We have recently demonstrated that c-Jun N-terminal kinase 3 (JNK3) is a key modulator of the enhanced osteogenic potential of stem cells derived from children when compared to those derived from adults. In this study, we formulated a JNK3-activator nanoparticle (JNK3*) that recapitulates the immense osteogenic potential of juvenile cells in adult stem cells by facilitating JNK3 activation. Moreover, we aimed to functionalize a collagen-based scaffold by incorporating the JNK3* in order to develop an advanced platform capable of accelerating bone healing by recruitment of host stem cells. Our data, in vitro and in vivo, demonstrated that the immense osteogenic potential of juvenile cells could be recapitulated in adult stem cells by facilitating JNK3 activation. Moreover, our results revealed that the JNK3* functionalized 3D scaffold induced the fastest bone healing and greatest blood vessel infiltration when implanted in critical-size rat calvarial defects in vivo. JNK3*scaffold fastest bone healing in vivo was associated with its capacity to recruit host stem cells to the site of injury and promote angiogenic-osteogenic coupling (e.g. Vegfa, Tie1, Runx2, Alp and Igf2 upregulation). In summary, this study has demonstrated the potential of harnessing knowledge of age-altered stem cell mechanobiology in order to develop a materials-based functionalization approach for the repair of large tissue defects.Xylopic acid (XA), a diterpene kaurene and the major active ingredient of the African spice Xylopia aethiopica (Annonaceae), is reported to possess anti-inflammatory and analgesic properties. Here, we investigated the therapeutic potential of XA for rheumatoid arthritis (RA), a debilitating autoimmune inflammatory disease characterized by joint damage, in the complete Freund's adjuvant (CFA)-induced arthritis model in rats. We synthesized bioinspired reconstituted high-density lipoprotein (rHDL) nanoparticles loaded with purified XA crystals (rHDL/XA) that passively accumulate in inflamed joints of CFA-induced arthritic rats. Treatment with rHDL/XA minimized mononuclear cell infiltration of CFA-induced arthritic sites and ameliorated disease burden. https://www.selleckchem.com/products/bapta-am.html Metabolomic and transcriptomic analyses revealed that the major molecular pathways perturbed following CFA-induced arthritis correlated with amino acid and lipid metabolism, which were restored to normal states by rHDL/XA treatment. This work demonstrates the anti-RA potential of XA in a nanoformulation and uncovers its underlying therapeutic mechanisms at the transcript and metabolite levels.Vitreous endo-tamponades are commonly used in the treatment of retinal detachments and tears. They function by providing a tamponading force to support the retina after retina surgery. Current clinical vitreous endo-tamponades include expansile gases (such as sulfur hexafluoride (SF6) and perfluoropropane (C3F8)) and also sislicone oil (SiO). They are effective in promoting recovery but are disadvantaged by their lower refractive indices and lower densities as compared to the native vitreous, resulting in immediate blurred vision after surgery and necessitating patients to assume prolonged face-down positioning respectively. While the gas implants diffuse out over time, the SiO implants are non-biodegradable and require surgical removal. Therefore, there is much demand to develop an ideal vitreous endo-tamponade that can combine therapeutic effectiveness with patient comfort. Polymeric hydrogels have since attracted much attention due to their favourable properties such as high water content, high clarity, suitable refractive indices, suitable density, tuneable rheological properties, injectability, and biocompatibility. Many design strategies have been employed to design polymeric hydrogel-based vitreous endo-tamponades and they can be classified into four main strategies. This review seeks to analyse these various strategies and evaluate their effectiveness and also propose the key criteria to design successful polymeric hydrogel vitreous endo-tamponades.Cancer immunotherapy, leveraging the host's coordinated immune system to fight against tumor has been clinically validated. However, the modest response owing to the multiple ways of tumor immune evasion is one of the challenges in cancer immunotherapy. Tumor associated macrophages (TAMs), as a major component of the leukocytes infiltrating in all tumors, play crucial roles in driving cancer initiation, progress and metastasis via multiple mechanisms such as mediating chronic inflammation, promoting angiogenesis, taming protective immune responses, and supporting migration and intravasation. TAMs targeted therapeutics have achieved remarkable successes in clinical trials mostly through the use of small-molecule agents and antibodies. However, efforts for further application have met with challenges of limited efficacy and safety. Nanomaterials can provide versatile approaches to realize the superior spatiotemporal control over immunomodulation to amplify immune responses, ultimately enhancing the therapeutic benefits and reducing toxicity. Here, the potential drugs used in TAM-centered cancer treatment in clinic are summarized and the recent advances of TAMs targeted nanomedicines in this filed are highlighted. More importantly, we focus on how nanomedicine can exert their advantages in spatial and temporal control of immunomodulation.Neural stem cells (NSCs) transplantation at the injury site of central nerve system (CNS) makes it possible for neuroregeneration. Long-term cell survival and low proliferation, differentiation, and migration rates of NSCs-graft have been the most challenging aspect on NSCs application. New multichannel electrical stimulation (ES) device was designed to enhance neural stem cells (NSCs) differentiation into mature neurons. Compared to controls, ES at nanoscale topography enhanced the expression of mature neuronal marker, growth of the neurites, concentration of BDNF and electrophysiological activity. RNA sequencing analysis validated that ES promoted NSC-derived neuronal differentiation through enhancing autophagy signaling. Emerging evidences showed that insufficient or excessive autophagy contributes to neurite degeneration. Excessive ES current were able to enhance neuronal autophagy, the neuronal cells showed poor viability, reduced neurite outgrowth and electrophysiological activity. Well-controlled autophagy not only protects against neurodegeneration, but also regulates neurogenesis.