Recent electronics technology development has provided unprecedented opportunities for enabling implantable bioelectronics for long-term disease monitoring and treatment. Current electronics-tissue interfaces are characterized by weak physical interactions, suffering from potential interfacial failure or dislocation during long-term application. On the other hand, some new technologies can be used to achieve robust electronics-tissue interfaces; however, such technologies are limited by potential risks and the discomfort associated with postdetachment of the bioelectronics. Here, a hydrogel-based electronicstissue interface based on the exploitation of dynamic interactions (such as boronate-diol complexation) that features an interfacial toughness over 400 J m −2 is presented. Moreover, these hydrogel adhesion layers are also triggerdetachable by dissociating the dynamic complexes (i.e., addition of glucose). These hydrogel-based bioelectronic interfaces enable the in vivo recording of physiological signals (i.e., electromyograph, blood pressure, or pulse rates). Upon mild triggering, these bioelectronics can be easily detached without causing any damage, trauma, or discomfort to the skin, tissues, and organs. This kind of trigger-detachable hydrogel adhesives offer general applicability in bioelectronic interfaces, exhibiting promising utility in monitoring, modulating, and treating diseases where temporary monitoring of physiologic signals, interfacial robustness, and postremoval of bioelectronics are required.

Hydrogel bioadhesion technology has offered unprecedented opportunities in minimally-invasive surgeries, which are routinely performed to reduce postoperative complication, recovery time, and patient discomfort. Existing hydrogelbased adhesives are challenged either by their inherent weak adhesion under wet and dynamic conditions, or potential immunological side-effects, especially for synthetic hydrogel bioadhesives. Here, a kind of synthetic hydrogel bioadhesives from a variety of polymer precursors are reported, featuring instant formation of tough biointerface, allowing for wet and robust adhesion with highly dynamic biological tissues. Moreover, by getting rid of monomers during the hydrogel fabrication, these hydrogel adhesives do not cause any inflammatory response during the in vivo wound sealing, promising for immediate vascular defects repairing and surgical hemostasis. Additionally, they could also serve as human-electronics interfacing materials, enabling bioelectronics implantation for real-time physiological and clinical monitoring.

Ischemic stroke, which is the second highest cause of death and the leading cause of disability, represents ~71% of all strokes globally. Some studies have found that the key elements of the pathobiology of stroke is immunity and inflammation. Microglia are the first line of defense in the nervous system. After stroke, the activated microglia become a double-edged sword, with distinct phenotypic changes to the deleterious M1 types and neuroprotective M2 types. Therefore, ways to promote microglial polarization toward M2 phenotype after stroke have become the focus of attention in recent years. In this review, we discuss the process of microglial polarization, summarize the alternation of signaling pathways and epigenetic regulation that control microglial polarization in ischemic stroke, aiming to find the potential mechanisms by which microglia can be transformed into the M2 polarized phenotype.

Hydrogel bioadhesives have emerged as one of the most promising alternatives to sutures and staples for wound sealing and repairing, owing to their unique advantages in biocompatibility, mechanical compliance, and minimally invasive manipulation. However, only a few hydrogel bioadhesives have been successfully used for gastric perforation repair, due to their undesirable swelling when in direct contact with extremely acidic gastric fluids, and are thereby accompanied by a gradually deteriorating adhesion performance. Herein, an acid-tolerant hydrogel (ATGel) bioadhesive is developed, which integrates two distinct components, an acid-tolerant hydrogel substrate and an adhesive polymer brush layer. The ATGel bioadhesive can form instant, atraumatic, fluid-tight, and sutureless sealing of gastric perforation, and enable robust biointerfaces in direct contact with gastric fluids, addressing the key limitations with sutures and commercially-available tissue adhesives. Moreover, in vivo investigation on gastric perforation of rat model validates the proposed acid-tolerant bioadhesion, and identifies the mechanisms for accelerated gastric perforation repair through alleviated inflammation, which suppresses fibrosis and enhances angiogenesis.

High molecular weight hyaluronic acid (HMW-HA) and low molecular weight hyaluronic acid (LMW-HA) were mixed at different ratios and cross-linked with 1,4-butanediol diglycidyl ether (BDDE) to prepare five hyaluronic acid hydrogels A–E.

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Brain arteriovenous malformations (AVMs) are congenital vascular abnormality in which arteries and veins connect directly without an intervening capillary bed. So far, the pathogenesis of brain AVMs remains unclear. Here, we found that Wilms' tumour 1‐associating protein (WTAP), which has been identified as a key subunit of the m6A methyltransferase complex, was down‐regulated in brain AVM lesions. Furthermore, the lack of WTAP could inhibit endothelial cell angiogenesis in vitro. In order to screen for downstream targets of WTAP, we performed RNA transcriptome sequencing (RNA‐seq) and Methylated RNA Immunoprecipitation Sequencing technology (MeRIP‐seq) using WTAP‐deficient and control endothelial cells. Finally, we determined that WTAP regulated Desmoplakin (DSP) expression through m6A modification, thereby affecting angiogenesis of endothelial cells. In addition, an increase in Wilms' tumour 1 (WT1) activity caused by WTAP deficiency resulted in substantial degradation of β‐catenin, which might also inhibit angiogenesis of endothelial cells. Collectively, our findings revealed the critical function of WTAP in angiogenesis and laid a solid foundation for the elucidation of the pathogenesis of brain AVMs.

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