Injectable hydrogel adhesives integrating both rapid adhesion to wet tissues and anti‐swelling in humid environments are highly desired for fast hemostasis and wound sealing in surgical applications. Herein, utilizing the synergistic effect of thermo‐sensitive shrinkable nano‐micelle gelators and small molecular adhesive moieties, an injectable hydrogel with rapid‐adhesion and anti‐swelling properties (RAAS hydrogel) is fabricated. The RAAS hydrogel can undergo ultrafast gelation to achieve wet adhesion within 2 s of ultraviolet illumination and exhibit an outstanding anti‐swelling performance with non‐expansion of volume during the whole degradation process. It also presents good biocompatibility and low risk of hemolysis. Its fast hemostasis is demonstrated in diverse hemorrhage models with injuries in the liver, artery, heart, cranial vessel, and brain cortex in small animals. Importantly, its volume stability in humid internal environment can maintain the strong adhesion strength and avoid compression injury to spinal cord when applied for dura sealing. These data suggest that the injectable RAAS hydrogel holds potential for the applications of fast hemostasis and wound sealing with the benefits of stable adhesion and reducing the risk of tissue compression injury.

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Senolytics are a class of drugs that selectively eliminate senescent cells and ameliorate senescence-associated disease. Studies have demonstrated the accumulation of senescent disc cells and the production of senescence-associated secretory phenotype decrease the number of functional cells in degenerative tissue. It has been determined that clearance of senescent cell by senolytics rejuvenates various cell types in several human organs, including the largest avascular structure, intervertebral disc (IVD). The microvasculature in the marrow space of bony endplate (BEP) are the structural foundation of nutrient exchange in the IVD, but to date, the anti-senescence effects of senolytics on senescent vascular endothelial cells in the endplate subchondral vasculature remains unclear. In this study, the relationships between endothelial cellular senescence in the marrow space of the BEP and IVD degeneration were investigated using the aged mice model. Immunofluorescence staining was used to evaluate the protein expression of P16, P21, and EMCN in vascular endothelial cells. Senescence-associated β-galactosidase staining was used to investigate the senescence of vascular endothelial cells. Meanwhile, the effects of senolytics on cellular senescence of human umbilical vein endothelial cells were investigated using a cell culture model. Preliminary results showed that senolytics alleviate endothelial cellular senescence in the marrow space of BEP as evidenced by reduced senescence-associated secretory phenotype. In the aged mice model, we found decreased height of IVD accompanied by vertebral bone mass loss and obvious changes to the endplate subchondral vasculature, which may lead to the decrease in nutrition transport into IVD. These findings may provide evidence that senolytics can eliminate the senescent cells and facilitate microvascular formation in the marrow space of the BEP. Targeting senescent cellular clearance mechanism to increase nutrient supply to the avascular disc suggests a potential treatment value of senolytics for IVD degenerative diseases.

Co-flow microfluidics and phenolic hydroxyl derivative of carboxymethylcellulose (CMC-Ph) provide a promising strategy for cell-enclosed microcapsules in combination with BMP-2 gene and Tet-on system modified BMSCs and then controlled BMP-2 protein released effectively as well as promoted the osteogenic differentiation of BMSCs.

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