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Newly discovered microprotein linked to type 2 diabetes, shows promise as a precision treatment

A previously unknown microprotein hidden within the human mitochondrial genome may help explain certain forms of type 2 diabetes and could point toward a new precision medicine approach to treating it, according to a new USC study.

Obesity and type 2 diabetes are among the fastest-growing threats to human health, yet their genetic underpinnings remain only partly understood. While most disease-gene research focuses on the larger set of DNA found in the nucleus within cells, the much smaller genome found in mitochondria—cells’ energy factories—is now known to encode a family of microproteins with wide-ranging biological effects.

The new study adds a striking example to that list, said Pinchas Cohen, the study’s senior author, USC Distinguished Professor and dean of the USC Leonard Davis School of Gerontology. The findings were published in the journal Theranostics.

Obstructive sleep apnea in people with epilepsy: Modifying risk

Obstructive sleep apnea (OSA) is a common but underdiagnosed and undertreated sleep disorder among people with epilepsy (PWE). In PWE, this sleep disorder is often managed as a comorbid condition rather than a contributor to epilepsy outcomes. For many years, OSA has been associated with higher seizure burden and interictal epileptiform discharges. Emerging evidence links OSA to late onset epilepsy (LOE) and increased risk markers for sudden unexpected death in epilepsy (SUDEP). This evidence also suggests that treating OSA with continuous positive airway pressure may improve seizure control. This critical review of the literature posits that OSA should be viewed as a modifiable risk factor for PWE. We apply the Bradford Hill criteria for causation as a framework to appraise the evidence connecting OSA with seizure severity, incident LOE, and SUDEP risk.

Oil droplets remodel themselves, swallow their surroundings like living cells

NYU researchers have made microscopic oil droplets in water do something usually reserved for living cells: change shape in complex, controllable ways and even engulf their surroundings.

The findings, published in Nature Communications, show that some of life’s signature behaviors—like morphing into complex shapes and capturing material—can emerge from physics and chemistry alone, without genes, proteins or active cellular machinery.

One of life’s defining features is morphogenesis—the ability of cells and tissues to reshape themselves, form compartments and engulf material from their surroundings. These remarkable transformations normally rely on a sophisticated molecular toolkit.

Human study links reduced inflammation to later myopia onset

University of Oklahoma College of Medicine researcher Jody Summers, Ph.D., has long hypothesized that inflammation plays a role in the development of myopia, or nearsightedness, in which close-up vision is clear but distance vision is blurry. Her laboratory experiments have been convincing, and now she has preliminary human data to support the theory.

Summers, a professor of cell biology, and R. Michael Siatkowski, M.D., MBA, professor and chair of the Dean McGee Department of Ophthalmology at the OU College of Medicine, reviewed the medical records of nearly 200 patients age 22 or younger who received eye exams at OU Health Dean McGee Eye Institute. About half were healthy, while the rest had juvenile idiopathic arthritis (JIA) and were being treated with anti-inflammatory drugs. They were having exams because JIA, an autoimmune disease that causes chronic inflammation, can affect the eyes.

The research was presented at the 2026 ARVO Annual Meeting, held in Denver, CO, May 3–7, 2026.

A digitally controlled silicon quantum processing unit

A silicon quantum processing unit executes high-fidelity multiqubit circuits, with all time-varying control signals generated by a digitally programmed cryogenic complementary metal–oxide–semiconductor controller and delivered to the low-noise, exchange-only qubit device through a high-density superconducting ribbon cable.

AI tech proactively prevents subway door entrapment accidents

A research team led by Professor Jo Woon Chong of the School of Electronic and Electrical Engineering at Sungkyunkwan University (SKKU), in collaboration with researchers from KAIST and Texas Tech University in the United States, has developed the Passenger Movement Estimation System (PMES). This AI-based system predicts passenger movements using CCTV footage to prevent subway door entrapment accidents before they occur.

Overcoming the limitations of conventional reactive methods, in which sensors trigger only after a passenger has entered the danger zone, the system proactively identifies risks before passengers reach the boarding area. The findings are published in IEEE Transactions on Intelligent Transportation Systems.

Chong, who has led research at Sungkyunkwan University on human-centered AI, multimodal signal processing and AI-embedded systems, oversaw the study. Hee Jo, the first author and a Ph.D. student, led the data analysis and AI model design.

Personalized gene therapy helps teen with rare form of severe epilepsy walk independently

SCN2A-related developmental epileptic encephalopathy (DEE) is a rare, severe form of childhood epilepsy and one of the most common causes of monogenic autism. The condition is caused by single mutations in the sodium voltage-gated channel alpha subunit (SCN2A) gene, which controls the flow of sodium ions into neurons. These mutations promote abnormal brain excitability, resulting in uncontrolled seizures along with developmental delays, autism, movement problems and gastrointestinal issues. Most of these mutations are de novo (not inherited from a parent) and arise spontaneously.

Traditional antiseizure medications are often ineffective and do not address the underlying genetic cause of SCN2A-related DEE.

Now, an international team of researchers led by the University of California San Diego and Rady Children’s Institute for Genomic Medicine has treated two children with the condition using gene therapy tailored to each child’s specific SCN2A mutation.

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