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Faster fracture tests offer path to more sustainable material choices

Recycled materials promise a cleaner future, but recycled content alone does not necessarily make a product sustainable. At Georgia Tech’s Daedalus Lab, assistant professor Christos Athanasiou and postdoctoral researcher Danqi Sun are working to provide greater certainty to designers and engineers by rethinking how materials are tested for their fracture characteristics.

Their article in Science Advances details a new testing protocol that reduces costs, increases speed and simulates real-world conditions.

Materials shape nearly every part of modern life, from packaging and consumer products to bridges and medical devices. Choosing the right material involves balancing durability, cost, manufacturability and environmental impact. Yet those decisions are not always guided by a clear understanding of how materials age and fail under real-world conditions, especially for recycled materials like plastics.

Chinese researchers map epigenetic control of congenital heart defects

The findings have direct implications for clinical practice and future research. For genetic screening, the study provides a clear priority: CHD7 for outflow‑tract defects, CHD4 for chamber‑patterning anomalies, and CHD8 for ventricular dysfunction. This prioritization can improve diagnostic efficiency. Therapeutically, while directly targeting remodelers is risky due to their broad expression, identifying their downstream pathways—such as those regulating cardiomyocyte proliferation or metabolism—may offer safer drug targets. Furthermore, future studies combining time‑resolved multi‑omics and combinatorial genetics could uncover how these proteins coordinate across development, potentially paving the way for precise, temporally controlled epigenetic therapies.

A team from China has published (DOI: 10.1007/s12519-026–01049-y) this definitive synthesis in World Journal of Pediatrics. The review systematically evaluates the current evidence from human genetics, animal models, and stem‑cell systems to assign specific cardiac functions to different CHD family members. The findings offer a new conceptual map for understanding the epigenetic control of heart development and disease.

The study’s key contribution is its systematic analysis of the evidence, which reveals a clear division of labor among CHD proteins. CHD7, the gene most frequently mutated in CHARGE syndrome (an acronym for Coloboma, Heart defects, Atresia choanae, Retarded growth, Genital abnormalities, and Ear abnormalities) syndrome, shows the strongest link to cardiac development, playing a dominant role in building the heart’s early structure. In contrast, CHD3 and CHD4 act as “identity guardians,” ensuring that heart cells commit to the correct fate during chamber formation. For CHD8, while evidence is still emerging, it appears to regulate later ventricular growth and functional maturation. Notably, although these proteins seem to act at different stages—CHD7 early, CHD4 mid, and CHD8 late—the review emphasizes that direct proof of their coordinated action is lacking.

One Common Sweetener May Increase Stroke Risk by Damaging The Brain’s Protective Barrier

The blood-brain barrier surrounds the blood vessels that run through the brain, letting in oxygen and nutrients while keeping out toxins and pathogens. It’s an absolutely essential line of defense that protects the brain from damage.

Researchers now believe they have discovered a significant threat to this barrier and its stability – and from something we’re willingly putting into our bodies.

Erythritol has been used as an artificial sweetener for decades.

Vaccine therapy for pediatric highgrade glioma: current landscape, challenges, and future directions NeuroOncology

Pediatric high-grade gliomas (pHGG) are among the most aggressive childhood brain tumors, with limited treatment options and poor prognosis. Vaccine-based immunotherapy offers a promising strategy by leveraging tumor-specific or associated antigens to stimulate durable anti-tumor immune responses with minimal toxicity.

This review outlines the scientific rationale for vaccine therapies in pHGG, detailing key targets such as glioma-associated antigens (EphA2, IL-13Rα2, survivin), driver mutation–derived neoantigens (H3.3K27M, TP53, IDH1), and viral antigens (CMV pp65). We evaluate current vaccine platforms, including peptide vaccines, dendritic cell vaccines, mRNA-based vaccines, and neoantigen-personalized approaches, highlighting early-phase clinical trial results that demonstrate safety and immunogenicity. Despite encouraging preliminary data, several challenges hinder clinical translation, including the distinct immune environment in the central nervous system, intratumoral heterogeneity, low mutational burden, immunosuppressive microenvironments, steroid use, and logistical hurdles in vaccine production and trial design. Future research must address these barriers through optimized antigen selection, combinatorial therapies, novel delivery systems, and pediatric-specific immune profiling.

With continued multidisciplinary collaboration, vaccine therapies may emerge as a meaningful addition to the therapeutic arsenal for children with pHGG.

Synthetic tumor data helps AI improve long-read cancer mutation detection

A research team at The University of Hong Kong (HKU), has developed ClairS—a deep-learning algorithm that significantly improves the detection of cancer mutations using long-read sequencing. Tested on breast cancer, lung cancer and melanoma cell line datasets, ClairS has demonstrated high accuracy across various cancer types and sequencing conditions.

The team was led by Professor Ruibang Luo, assistant director of Learning Experience & Student Enrichment and associate head of the Department of AI & Data Science at the School of Computing and Data Science (CDS) at HKU. The findings are published in the journal Nature Methods. ClairS is open source and available on GitHub.

Inherited gene variants may shape CAR-T therapy benefits and toxic side effects

Chimeric antigen receptor (CAR)-T cell therapy, which reprograms an individual’s immune cells to seek out and destroy certain cancer cells, has revolutionized treatment for blood cancers such as lymphoma. But in some patients, the treatment can cause serious side effects. New research led by investigators at the Mass General Brigham Cancer Institute, the Broad Institute of MIT and Harvard, and Dana-Farber Cancer Institute has shown that patients’ inherited genetic makeup can influence whether they benefit from CAR-T cell therapy or experience toxicity from the treatment. The results are published in Science Immunology.

“These findings have important implications for understanding how CAR-T cells behave in patients since each CAR-T cell product is unique to the person from whom it is manufactured, unlike all prior forms of therapy, which are identical across patients,” said lead author Mark B. Leick, M.D., an oncologist at the Mass General Brigham Cancer Institute.

For the study, Leick and his colleagues sequenced the entire genomes of more than 200 patients with aggressive lymphoma from two major clinical trials of CAR-T cell therapy. In one of the trials, patients with T cells with variants that silenced the STXBP2 gene tended to experience toxicity related to CAR-T cell therapy. Also, donor T cells engineered to lack STXBP2 and/or express these STXBP2-silencing variants triggered inflammation.

Low-Frequency Ultrasound Attacks Oral Cancer Cells

When Ajay Tijore was a postdoctoral researcher in mechanobiologist Michael Sheetz’s lab at the National University of Singapore, he and his team studied how mechanical strain affected cancer cells. A few years ago, the researchers found that low-frequency ultrasound waves triggered mechanical stress that killed several invasive cancer cell types.1 “That was kind of a big revelation… Eureka moment,” said Tijore.

When he started his own lab at the Indian Institute of Science in 2021, Tijore hoped to contribute to Indian society. With India accounting for one-third of the oral cancer cases worldwide, Tijore sought to investigate whether low-frequency ultrasound could also target oral cancer cells.2

Now, Tijore and his team found that patient-derived oral cancer cells are susceptible to low-frequency ultrasound due to their distinct biomechanical properties compared to healthy cells.3 The team’s findings, published in Materials Today Bio, highlight the potential of the non-invasive approach in oral cancer therapy.

Gene therapy reverses complete congenital night blindness in mice, improving vision

A new preclinical study suggests that gene augmentation therapy may restore sight in a severe form of inherited night blindness. The work, reported in Gene Therapy, targets complete congenital stationary night blindness (cCSNB), a disorder in which the retinal circuitry fails to generate reliable visual responses from birth. In mouse models, treatment improved both retinal function and visual performance, offering a promising blueprint for future human therapies.

The researchers focused on augmenting gene activity to compensate for the underlying molecular defect driving defective photoreceptor signaling. Rather than attempting to edit the genome directly, the approach delivers functional genetic instructions to retinal cells, aiming to re-establish healthier visual transduction. This strategy is designed for conditions where disease-causing pathways can be partially rescued by restoring protein expression levels.

Using viral delivery, the team administered a therapeutic vector into the eyes of affected mice. After treatment, they monitored retinal function with electrophysiological assays that quantify how well retinal neurons respond to light. The results showed a measurable shift toward more normal response patterns, indicating that the treated retinas regained function rather than merely delaying degeneration.

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