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In nanocomposite electrodes, besides the synergistic effect that takes advantage of the merits of each component, phase interfaces between the components would contribute significantly to the overall electrochemical properties. However, the knowledge of such effects is far from being well developed up to now. The present work aims at a mechanistic understanding of the phase interface effect in C@TiO2 coreâ€"shell nanocomposite anode which is both scientifically and industrially important. Firstly, amorphous C, anatase TiO2 and C@anatse-TiO2 electrodes are compared. The C@anatase-TiO2 shows an obvious higher specific capacity (316.5 mAh gâˆ'1 at a current density of 37 mA gâˆ'1 after 100 cycles) and Li-ion diffusion coefficient (4.0 × 10â€"14 cm2 sâˆ'1) than the amorphous C (178 mAh gâˆ'1 and 2.9 × 10â€"15 cm2 sâˆ'1) and anatase TiO2 (120 mAh gâˆ'1 and 1.6 × 10â€"15 cm2 sâˆ'1) owing to the C/TiO2 phase interface effect. Then, C@anatase/rutile-TiO2 is obtained by a heat treatment of the C@anatase-TiO2. Due to an anatase-to-rutile phase transformation and diffusion of C along the anatase/rutile phase interface, additional abundant C/TiO2 phase interfaces are created. This endows the C@anatase/rutile-TiO2 with further boosted specific capacity (409.4 mAh gâˆ'1 at 37 mA gâˆ'1 after 100 cycles) and Li-ion diffusion coefficient (3.2 × 10â€"13 cm2 sâˆ'1), and excellent rate capability (368.6 mAh gâˆ'1 at 444 mA gâˆ'1). These greatly enhanced electrochemical properties explicitly reveal phase interface engineering as a feasible way to boost the electrochemical performance of nanocomposite anodes for Li-ion batteries. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a devastating trauma that leads to irreversible motor and sensory dysfunction and is, so far, without effective treatment. Recently, however, nano‐sized extracellular vesicles derived from preconditioned mesenchymal stem cells (MSCs) have shown great promise in treating various diseases, including SCI. In this study, we investigated whether extracellular vesicles (MEVs) derived from MSCs pretreated with melatonin (MT), which is well recognized to be useful in treating diseases, including Alzheimer's disease, non‐small cell lung cancer, acute ischemia‐reperfusion liver injury, chronic kidney disease, and SCI, are better able to promote functional recovery in mice after SCI than extracellular vesicles derived from MSCs without preconditioning (EVs). MEVs were found to facilitate motor behavioral recovery more than EVs and to increase microglia/macrophages polarization from M1‐like to M2‐like in mice. Experiments in BV2 microglia and RAW264.7 macrophages confirmed that MEVs facilitate M2‐like polarization and also showed that they reduce the production of reactive oxygen species (ROS) and regulate mitochondrial function. Proteomics analysis revealed that ubiquitin‐specific protease 29 (USP29) was markedly increased in MEVs, and knockdown of USP29 in MEVs (shUSP29‐MEVs) abolished MEVs‐mediated benefits in vitro and in vivo. We then showed that USP29 interacts with, deubiquitinates and therefore stabilizes nuclear factor‐like 2 (NRF2), thereby regulating microglia/macrophages polarization. In NRF2 knockout mice, MEVs failed to promote functional recovery and M2‐like microglia/macrophages polarization. We also showed that MT reduced global N6‐methyladenosine (m6A) modification and levels of the m6A "writer" methyltransferase‐like 3 (METTL3). The stability of USP29 mRNA in MSCs was enhanced by treatment with MT, but inhibited by overexpression of METTL3. This study describes a very promising extracellular vesicle‐based approach for treating SCI. [ABSTRACT FROM AUTHOR]

High mobility group box (HMGB) consists primarily of HMGB1, HMGB2, and HMGB3 proteins. Although abnormal HMGB expression is associated with various tumors, the relationship with gastric cancer (GC) remains unclear. In this study, HMGB1, HMGB2, and HMGB3 expression was analyzed using the Oncomine and TCGA databases. Correlations between HMGB1, HMGB2, and HMGB3 and clinicopathological factors were analyzed. cBioPortal was used to analyze HMGB1, HMGB2, and HMGB3 genetic alterations and its gene regulation network in GC tissue. HMGB1, HMGB2, and HMGB3 expression was higher in tumor tissues than in normal tissues, especially in GC. High HMGB1, HMGB2, and HMGB3 expression may predict a poor prognosis among patients with GC (hazard ratios [HR] = 1.90; 95% confidence interval [CI]: [1.30−2.78]) and human digestive system neoplasm (HR = 1.85; 95% CI [1.64−2.10]). These findings suggest that HMGB1, HMGB2, and HMGB3 may be useful prognostic indicators for patients with GC. [ABSTRACT FROM AUTHOR]

Rationale and Objectives: Secondary vertebral compression fractures (SVCF) are very common in patients after vertebral augmentation (VA). The aim of this study was to establish a radiomic-based model to predict SVCF and specify appropriate treatment strategies., Materials and Methods: Patients diagnosed with osteoporotic vertebral compression fracture (OVCF) and undergoing VA surgery at our center between 2017 and 2021 were subject to a retrospective analysis. Radiological features of the T6-L5 vertebrae were derived from CT images. Clustering analysis, t-test, and LASSO (least absolute shrinkage and selection operator) regression were used to identify the optimization characteristics. A radiological signature model was constructed through the best combination of 13 machine learning algorithms. Radiomics signature was integrated with clinical characteristics into a nomogram for clinical applications. The model reliability was assessed by receiver operating characteristic (ROC) curve, calibration curve, clinical decision analysis (DCA), log-rank test, and confusion matrix., Results: A total of 470 eligible patients (81 with SVCF and 389 without) were identified in the clinical cohort. Eight radiomics features were identified and incorporated into machine learning, and "XGBoost" model showed the best performance. Final logistic nomogram included radiomics signature (P < 0.001), bone cement volume (P = 0.034), and T-scores of L1-L4 (P = 0.001), and showed satisfactory prediction capability in training set (0.986, 95%CI 0.969-1.000) and verification set (0.884, 95%CI 0.823-0.946)., Conclusion: Our radiomics-clinical model based on machine learning showed potential to prospectively predict SVCF after VA and provide precise treatment strategies., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Association of University Radiologists. Published by Elsevier Inc. All rights reserved.)

RNA N 6 -methyladenosine (m 6 A) modification is involved in diverse biological processes. However, its role in spinal cord injury (SCI) is poorly understood. The m 6 A level increases in injured spinal cord, and METTL3, which is the core subunit of methyltransferase complex, is upregulated in reactive astrocytes and further stabilized by the USP1/UAF1 complex after SCI. The USP1/UAF1 complex specifically binds to and subsequently removes K48-linked ubiquitination of the METTL3 protein to maintain its stability after SCI. Moreover, conditional knockout of astrocytic METTL3 in both sexes of mice significantly suppressed reactive astrogliosis after SCI, thus resulting in widespread infiltration of inflammatory cells, aggravated neuronal loss, hampered axonal regeneration, and impaired functional recovery. Mechanistically, the YAP1 transcript was identified as a potential target of METTL3 in astrocytes. METTL3 could selectively methylate the 3'-UTR region of the YAP1 transcript, which subsequently maintains its stability in an IGF2BP2-dependent manner. In vivo , YAP1 overexpression by adeno-associated virus injection remarkably contributed to reactive astrogliosis and partly reversed the detrimental effects of METTL3 knockout on functional recovery after SCI. Furthermore, we found that the methyltransferase activity of METTL3 plays an essential role in reactive astrogliosis and motor repair, whereas METTL3 mutant without methyltransferase function failed to promote functional recovery after SCI. Our study reveals the previously unreported role of METTL3-mediated m 6 A modification in SCI and might provide a potential therapy for SCI. SIGNIFICANCE STATEMENT Spinal cord injury is a devastating trauma of the CNS involving motor and sensory impairments. However, epigenetic modification in spinal cord injury is still unclear. Here, we propose an m 6 A regulation effect of astrocytic METTL3 following spinal cord injury, and we further characterize its underlying mechanism, which might provide promising strategies for spinal cord injury treatment., Competing Interests: The authors declared no competing financial interests., (Copyright © 2023 the authors.)

In nanocomposite electrodes, besides the synergistic effect that takes advantage of the merits of each component, phase interfaces between the components would contribute significantly to the overall electrochemical properties. However, the knowledge of such effects is far from being well developed up to now. The present work aims at a mechanistic understanding of the phase interface effect in C@TiO 2 core-shell nanocomposite anode which is both scientifically and industrially important. Firstly, amorphous C, anatase TiO 2 and C@anatse-TiO 2 electrodes are compared. The C@anatase-TiO 2 shows an obvious higher specific capacity (316.5 mAh g -1 at a current density of 37 mA g -1 after 100 cycles) and Li-ion diffusion coefficient (4.0 × 10 -14 cm 2 s -1 ) than the amorphous C (178 mAh g -1 and 2.9 × 10 -15 cm 2 s -1 ) and anatase TiO 2 (120 mAh g -1 and 1.6 × 10 -15 cm 2 s -1 ) owing to the C/TiO 2 phase interface effect. Then, C@anatase/rutile-TiO 2 is obtained by a heat treatment of the C@anatase-TiO 2 . Due to an anatase-to-rutile phase transformation and diffusion of C along the anatase/rutile phase interface, additional abundant C/TiO 2 phase interfaces are created. This endows the C@anatase/rutile-TiO 2 with further boosted specific capacity (409.4 mAh g -1 at 37 mA g -1 after 100 cycles) and Li-ion diffusion coefficient (3.2 × 10 -13 cm 2 s -1 ), and excellent rate capability (368.6 mAh g -1 at 444 mA g -1 ). These greatly enhanced electrochemical properties explicitly reveal phase interface engineering as a feasible way to boost the electrochemical performance of nanocomposite anodes for Li-ion batteries., (© 2021 IOP Publishing Ltd.)