The medical community has expressed significant interest in the development of new types of artificial bones that mimic natural bones. In this study, computed tomography (CT)-guided fused deposition modeling (FDM) was employed to fabricate polycaprolactone (PCL)/hydroxyapatite (HA) and PCL 3D artificial bones to mimic natural goat femurs. The in vitro mechanical properties, in vitro cell biocompatibility, and in vivo performance of the artificial bones in a long load-bearing goat femur bone segmental defect model were studied. All of the results indicate that CT-guided FDM is a simple, convenient, relatively low-cost method that is suitable for fabricating natural bonelike artificial bones. Moreover, PCL/HA 3D artificial bones prepared by CT-guided FDM have more close mechanics to natural bone, good in vitro cell biocompatibility, biodegradation ability, and appropriate in vivo new bone formation ability. Therefore, PCL/HA 3D artificial bones could be potentially be of use in the treatment of patients with clinical bone defects.

Molecular composites comprising poly(p-sulfophenylene terephthalamide) (sPPTA), a sulfonated polyaramid rigidrod polyelectrolyte, and flexible-chain poly(vinyl alcohol) (PVA) were prepared by a green and easy-to-scale-up water casting method. Influence of sPPTA on the microstructure and properties of the molecular composites was systematically investigated. Fourier transform infrared spectroscopy confirms the existence of hydrogen bonding between sPPTA and PVA. Wide-angle X-ray diffraction patterns do not show the characteristic of neat sPPTA crystalline aggregates in the composites even when the sPPTA content is as high as 33 wt %, suggesting that the strong interaction between sPPTA and PVA prevents the self-aggregation of sPPTA and leads to the formation of PVA/sPPTA complexes inside the composites. Transmission electron microscopy shows that sPPTA has good compatibility with PVA, and nanoscale fibril-like supramolecular assemblies dispersing uniformly in the composites become observable with the increase of sPPTA content. Moreover, the PVA/sPPTA complexes have a strong effect on the melt point, crystallinity, mechanical properties, and thermal stability of PVA. The PVA/sPPTA composites exhibit both high strength and high ductility. When the content of sPPTA is 5 wt %, the PVA/sPPTA composite exhibits the best mechanical properties, with a tensile strength of 169 ± 13 MPa, which is 54% higher than that of neat PVA (110 ± 10 MPa). Surprisingly, the reinforcement factor is even superior to that of multiwalled carbon nanotubes, vapor grown carbon fibers, and nanodiamonds previously reported for the reinforcement of PVA nanocomposites. Moreover, the PVA/sPPTA molecular composites have a relatively low modulus but a much larger elongation at break than prefabricated nanocomposites, showing good ductility. The strong and tough PVA/sPPTA molecular composites can be potentially used as high performance membranes or fibers in the future.

The (3-aminopropyl)triethoxysilane (APTES) self-assembled monolayer (SAM) has been widely used in fundamental research and engineering applications; however, characterization of its surface wetting properties remains problematic. Surface wetting properties of the APTES SAM were systematically investigated using different contact angle measurement techniques. The observed unique nonideal wetting was related to the APTES SAM structure, including surface hydrogen bond formation, the surface roughness, and the effect of water penetration. The contact angle decreased dramatically with the residence time on the APTES SAM surface, and a special contact angle hysteresis phenomenon was observed. The contact angle could be distorted by the calculation method used for the nonideal APTES SAM surface. Values calculated by the tangent-leaning method were thought to be more accurate and credible. Our findings demonstrated that static advancing contact angles were the most stable and credible for characterizing the APTES SAM surface wettability.

Traumatic spinal cord injury (SCI) is caused by external physical impacts and can induce complex cascade events, sometimes converging to paralysis. Existing clinical drugs to traumatic SCI have limited therapeutic efficacy because of either the poor blood–spinal cord barrier (BSCB) permeability or a single function. Here, we suggest a “pleiotropic messenger” strategy based on near-infrared (NIR)–triggered on-demand NO release at the lesion area for traumatic SCI recovery via the concurrent neuroregeneration and neuroprotection processing. This NO delivery system was constructed as upconversion nanoparticle (UCNP) core coated by zeolitic imidazolate framework–8 (ZIF-8) with NO donor (CysNO). This combined strategy substantial promotes the repair of SCI in vertebrates, ascribable to the pleiotropic effects of NO including the suppression of gliosis and inflammation, the promotion of neuroregeneration, and the protection of neurons from apoptosis, which opens intriguing perspectives not only in nerve repair but also in neurological research and tissue engineering.

TRIM66 belongs to the family of tripartite motif (TRIM)-containing proteins. Alterations in TRIM proteins have been implicated in several malignancies. This study was aimed at elucidating the expression and biological function of TRIM66 in osteosarcoma. Here, TRIM66 expression level was higher in osteosarcoma tissues than in normal tissues. High TRIM66 expression was correlated with high rate of local recurrence and lung metastasis, and short survival time. Then, we found that knockdown of TRIM66 in two osteosarcoma cell lines, MG63 and HOS, significantly inhibited cell proliferation and induced G1-phase arrest. Moreover, inhibition of TRIM66 in osteosarcoma cells significantly induced cell apoptosis, while remarkably inhibited cell migration, invasion as well as tumorigenicity in nude mice. Gene set enrichment analysis in Gene Expression Omnibus dataset revealed that apoptosis, epithelial-mesenchymal transition (EMT) and transforming growth factor-β (TGF-β) signaling pathway-related genes were enriched in TRIM66 higher expression patients, which was confirmed by western blot analysis in osteosarcoma cells with TRIM66 silenced. In conclusion, TRIM66 may act as an oncogene through suppressing apoptosis pathway and promoting TGF-β signaling in osteosarcoma carcinogenesis. TRIM66 may be a prognostic factor and potential therapeutic target in osteosarcoma.