relieve kynurenine-induced immunosuppression in CD8+ T cells.

Gene therapy for deafness approved

The world’s first gene therapy for deafness received approval from the U.S. Food and Drug Administration today. The treatment, from biotech company Regeneron, targets hearing loss caused by inherited mutations in the OTOF gene, which encodes otoferlin, a protein that allows the inner ear’s hair cells to sense and transmit sound to the brain. Patients receive a one-time ear injection containing viral vectors that carry a working copy of the OTOF gene into their cells. In a clinical trial, nine of 12 deaf children who initially received the Regeneron therapy gained enough hearing to stop using cochlear implants; three within that group ended up having normal hearing. Although many gene therapies cost $1 million or more, Regeneron said its treatment, called Otarmeni, will be free in the United States.

Eli Lilly & Co. and researchers in China are also developing gene therapies for OTOF mutations, which account for up to 3% of cases of inherited deafness. One U.S.-Chinese team reported in Nature this week that among 24 patients, including some adults, hearing improvements have lasted more than 2 years in some cases, NPR reports. Researchers eventually hope to treat other types of genetic deafness as well, but those attempts face more challenges. For example, for some disorders, it may be necessary to regenerate lost hair cells. In others, targeting the wrong cell type could damage hearing.

Label-free optical imaging enables automated measurement of human white matter microstructure

White matter pathways allow distant parts of the brain to communicate, supporting memory, emotion, and language. One such pathway, the uncinate fasciculus, connects the front of the temporal lobe with regions of the frontal cortex involved in decision-making and social behavior. Despite its importance, little is known about the microscopic structure of this tract in the human brain.

Traditional techniques such as electron microscopy can reveal fine details, but they often fail when applied to postmortem human tissue, which is frequently degraded.

In a study published in Biophotonics Discovery, researchers report a new way to examine white matter structure in postmortem human brains.

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