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Developing superporous hemostatic sponges with simultaneously enhanced permeability and mechanical properties remains challenging but highly desirable to achieve rapid hemostasis for non-compressible hemorrhage. Typical approaches to improve the permeability of hemostatic sponges by increasing porosity sacrifice mechanical properties and yield limited pore interconnectivity, thereby undermining the hemostatic efficacy and subsequent tissue regeneration. Herein, we propose a temperature-assisted secondary network compaction strategy following the phase separation-induced primary compaction to fabricate the superporous chitosan sponge with highly-interconnected porous structure, enhanced blood absorption rate and capacity, and fatigue resistance. The superporous chitosan sponge exhibits rapid shape recovery after absorbing blood and maintains sufficient pressure on wounds to build a robust physical barrier to greatly improve hemostatic efficiency. Furthermore, the superporous chitosan sponge outperforms commercial gauze, gelatin sponges, and chitosan powder by enhancing hemostatic efficiency, cell infiltration, vascular regeneration, and in-situ tissue regeneration in non-compressible organ injury models, respectively. We believe the proposed secondary network compaction strategy provides a simple yet effective method to fabricate superporous hemostatic sponges for diverse clinical applications. Developing porous hemostatic sponges remains challenging. Here, authors proposed a temperature-assisted secondary network compaction strategy following the phase separation induced primary compaction to fabricate the superporous chitosan sponges.

Objective The association between Metabolic Syndrome (MetS), its components, and the risk of osteoarthritis (OA) has been a topic of conflicting evidence in different studies. The aim of this present study is to investigate the association between MetS, its components, and the risk of OA using data from the UK Biobank. Methods A prospective cohort study was conducted in the UK Biobank to assess the risk of osteoarthritis (OA) related to MetS. MetS was defined according to the criteria set by the International Diabetes Federation (IDF). Additionally, lifestyle factors, medications, and the inflammatory marker C-reactive protein (CRP) were included in the model. Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI). The cumulative risk of OA was analyzed using Kaplan–Meier curves and log-rank tests. To explore potential nonlinear associations between MetS components and OA risk, a restricted cubic splines (RCS) model was employed. In addition, the polygenic risk score (PRS) of OA was calculated to characterize individual genetic risk. Results A total of 45,581 cases of OA were identified among 370,311 participants, with a median follow-up time of 12.48 years. The study found that individuals with MetS had a 15% higher risk of developing OA (HR = 1.15, 95%CI:1.12–1.19). Additionally, central obesity was associated with a 58% increased risk of OA (HR = 1.58, 95%CI:1.5–1.66), while hyperglycemia was linked to a 13% higher risk (HR = 1.13, 95%CI:1.1–1.15). Dyslipidemia, specifically in triglycerides (HR = 1.07, 95%CI:1.05–1.09) and high-density lipoprotein (HR = 1.05, 95%CI:1.02–1.07), was also found to be slightly associated with OA risk. When stratified by PRS, those in the high PRS group had a significantly higher risk of OA compared to those with a low PRS, whereas no interaction was found between MetS and PRS on OA risks. Furthermore, the presence of MetS significantly increased the risk of OA by up to 35% in individuals with elevated CRP levels (HR = 1.35, 95% CI:1.3–1.4). Conclusion MetS and its components have been found to be associated with an increased risk of OA, particularly in individuals with elevated levels of CRP. These findings highlight the significance of managing MetS as a preventive and intervention measure for OA.

Objective To compare the neurological recovery between patients with adequate and inadequate immediate spinal cord expansion after sufficient decompression in degenerative cervical myelopathy (DCM). Methods Twenty-seven patients subjected to French-door laminoplasty underwent the guidance of intraoperative ultrasound (IOUS) and were prospectively included. The modified Japanese Orthopedic Association (mJOA) score was evaluated before surgery and at 12 months postoperatively. The maximum spinal cord compression (MSCC) after sufficient decompression was calculated on the IOUS image; patients were divided into adequate (MSCC ≥ 0.95) and inadequate (MSCC < 0.95) expansion groups according to the MSCC. The mJOA score, spinal cord hyperechogenicity, age at surgery, symptom duration, occupational rate of the spinal canal, and the minimum anteroposterior diameter of the spinal cord between the two groups were compared. Results Initially, 2 cases showed residual compression on IOUS; after further decompression, all patients acquired sufficient decompression. All patients achieved improvements in mJOA scores with an average recovery rate of 68.6 ± 20.3%. The recovery rate of the mJOA score of the inadequate expansion group was significantly inferior to that of the adequate expansion group (59.2 ± 21.7% versus 76.2 ± 16.2%, p = 0.028). The spinal cord hyperechogenicity was more common in the inadequate expansion group, while the spinal cord anteroposterior diameter of the inadequate expansion group was significantly smaller than that of the adequate expansion group. Conclusions The application of IOUS in French-door laminoplasty could help to confirm sufficient decompression for the treatment of DCM. Inadequate spinal cord expansion after sufficient decompression had the high possibility of predicting less satisfactory neurological recovery of DCM. Key Points • The intraoperative ultrasound revealed that not all degenerative cervical myelopathy patients acquired adequate spinal cord expansion after sufficient decompression. • Patients who failed to acquire adequate spinal cord expansion commonly combined with spinal cord hyperechogenicity and trended to achieve less satisfactory neurological recovery after surgical decompression. • Inadequate spinal cord expansion after sufficient decompression had the high possibility of predicting less satisfactory neurological recovery of patients with degenerative cervical myelopathy.

This study investigates the association between handgrip strength, walking pace, and the incidence of degenerative cervical myelopathy (DCM) using the UK Biobank dataset. We analyzed data from 364,716 UK Biobank participants without prior neurological conditions. Handgrip strength was measured with a dynamometer, and walking pace was self-reported. Cox proportional hazards models assessed hazard ratios (HRs) and 95% confidence intervals (CIs) for DCM development. The cohort, with an average age of 56.2 years (SD, 8.1) and 47.4% male, was followed for a median of 12.6 years. During this period, 3,993 participants (1.1%) developed DCM. A significant inverse correlation was found between handgrip strength and DCM incidence (P for trend < 0.001), with decreasing HRs for DCM across quartiles of increasing grip strength: HRs were 0.70 (95% CI: 0.64-0.76), 0.62 (95% CI: 0.57-0.68), and 0.59 (95% CI: 0.54-0.66) for the second, third, and fourth quartiles, respectively. Participants with average or brisk walking paces had a lower DCM risk (HR, 0.55; 95% CI: 0.50-0.61 and HR, 0.48; 95% CI: 0.43-0.54) compared to slow walkers. The greatest risk reduction was in those with both higher handgrip strength and faster pace (HR, 0.39; 95% CI: 0.34-0.44). Handgrip strength and walking pace are inversely associated with DCM incidence, suggesting their potential as cost-effective screening tools for identifying individuals at risk for DCM.

Intervertebral disc degeneration (IVDD) is a prevalent chronic spinal condition characterized by the deterioration of the intervertebral discs (IVD), leading to structural damage and associated pain. This degenerative process is closely linked to oxidative stress injury, which plays a pivotal role in its onset and progression. Oxidative stress in IVDD results from the excessive production of reactive oxygen species (ROS) and impaired ROS clearance mechanisms, disrupting the redox balance within the intervertebral disc. Consequently, oxidative stress contributes to the degradation of the extracellular matrix (ECM), promotes cell apoptosis, and exacerbates disc tissue damage. Current treatment options for IVDD face significant challenges in effectively alleviating the oxidative stress-induced damage and facilitating disc tissue repair. However, recent advancements in biomaterials have opened new avenues of hope for IVDD treatment by addressing oxidative stress. In this review, we first provide an overview of the pathophysiological process of IVDD and explore the mechanisms and pathways associated with oxidative stress injury. Then, we delve into the current research on antioxidant biomaterials employed in the treatment of IVDD, and outline the advantages and limitations of hydrogel, nanomaterials, polyphenol and inorganic materials. Finally, we propose the future research direction of antioxidant biomaterials in IVDD treatment. The main idea of this review is shown in Scheme 1. [Display omitted] •The mechanisms of oxidative stress damage in intervertebral disc degeneration are discussed.•The pathophysiological changes that occur during the process of the intervertebral disc degeneration are discussed.•Recent findings on antioxidant biomaterials for the treatment of intervertebral disc degeneration are summarized.•The future applications of antioxidant biomaterials in the intervertebral disc degeneration are prospected.

Intervertebral disc degeneration (IDD) has been considered as the primary pathological mechanism that underlies low back pain. Understanding the molecular mechanisms underlying human IDD is imperative for making strategies to treat IDD-related diseases. Herein, we report the molecular programs, lineage progression patterns, and paths of cellular communications during the progression of IDD using single-cell RNA sequencing (scRNA-seq) on nucleus pulposus (NP) cells from patients with different grades of IDD undergoing discectomy. New subtypes of cells and cell-type-specific gene signatures of the metabolic homeostatic NP cells (Met NPC), adhesive NP cells (Adh NPC), inflammatory response NP cells (IR NPC), endoplasmic reticulum stress NP cells (ERS NPC), fibrocartilaginous NP cells (Fc NPC), and CD70 and CD82 + progenitor NP cells (Pro NPC) were identified. In the late stage of IDD, the IR NPC and Fc NPC account for a large proportion of NPC. Importantly, immune cells including macrophages, T cells, myeloid progenitors, and neutrophils were also identified, and further analysis showed that significant intercellular interaction between macrophages and Pro NPC occurred via MIF (macrophage migration inhibitory factor) and NF-kB signaling pathways during the progression of IDD. In addition, dynamic polarization of macrophage M1 and M2 cell subtypes was found in the progression of IDD, and gene set functional enrichment analysis suggested a significant role of the macrophage polarization in regulating cell metabolism, especially the Pro NPC. Finally, we found that the NP cells in the late degenerative stage were mainly composed of the cell types related to inflammatory and endoplasmic reticulum (ER) response, and fibrocartilaginous activity. Our results provided new insights into the identification of NP cell populations at single-cell resolution and at the relatively whole-transcriptome scale, accompanied by cellular communications between immune cells and NP cells, and discriminative markers in relation to specific cell subsets. These new findings present clues for effective and functional manipulation of human IDD-related bioremediation and healthcare.

Biomolecule‐reinforced graphene materials (Bio‐RGMs) have emerged as versatile matrices for biomedical and tissue engineering applications, owing to the combination of graphene‐based materials (GMs) with biomolecular components and their synergistic effects. In this review, an overview of the design, synthesis, structural/functional regulation, and bone engineering applications of various Bio‐RGMs is provided. Both covalent and noncovalent methods for conjugating biomolecules onto GMs, followed by an exploration of the structural diversity of Bio‐RGMs, ranging from 1D nanofibers to 2D membranes and 3D scaffolds/hydrogels/aerogels are discussed. Techniques such as electrospinning, self‐assembly, freeze‐drying, 3D printing, and templated synthesis are highlighted for their roles in designing and fabricating Bio‐RGM architectures. Additionally, specific properties and functions endowed to Bio‐RGMs by biomolecule conjugation, including biocompatibility, cytotoxicity, antibacterial activity, drug delivery ability, and fluorescent sensing are examined. Finally, recent advance is showcased in fabricating Bio‐RGMs for the bone tissue engineering applications of bone repair, regeneration, grafting, drug/cell delivery, and tumor inhibition, and further, the potential of Bio‐RGMs for preclinical applications is analyzed. It is believed that this review will deepen readers’ understanding of biomolecule–GM interactions and inspire the development of innovative Bio‐RGMs for advanced biomedical and tissue engineering applications. Biomolecule‐reinforced graphene materials (Bio‐RGMs) exhibit synergistic merits of biomolecules and graphene materials, revealing wide applications in various fields. This prehensive review focuses on the design and structural/functional regulations of Bio‐RGMs with high biocompatibility, cytotoxicity, antibacterial activity, controlled drug delivery, and fluorescent sensing, and further presents recent advances in the bioactive Bio‐RGMs for bone tissue engineering applications.

To analyze the correlations between intraoperative ultrasound and MRI metrics of the spinal cord in degenerative cervical myelopathy and identify novel potential predictive ultrasonic indicators of neurological recovery for degenerative cervical myelopathy. Twenty-two patients who underwent French-door laminoplasty for multilevel degenerative cervical myelopathy were followed up for 12 months. The Japanese Orthopedic Association (JOA) scores were assessed preoperatively and 12 months postoperatively. Maximum spinal cord compression and compression rates were measured and calculated using both intraoperative ultrasound imaging and preoperative T2-weight (T2W) MRI. Signal change rates of the spinal cord on preoperative T2W MRI and gray value ratios of dorsal and ventral spinal cord hyperechogenicity on intraoperative ultrasound imaging were measured and calculated. Correlations between intraoperative ultrasound metrics, MRI metrics, and the recovery rate JOA scores were analyzed using Spearman correlation analysis. The postoperative JOA scores improved significantly, with a mean recovery rate of 65.0 ± 20.3% ( < 0.001). No significant correlations were found between the operative ultrasound metrics and MRI metrics. The gray value ratios of the spinal cord hyperechogenicity was negatively correlated with the recovery rate of JOA scores (ρ = -0.638, = 0.001), while the ventral and dorsal gray value ratios of spinal cord hyperechogenicity were negatively correlated with the recovery rate of JOA-motor scores (ρ = -0.582, = 0.004) and JOA-sensory scores (ρ = -0.452, = 0.035), respectively. The dorsal gray value ratio was significantly higher than the ventral gray value ratio ( < 0.001), while the recovery rate of JOA-motor scores was better than that of JOA-sensory scores at 12 months post-surgery ( = 0.028). For degenerative cervical myelopathy, the correlations between intraoperative ultrasound and preoperative T2W MRI metrics were not significant. Gray value ratios of the spinal cord hyperechogenicity and dorsal and ventral spinal cord hyperechogenicity were significantly correlated with neurological recovery at 12 months postoperatively.

Intervertebral disc degeneration (IDD) induced lower back pain is a main cause of disability, resulting in a substantial workforce loss worldwide and placing a substantial burden on the global economy and healthcare systems. However, no effective disease‐modifying therapies presently exist for IDD or its related pathologies. Single‐cell sequencing analyses reveal progressive M1 macrophage polarization in NP cells correlating with IDD severity, underscoring the therapeutic imperative for dual‐targeting agents addressing both inflammatory dysregulation and matrix homeostasis. β‐mangostin (β_Man) is screened to be proven to possess potential therapeutic effects in alleviating IDD. β_Man possesses anti‐inflammatory capabilities, which include remodeling the homeostasis of the extracellular matrix, regulating macrophage polarization, and inhibiting apoptosis in the nucleus pulposus. TET2‐Prkcg exerts significant regulatory functions downstream of β_Man. Mechanically, β_Man mediated reduction of TET2 maintains the DNA methylation of Prkcg rather than hydroxymethylation, which promotes mitophagy and alleviates the inflammatory microenvironment. β_Man represents a promising novel therapeutic strategy for IDD treatment. The TET2‐Prkcg axis emerges as a novel therapeutic target for IDD treatment. β‐Mangostin alleviates intervertebral disc degeneration through dual modulation of macrophage polarization and the TET2‐Prkcg axis in nucleus pulposus cells.

Spinal cord injury (SCI) causes neuroinflammation, neuronal death, and severe axonal connections. Alleviating neuroinflammation, protecting residual cells and promoting neuronal regeneration via endogenous neural stem cells (eNSCs) represent potential strategies for SCI treatment. Extracellular vesicles (EVs) released by mesenchymal stem cells have emerged as pathological mediators and alternatives to cell-based therapies following SCI. In the present study, EVs isolated from untreated (control, C-EVs) and TGF-β1-treated (T-EVs) mesenchymal stem cells were injected into SCI mice to compare the therapeutic effects and explore the underlying mechanisms. Our study demonstrated for the first time that the application of T-EVs markedly enhanced the proliferation and antiapoptotic ability of NSCs in vitro. The infusion of T-EVs into SCI mice increased the shift from the M1 to M2 polarization of reactive microglia, alleviated neuroinflammation, and enhanced the neuroprotection of residual cells during the acute phase. Moreover, T-EVs increased the number of eNSCs around the epicenter. Consequently, T-EVs further promoted neurite outgrowth, increased axonal regrowth and remyelination, and facilitated locomotor recovery in the chronic stage. Furthermore, the use of T-EVs in Rictor−/− SCI mice (conditional knockout of Rictor in NSCs) showed that T-EVs failed to increase the activation of eNSCs and improve neurogenesis sufficiently, which suggested that T-EVs might induce the activation of eNSCs by targeting the mTORC2/Rictor pathway. Taken together, our findings indicate the prominent role of T-EVs in the treatment of SCI, and the therapeutic efficacy of T-EVs for SCI treatment might be optimized by enhancing the activation of eNSCs via the mTORC2/Rictor signaling pathway. [Display omitted] •TGF-β1 could alter MSC-derived EVs production.•T-EVs might be a promising therapeutic approach for treating SCI.•T-EVs optimize therapeutic efficacy by enhancing the activation of eNSCs via the mTORC2/Rictor pathway.