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Two prostate cancer mutations reveal opposite responses to ferroptosis therapy

A new study by researchers at The University of Texas MD Anderson Cancer Center has identified genetic factors that determine whether prostate cancers are susceptible to a type of cell death known as ferroptosis. These findings, published in Nature Communications, could help guide treatment strategies for patients whose tumors do not respond to current treatment options.

The study was led by Di Zhao, Ph.D., associate professor, and Boyi Gan, Ph.D., professor, both of Experimental Radiation Oncology.

“Prostate cancer is such a genetically diverse cancer that there are many possible treatment options, so getting patients on the right treatment as quickly as possible is crucially important,” Zhao said. “The two genetic findings in this study could help identify some patients who are more likely to respond, as well as some patients who are significantly less likely.”

The world’s first ultra-compact semiconductor chip for biosignal measurement

A research team led by Prof. Junghyup Lee of the Department of Electrical Engineering and Computer Science at DGIST has become the first in the world to develop a “time-interleaved noise-shaping SAR ADC (analog-to-digital converter)” semiconductor chip capable of simultaneously measuring multiple biosignals, including electrocardiograms (ECG) and electromyograms (EMG). The team developed this technology in an actual semiconductor chip and successfully completed functional validation. Their findings were presented at the IEEE Symposium on VLSI Technology & Circuits (VLSI 2026), held in Honolulu, June 14–18.

Accurately measuring multiple biosignals using wearable devices such as smartwatches requires meeting several demanding conditions. These include “ultra-high input impedance (resistance)” to prevent signal loss even when no sweat is present on the skin or when contact is loose (dry or non-contact electrodes), a “wide input range” to prevent signal distortion caused by vigorous movement, and “ultra-low power consumption” for long-term operation. However, conventional measurement approaches have struggled to satisfy all these requirements simultaneously within a single chip.

Lee’s research team addressed this challenge by proposing a novel “time-interleaved third-order noise-shaping SAR ADC” architecture in which circuit blocks that consume significant power and chip area are shared across multiple channels, while only essential components (the residual capacitor banks) are allocated separately to each channel. This approach dramatically reduced the circuit area and power consumption required for multichannel systems, enabling an ultra-compact, ultra-low-power chip.

Common nanostructures may explain shared photoproperties in two widespread dark materials

A newly developed framework for understanding the photoproperties of both natural organic matter and eumelanin, a natural pigment responsible for dark colors in organisms, may inspire advanced sustainable technologies, scientists say.

Although they are some of the most widespread substances on Earth, not much is known about eumelanin or natural organic matter (NOM)—a dark-colored substance formed by the decomposition of biological material. In humans, eumelanin is a vital pigment in skin and other tissues that protects cells from damage caused by ultraviolet radiation. In nature, NOM gives rivers and soils their color and affects light-driven reactions like photosynthesis.

Although these compounds have been studied individually for decades, researchers in a new study, by scrutinizing them alongside each other, have shown that eumelanin and NOM have common properties beyond their dark colors.

Brainwide blood volume reflects opposing neural populations

An interesting new approach to more accurately predicting blood flow in the mouse brain based on the activity of neurons correlated positively or negatively with arousal (as measured by whisking). Neuropixels and functional ultrasound imaging were used to simultaneously record from neurons and map blood flow, allowing the authors to derive their model.


Combined functional ultrasound imaging and Neuropixels recording of mouse brains identify two neuronal populations with opposing arousal-related activity and distinct haemodynamic response functions, that occur throughout the brain.

Resilience to autosomal dominant Alzheimer’s disease in a Reelin-COLBOS heterozygous man

Fascinating case study on the neuroprotective effects of a mutant reelin allele (RELN–COLBOS) which delayed disease progression in a patient with autosomal dominant Alzheimer’s disease (ADAD). A promising therapeutic target!


Case report of an individual heterozygous for a rare RELN–COLBOS variant that confers resilience, via a gain-of-function mechanism, to Alzheimer’s disease.

Newfound biomarkers may someday help clinicians better detect—and possibly cure—Lyme disease

Lyme disease can be easiest to treat in its earliest stages, but current tests often miss infections during that critical window and cannot tell whether bacteria are still present or were cleared years ago. New research led by Tufts University School of Medicine suggests that a group of immune molecules called anti-lipid antibodies may address these shortcomings.

The findings, published in Infection and Immunity, could lead to improved tests that identify Lyme disease earlier, when antibiotics can best prevent more debilitating disease. They also may help clinicians better identify patients who continue to experience symptoms of infection after treatment—and potentially find new drug targets to help them.

Nearly half a million Americans are diagnosed and treated for Lyme disease each year. Caused by the bacterium Borrelia burgdorferi and spread through the bite of infected blacklegged ticks (also known as deer ticks), the disease can lead to arthritis, neurological problems and heart complications if untreated.

Common brain cancer mutation changes DNA shape to drive progression, exposing therapeutic target

A new study from researchers at The University of Texas MD Anderson Cancer Center has uncovered how one of the most common genetic alterations in glioma rewires the cancer cell genome to fuel tumor progression, suggesting a potential new therapeutic strategy for patients with ATRX-mutant gliomas.

The findings show that mutations in the ATRX gene fundamentally reprogram the epigenome and change the three-dimensional structure of chromatin, creating new interactions that activate developmental programs that tumors exploit to grow and spread. Targeting one of the genes downstream of ATRX in preclinical models—particularly in the HOXA family—slowed cancer progression.

The study, published in Nucleic Acids Research, was co-led by Jason Huse, M.D., Ph.D., professor of Anatomic Pathology, and Kunal Rai, Ph.D., professor of Genomic Medicine, with major contributions from Prit Benny Malgulwar, Ph.D., instructor of Translational Molecular Pathology, Anand Singh, Ph.D., senior research scientist in Genomic Medicine, and Ajay Saw, Ph.D., previous postdoctoral fellow in Genomic Medicine.

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