BACKGROUND:Spinal cord injury (SCI) induces gut microbiota dysbiosis, which significantly affects recovery. Buyang Huanwu Decoction (BHD), a traditional Chinese medicine formula, has shown therapeutic effects on SCI. Although BHD is known to modulate gut microbiota, whether its benefits are mediated through the gut-spinal cord axis remains unclear. METHODS:A rat SCI model was established. BHD was administered orally, and fecal microbiota transplantation (FMT) from BHD-treated rats (BHD-FMT) was performed to assess neuroprotective and gut-protective effects. Behavioral testing, histology, and immunofluorescence evaluated motor recovery, inflammation, and neuroregeneration. Gut microbiota profiling was performed using 16S rDNA sequencing and metagenomics, while targeted metabolomics quantified tryptophan metabolites. Transcriptomics validated key pathways, and a microbiota-metabolite-signaling network was constructed. RESULTS:BHD significantly improved motor function, reduced spinal inflammation, and promoted neuronal survival and axonal regeneration. It restored gut function, reduced colonic inflammation, and enhanced ZO-1 and Occludin expression, which were further confirmed by FMT. BHD-FMT reshaped the gut microbiota and enriched Lactobacillus johnsonii, which correlated positively with recovery. Metabolomics showed increased tryptophan metabolites, including indole-3-lactic acid (ILA) and indole-3-propionic acid (IPA), with ILA strongly associated with functional improvement. Transcriptomic analysis and Western blot validation demonstrated that BHD-FMT activated the AhR-PI3K/Akt pathway, which was suppressed by an AhR antagonist. CONCLUSION:BHD promotes neuroregeneration after SCI by reshaping gut microbiota and enhancing tryptophan metabolism, potentially exerting its effects through the L. johnsonii-ILA-AhR-PI3K/Akt network. These findings reveal a gut-spinal cord axis-mediated mechanism of BHD and highlight microecological targets for SCI therapy.

Objectives Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterised by synovial inflammation and joint destruction, in which fibroblast-like synoviocytes (FLS) play a pivotal role through their hyperproliferative, invasive and inflammatory properties. The salt-inducible kinase (SIK) family regulates inflammatory responses, yet the role of its isoform SIK3 in RA and the therapeutic potential of its inhibition remain unclear. This study investigates the effects of HG-9-91-01, a potent SIK inhibitor, on RA-FLS pathogenicity and disease progression. Methods The impact of HG-9-91-01 on human MH7A cells was assessed using cell counting kit-8, 5-ethynyl-2′-deoxyuridine, flow cytometry, wound healing and Transwell assays. RNA sequencing, bioinformatics analyses and western blot analysis were employed to explore the underlying mechanisms. The therapeutic efficacy of HG-9-91-01 was evaluated in a murine collagen-induced arthritis (CIA) model through clinical scoring, histopathology and micro-CT imaging. Results SIK3 was significantly upregulated in RA synovial tissues and correlated with disease activity. HG-9-91-01 potently inhibited MH7A cell proliferation, migration and invasion while promoting apoptosis. Transcriptomic and molecular analyses revealed that these effects were mediated through the concurrent suppression of the phosphoinositide 3-kinase-protein kinase B (PI3K-Akt) and nuclear factor kappa B (NF-κB) signalling pathways, leading to downstream modulation of Bcl-2-associated X protein, B-cell lymphoma 2, inducible nitric oxide synthase, tumour necrosis factor-α and matrix metalloproteinase-9. In CIA mice, HG-9-91-01 administration markedly alleviated arthritis severity, synovitis, cartilage degradation and bone erosion. Conclusions Our findings demonstrate that HG-9-91-01 attenuates RA progression by directly targeting FLS pathogenicity via dual inhibition of PI3K-Akt and NF-κB signalling, highlighting the therapeutic potential of SIK family inhibition in RA.

Spinal cord injury (SCI) leads to sustained oxidative damage and inflammatory activation, processes that are mutually reinforcing and ultimately hinder neural regeneration. This paper introduces cerium–kaempferol coordination nanoparticles (CeKaeNCs), a nanotherapeutic platform specifically engineered through metal–phenol coordination to concurrently neutralize reactive oxygen species and modulate the inflammatory microenvironment. CeKaeNCs integrate the enzyme-mimetic antioxidant capabilities of redox-active cerium with the anti-inflammatory attributes of the natural flavonoid kaempferol into a singular, stable nanostructure. CeKaeNCs demonstrate broad-spectrum ROS scavenging and effectively diminish pro-inflammatory macrophage activation, while simultaneously promoting a shift toward an anti-inflammatory phenotype. These effects surpass those observed with either free cerium or kaempferol alone. Furthermore, these beneficial actions preserve tissue integrity, promote axonal repair and remyelination, reduce glial scar formation, facilitate synaptic reconstruction, and ultimately enhance functional recovery. This research highlights the potential of rationally designed metal–polyphenol nanoplatforms to interrupt the detrimental feedback loop of oxidative stress and inflammation, thereby presenting a versatile, multifunctional approach for central nervous system repair.

Spinal cord injury (SCI) induces persistent inflammation, excessive oxidative stress and mitochondrial dysfunction, creating a hostile pathological microenvironment that greatly hinders neural regeneration and functional recovery. Native exosomes derived from M2 macrophages exhibit poor stability and limited functional diversity within the lesion microenvironment. In this study, we preconditioned M2 macrophages with 4-OI to produce engineered exosomes (4-OI@exo) with dual anti-inflammatory and mitochondria-protective functions. In vitro experiments revealed that 4-OI@exo markedly suppressed M1 macrophage polarization, eliminated intracellular reactive oxygen species (ROS), restored mitochondrial membrane potential and inhibited aberrant mitochondrial fission, thereby alleviating neuronal apoptosis caused by inflammatory stress. To achieve controllable delivery of exosomes, we developed a ROS-responsive SilMA-PBA/PVA hydrogel. This exosomes-loaded SilMA-PBA/PVA hydrogel delivery system (Gel@exo) enables on-demand release of exosomes and sustained therapeutic effects at lesion sites with elevated ROS levels. In vivo results revealed that the Gel@exo system exhibited excellent biocompatibility. It modulates local immune responses, preserves the integrity of neural structures, promotes neural repair, and substantially improves motor and sensory functions in SCI rats. By combining engineered exosomes with smart responsive biomaterials, this study offers a novel strategy for SCI treatment and holds promising potential for clinical translation.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis, primarily affecting symmetric small joints. Deucravacitinib, a novel oral highly selective tyrosine kinase 2 (TYK2) inhibitor, has shown promise in treating various immune-mediated diseases. This study aimed to explore the therapeutic effects and underlying mechanisms of deucravacitinib in RA. The anti-proliferative effects of deucravacitinib were assessed using the CCK-8 assay, while its pro-apoptotic activity in MH7A cells was evaluated via flow cytometry. Cell wound healing assay and transwell assays were employed to determine the migration and invasive capabilities of MH7A cells. RNA sequencing (RNA-seq) was conducted to identify differentially expressed genes following deucravacitinib treatment. Network pharmacology and molecular docking analyses were utilized to predict potential anti-arthritic targets. The impact of deucravacitinib on the TYK2/STAT3 (signal transducer and activator of transcription) and PI3K(phosphoinositide3-kinase)/AKT(protein kinases B) signaling pathways was investigated. In vivo, a collagen-induced arthritis (CIA) mouse model was treated with low-dose deucravacitinib (5 mg/kg/d) for 21 days, and its anti-arthritic effects were evaluated. In vitro, deucravacitinib significantly inhibited MH7A cell proliferation and induced apoptosis, while also reducing cell migration and invasion. Mechanistically, deucravacitinib upregulated Bax (Bcl-2-associated X protein) expression and downregulated Bcl-2 (B-cell lymphoma 2), MMP-2(Matrix Metalloproteinase-2), and MMP-9(Matrix Metalloproteinase-9) mRNA levels, likely through inhibition of the TYK2/STAT3 and PI3K/AKT pathways. In vivo, deucravacitinib alleviated toe swelling, reduced arthritis scores, and decreased mRNA levels of Bcl-2, MMP-2, and MMP-9 in CIA mice. Histopathological analysis revealed improved joint integrity and reduced bone erosion. Deucravacitinib demonstrates significant anti-arthritic potential by inhibiting synovial fibroblast proliferation, migration, and invasion while promoting apoptosis. These effects are mediated through suppression of the TYK2/STAT3 and PI3K/AKT signaling pathways, suggesting its promise as a therapeutic agent for RA.

The field of bone defect repair continues to face numerous challenges. Therefore, the development of effective bone regeneration materials remains urgently needed. This study fabricated a microchannel sponge scaffold (MS) with the assistance of 3D printing. Experimental results showed that MS increased clot porosity and mechanical stability. And MS-treated blood clots significantly enhanced cell migration compared with ordinary clots. In in vitro cell experiments, the MS loaded with blood clots and vascular endothelial growth factor (VEGF) significantly upregulated the expression levels of osteogenesis- and angiogenesis-related genes, promoting both angiogenesis as well as osteogenic differentiation. In vivo hemostasis experiments revealed that the MS significantly reduced blood loss and hemostasis time, when compared with commercially available gelatin hemostatic sponges (C-Sponge). Furthermore, in vivo experiments utilizing a rat cranial defect model indicated that the MS provided substantial support for bone defects and stimulated bone tissue formation. At 8 weeks post-transplantation, the Blood-UMS600-V group had the highest Bone Mineral Density (BMD) and Bone Volume Fraction (BV/TV) with significant differences from other groups. Histological staining revealed accelerated bone repair mechanisms involving increased collagen deposition and enhanced angiogenesis. Conclusively, MS holds clinical potential for treating bone defect bleeding and improving bone healing.

Spinal cord injury (SCI) results in irreversible neurological damage primarily due to secondary processes such as oxidative stress, inflammation, and mitochondrial dysfunction, which hinder functional recovery and currently lack effective targeted treatments. Developing bioactive scaffolds that can dynamically reshape this pathological environment is essential for facilitating neural repair. In this study, we present a ROS-responsive hydrogel scaffold synthesized from quaternized chitosan (QCS) and tannic acid (TA), which is further functionalized with Cu/Zn MOF, designed to create a neuro-permissive microenvironment. By taking advantage of the elevated oxidative levels present at the injury site, this hydrogel functions as an "on-demand" therapeutic system. It demonstrates significant antioxidative properties by effectively scavenging intracellular ROS and preserving mitochondrial function, thereby preventing neuronal apoptosis. Concurrently, the composite regulates the immune microenvironment by inhibiting the polarization of pro-inflammatory M1 macrophages while promoting the reparative M2 phenotype. This dual approach of anti-inflammatory and antioxidative regulation significantly reduces astrogliosis and establishes a favorable permissive environment for tissue reconstruction. In vivo assessments reveal that the Cu/Zn MOF@gel significantly enhances axonal regeneration and remyelination, leading to considerable improvements in both electrophysiological conduction and locomotor function recovery. This study underscores the potential of ROS-responsive hydrogels functionalized with MOFs as a promising therapeutic strategy for addressing oxidative and inflammatory challenges in SCI.

Osteoarthritis (OA) is a chronic joint disease characterized by structural cartilage damage and inflammatory changes in the synovium. The macrophage response, especially the activation of M1-type macrophages, represents a key mechanism underlying OA pathogenesis. Rheumatic and immune-related disorders may benefit from sinomenine treatment, a natural substance with immunomodulatory and anti-inflammatory properties. Here, human synovial tissues were collected from OA patients and healthy controls (n = 6 per group), and an ACLT-induced OA rat model was established (n = 6 per group). In vitro experiments were performed in RAW264.7 macrophages and SW1353 chondrocytes with three independent biological replicates for each experiment. These experiments were performed to investigate the regulatory effects of sinomenine on M1/M2 macrophage polarization and inflammatory cytokine expression. An ACLT-induced OA rat model was used to determine the effects of sinomenine on cartilage lesions, synovial inflammatory responses, and matrix metabolic alterations. Primary outcomes were M1/M2 macrophage polarization status and synovial inflammatory response. Secondary outcomes included cartilage matrix metabolic changes and chondrocyte function. Sinomenine dramatically increased CD206 levels in macrophages and suppressed LPS-induced iNOS expression (P < 0.001). Additional research revealed that sinomenine altered macrophage polarization by increasing IL-10 levels in M2 macrophages and decreasing TNF-α levels in M1 macrophages (P < 0.001). Sinomenine significantly decreased synovial inflammation and cartilage damage in OA rats and restored cartilage matrix homeostasis. Immunohistochemistry revealed that sinomenine reduced MMP13 expression and increased COL2 synthesis (P < 0.001). This study confirms that sinomenine can alleviate synovial inflammation and promote cartilage repair in OA by modulating macrophage polarization, suggesting a novel strategy for OA treatment.

3D‐printed titanium implants are extensively utilized in bone reconstruction. However, their bioinertness and lack of antibacterial activity increase risks of aseptic loosening and implant‐associated infection—the primary causes of implant failure. To address these limitations, we developed a dual‐functional 3D‐printed porous titanium–hydrogel composite scaffold to enhance the osteogenic and antibacterial capacities of titanium. This composite scaffold was fabricated by integrating quaternized chitosan (QCS)/aldehyde‐terminated Pluronic F127 (PF127‐CHO) hydrogel loaded with magnesium ions (Mg2+) and zeolitic imidazolate framework‐8 (ZIF‐8) into polydopamine‐coated 3D‐printed porous titanium scaffold. The composite scaffold exhibited sustained and controlled release of Mg2+ and ZIF‐8 with enhanced binding strength at titanium–hydrogel interface. In vitro experiments demonstrated that the composite scaffold possessed favorable biocompatibility, promoted the adhesion and proliferation of MC3T3‐E1 cells, and facilitated their osteogenic differentiation through synergistic effect of Mg2+ and ZIF‐8. Furthermore, it also inhibited bacterial growth via synergistic action of QCS/PF127‐CHO hydrogel and ZIF‐8. In vivo experiments confirmed enhanced bone ingrowth into the composite scaffold and its effective antibacterial activity. In summary, this composite scaffold provides a promising strategy to simultaneously improve the osteogenic and antibacterial capacities of titanium implants.

Osteoporosis (OP) is a systemic disease characterized by a reduction in the number of trabecular bone structures and damage to the bone microstructure. It is commonly found in people who are aging or have estrogen deficiency. Oxidative stress and chronic inflammation caused by pathological factors such as aging and estrogen deficiency are key pathogenic factors. Betulinic acid (BA), a natural pentacyclic triterpenoid compound, exhibits anti‑inflammatory and antioxidant biological effects. However, its role and potential mechanisms in the inflammatory injury of osteoblasts in OP remain unclear. In the present study, in vivo experiments were conducted using an ovariectomized (OVX) rat model of OP, with bone microstructure analyzed by micro‑CT, protein expression detected by immunohistochemistry, and serum inflammatory factors measured by ELISA. BA was revealed to alleviate bone loss in OVX rats and inhibit the expression of NOD‑like receptor pyrin domain‑containing 3 (NLRP3), Asc and caspase‑1 in the femur of OVX rats, as well as suppress the release of inflammatory factors such as interleukin‑1 β, interleukin‑6, and tumor necrosis factor‑αin the serum of rats. The inflammatory injury osteoblast model of BA intervention was also studied with hydrogen peroxide (H2O2) in vitro, with reactive oxygen species (ROS) levels assessed by fluorescence assay, osteogenic differentiation evaluated by ALP staining and alizarin red staining, and autophagy‑related proteins detected by western blotting. BA pretreatment reduced production of ROS, inhibited expression of NLRP3 and downstream pathway activation, improved alkaline phosphatase activity, mineralization ability, and osteogenic differentiation ability of MC3T3‑E1 cells. Administration of BA increased the autophagy of MC3T3‑E1 cells treated with H2O2, which was confirmed by the increased expression levels of LC3b II and Beclin‑1 and the decreased expression levels of P62. In addition, BA could enhance the phosphorylation of AMPK in MC3T3‑E1 cells treated with H2O2 and reduce the phosphorylation of mTOR, but this effect could be rescued by Compound C (an AMPK blocker). BA can protect osteoblasts from inflammatory injury by reducing the production of ROS and inhibiting the activation of NLRP3 through autophagy mediated by the AMPK/mTOR pathway.

Rationale:Spinal cord injury (SCI) triggers a complex secondary injury process characterized by inflammation, neuronal loss, extracellular matrix (ECM) disruption, and limited endogenous repair. Although cell-based therapies hold potential for SCI treatment, their efficacy is often constrained by poor lesion targeting, inadequate persistence after delivery, and limited temporal control over therapeutic factor release. Methods:To address these limitations, we developed a macrophage-based mRNA delivery platform by electroporating CCR2 positive (CCR2+) macrophages with ANXA1, GDNF, and CTGF mRNAs. In vitro, we assessed transfection efficiency, cell viability, secretion kinetics of therapeutic proteins, anti-inflammatory activity, and neuroprotective and regenerative effects. In vivo, using a mouse SCI model, we evaluated lesion-site accumulation, inflammatory regulation, tissue repair, electrophysiological recovery, transcriptomic alterations, and behavioral outcomes. Results:Following electroporation, CCR2⁺ macrophages efficiently expressed ANXA1, GDNF, and CTGF while maintaining high viability, with no marked shift toward CD86- or CD206-associated phenotypes. These engineered macrophages showed enhanced accumulation at the lesion site and sustained therapeutic protein secretion for up to 14 days. In vitro, they protected neuronal cells against oxidative stress-induced injury and promoted neurite outgrowth. In vivo, they attenuated inflammation, improved the local repair microenvironment, and promoted axonal regeneration, remyelination, and ECM remodeling, accompanied by partial recovery of electrophysiological and motor function after SCI. RNA-seq analysis further supported broad changes in pathways related to immune regulation, neural repair, myelination, and matrix remodeling. Conclusions:CCR2-enriched macrophages engineered with reparative mRNAs may represent a promising treatment strategy for SCI. By linking CCR2-associated lesion accumulation with multimodal reparative activity, this cell-based platform provides a potential approach for coordinated microenvironmental regulation and tissue repair.

Arginine, as a semi-essential amino acid, plays a pivotal role in bone metabolism and orthopedic diseases. Beyond its function in protein synthesis, arginine serves as a crucial precursor for Nitric Oxide (NO), polyamines, and proline, profoundly influencing osteoblast differentiation, osteoclast activation, immune responses, and angiogenesis. Research indicates that abnormalities in arginine metabolism—such as imbalances in NO synthase activity, upregulation of arginase, or abnormal expression of protein arginine methyltransferases—are closely associated with the onset and progression of osteoporosis, rheumatoid arthritis, osteoarthritis, and bone tumors. Simultaneously, the arginine pathway intertwines with oxidative stress, inflammatory responses, and epigenetic regulation, forming a complex “metabolism-immunity-bone” network. In materials science, arginine has been integrated into various biomaterial systems, including Poly (lactic-co-glycolic acid) (PLGA) scaffolds, chitosan hydrogels, hydroxyapatite composites, and RGD-functionalized polymers, significantly enhancing osteogenic, angiogenic, and immunomodulatory capabilities. Despite ongoing research advancements, challenges persist in understanding the environment-dependent effects of arginine, optimizing dosage, and achieving clinical translation. This review systematically summarizes the mechanistic roles of arginine in bone metabolism regulation and its application progress in engineered materials, offering novel therapeutic insights and research directions for preventing and treating diseases such as osteoporosis, arthritis, and bone tumors.

Osteoarthritis (OA) is a low-grade inflammatory disease that is highly associated with severe hyperplasia of the synovial membrane and the degeneration of cartilage. Interleukin-10 (IL-10), has been extensively studied, while its receptor, IL-10Rα, has not been widely mentioned in the context of OA. A significant difference is found in the expression of IL-10Rα in synovial macrophages from normal and OA patients, along with a marked increase in the glycolytic activity of synovial macrophages. In IL-10RαLysm OA mice, the specific deficiency of IL-10Rα exacerbated the progression of OA. Mechanistically, hypoxia-inducible factor-1α (HIF-1α) is identified as a key transcription factor, and its inhibition significantly weakened the glycolytic process. Additionally, differences in ferroptosis of chondrocytes are observed. After co-culturing the two types of cells in vitro, a significant connection is found between the glycolytic state of synovial macrophages and the ferroptosis of chondrocytes. To achieve targeted therapy, MI@UN, a biomimetic nanoparticle encapsulating NO-prednisolone in UIO-66-NH2, surface-modified with IL-10, and coated with macrophage membranes (MM), is developed. It significantly slows osteoarthritis progression in mice. This offers new insights into OA pathogenesis, highlighting IL-10Rα as a therapeutic target and supporting MI@UN's translational use for OA treatment.

OBJECTIVE:This study aimed to compare the clinical outcomes of patients with AOSpine A3 or A4 thoracolumbar fractures presenting with neurological deficits treated with endoscopic decompression combined with percutaneous pedicle screws fixation (endoscopic minimally invasive surgery, EMIS) or conventional open surgery (OS). METHODS:Data of patients with AOSpine A3 or A4 thoracolumbar fractures with neurological deficits who were treated with EMIS or OS between June 2019 and July 2021 were extracted from the electronic database. Various clinical outcomes were compared between the 2 cohorts. RESULTS:Among the 231 patients who were followed up for more than 2 years, 107 were in the EMIS cohort and 124 were in the OS cohort. Compared with the OS cohort, the EMIS cohort had longer operative time (p<0.05), but the intraoperative blood loss, incision length and hospital stay were significantly reduced (p<0.05). At both postoperative and final follow-up assessments, the EMIS cohort demonstrated significantly better visual analogue scale and Oswestry Disability Index outcomes compared to the OS cohort (p<0.05). Both cohorts maintained similar correction of spinal canal erosion rate, percentage of anterior vertebral height and sagittal Cobb angle after surgery and at the last follow-up (p>0.05). According to American Spinal Injury Association classification, the 2 cohorts had similar neurological recovery at the last follow-up (p>0.05). CONCLUSION:In comparison to OS, EMIS treatment for AOSpine A3 or A4 thoracolumbar fractures with neurological deficits has shown comparable clinical efficacy while significantly reducing surgical trauma.

Titanium cage subsidence remains a common complication following anterior cervical corpectomy and fusion. 3D printing technology can optimize titanium cages, including high geometric matching and unique porous graded structures, providing a better option for improving titanium cage subsidence. This study aims to evaluate the mechanical properties of 3D-printed titanium cages and compare them with those of conventional titanium cages, providing preclinical data for future clinical trials. The samples were divided into a 3D-printed titanium cage group and a conventional titanium cage group, with 5 samples in each group. A static compression test was conducted using the American Society for Testing and Materials (ASTM) F2077-14 standard to evaluate the stiffness of the titanium cages. A static subsidence test was conducted using the ASTM F2267-04 standard to evaluate the stiffness (Kp) of the test blocks in different groups of Sawbone. The larger the Kp value, the smaller the tendency of titanium cage subsidence. In the static compression test, the stiffness of the 3D-printed titanium cage and the conventional titanium cage were (6562.60 ± 390.72) N/mm and (10252.40 ± 704.07) N/mm, respectively, with a statistically significant difference (P < 0.05). In the static subsidence test, the stiffness of the 3D-printed titanium cage system and the conventional titanium cage system were (258.60 ± 7.99) N/mm and (221.00 ± 20.36) N/mm, respectively, with a statistically significant difference (P < 0.05). Additionally, the stiffness (Kp value) of the test block for the 3D-printed titanium cage in the static subsidence test was 270 N/mm, while the Kp value of the test block in the conventional titanium cage static subsidence test was 226 N/mm, indicating a 19.5

Posterior laminectomy is a standard treatment for thoracic ossification of the ligamentum flavum (TOLF), but it often leads to neurological deterioration during surgery. This study aimed to reduce iatrogenic neurological deterioration by using an S8 navigation system combined with an ultrasonic osteotome for three-dimensional real-time dynamic visualization decompression. A retrospective analysis was conducted on patients who underwent laminectomy and internal fixation for TOLF in our centre from January 2016 to January 2023. Patients were divided into a visualization group (S8 navigation + ultrasonic bone scalpel) and a control group (ultrasonic bone scalpel) based on the use of three-dimensional real-time dynamic visualization decompression technology. Intraoperative multimodal neuroelectrophysiological monitoring (IONM) was used to collect somatosensory evoked potential and motor evoked potential data. We compared the incidence of intraoperative neurological deterioration indicated by IONM alarms between the two groups. Neurological and motor functions were assessed via the American Spinal Injury Association (ASIA) classification system and the modified Japanese Orthopaedic Association (m-JOA) score for thoracic myelopathy. Follow-ups were conducted at 1, 3, 6, and 12 months postsurgery, and the data from both groups were compared. Other clinical indicators included decompression time per laminectomy segment, intraoperative blood loss, intraoperative dural ossification, hospitalization duration, and drainage tube placement time. We also analysed intraoperative and postoperative complications. A total of 91 patients with thoracic ossification of the ligamentum flavum were included, with a follow-up period of 12–18 months. The visualization group consisted of 41 patients, and the control group included 50 patients. The incidence of neurological deterioration indicated by IONM in the visualization group (9.8

Owing to their unique biological effects and physicochemical properties, nanomaterials have garnered substantial attention in the field of bone tissue engineering (BTE), targeting the repair and restoration of impaired bone tissue. In recent years, strategies for the design and optimization of nanomaterials through thiolation modification have been widely applied in BTE. This review concisely summarizes the categories of nanomaterials commonly used in BTE and focuses on various strategies for the modification of nanomaterials via thiolation. A multifaceted analysis of the mechanisms by which thiolated nanomaterials enhance nanomaterial–cell interactions, promote drug loading and release, and modulate osteogenic differentiation is presented. Furthermore, this review introduces biomedical applications of thiolated nanomaterials in BTE, including as scaffold components for bone regeneration, coatings for bone implants, and drug delivery systems. Finally, the future perspectives and challenges in the development of this field are discussed. Thiolation modification strategies provide a platform for developing new ideas and methods for designing nanomaterials for BTE and are expected to accelerate the development and clinical translation of novel bone repair materials.

BACKGROUND:Saccharomyces boulardii shows great promise as a treatment for osteoporosis since it plays a crucial role in protecting against inflammatory bone loss and demonstrates exceptional resilience to gastrointestinal stress during oral administration. This study delved into the impacts of gastrointestinal stress on S. boulardii and the corresponding adaptive mechanisms employed by the yeast at the membrane level using physiological methodologies. RESULTS:The findings demonstrated that exposure to gastrointestinal stress compromised cellular integrity, resulting in cell wall rupture and the subsequent leakage of intracellular contents. To mitigate the adverse effects of gastrointestinal stress, S. boulardii activated several membrane-associated defense strategies. Notably, there was a decrease in membrane fluidity, and significant alterations in fatty acid composition, including a higher proportion of unsaturated fatty acids. Additionally, intracellular ergosterol and glutathione levels were substantially elevated, contributing to the stabilization of the cell membrane and minimizing damage caused by gastrointestinal stress. CONCLUSIONS:Taken together, the comprehensive analysis presented in this study offers valuable insights into the mechanisms underlying salt tolerance in S. boulardii. These results support the enhancement of the application of probiotics in osteoporosis, especially for oral administration requiring resistance to gastrointestinal stress.