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Any sort of wound injury leads to the destruction of skin integrity and wound formation, causing millions of deaths every year and accounting for 10% of death rate insight into various diseases. The ideal biological wound dressings are expected to possess extraordinary mechanical characterization, cytocompatibility, adhesive properties, antibacterial properties, and conductivity of endogenous electric current to enhance the wound healing process. Recent studies have demonstrated that biomedical hydrogels can be used as typical wound dressings to accelerate the whole healing process due to them having a similar composition structure to skin, but they are also limited by ideal biocompatibility and stable mechanical properties. To extend the number of practical candidates in the field of wound healing, we designed a new structural zwitterion poly[3-(dimethyl(4-vinylbenzyl) ammonium) propyl sulfonate] (SVBA) into a poly-acrylamide network, with remarkable mechanical properties, stable rheological property, effective antibacterial properties, strong adsorption, high penetrability, and good electroactive properties. Both in vivo and in vitro evidence indicates biocompatibility, and strong healing efficiency, indicating that poly (AAm-co-SVBA) (PAS) hydrogels as new wound healing candidates with biomedical applications.

An electrical signal is the key basis of normal physiological function of the nerve, and the stimulation of the electric signal also plays a very special role in the repair process of nerve injury. Electric stimulation is shown to be effective in promoting axonal regeneration and myelination, thereby promoting nerve injury repair. At present, it is considered that electric conduction recovery is a key aspect of regeneration and repair of long nerve defects. Conductive neural scaffolds have attracted more and more attention due to their similar electrical properties and good biocompatibility with normal nerves. Herein, PCL and MXene-PCL nerve guidance conduits (NGCs) were prepared; their effect on nerve regeneration was evaluated in vitro and in vivo. The results show that the NGCs have good biocompatibility in vitro. Furthermore, a sciatic nerve defect model (15 mm) of SD rats was made, and then the fabricated NGCs were implanted. MXene-PCL NGCs show similar results with the autograft in the sciatic function index, electrophysiological examination, angiogenesis, and morphological nerve regeneration. It is possible that the conductive MXene-PCL NGC could transmit physiological neural electric signals, induce angiogenesis, and stimulate nerve regeneration. This paper presents a novel design of MXene-PCL NGC that could transmit self-originated electric stimulation. In the future, it can be combined with other features to promote nerve regeneration.

Background Apart from the current understanding of enzyme function, the mechanism of ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) deficiency-associated osteoporosis is unknown. We aimed to explore the changes in the expression of signaling pathways of bone tissues involved in Enpp1 deficiency. Methods The body weights and morphology and histology of the bones of male Enpp1 knockout (KO) and wild-type (WT) mice were assessed. The humeri of WT and Enpp1 KO mice at 12 weeks of age were subjected to high-throughput quantitative molecular measurements, and bioinformatics analysis was performed. Proteins from humeri and calvarial pre-osteoblasts (Pobs) were used to verify the differentially expressed signaling pathways and to explain the mechanism of Enpp1 deficiency-associated osteoporosis. Results Enpp1 KO mice had significantly lower body weight and trabecular bone mass in the hindlimbs than WT mice. Proteomics and immunoblotting showed that Enpp1 deletion downregulated the expression of the p38 mitogen-activated protein kinase (MAPK) signaling pathway in bones. Lysophosphatidic acid (LPA) was involved in activating the MKK3/p38 MAPK/PCNA pathway and proliferating Pobs in Enpp1 KO mice, whereas a p38 MAPK inhibitor suppressed the LPA-induced pro-proliferation phenotype (p < 0.05). Conclusion The inhibition of MKK3/p38 MAPK/PCNA pathway plays an important role in the development of osteoporosis caused by Enpp1 deficiency, and LPA partially rescued the proliferation of pre-osteoblasts via the MKK3/p38 MAPK/PCNA pathway.

Objects. Human umbilical cord Wharton jelly cells (HUCWJCs) treatment has been proven to be a useful treatment approach for various inflammatory diseases. This study investigated the therapeutic effect and mechanism of HUCWJCs on D-galactose-induced osteoporosis in mice. Methods. Sixteen male mice were randomly divided into 4 groups: control (ordinary feeding), D-gal (D-galactose) group, D-gal + MSC (human umbilical cord Wharton jelly cells), and D-gal + MSC-TNFα groups. Except for the control group (fed with same amount of saline solution), other mice received gastric feeding of 250 mg/kg D-galactose every day for 8 weeks. TNFα (10 ng/mL for 24 h) cocultured or noncocultured HUCWJCs (5 × 105) were suspended in 0.1 ml of sterile PBS and injected into tail veins every other week in D-gal + MSC-TNFα and D-gal + MSC groups, respectively, and only 0.1 ml of sterile PBS for control and D-gal groups. The bone mass was detected by qPCR, ELISA, microcomputed tomography (μCT), and hematoxylin-eosin staining. Proliferation, apoptosis, and differentiation of periosteal-derived osteoblasts (POB) were assessed. Transwell assay and scratch healing were performed to detect POB migration and invasion ability. The effect of HUCWJCs on POB signaling pathway expression was evaluated by immunoblotting. Results. The malondialdehyde (MDA) in serum was higher and superoxide dismutase (SOD) was lower in the D-gal group compared to the other groups ( p < 0.05 ). Mice in D-gal group showed significantly decreased bone mass when compared to the control group, while HUCWJCs treatment partially rescued the phenotype, as demonstrated by μCT and histology ( p < 0.05 ). Mechanically, HUCWJCs treatment partially promoted proliferation and migration and decreased apoptosis of POB induced by oxidative stress via activating the mitogen-activated protein kinase (MAPK) signaling pathway. Conclusion. HUCWJCs can prevent the progression of osteoporosis by inhibiting oxidative stress, which may act by regulating osteoblasts fate through the MAPK signaling pathway.

Background Numerous complications of lumbar fusion surgery have been reported, with adjacent segment disease (ASD) being one of the most important. Few studies describe the effect of sagittal, horizontal screw angles and distance of pedicle screw apex to superior endplate on the incidence of ASD in lumbar spine. The purpose of this retrospective study is to evaluate the hypothesis that unsatisfactory pedicle screw insertion positions would increase the likelihood of ASD. Methods Outpatients with lumbar spinal stenosis underwent posterolateral lumbar fusion at L4-S1 with a least 2-year follow-up were studied. ASD at L3–L4 was defined as a condition in which intervertebral disk narrowing, posterior vertebral opening, and vertebral slippage progress at the last follow-up in comparison with the postoperative. Independent t test was performed to compare data between two groups; Spearman analysis was performed to analyze the relationship between two continuous variables. Multivariate binary logistic models were performed to identify the independent risk factors of ASD. The receiver operating characteristic (ROC) curve was performed to measure model discrimination and Hosmer–Lemeshow (H–L) test was used to measure calibration. ROC curve evaluated the discrimination ability of sagittal screw angle and distance in predicting incidence of ASD. Results Patients in ASD group exhibit higher incidence of osteoporosis, higher Visual analogue scale (VAS), Oswestry disability index (ODI), bigger sagittal screw angle, shorter distance of pedicle screw apex to superior endplate than those in non-ASD group (p < 0.05). VAS, ODI at the last follow-up were positively correlated with Pfirrmann grade of L3–4 disk and sagittal screw angle, while negatively correlated with distance of screw apex to superior endplate (p < 0.05). Multivariate binary logistic model indicated that follow-up time (odds ratio [OR] 1.637, 95% confidence interval [CI] 1.186–2.260), distance of screw apex to superior endplate (OR 0.150, 95% CI 0.067–0.336), sagittal screw angle (OR 2.404, 95% CI 1.608–3.594) were statistically significant. The models showed great discrimination and calibration. The area under the curve of ASD identified by sagittal angle and distance was 0.895 and the cut-off values were 5.500° and 6.250 mm, respectively. Conclusion Sagittal screw angle and distance of screw apex to superior endplate were significantly associated with the risk of ASD.

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