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Deep-learning algorithms enhance mutation detection in cancer and RNA sequencing

Researchers from the Faculty of Engineering at The University of Hong Kong (HKU) have developed two innovative deep-learning algorithms, ClairS-TO and Clair3-RNA, that significantly advance genetic mutation detection in cancer diagnostics and RNA-based genomic studies.

The pioneering research team, led by Professor Ruibang Luo from the School of Computing and Data Science, Faculty of Engineering, has unveiled two groundbreaking deep-learning algorithms—ClairS-TO and Clair3-RNA—set to revolutionize genetic analysis in both clinical and research settings.

Leveraging long-read sequencing technologies, these tools significantly improve the accuracy of detecting genetic mutations in complex samples, opening new horizons for precision medicine and genomic discovery. Both research articles have been published in Nature Communications.

Brewing possibilities: Using caffeine to edit gene expression

What if a cup of coffee could help treat cancer? Researchers at the Texas A&M Health Institute of Biosciences and Technology believe it’s possible. By combining caffeine with the use of CRISPR—a gene-editing tool known as clustered regularly interspaced short palindromic repeats—scientists are unlocking new treatments for long-term diseases, like cancer and diabetes, using a strategy known as chemogenetics.

The work is published in the journal Chemical Science.

Yubin Zhou, professor and director of the Center for Translational Cancer Research at the Institute of Biosciences and Technology, specializes in utilizing groundbreaking tools and technology to study medicine at the cellular, epigenetic and genetic levels. Throughout his career and over 180 publications, he has sought answers to medical questions by using highly advanced tools like CRISPR and chemogenetic control systems.

Several Psychiatric Disorders Share The Same Root Cause, Study Suggests

Researchers have discovered that eight different psychiatric conditions share a common genetic basis.

A study published in early 2025 pinpointed specific variants among those shared genes, showing how they behave during brain development.

The US team found many of these variants remain active for extended periods, potentially influencing multiple developmental stages – and offering new targets for treatments that could address several disorders at once.

How your life story leaves epigenetic fingerprints on your immune cells

The COVID-19 pandemic gave us tremendous perspective on how wildly symptoms and outcomes can vary between patients experiencing the same infection. How can two people infected by the same pathogen have such different responses? It largely comes down to variability in genetics (the genes you inherit) and life experience (your environmental, infection, and vaccination history).

These two influences are imprinted on our cells through small molecular alterations called epigenetic changes, which shape cell identity and function by controlling whether genes are turned “on” or “off.”

Salk Institute researchers are debuting a new epigenetic catalog that reveals the distinct effects of genetic inheritance and life experience on various types of immune cells. The new cell type-specific database, published in Nature Genetics, helps explain individual differences in immune responses and may serve as the foundation for more effective and personalized therapeutics.

For decades, memory-like responses in immune cells have remained unexplained

Katherine Y. King & team now identify epigenetic changes in hematopoietic stem and progenitor cells in a mycobacterial infection model that are retained in downstream macrophages, providing mechanistic mediators of innate immune memory and explaining persistence of central trained immunity.


1Graduate Program in Cancer and Cell Biology.

2Department of Pediatrics, Division of Infectious Disease, Texas Children’s Hospital and Baylor College of Medicine.

3Stem Cells and Regenerative Medicine Center.

4Department of Molecular and Human Genetics.

Dr. Natalie Yivgi-Ohana, Ph.D. — CEO, Minovia — Harnessing The Therapeutic Power Of Mitochondria

Dr. Natalie Yivgi-Ohana, Ph.D. — CEO, Minovia Therapeutics — Harnessing The Therapeutic Power Of Mitochondria


Is Co-Founder and CEO of Minovia Therapeutics (https://minoviatx.com/), a biotech company dedicated to rapidly advance life-changing therapies that address the unmet need of serious and complex mitochondrial diseases, and are the first clinical-stage company to develop a mitochondrial transplantation approach to treat a broad range of indications generated by a mitochondrial dysfunction which lead to rare-genetic or age-related diseases.

Dr. Yivgi-Ohana has twenty years of experience in mitochondrial research and received her Ph.D. in Biochemistry at The Hebrew University, after which she completed her postdoctoral fellowship at the Weizmann Institute of Science.

Dr. Yivgi-Ohana also has her B.Sc., Medical Sciences Ben-Gurion University of the Negev and her Master’s Degree, Human Reproduction Bar-Ilan University.

Dr. Yivgi-Ohana founded Minovia with a passion to help children and adults with mitochondrial diseases worldwide.

Scientists Uncover Potential “Two-in-One” Treatment for Diabetes and Heart Disease

Earlier work linked the experimental drug ‘IC7Fc’ to improvements in type 2 diabetes, and new research now points to a possible role in cardiovascular health as well. Scientists report that the compound may lower the risk of heart disease by reducing harmful cholesterol in the bloodstream and calming inflammatory activity that damages blood vessels over time.

The findings come from a preclinical study published in Science Advances, led by researchers at Leiden University Medical Centre in the Netherlands in collaboration with Monash University and other international partners.

In experiments involving mice genetically predisposed to heart disease, treatment with IC7Fc led to clear reductions in blood fat (triglycerides) and cholesterol, markers closely linked to the development of cardiovascular complications.

Altered Molecular Composition of a Specific Subset of Prefrontal Cortical Excitatory Synapses in Schizophrenia

JNeurosci: Lorincz et al. provide novel insights into the molecular mechanisms underlying excitatory synaptic dysfunction in schizophrenia.

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Abnormal excitatory synaptic transmission in the human prefrontal cortex has been implicated in the pathophysiology of schizophrenia based primarily on genetic evidence. However, changes in synaptic function cannot be predicted from altered gene expressions, but determining the amount, density, and subsynaptic distribution of synaptic proteins is the only reliable indirect readout of function. Detecting proteins in individual synapses of human postmortem tissues has been severely constrained by technical limitations. Here we overcome this limitation by optimizing a high-resolution, quantitative localization method to facilitate antigen recognition at excitatory synapses in postmortem brains of both sexes.

Stress-reduction molecule has potential to treat aging and metabolic disorders

University of Queensland researchers say the discovery of a new stress reduction role for a naturally occurring molecule in the body could lead to new drugs and treatment for metabolic disorders and aging.

Professor Steven Zuryn, a molecular geneticist from UQ’s Queensland Brain Institute, was part of a team that found that very small RNA molecules, called microRNAs, bind to genes and prevent them from being over-activated.

MicroRNAs were discovered in C. elegans about 30 years ago and have since been shown to be important in human health and disease. This initial discovery led to the 2024 Nobel Prize in Physiology or Medicine.

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