Spine disorders affect 619 million people globally and are a leading cause of disability, yet AI-assisted diagnosis remains limited by the lack of level-aware, multimodal datasets. Clinical decision-making for spine disorders requires sophisticated reasoning across X-ray, CT, and MRI at specific vertebral levels. However, progress has been constrained by the absence of traceable, clinically-grounded instruction data and standardized, spine-specific benchmarks. To address this, we introduce SpineMed, an ecosystem co-designed with practicing spine surgeons. It features SpineMed-450k, the first large-scale dataset explicitly designed for vertebral-level reasoning across imaging modalities with over 450,000 instruction instances, and SpineBench, a clinically-grounded evaluation framework. SpineMed-450k is curated from diverse sources, including textbooks, guidelines, open datasets, and $\sim$1,000 de-identified hospital cases, using a clinician-in-the-loop pipeline with a two-stage LLM generation method (draft and revision) to ensure high-quality, traceable data for question-answering, multi-turn consultations, and report generation. SpineBench evaluates models on clinically salient axes, including level identification, pathology assessment, and surgical planning. Our comprehensive evaluation of several recently advanced large vision-language models (LVLMs) on SpineBench reveals systematic weaknesses in fine-grained, level-specific reasoning. In contrast, our model fine-tuned on SpineMed-450k demonstrates consistent and significant improvements across all tasks. Clinician assessments confirm the diagnostic clarity and practical utility of our model's outputs.

ABSTRACT Previous optogenetic bioelectronic systems have enabled a highly selective way of modulating neural populations by delivering a certain wavelength of light to engage with exogenously expressed light‐sensitive proteins, which lay the foundation of therapeutic interventions of neural circuits. However, real‐time biofeedback and strategic modulation are crucial for adjusting customized clinical treatment adjustment. To achieve this purpose, we integrated illumination, temperature, and electromyographic (EMG) sensing elements into the optogenetic bioelectronic system to avoid overexposure caused by localized overheating and to provide functional recovery evaluation during neural regeneration, which guides the in situ adjustment of the intensity, frequency, and duration of illumination parameters controlled by a wireless connected programmable external control board. In this study, both in vitro and in vivo experiments were performed to examine the optical, thermal, and electrical characteristics of our bioelectronic system. On this basis, we demonstrated a series of standardized EMG results to evaluate the recovery condition and modify the illumination parameters of each test rat. Combining temperature monitoring feedback and EMG signaling feedback, our optogenetic bioelectronic system enables strategic optogenetic spinal cord injury (SCI) treatment through real‐time illumination modulation to achieve customized spinal cord injury treatment.

Intervertebral disc degeneration (IVDD), a major contributor to chronic low back pain (LBP), involves progressive extracellular matrix (ECM) degradation and limited self-repair. Current therapies alleviate symptoms but fail to halt degeneration, driving interest in endogenous stem cell-based regeneration. Endogenous stem/progenitor cells within disc niches exhibit regenerative potential through ECM synthesis, anti-inflammatory signaling, and exosomal miRNA-mediated repair. Preclinical studies highlight mesenchymal stem cell (MSC) transplantation and reprogramed induced pluripotent stem cells (iPSCs) in restoring disc hydration and reducing pain, while early clinical trials report symptomatic relief (e.g., 70% pain reduction) but incomplete structural recovery. Challenges include the disc’s hostile microenvironment (hypoxia and nutrient deprivation), age-related depletion of endogenous stem/progenitor cells, and impaired cell homing under mechanical stress. Emerging strategies target epigenetic modulation, biomimetic scaffolds, and combination therapies to enhance cell survival and integration. Despite promising preclinical outcomes, clinical translation requires overcoming microenvironmental barriers and refining delivery systems. Future efforts should prioritize large-animal validation and biomarker-guided approaches to bridge the gap between experimental success and therapeutic application.

OBJECTIVE: This study aimed to investigate the impact of paraspinal muscle (PSM) degeneration on coronal balance in patients with degenerative lumbar scoliosis (DLS). METHODS: In this retrospective cross-sectional study, 127 DLS patients who underwent spinal fusion surgery were reviewed. Preoperative x-rays and magnetic resonance images were used to assess PSM degeneration, measured by the cross-sectional area (CSA) and fat infiltration rate (FIR) of the multifidus (MF) and erector spinae (ES) muscles. The ratios of the convex to concave sides, namely RCSA and RFIR, were calculated. Coronal balance was classified into types A, B, and C based on the coronal balance distance. One-way analysis of variance and multiple logistic regression were performed to analyze PSM parameters and risk factors for imbalance. RESULTS: Significant differences were found among the coronal balance types in the RFIR of MF (P = 0.009), RCSA of ES (P < 0.001), FIR of ES (P = 0.017), and RFIR of ES (P = 0.001). Multiple logistic regression identified the RCSA and RFIR of ES as significant for type B imbalance, while the RFIR of MF and FIR of ES were significant for type C. CONCLUSIONS: PSM degeneration, particularly in the MF and ES muscles, significantly affects coronal balance in DLS patients. Preoperative evaluation of these factors is essential for optimizing surgical outcomes.

BACKGROUND:Osteoporosis is an increasingly prevalent public health concern in ageing populations. While traditional risk factors such as ageing, hormonal status, and physical inactivity are well-recognized, the role of sleep quality in osteoporosis risk remains understudied. This study aimed to investigate the prospective association between sleep quality and the risk of developing osteoporosis among older adults. METHODS:We conducted a prospective cohort study using data from the English Longitudinal Study of Ageing (ELSA). A total of 5958 osteoporosis-free participants aged ≥50 years were recruited at wave 4 (2008-2009) and followed up across waves 5 to 8 (2016-2017), with a maximum follow-up of 8 years. Sleep quality was assessed using a validated four-item questionnaire (score range: 4-16), and categorized as good (4 ≤ score ≤ 7), intermediate (8 ≤ score ≤ 11), and poor (12 ≤ score ≤ 16) sleep quality groups. Incident osteoporosis was identified via self-reported physician diagnosis. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs), adjusting for demographic, socioeconomic, lifestyle, and health-related covariates including sleep duration. RESULTS:During the 8-year follow-up, 319 participants (5.36 %) developed osteoporosis. Compared to those with poor sleep quality, the risk of osteoporosis was significantly lower in the intermediate (adjusted HR = 0.64, 95 % CI: 0.49-0.85) and good sleep quality groups (adjusted HR = 0.54, 95 % CI: 0.39-0.73). A significant dose-response relationship was observed (P for trend <0.001). These associations remained robust among participants with normal sleep duration (6-9 h). Subgroup analyses revealed that the associations were particularly significant in adults aged 60-80 years, those who were married or cohabiting, and individuals with hypertension, even after Bonferroni correction. CONCLUSIONS:Higher sleep quality was significantly associated with a reduced risk of osteoporosis among older adults. These findings suggest that sleep quality may be a potentially modifiable behavioral factor related to osteoporosis risk, warranting further investigation in future longitudinal and interventional studies.

The central nervous system (CNS) barrier obstructs therapeutic component entrance and hinders the therapy efficiency of CNS diseases. An ideal delivery system should penetrate and concentrate in the CNS without safety concerns. Nanovesicles (NVs) are a popular delivery tool, because of their biological homology, inherent homing effects, and capacity to penetrate barriers. However, the delivery efficacy of NVs is insufficient for CNS disease therapy, and the mechanism for barrier penetration remains elusive. Herein, nanovesicles (NVs) were extruded from mesenchymal stem cells and modified by a lesion tissue affinity peptide (CAQK) for spinal cord injury (SCI) therapy. The NVs penetrated endothelial barriers effectively in vitro. Subsequently, the CNS barrier penetration capacity of the CAQK-conjugated NVs (CNVs) was verified in vivo in spinal cord injury (SCI) and the temporary middle cerebral artery occlusion (t-MCAO) mouse models. Furthermore, the endothelial barrier penetration of CNVs depended on the active endocytosis by endothelial cells. After endocytosis, the Rab11+ endosome was identified to mediate a transcellular transcytosis to transport CNVs across the barrier. In the SCI model, CNVs promoted the lesion tissue accumulation, leading to improvement in the neural functional recovery. In summary, we developed a natural NV tool for SCI therapy, employing the inherent CNS barrier penetration capacity and enhanced lesion tissue homing characteristics of NVs. The NVs crossed the CNS barriers via active endocytosis, followed by Rab11+ endosome-mediated transcytosis. The CNV exhibited good delivery efficacy and therapeutic effects in CNS diseases and has the potential for clinical translation.

Stem cells hold great promise for repairing degenerated nucleus pulposus (NP) in intervertebral disc degeneration (IVDD) via differentiating into NP-like cells and replenishing the extracellular matrix (ECM). However, the harsh environment in degenerated NP contributes to poor survival, low differentiation efficiency, and matrix catabolism, hampering stem cells' long-term transplantation and efficacy. Herein, a hyaluronic acid (HA)-based hydrogel (Pep-aGel) functionalized with collagen mimetic peptide and amination is fabricated to deliver glycoengineered stem cells for NP repair. The peptide (GFOGER), which contains the integrin recognition sequence of collagen, is selectively bound to the upregulated integrin-β1 of glycoengineered stem cells, thereby promoting their NP-like differentiation. The amination introduced amino groups in hydrogel and further enhanced the integration of cell-secreted glycosaminoglycans (GAGs) on the HA chains, which mimicked the biosynthesis of Aggrecan, creating an NP-like nanostructure in the hydrogel. Pep-aGel loading with glycoengineered cells showed injectable properties and significantly improved disc height, extracellular matrix content, and GAG deposition in rat degenerated discs. This approach established a self-sufficient system that consists of NP cell replenishment, in situ ECM supply, and GAG anchoring, which may offer a concise, yet synergistic, strategy for the regeneration of IVDD.

Mechanotransduction refers to the cellular mechanism by which mechanical cues from the extracellular matrix (ECM) are sensed and transduced into biochemical signals, playing a critical role in regulating stem cell differentiation. In degenerative intervertebral disc (IVD) disease, the mechanical microenvironment undergoes pathological alterations, most notably a marked increase in ECM stiffness. This aberrant mechanical milieu disrupts cellular fate decisions and poses a critical barrier to successful endogenous regeneration. To address this limitation, poly(acrylamide-co-acrylic acid) (P(AAm-co-AA)) microgels with tunable elastic moduli were synthesized via inverse emulsion polymerization. These microgels were subsequently functionalized with polydopamine (PDA) to enhance cellular adhesion, thereby facilitating cytoskeletal remodeling and activation of mechanotransductive signaling pathways. Notably, a compliant matrix with an elastic modulus of approximately 2 kPa was found to enhance nucleus pulposus (NP)-like differentiation of adipose-derived mesenchymal stem cells in differentiation-inducing medium, as evidenced by significantly upregulated expression of NP marker genes (COL2, ACAN, SOX9). This effect was correlated with the translocation of yes-associated protein 1 (YAP).In vivostudies demonstrated that implantation of these microgels into degenerated discs led to restoration of disc height and increased ECM deposition within the NP region, as demonstrated by imaging and immunohistochemical results. Collectively, this work highlights the potential of microgel-based delivery platforms with tunable mechanical properties as a promising strategy to facilitate stem cell differentiation and promote IVD regeneration.

Scarring is an insurmountable obstacle for axonal regeneration in recovery from spinal cord injury (SCI). It impedes the repair effects of therapeutic targets in cortical neurons, such as PTEN−/− and hyper-IL-6, which cannot break through dense scar barriers to reconstruct neural circuits. However, methods for eliminating this process remain elusive. Here, we conducted a multiomics analysis of SCI and identified FBXL12 as an effective target for inhibiting scarring, further promoting spontaneous crossing of axons at the epicenter. We identified N6-Methyladenosine (m6A) modification as the predominant mRNA modification in SCI, with Fbxl12 being a major modification target. Furthermore, m6A modification specifically promoted FBXL12 synthesis in activated microglia. The overexpression of FBXL12 in microglia contributed to its homogeneous distribution and maintained a “scar-less healing” phenotype. Remarkably, FBXL12 therapy effectively reduced extracellular matrix deposition and decreased the scar area by ~70%. Importantly, axons grew through the epicenter and reached a length of more than 2.4 mm 56 days post-SCI, significantly improving motor function and reconstructing the neural circuit. Mechanistically, FBXL12 promoted cytoskeletal reorganization and migration in microglia by catalyzing the K63-linked ubiquitylation of Myosin heavy chain 14 (MYH14). Together, our results identify m6A-FBXL12-MYH14 axis as a novel cytoskeletal reorganization pathway in activated microglia and suggest FBXL12 as an effective target for a novel microglia-based approach to facilitate scarless functional recovery in SCI.

ABSTRACT Purpose Understanding the risk factors associated with unscheduled readmission following lateral lumbar interbody fusion (LLIF) is crucial for mitigating the occurrence of these costly events. This study aims to ascertain the incidence and factors of unscheduled hospital readmission subsequent to LLIF. Methods A retrospective analysis was conducted on patients who underwent LLIF at our institution from March 2016 to February 2023. Instances of unscheduled hospital readmission after LLIF were meticulously recorded, including baseline demographics, characteristics of spine pathology, surgical interventions, duration between two hospitalizations, and hospitalization costs and duration. Reasons for readmission were categorized based on their etiology. A case–control methodology was employed to compare unscheduled hospital readmission patients against planned readmission patients due to staged surgery. Parametric data were analyzed with a two‐tailed T‐test, nonparametric data with the Wilcoxon rank‐sum test, and categorical data with the χ 2 test. Results A total of 1521 patients who received LLIF at our institution were included in the study. A total of 59 patients (3.88%) were unscheduled readmitted due to adjacent segment disease (ASD), cage subsidence, the original surgical segments remaining narrow, spondylodiscitis, and pain. 51 patients (3.35%) experienced reoperation, predominantly attributable to ASD. Compared to planned readmission patients, unscheduled readmission patients tended to be younger, had a lower likelihood of having scoliosis, and were more likely to have short‐segment surgery and higher initial hospitalization costs. Among unscheduled readmission patients, patients receiving short‐segment surgery, as well as those who paid less during the initial hospitalization, demonstrated a higher likelihood of a 90‐day readmission rate. Conclusion Our findings indicated the heightened risks of unscheduled hospital readmission after LLIF. Taking targeted measures against these risk factors is expected to reduce the healthcare burden caused by unplanned readmissions in the future.

Background: Lateral lumbar interbody fusion (LLIF) is a minimally invasive fusion technique that can be performed with lateral plate. Insufficient contact between the endplate and bone graft may result in cage subsidence. This study aimed to investigate the potential risk factor for high-grade cage subsidence (HCS) occurring after LLIF supplemented with lateral plate. Methods: Between June 2017 and February 2023, 121 patients (48 males, 73 females; mean age 63.0 years; minimum follow-up period 12 months) undergoing LLIF supplemented with lateral plate were retrospectively reviewed. The incidence of HCS was assessed, and patients were categorized into HCS group or non-HCS group based on the occurrence of HCS. A revision surgery of posterior pedicle screw fixation was performed in patients with cage subsidence and complained with intolerable back pain or radicular symptoms. Comparative analyses were performed on demographic characteristics, surgical variables, and parameters related to endplate-bone graft contact between the two groups. Multivariable logistic regression analysis was employed to identify the potential risk factors associated with HCS. The receiver operating characteristic (ROC) analysis was used to calculate the cutoff values for the risk factors. Clinical outcomes were evaluated using Oswestry Disability Index (ODI), and radiographic fusion at the final follow-up was assessed based on the Bridwell grading system. Results: The HCS group comprised 12 patients, while the non-HCS group included 109 patients. The incidence of HCS occurring after LLIF supplemented with lateral plate was 9.9 %. Compared to non-HCS group, patients in HCS group had lower sagittal and coronal endplate-bone graft contact rates and larger cage-endplate angles. Low sagittal (OR, 1.099; 95 % CI, 1.033-1.169; P =0.003) and low coronal (OR, 1.149, 95 % CI, 1.061-1.243, P =0.001) endplate-bone graft contact rates were determined to be correlated with HCS. The cutoff value of the sagittal and coronal endplate-bone graft contact rate was 63.5 % and 60.9 %. Eleven (91.7 %) patients in HCS group underwent revision posterior pedicle screw fixation. Both HCS and non-HCS groups experienced significant improvements in ODI at the final follow-up, while there were no differences between groups. Ninety-five (87.2 %) patients in non-HCS group, and nine (81.8 %) of the 11 patients who underwent revision surgery in HCS group achieved radiographic fusion at the final follow-up. Conclusions: The incidence of HCS occurring after LLIF supplemented with lateral plate was 9.9%. Insufficient endplate-bone graft contact is an important risk factor of HCS, and sagittal and coronal endplate-bone graft contact rates can be used as effective predictors for HCS.

Circular RNAs (circRNAs) play a critical regulatory role in degenerative diseases; however, their functions and therapeutic applications in intervertebral disc degeneration (IVDD) have not been explored. Here, we identified that a novel circATXN1 highly accumulates in aging nucleus pulposus cells (NPCs) accountable for IVDD. CircATXN1 accelerates cellular senescence, disrupts extracellular matrix organization, and inhibits mitochondrial respiration. Mechanistically, circATXN1, regulated by heterogeneous nuclear ribonucleoprotein A2B1-mediated splicing circularization, promotes progerin translocation from the cell nucleus to the cytoplasm and inhibits the expression of insulin-like growth factor 1 receptor (IGF-1R). To demonstrate the therapeutic potential of circATXN1, siRNA targeting the backsplice junction of circATNX1 was screened and delivered by tetrahedral framework nucleic acids (tFNAs) due to their unique compositional and tetrahedral structural features. Our siRNA delivery system demonstrates superior abilities to transfect aging cells, clear intracellular ROS, and enhanced biological safety. Using siRNA–tFNAs to silence circATXN1, aging NPCs exhibit reduced mislocalization of progerin in the cytoplasm and up-regulation of IGF-1R, thereby demonstrating a rejuvenated cellular phenotype and improved mitochondrial function. In vivo, administering an aging cell-adapted siRNA nucleic acid framework delivery system to progerin pathologically expressed premature aging mice (zmpste24−/−) can ameliorate the cellular matrix in the nucleus pulposus tissue, effectively delaying IVDD. This study not only identified circATXN1 functioning as a cell senescence promoter in IVDD for the first time, but also successfully demonstrated its therapeutic potential via a tFNA-based siRNA delivery strategy.

The extensive degeneration of functional somatic cells and the depletion of endogenous stem/progenitor populations present significant challenges to tissue regeneration in degenerative diseases. Currently, a cellular reprogramming approach enabling directly generating corresponding progenitor populations from degenerative somatic cells remains elusive. The present study focused on intervertebral disc degeneration (IVDD) and identified a three-factor combination (OCT4, FOXA2, TBXT [OFT]) that could induce the dedifferentiation-like reprogramming of degenerative nucleus pulposus cells (dNPCs) toward induced notochordal-like cells (iNCs). Single-cell transcriptomics dissected the transitions of cell identity during reprogramming. Further, OCT4 was found to directly interact with bromodomain PHD-finger transcription factor to remodel the chromatin during the early phases, which was crucial for initiating this dedifferentiation-like reprogramming. In rat models, intradiscal injection of adeno-associated virus carrying OFT generated iNCs from in situ dNPCs and reversed IVDD. These results collectively present a proof-of-concept for dedifferentiation-like reprogramming of degenerated somatic cells into corresponding progenitors through the development of a factor-based strategy, providing a promising approach for regeneration in degenerative disc diseases.

Background Lateral lumbar interbody fusion (LLIF) is a minimally invasive fusion technique that can be performed with lateral plate. Insufficient contact between the endplate and bone graft in the fusion segment may result in instability and subsequent cage subsidence. This study aimed to investigate the potential correlation between endplate-bone graft contact and high-grade cage subsidence (HCS) occurring after LLIF supplemented with lateral plate. Method Between June 2017 and February 2023, 122 patients (47 males, 75 females; mean age 62.7 years; minimum follow-up period 12 months) undergoing LLIF supplemented with lateral plate were retrospectively reviewed. The incidence of HCS was assessed, and patients were categorized into HCS group or non-HCS group based on the occurrence of HCS. Comparative analyses were performed on demographic characteristics, surgical variables, and parameters related to endplate-bone graft contact between the two groups. Multivariable logistic regression analysis was employed to identify the potential risk factors associated with HCS. Results The HCS group comprised 13 patients, while the non-HCS group included 109 patients. The incidence of HCS occurring after LLIF supplemented with lateral plate was 10.7%. The sagittal contact rate of endplate-bone graft (OR, 0.844; 95% CI, 0.766–0.931; P < 0.001) and inferior cage-endplate angle (OR, 1.869, 95% CI, 1.215–2.873, P = 0.004) were determined to be significantly correlated with HCS occurring after LLIF supplemented with lateral plate. Compared to non-HCS group, the patients in HCS group had a lower sagittal contact rate of endplate-bone graft and a larger inferior cage-endplate angle. Conclusion The incidence of HCS occurring after LLIF supplemented with lateral plate was 10.7%. HCS was significantly associated with insufficient sagittal endplate-bone graft contact. Further study aiming to optimize the sagittal endplate-cage contact in the procedure of LLIF supplemented with lateral plate are warranted to enhance clinical outcomes.

Spinal cord injuries impose a notably economic burden on society, mainly because of the severe after-effects they cause. Despite the ongoing development of various therapies for spinal cord injuries, their effectiveness remains unsatisfactory. However, a deeper understanding of metabolism has opened up a new therapeutic opportunity in the form of metabolic reprogramming. In this review, we explore the metabolic changes that occur during spinal cord injuries, their consequences, and the therapeutic tools available for metabolic reprogramming. Normal spinal cord metabolism is characterized by independent cellular metabolism and intercellular metabolic coupling. However, spinal cord injury results in metabolic disorders that include disturbances in glucose metabolism, lipid metabolism, and mitochondrial dysfunction. These metabolic disturbances lead to corresponding pathological changes, including the failure of axonal regeneration, the accumulation of scarring, and the activation of microglia. To rescue spinal cord injury at the metabolic level, potential metabolic reprogramming approaches have emerged, including replenishing metabolic substrates, reconstituting metabolic couplings, and targeting mitochondrial therapies to alter cell fate. The available evidence suggests that metabolic reprogramming holds great promise as a next-generation approach for the treatment of spinal cord injury. To further advance the metabolic treatment of the spinal cord injury, future efforts should focus on a deeper understanding of neurometabolism, the development of more advanced metabolomics technologies, and the design of highly effective metabolic interventions.

ObjectiveLower limb discrepancy (LLD) was frequently observed in patients with idiopathic scoliosis (IS), potentially associated with etiopathogenesis. Although sole lifts had been proposed as a conservative treatment for IS, evidence supporting their efficacy was limited. This study aimed to assess the effects of sole lift intervention on pediatric patients with mild IS, specifically focusing on thoracolumbar/lumbar (TL/L) curvature.MethodsTwenty patients, with an average age of 12.3 ± 3.1 years and presenting mild TL/L curve (15.6° ± 6.2°), were selected from a pool of 267 pediatric IS patients in the outpatient of our spine center from February 2023 to August 2023. Inclusion criteria comprised a main TL/L curve ranging between 10° and 40°, the lower limb positioned at the convexity of the main curve, and LLD of less than 2 cm; individuals requiring bracing or surgical intervention were excluded. Custom sole lifts were used to address the shorter lower limb with the objective of leveling the pelvis. Radiographic evaluations were conducted both before and after intervention using standing full spine posteroanterior radiographs and full leg length radiographs. Statistical analysis was undertaken to evaluate curve correction and its associations with other influencing factors.ResultsThe mean structural and functional LLD were 7.1 ± 4.5 mm and 7.1 ± 4.1 mm, respectively. Among the 20 patients, four exhibited structural LLD greater than 10 mm. The average follow‐up duration was 6.4 ± 1.9 months (range: 3–8 months). Following sole lift intervention (7.0 ± 3.0 mm), a significant reduction was observed in the TL/L curve compared to the pre‐sole lifting measurements (15.6° ± 6.2° vs. 12.1° ± 7.2°, p < 0.001), as well as a notable decrease in the thoracic curve (12.2° ± 4.0° vs. 8.6° ± 6.3°, p = 0.064). Nine patients experienced a significant curve reduction of ≥5°, while eight showed a reduction between 0° and 5°; however, two patients exhibited no change in curve magnitude. Furthermore, the correction rate of the TL/L curve correlated significantly with functional LLD (r = −0.484, p = 0.030) and pelvic obliquity (r = −0.556, p = 0.011), highlighting the active pelvic compensation in maintaining balance between the spine and lower limbs. Conversely, no significant correlation was observed between curve correction and structural LLD (p > 0.05). Additionally, even after adjusting for other influencing factors, the TL/L Cobb angle remained significantly different between pre‐ and post‐sole lifting (p = 0.037).ConclusionThis study confirmed the effectiveness of sole lift intervention in correcting TL/L and thoracic curves among the mild IS children with a main TL/L curve, providing a supplementary conservative treatment option for patients with the lower limb at the convexity of the main curve. Moreover, our findings underscored the active compensation of the lower limbs and the pelvis in the etiopathogenesis of IS, highlighting the importance of considering their influence in treatment strategies.

Background: Skeleton involvement is one of the most significant aspects of Gaucher disease (GD). However, the treatment for spinal involvement in GD among patients undergoing enzyme replacement therapy (ERT) is poorly characterized. We present a case of progressive kyphotic spinal deformity in a young child caused by vertebral involvement, which was managed by posterior spinal fusion without anterior spinal release under ERT. Case presentation: This is a retrospective study. A 10-year-old boy presenting with progression kyphosis (thoracic kyphotic angle of 113°) associated with type-IIIb GD had undergone posterior spinal fusion with segmental pedicle screw fixation (from T6-L3) and Ponte osteotomy. The patient went back to school without further brace protection. Proximal junctional kyphosis (PJK) was observed at 4 months postoperatively. Revision surgery was performed to prevent neurological impairment. Additional posterior spinal fusion from T2–T6 and decompressive laminectomy were performed during the revision surgery. A 2-year follow-up showed no recurrence of PJK and solid fusion was achieved in the patient under ERT and brace protection. Conclusions: Posterior spinal fusion without anterior spinal release is a good treatment option for severe spinal deformity in patients with GD. However, the fusion level and reinforced fixation require careful consideration. Revision surgery and brace protection is needed as long as PJK is observed.

With a booming aging population worldwide, bone and joint degenerative diseases have gradually become a major public health focus, attracting extensive scientific attention. However, the effective treatments of these degenerative diseases have been confined to traditional medications and surgical interventions, which easily lead to the possibility of drug abuse or loss of physiological function to varying degrees. Recently, given that the development of reprogramming has overcome shackles in the field of degenerative diseases, direct reprogramming would provide a new concept to accelerate progress in the therapy of bone and joint degenerative diseases. The process of direct reprogramming would directly induce ordinary somatic cells to the desired targeted cells without passing through pluripotent cell states. In this review, we summarize some direct reprogramming of cells that has been attempted for the repair of common bone and joint degenerative diseases, such as osteoarthritis, osteoporosis-related fracture and intervertebral disc degeneration. However, it is inevitable that some obstacles, such as accurate transcription factors, an appropriate extracellular microenvironment and efficient delivery carriers in vivo, need to be resolved. In addition, developmental and promising directions associated with direct reprogramming have attracted public attention. Investigation of the regulation of the transient genome, metabolic conversion and cellular skeleton would provide superior potential candidates for the revolution of direct reprogramming. The aim of direct reprogramming is to directly provide target cells for cell therapy and even tissue reconstruction in bone and joint degenerative diseases. Moreover, the development of direct reprogramming have potential to achieve repair and even reconstruct in situ, which would be breakthrough effect for the repair of bone and joint degenerative diseases. The advance of direct reprogramming has opened numerous opportunities for new therapeutic strategies in regenerative medicine.

Bladder cancer (BC), a urologic disease, commonly occurs globally and is very invasive. Patients with invasive BC have low 5-year survival rate. Hence, the mechanisms underlying BC development and progression should be elucidated. MicroRNAs (miRNAs), as common noncoding RNAs, are receiving increasing attention because of their biological functions. The irregular expression patterns of miRNAs are linked to BC occurrence; therefore, determining the functions of miRNAs in abnormally expressed BC tissues might enable to elucidate the pathogenetic mechanism of BC and offer new markers for the prognosis, diagnosis, and therapy of BC. Here, we consolidate the primary roles of miRNAs with atypical expression in BC development as well as their association with BC pathological grades and chemotherapy resistance development in patients with BC.