Dr. Hye Jin Nam’s team at the Korea Research Institute of Chemical Technology (KRICT), in collaboration with Professors Dong Hyun Jo and Sangsu Bae at Seoul National University College of Medicine, found that autophagy induction via nutrient deprivation or mTOR inhibition markedly enhances the efficiency of HR-based CRISPR–Cas9 gene editing up to threefold.

A daily dose of almonds improved key health markers for people with metabolic syndrome in a study led by scientists at Oregon State University’s Linus Pauling Institute and the OSU College of Health.

Harnessing the artificial intelligence (AI) driven platform, IDentif.AI, researchers from the Institute for Digital Medicine (WisDM), Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), Cancer Science Institute of Singapore, NUS and the Shu Chien-Gene Lay Department of Bioengineering at the University of California San Diego, sought to uncover sex-specific drug combinations that may slow or halt AVS progression. IDentif.AI optimised drug combinations to inhibit aortic valve myofibroblast activation—a hallmark of AVS which refers to a process causing valve cells to stiffen and scar—in female and male valve cells isolated from laboratory models. The AI platform pinpointed a list of female-biased combinations (e.g. Y-27632/SB-203580/SD-208) that were more effective in addressing AVS in female cells, while AI-optimised male-biased combinations (e.g.  LY294002/Irosustat/TM5441) were notably more effective in male cells.

CHAF1B, a histone chaperone component of the chromatin assembly factor-1 complex, is overexpressed in multiple cancers and linked to tumor progression, but its role in lung squamous-cell carcinoma (LUSC) remained unclear. This study identifies CHAF1B as a critical oncogenic driver in LUSC through integrated bioinformatics, in vitro experiments, and in vivo models. Analysis of the GSE68793 LUSC dataset via weighted gene co-expression network analysis (WGCNA) highlighted CHAF1B as a top hub gene enriched in cell cycle regulation pathways. Immunohistochemistry of 126 LUSC tissues confirmed CHAF1B overexpression compared to adjacent normal tissues, with higher expression correlating significantly with advanced tumor stages and poor patient survival. Functional assays demonstrated that CHAF1B knockdown suppressed LUSC cell proliferation, induced S-phase cell cycle arrest, and reduced colony formation. In mouse xenograft models, CHAF1B silencing markedly inhibited tumor growth, underscoring its pro-tumorigenic role.