Transition metal dichalcogenides (TMDs) have received considerable attention due to their strong absorption in the near‐infrared (NIR) region, strong spin‐orbit coupling, and excellent photothermal conversion efficiency (PCE). Herein, CoFeMn dichalcogenide nanosheets (CFMS NSs) are prepared via facile vulcanization of a lamellar CoFeMn‐layered double hydroxide (LDH) precursor followed by polyvinyl pyrrolidone modification (to give CFMS‐PVP NSs), and found to show excellent photoacoustic (PA) imaging and synergistic photothermal/chemodynamic therapy (PTT/CDT) performance. The as‐prepared CFMS‐PVP NSs inherit the ultrathin morphology of the CoFeMn‐LDH precursor and exhibit an outstanding photothermal performance with a η of 89.0%, the highest PCE reported to date for 2D TMD materials. Moreover, 50% of maximum catalytic activity (Michaelis–Menten constant, K _m ) is attained by CFMS‐PVP NSs with 0.26 × 10 ⁻³ m H ₂ O ₂ at 318 K, markedly lower than the endogenous concentration of H ₂ O ₂ inside tumor cells. In addition, complete apoptosis of HepG2 cancer cells and complete tumor elimination in vivo are observed after treatment with CFMS‐PVP NSs at a low dose, substantiating the NSs’ remarkable PTT/CDT efficacy. This work provides a new and facile approach for the synthesis of high‐quality multicomponent TMD nanosheets with precise process control, the potential for mass production, and outstanding performance, providing great promise in cancer theranostics.

Exosomes are a subset of small, membrane-bound extracellular vesicles that are important for communication among cells. They originate from the cell membrane during endocytic internalization, and are stable in biological fluids, including blood and synovial fluids. Increasing knowledge is emerging about exosomes in joint diseases, including osteoarthritis, rheumatoid arthritis, osteonecrosis of the femoral head, and others. Exosomes in synovial fluid can lead to inflammation, degeneration of cartilage, and destruction of joints. Exosomes in blood have diagnostic value in the early disease stage or for complicated conditions of joint diseases. Exosomes from stem cells could delay diseases and repair joints. For a comprehensive understanding about the emerging role of exosomes in joint diseases, we introduced the isolation and verification of exosomes from synovial fluid, reviewed the physiological and pathological effects of exosomes on joints, and discussed the diagnostic value and therapeutic potential of exosomes in joint diseases. In the future, immunologically active exosomes and engineered exosomes will of interest in the joint diseases. Challenges in the field of exosomes in joint-disease research include complex and expensive isolation, detection of contributing molecular, effectiveness and safety evaluation. In summary, challenges remain, but the field of exosomes in joint diseases has potential, including in mechanisms, diagnoses and therapies.

Glucocorticoids play a pivotal role in the proliferation of osteoblasts, but the underlying mechanism has not been successfully elucidated. In this report, we have investigated the molecular mechanism which elucidates the inhibitory effects of dexamethasone on murine osteoblastic MC3T3-E1 cells. It was found that the inhibitory effects were largely attributed to apoptosis and G1 phase arrest. Both the cell cycle arrest and apoptosis were dependent on glucocorticoid receptor (GR), as they were abolished by GR blocker RU486 pre-treatment and GR interference. G1 phase arrest and apoptosis were accompanied with a p53-dependent up-regulation of p21 and pro-apoptotic genes NOXA and PUMA. We also proved that dexamethasone can’t induce apoptosis and cell cycle arrest when p53 was inhibited by p53 RNA interference. These data demonstrate that proliferation of MC3T3-E1 cell was significantly and directly inhibited by dexamethasone treatment via aberrant GR activation and subsequently P53 activation.