Recent advances in immunotherapy have shown remarkable success across multiple solid tumor types, revitalizing interest in immune-modulating strategies for osteosarcoma (OS). Within the complex tumor microenvironment (TME), immune cells exhibit dual regulatory roles-exerting critical regulatory influences on both tumorigenesis and disease progression while simultaneously serving as therapeutic targets. Particularly in OS, the dynamic interplay between malignant cells and the unique bone microenvironment manifests through intricate immune cell-mediated crosstalk. This comprehensive review analyzes the paradoxical roles of immune cell subsets in OS pathophysiology, detailing their tumor-promoting versus tumor-suppressing functions. Furthermore, we systematically evaluate recent progress in immune cell-targeted therapeutic approaches, including adoptive cell therapies and macrophage reprogramming strategies. The review encompasses current clinical applications and emerging preclinical innovations, providing valuable insights for optimizing immunotherapeutic approaches in OS management.

Cardiovascular diseases (CVDs) continue to drive global mortality rates, underscoring an urgent need for advancements in healthcare solutions. The development of point‐of‐care (POC) devices that provide rapid diagnostic services near patients has garnered substantial attention, especially as traditional healthcare systems face challenges such as delayed diagnoses, inadequate care, and rising medical costs. The advancement of machine learning techniques has sparked considerable interest in medical research and engineering, offering ways to enhance diagnostic accuracy and relevance. Improved data interoperability and seamless connectivity could enable real‐time, continuous monitoring of cardiovascular health. Recent breakthroughs in computing power and algorithmic design, particularly deep learning frameworks that emulate neural processes, have revolutionized POC devices for CVDs, enabling more frequent detection of abnormalities and automated, expert‐level diagnosis. However, challenges such as data privacy concerns and biases in dataset representation continue to hinder clinical integration. Despite these barriers, the translational potential of machine learning‐assisted POC devices presents significant opportunities for advancement in CVDs healthcare.

Ewing sarcoma breakpoint region 1 (EWSR1) fusion with Friend leukemia integration 1 transcription factor (FLI1) induced by a translocation of chromosome 11 with 22 contributes to Ewing sarcoma development. To date, the precise molecular mechanisms about EWSR1/FLI1 involving in Ewing sarcoma development remains to be defined. This study explored the potential critical gene targets of EWSR1/FLI1 knockdown in Ewing sarcoma cells on the gene expression profile based on online dataset, performed Limma algorithm for differentially expressed genes identification, constructed the transcriptional factor (TF)-gene regulatory network based on integrate transcriptional regulatory element database (TRED). The data showed up- and down-regulation of differentially expressed genes over time and peaked at 72 h after EWSR1/FLI1 knockdown in Ewing sarcoma cells. SMAD3 were up-regulated and FLI1, MYB, E2F1, ETS2, WT1 were down-regulated with more than half of their targets were down-regulated after EWSR1/FLI1 knockdown. The Gene Ontology (GO) and pathway annotation of these differentially expressed genes showed a consistent trend in each group of samples. Totally, there were 355 differentially expressed genes occurring in all five comparison groups of different time points, in which 39 genes constructed a dysregulated TF-gene network in Ewing sarcoma cell line A673 after EWSR1/FLI1 knockdown. These data demonstrated that knockdown of EWSR1/FLI1 expression led to transcriptome changes in Ewing sarcoma cells and that Ewing sarcoma development and progression caused by altered EWSR1/FLI1 expression may be associated with more complex transcriptome changes.

Osteoporosis (OP) is a metabolic bone disease characterized by reduced bone mass and deterioration of bone microstructure. Current pharmacological treatments are often associated with significant side effects and poor patient compliance. In recent years, food bioactives—such as polyphenols, carotenoids, and saponins—have attracted growing interest for their multi-target and low-toxicity profiles in the prevention and management of OP. This review systematically elaborates the protective roles and underlying molecular mechanisms of these compounds against OP. Polyphenols exert beneficial effects through antioxidant, anti-inflammatory, and bone metabolism-regulating properties, as well as via modulation of the gut–bone axis. Their mechanisms involve key signaling pathways, including PI3K/Akt, sirtuin 1 (SIRT1)/forkhead box O3a (FOXO3a), Hippo/YAP, reactive oxygen species (ROS)/HIF-1α, and Wnt/β-catenin. Carotenoids, which are potent antioxidants, contribute to a reduced risk of OP by alleviating oxidative stress and cellular senescence, including the senescence-associated secretory phenotype (SASP). Saponins regulate bone remodeling bidirectionally through pathways such as PI3K/Akt/mTOR, bone morphogenetic protein 2 (BMP-2)/runt-related transcription factor 2 (Runx2), and RANKL/osteoprotegerin (OPG). They also inhibit NF-κB/mitogen-activated protein kinase (MAPK) signaling and downregulate osteoclast-related transcription factors, including c-Fos and NFATc1. Given their efficacy and safety, food bioactives represent a valuable source of novel nutraceuticals for bone health.