Like a phoenix rising from the ashes, our skin tissue—and in fact many types of epithelial tissue that lines and covers the body’s organs—can respond to death and destruction with a burst of regeneration. This phenomenon, known as compensatory proliferation, was first described in the 1970s in fly larvae, which regrew fully functional wings after their epithelial tissue had been severely damaged by high-dose radiation. Since then, this surprising ability has been documented in many species, including humans, yet its molecular basis has remained unclear.
A new study from the Weizmann Institute of Science, published in Nature Communications, reveals that the very enzymes responsible for cellular destruction—caspases—may also render certain cells resistant to death, enabling damaged tissue not only to regenerate but even to become more resilient.
Unfortunately, this same mechanism may be hijacked by many types of cancer and may help explain why some tumors recur in a more aggressive and treatment-resistant form. The new findings could thus open avenues for therapies that speed up wound repair and help prevent cancer relapse.
This machine learning model was trained on a large multicenter dataset of unruptured intracranial aneurysms to predict future rupture risk across international cohorts, supporting more precise and personalized treatment decisions.
Question Can a machine-learning model (MLM) predict the rupture risk of unruptured intracranial aneurysms (UIAs) using prerupture data?
Findings In this prognostic study of 11 579 UIAs from a cohort of 8,846 patients, an MLM trained on prerupture clinical and morphological data demonstrated robust performance in both internal and external validation, including on aneurysms smaller than 10 mm.
Meaning The findings of this study suggest that an MLM may improve risk stratification and inform treatment decision-making for patients with UIAs, providing additional guidance even for smaller aneurysms traditionally considered low risk.
A new study published in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in patients with an aggressive subtype of triple-negative breast cancer.
Led by Khandan Keyomarsi, Ph.D., professor of Experimental Radiation Oncology, the study shows that simultaneous inhibition of ATR and PKMYT1 triggers a type of cell death in Rb1-deficient breast cancer models.
Using genomic profiling, proteomics and patient-derived xenografts, the researchers found that loss of Rb1—a gene important for normal cell division—disrupts DNA repair processes and forces tumor cells to rely on ATR and PKMYT1 dependent pathways for survival, creating a vulnerability that can be selectively targeted.
New research from the University of Virginia School of Medicine is revealing why traumatic brain injury increases the chance of developing Alzheimer’s disease—and the discovery is pointing to a potential strategy to prevent the progressive brain disorder.
John Lukens, director of UVA’s Harrison Family Translational Research Center in Alzheimer’s and Neurodegenerative Diseases—housed within the Paul and Diane Manning Institute of Biotechnology—and his team discovered that even one mild traumatic brain injury can set off damaging changes, paving the way for the development of Alzheimer’s.
“Our findings indicate that fixing brain drainage following head trauma can provide a much-needed strategy to limit the development of Alzheimer’s disease later in life,” said Lukens, part of UVA’s Department of Neuroscience and its Center for Brain Immunology and Glia, and author on the new study published in Cell Reports.
Malaria continues to place a substantial burden on many emerging economies, contributing to significant loss of life, long-term disability, and economic disruption. According to the World Health Organization, the disease accounts for about 600,000 deaths each year, with the highest impact in low- and middle-income regions where access to prompt diagnosis and treatment remains limited.
CADskills is a medical device startup based in Ghent, Belgium. Their expertise lies in patient-specific implants, with a focus on CMF and neurosurgery patients. What is putting them in Materialise’s spotlight however, is their AMSJI: a revolutionary 3D-printed titanium jaw implant that will make life better for extreme maxillary atrophy sufferers. Now there’s something to […]
The mechanosensitive LPHN2 expressed at the tips of stereocilia in cochlear hair cells is identified as a modulator in the auditory process by interacting with MET channel components, which contributes to the Ca2+ response and neurotransmitter release in cochlear hair cells in response to mechanical stimulation.
A research team affiliated with UNIST has made a advancement in controlling spin-based signals within a new magnetic material, paving the way for next-generation electronic devices. Their work demonstrates a method to reversibly switch the direction of spin-to-charge conversion, a key step toward ultra-fast, energy-efficient spintronic semiconductors that do not require complex setups or strong magnetic fields.
Led by Professor Jung-Woo Yoo from the Department of Materials Science and Engineering and Professor Changhee Sohn from the Department of Physics at UNIST, the team has experimentally shown that within the altermagnetic material ruthenium oxide (RuO₂), the process of converting spin currents into electrical signals can be precisely controlled and flipped at will.
This breakthrough is expected to accelerate the development of low-power devices capable of processing information more efficiently than current technologies. The study is published in the journal Nano Letters.