Children with idiopathic short stature respond differently to growth hormone therapy, making treatment outcomes difficult to predict. Researchers from South Korea developed a mathematical model to better capture these individual differences in growth response over time. By analyzing treatment and patient characteristics, the study offers new insights into why some children may experience greater catch-up growth than others—and points toward a more personalized approach to predicting outcomes before therapy begins.

Fungal bloodstream infections can be life-threatening, and accurately identifying the causative fungal species is important for clinicians to administer appropriate treatment. In a recent study, researchers from Japan developed an innovative workflow that uses various genomic and sequence-analysis techniques to identify fungal species in blood samples much faster than conventional methods. Their approach could help patients receive the most effective treatment for their specific fungal infection as soon as possible.

Bacterial toxins can create pores in epithelial cell membranes, threatening cell survival and weakening the body’s protective barriers. Yet when these barriers are breached, cells may have an unexpected response. Researchers at Juntendo University investigated a lipid signaling pathway involving 12-HHT and BLT2 to understand what happens inside cells after toxin-induced membrane damage. Their study sheds new light on the cellular events that unfold as damaged cells fight to recover from injury.

Solid tumors resist CAR cell therapy through antigen heterogeneity, poor infiltration, and an immunosuppressive microenvironment. A new review argues that oncolytic viruses and CAR cells should be co-designed as an integrated, self-amplifying therapeutic system rather than simply combined. The authors describe how oncolytic viruses can install new targets, remodel the tumor microenvironment, and deliver local immune support, outlining engineering strategies, translational challenges, and future directions for next-generation solid tumor immunotherapy.

As we grow older, our bodies accumulate “zombie cells”—living cells that have stopped dividing or functioning normally—but linger in our tissues, contributing to chronic inflammation and age-related diseases. A new study led by Albert Einstein College of Medicine researchers and published today in Nature Aging helps explain why these cells, formally known as senescent cells, become increasingly difficult to eliminate. The research also points to a potential strategy for helping the body rid itself of these cells.

A research team led by Associate Professor Yohei Funakoshi, Associate Professor Kimikazu Yakushijin, and Professor Hironobu Minami of the Division of Medical Oncology/Hematology at Kobe University Hospital, together with Associate Professor Goh Ohji of the Division of Infectious Disease Therapeutics and Takaji Matsutani of Anymics Inc., has developed the pGen-SHM plot. The method combines the generation probability (pGen) of individual B-cell receptor (BCR) sequences with somatic hypermutation (SHM) associated with antigen-driven maturation. This enables the visualization and objective assessment of the maturation of the BCR repertoire after allogeneic hematopoietic stem cell transplantation (allo-HSCT).