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Category: biotech/medical – Page 164

Nanobody hitchhikers boost immunotherapy potency in cancer treatment

Researchers led by John T. Wilson, Vanderbilt University associate professor of chemical and biomolecular engineering and biomedical engineering, have developed a new approach using a molecularly designed nanobody platform that seeks to make immunotherapy more effective in the treatment of cancer.

The research, “Potentiating Cancer Immunotherapies with Modular Albumin-Hitchhiking Nanobody-STING Agonist Conjugates,” is published in Nature Biomedical Engineering.

Immunotherapy is revolutionizing cancer treatment, but few patients benefit from the treatment, according to researchers. However, Wilson and his Immunoengineering Lab at Vanderbilt, along with collaborators at Vanderbilt University Medical Center, SOMBS, and the College of Arts and Sciences, aim to solve this problem.

New study reveals genetic link between brain criticality and human cognition

A new study has revealed compelling evidence that brain criticality—a dynamic balance between neural excitation and inhibition—has a strong genetic foundation and is associated with cognitive performance. The research was published on June 23 in the Proceedings of the National Academy of Sciences.

Led by Prof. Liu Ning from the Institute of Biophysics of the Chinese Academy of Sciences (CAS) and Prof. Yu Shan from the Institute of Automation of CAS, the team analyzed resting-state functional MRI (rs-fMRI) data from the Human Connectome Project S1200 release. The dataset included 250 , 142 , and 437 unrelated individuals, providing a robust framework for examining the heritability of critical brain dynamics.

The results showed that brain criticality is significantly influenced by , with stronger genetic effects observed in primary sensory cortices compared to higher-order association regions. These findings suggest that the capacity of the brain to maintain near-critical dynamics—previously associated with optimal information processing and cognitive flexibility—is, to a substantial degree, inherited.

Diglycerides Are Associated With An Older Biological Age

And an increased all-cause mortality risk…

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Insulin on edge: Study identifies stress-triggered gene behind diabetes

Researchers from Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damages pancreatic β-cells—the cells responsible for insulin production and blood sugar control—pushing them toward dysfunction. The findings highlight a promising new target for early intervention in type 2 diabetes. The study is published in the Journal of Biological Chemistry.

While many factors can contribute to type 2 diabetes, lifestyle, especially diet, plays a major role in its onset. Genetics matter, but poor eating habits can greatly increase the risk of developing what is now often called a “silent epidemic.”

“Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate , become impaired due to prolonged stress caused by poor dietary habits, a condition known as ,” said Naoki Harada, an associate professor at Osaka Metropolitan University’s Graduate School of Agriculture and lead author of this study.

Scientists use gene editing to correct harmful mitochondrial mutations in human cells

In a step toward treating mitochondrial diseases, researchers in the Netherlands have successfully edited harmful mutations in mitochondrial DNA using a genetic tool known as a base editor. The results, published in the open-access journal PLOS Biology, offer new hope for people with rare genetic conditions.

Mitochondria have their own small set of DNA. Mutations in this mitochondrial DNA can lead to a wide range of maternally inherited diseases, cancer, and aging-related conditions. While the development of CRISPR technology has given scientists new ways to correct mutations in nuclear DNA, this system cannot effectively cross the mitochondrial membrane and reach mitochondrial DNA.

In the new study, the researchers used a tool called a base editor—specifically, a DdCBE (double-stranded DNA deaminase toxin A-derived cytosine ). This tool allows scientists to change a single letter in the DNA code without cutting it, and it works on mitochondrial DNA.

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