With global life expectancy steadily increasing, the growing gap between lifespan and healthspan has placed the aging of the female reproductive system at the forefront of biomedical research. This process, which profoundly impacts fertility, quality of life, and long-term health, is no longer viewed simply through the lens of chronological age or menopause. Instead, a paradigm shift is underway, where aging is understood as a distinct biological process best quantified by multi-omics technologies and computational models known as "aging clocks." These tools—encompassing epigenetics, transcriptomics, proteomics, metabolomics, and microbiomics—provide a powerful, integrated framework to measure biological age, reveal tissue-specific vulnerabilities, and elucidate systemic aging patterns that chronological metrics fail to capture. While this research area is still evolving, the growing availability of high-quality datasets offers unprecedented opportunities to advance our understanding of reproductive aging, infertility, and pregnancy complications, moving towards more personalized and predictive healthcare.

Promoters are key DNA regions that control gene transcription, but their activity varies greatly across different cell types. This heterogeneity makes it difficult for existing computational methods to identify promoters reliably. A team led by Professors Zhangyu Mei and Hao Wu from Shandong University, China, has developed MuSE‑Promoter, a deep ensemble learning framework that combines multi‑scale feature fusion, transformer attention, and a learnable weighted ensemble of neural network and random forest. The system outperforms state‑of‑the‑art methods on human cell lines from different tissues and on Arabidopsis thaliana datasets, and shows excellent generalization in cross‑cell‑line and promoter–enhancer discrimination tasks.

Paligenosis defines a tightly controlled program through which terminally differentiated cells re‑enter the cell cycle and contribute to tissue repair after injury. This review systematically introduces the concept, the three sequential stages of paligenosis—mTORC1 suppression with autophagy initiation, followed by mTORC1 reactivation and stemness gene induction, and finally proliferation with lineage restoration—as well as the underlying molecular networks involving autophagy, metabolic rewiring, and epigenetic remodeling. The article then compares paligenosis with other forms of cellular plasticity such as dedifferentiation, transdifferentiation, epithelial‑mesenchymal transition, and induced pluripotency, highlighting its unique stepwise, reversible and intralineage nature. A major focus is the dual role of paligenosis: while it ensures efficient regeneration in tissues like the stomach and pancreas, its persistent or dysregulated activation under chronic stress or oncogenic signals can drive metaplasia, tumor initiation, metastasis and therapy resistance. The review closes by discussing biomarker prospects for distinguishing adaptive repair from malignant drift, and the therapeutic potential of modulating paligenotic pathways for regenerative medicine and cancer treatment.

N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNA, serves as a pivotal epitranscriptomic mark that dynamically regulates RNA metabolism—including stability, splicing, translation, and localization—thereby shaping cellular identity and function. This modification is installed by writer complexes (e.g., METTL3/METTL14), erased by demethylases (FTO, ALKBH5), and interpreted by reader proteins. Among these readers, YTHDF2 has emerged as a central regulator, primarily known for binding m6A-modified transcripts and promoting their decay, but recent evidence reveals a more complex role extending to m5C reading and even translational enhancement. YTHDF2 functions as a key integrator of intrinsic genetic programs and extrinsic environmental cues, critically governing hematopoietic stem cell (HSC) fate, immune cell development and activation, and tumor-immune interactions. This review synthesizes advances in understanding YTHDF2’s molecular mechanisms—spanning RNA-stability-dependent and -independent pathways—and its multifaceted roles in hematopoiesis, immunity, and cancer, highlighting its potential as a therapeutic target in immune-related diseases and malignancies.

A new approach to accurately imaging objects with complex shapes and varying degrees of "shininess" could enable high-precision applications in virtual and mixed reality settings, industrial inspection and medical imaging.

The rapid clinical validation of mRNA technology during the COVID‑19 pandemic has powerfully accelerated its application in oncology, and this comprehensive review provides a state‑of‑the‑art assessment of mRNA cancer vaccines. It systematically covers the molecular design principles of synthetic mRNA, the diverse antigen‑targeting strategies (from conventional tumor‑associated antigens to patient‑specific neoantigens and non‑canonical sources), the major delivery platforms (lipid nanoparticles, lipoplexes, protamine complexes, and cell‑based systems), and the mechanistic pathways by which these vaccines activate both cellular and humoral antitumor immunity. The review then synthesizes preclinical and clinical evidence across solid tumors—melanoma, pancreatic ductal adenocarcinoma, non‑small cell lung cancer, prostate cancer, glioblastoma—and hematologic malignancies, including acute myeloid leukemia, myelodysplastic syndromes, and multiple myeloma. It also critically discusses current challenges, such as the immunosuppressive tumor microenvironment, delivery barriers, and manufacturing complexities, before outlining future directions that involve next‑generation delivery systems, artificial intelligence‑driven vaccine design, and combination strategies with immune checkpoint inhibitors and adoptive T‑cell therapies.

Mono-ubiquitination of histone H2A lysine 119 (H2AK119Ub): its multifaceted role in biology and implication in diseases