Bupleuri Radix (BR), a cornerstone traditional Chinese medicine, has been used for millennia to treat liver and intestinal disorders, yet its dual nature as both a hepatoprotective agent and a potential hepatotoxin demands rigorous scientific examination. This innovative review systematically synthesizes the bidirectional effects of BR through the lens of the gut-liver axis, a biological framework that has transformed our understanding of drug metabolism and toxicity. Saikosaponins, the principal bioactive constituents of BR, undergo biotransformation by gut microbiota into metabolites with enhanced bioavailability, enabling them to regulate intestinal flora composition, strengthen intestinal barrier integrity, and alleviate inflammation through key signaling pathways including NF-κB, PI3K/Akt/mTOR, and STAT3. Simultaneously, BR and its components exert hepatoprotective effects through antioxidant, anti-inflammatory, and metabolic regulatory mechanisms. However, the review also critically examines evidence that saikosaponins and volatile oils may induce hepatotoxicity via oxidative stress and apoptotic pathways. The authors identify critical evidence gaps regarding the systematic interplay between BR's multi-component actions and the gut-liver axis, the toxicity of microbial metabolites, and clinical hepatotoxicity risk, proposing a future research agenda to optimize the safe and effective clinical application of this important medicinal herb.

Hematopoietic loss of chromosome Y (LOY) has emerged as one of the most prevalent somatic genomic alterations in aging males, yet its biological significance extends far beyond a mere marker of aging. This comprehensive review synthesizes current understanding of LOY, from its molecular origins in mitotic chromosome mis-segregation to its far-reaching clinical implications. Advances in detection technologies, including single-cell sequencing and bulk genomic approaches, have enabled robust identification of LOY across population scales. The review examines how inherited genetic variation, environmental exposures, and aging collectively contribute to LOY pathogenesis. Large-scale genome-wide association studies have revealed compelling epidemiological links between hematopoietic LOY and cardiovascular disease, neurodegenerative conditions, immune disorders, and cancer. Mechanistically, LOY drives altered gene expression, immune dysregulation, and clonal expansion of affected hematopoietic cells. Critically, CRISPR-based mouse and cellular models have recapitulated key disease phenotypes, establishing LOY as a functionally consequential form of somatic mosaicism with profound implications for disease susceptibility and male health disparities.

CAMBRIDGE, Mass., September 2 - Insilico Medicine (“Insilico”; HKEX: 3696), a clinical-stage generative artificial intelligence (AI)-driven drug discovery company, today announced the release of a series of frontier specialist models for chemistry and biology, trained through its MMAI Gym for Science framework. Across chemistry and biology, the models demonstrate state-of-the-art (SOTA) performance on more than 50 benchmark tasks.

BUFFALO, NY — September 2, 2026 — A new case report was published in Volume 13 of Oncoscience on July 29, 2026, titled “MRI in deciphering the superficial spread of cervical squamous cell carcinoma into the uterine corpus: A case report and literature review.”

A new study introduces a novel injectable composite microsphere that combines cells and biomaterials to significantly accelerate bone healing.

This is the first unequivocal record of the species outside its type locality in Dorset, UK, and the largest specimen known to date.

A new study in Science Bulletin reveals that maternal PAN2 protein is essential for early embryonic development by regulating mRNA poly(A) tail length. Using an oocyte-specific conditional knockout mouse model, researchers found that PAN2 deficiency causes embryos to arrest at the two-cell stage due to abnormal poly(A) tail elongation, maternal mRNA accumulation, and impaired zygotic genome activation. PAN2 recognizes substrates via the PAN3-PABPC1 complex, preferring tails lacking guanosine but enriched in uridine.