Liang Chen

Exosomes are nanosized extracellular vesicles actively secreted by various cell types, typically ranging from approximately 30 to 150 nm in diameter

Objective: To introduce the technical protocol of unilateral biportal endoscopy (UBE) in the treatment of patients with non-aggressive spinal benign tumors and evaluate its clinical efficacy and safety. Methods: A retrospective analysis was conducted on 14 patients (6 males, 8 females) with pathologically confirmed spinal benign tumors who underwent UBE surgery at Chongqing University Cancer Hospital between August 2021 and December 2023. Operative duration, total perioperative blood loss, and postoperative complications were recorded. Back pain visual analog scale (VAS) scores were compared preoperatively and at postoperative day 1, 3 months, 6 months, and the final follow-up. Preoperative and predischarge CT imaging findings were also assessed. Results: All 14 patients successfully underwent UBE surgery, with a mean operative duration of 77.5 ± 21.2 min and a mean blood loss of 17.5 ± 11.7 mL. Postoperative CT confirmed adequate lesions resection. Patients were followed up for 10–30 months (mean: 16.6 ± 5.4 months). VAS scores at all postoperative timepoints showed significant improvement compared to preoperative values ( P < 0.05). No tumor recurrence was observed during follow-up, and all patients resumed normal daily activities. Conclusion: UBE is a safe and effective surgical option for non-aggressive spinal benign tumors, achieving satisfactory lesions resection and favorable clinical outcomes.

Background Open surgery is commonly used for treating benign bone tumours and tumour-like lesions near the joints of the extremities. However, inappropriate resection margins may lead to incomplete lesion removal and subsequent local recurrence, while overly extensive dissection aggravates soft tissue injury and compromises periarticular joint function. Although uniportal endoscopic technique have been well established in minimally invasive spinal surgery, their utilization in juxta-articular benign bone lesions remains poorly defined with unclear patient selection criteria and medium-term oncological performance. This retrospective study aimed to summarize the appropriate indications for uniportal endoscopic technique in the treatment of benign bone tumours and tumour-like lesions adjacent to limb joints and evaluate its oncological safety and local control outcomes. Purposes By comparing the differences between the uniportal endoscopic technique and open surgery in treating benign bone tumours and tumour-like lesions adjacent to limb joints, this study aims to investigate the feasibility of the uniportal endoscopic technique. More importantly, it aims to evaluate and discuss the indications of uniportal endoscopic technique, as well as the medium-term oncological efficacy and safety. Methods A retrospective analysis was conducted on the clinical data of patients with benign bone tumours and tumour-like lesions near the joints of the extremities treated at the Affiliated Cancer Hospital of Chongqing University between October 2021 and December 2024. Among them, 53 patients were treated using the uniportal endoscopic technique, and 97 patients were treated using the open surgery. The follow-up period for all cases exceeded 12 months. All cases had a definitive pathological diagnosis preoperatively. The lesion size (maximum diameter) was recorded for indication stratification. Primary study endpoints focused on medium-term oncological outcomes, including local recurrence rate and lesion clearance status evaluated by serial follow-up computed tomography (CT). Secondary perioperative indicators including operation time, intraoperative blood loss, postoperative complications, and preoperative and postoperative Visual Analogue Scale (VAS) scores were collected for comparison. Surgical outcomes were evaluated using the modified Macnab criteria. Results All 150 patients included in this study completed the follow-up examinations. During follow-up, adequate radical lesion clearance was confirmed on serial CT examinations in all patients, and no local recurrence was detected in both the uniportal endoscopic technique group and the open surgery group. All lesions enrolled in this study had a maximum diameter less than 5 cm, and uniportal endoscopic technique achieved complete resection in these eligible cases, suggesting that a maximal diameter < 5 cm represents a reasonable size indication for this endoscopic technique. Postoperative imaging examinations indicated satisfactory bone healing in all patients. The mean operation time was 140.02 ± 39.67 min in the uniportal endoscopic technique group and 141.56 ± 36.90 min in the open surgery group, with no statistically significant difference between the two groups (P > 0.05). Intraoperative blood loss was significantly lower in the uniportal endoscopic technique group compared with the open surgery group [20.00 (15.00) mL vs. 50.00 (50.00) mL; P < 0.001]. No postoperative complications occurred in either group. Intra-group comparison: The VAS scores at various postoperative time points were significantly lower compared to the preoperative scores in both groups (P < 0.05), indicating statistically significant improvement postoperatively. The results of the modified Macnab criteria at the final follow-up indicated significant improvement in clinical symptoms for all patients, suggesting postoperative pain relief, functional recovery, and improved quality of life. Conclusion In conclusion, for juxta-articular benign bone tumours and tumour-like lesions with a maximum diameter less than 5 cm, uniportal endoscopic technique achieves equivalent radical resection efficacy compared with open surgery under strict indication screening. No local recurrence was observed in either group during follow-up, which suggests the favourable oncological safety of the uniportal endoscopic technique. Although the uniportal endoscopic technique had advantages in several perioperative indicators, these minimally invasive benefits should not serve as the primary basis for surgical decision-making.

Glucocorticoid-induced osteoporosis (GIOP) is the most common secondary osteoporosis, which characterized by the decreased bone strength and increased frac

Osteosarcoma (OS) is a highly aggressive primary bone malignancy that predominantly affects children and adolescents. Although surgical intervention and neoadjuvant therapy demonstrate efficacy in localized OS, postoperative survival rates remain suboptimal for patients with metastatic and recurrent OS. In recent years, immunotherapy has garnered considerable attention due to its promising efficacy across various solid tumors. However, the distinct immunosuppressive tumor microenvironment in OS restricts therapeutic response, as immunosuppressive states are further intensified in metastatic and recurrent lesions, thereby complicating immunotherapy efforts. Recent studies have found that metabolic reprogramming plays a crucial role in shaping the immunosuppressive tumor microenvironment of OS. Tumor cells can induce adaptive metabolic changes in immune cells through competitively consuming nutrients, accumulating immunosuppressive metabolites, and secreting exosomes. This subsequently diminishes their immune functions and promotes immune escape, which partially explains the poor efficacy of immunotherapy in OS. Thus, combining immunotherapy and metabolic-targeted drugs is a potential strategy for enhancing treatment efficacy against OS. This review focuses on the major characteristics of the immunosuppressive microenvironment in OS. It details how metabolic reprogramming in glucose, lipid, and amino acid metabolism remodels this environment and influences key immune cells, including tumor-associated macrophages (TAMs), T cells, and natural killer (NK) cells. It further explores the translational potential of combining metabolic interventions with immunotherapy to advance the clinical application in OS.

To construct an improved deep learning model that provides a more accurate and cost-effective solution for diagnosing abnormalities in the cervical physiol

Bone morphogenetic protein 9 (BMP9) is a cytokine with potent osteoinductive activity, although its precise regulatory mechanisms remain incompletely elucidated. NOTUM, a secreted palmitoleoyl-protein carboxylesterase, has an unclear role in osteogenic differentiation. This study aims to explore the role and mechanism of NOTUM in BMP9-induced osteogenic differentiation of mouse embryonic fibroblasts (MEFs). In the BMP9-induced osteogenic differentiation model, Notum was either overexpressed or silenced, and the expression of RUNX2 and OPN as well as osteogenic signaling pathways were assessed by q-PCR and Western blot. ALP staining and Alizarin Red staining were subsequently performed to determine ALP activity and matrix mineralization. Furthermore, the osteogenic effect of Notum was evaluated using an in vivo subcutaneous ectopic osteogenesis model, supplemented by histochemical staining and micro-CT analysis. BMP9 significantly downregulates NOTUM protein expression in MEF cells. NOTUM attenuated BMP9-induced expression of osteogenic markers RUNX2 and OPN, as well as ALP activity and matrix mineralization. In vivo ectopic osteogenesis assays yielded results consistent with in vitro observations. Mechanistically, NOTUM overexpression reduced β-catenin protein levels, while NOTUM knockdown elevated β-catenin accumulation during BMP9-mediated osteogenic differentiation. NOTUM overexpression up-regulated GSK-3β protein expression while suppressing its phosphorylation status during BMP9-induced osteogenesis, whereas NOTUM depletion produced the converse effects. Pharmacological activation of the Wnt/β-catenin signaling pathway rescued osteogenic marker expression, effectively counteracting NOTUM-mediated suppression of BMP9's osteogenic potential. NOTUM serves as a novel regulator of BMP9-Induced osteogenesis via modulation of the Wnt/β-Catenin Axis, Suggesting its potential as a therapeutic target for bone regeneration.

Tumor drug resistance exhibits substantial heterogeneity across cancer types, reflecting distinct molecular mechanisms in each malignancy. To characterize this complexity, we developed a pan-cancer transfer learning framework that integrates bulk RNA-seq data with a residual variational autoencoder (Res VAE) backbone. Five models were trained on the Genomics of Drug Sensitivity in Cancer (GDSC) dataset, which includes drug response profiles for 72 chemotherapeutic agents. Among them, three models are specially designed by incorporating variational autoencoders and large pretrained models (LLMs): the LLM large VAE (VAE_LL), the LLM small VAE (VAE_LS), and the LLM distillation VAE (VAE_LD). Random Forest (RF) and eXtreme Gradient Boosting (XGB) were included as ensemble learning baselines. After internal cross-validation, the top four models (VAE_LL, VAE_LD, XGB, and RF) were applied to five representative TCGA cohorts comprising 1,836 patients. For each cancer type, resistance to nine clinically relevant first-line drugs was modeled, resulting in 180 drug–cancer prediction tasks. Among all models, VAE_LD achieved the best overall performance, with a mean AUC of 0.81 and an F1 score of 0.92 on the GDSC benchmark, and maintained strong predictive power in the clinical validation phase. Interpretation analyses identified tumor-specific resistance biomarkers with clinical significance. In lung adenocarcinoma, elevated expression of TFF1 was repeatedly associated with resistance to Gefitinib and correlated with poor patient prognosis, indicating its potential as a therapeutic target. In glioblastoma, OPALIN, LTF, IL2RA, and SLC17A7 were implicated in Temozolomide resistance through pathways related to epithelial differentiation and angiogenesis. In conclusion, the VAE_LD model offers a high-performing and interpretable approach for predicting drug resistance across multiple tumor types. It supports the identification of clinically actionable biomarkers and provides a robust framework for precision oncology applications.

Extracellular vesicles (EVs) are nanoscale particles with a lipid bilayer membrane structure secreted by various cell types. Nearly all human cells secrete EVs, primarily mediating intercellular communication. In recent years, scientists have discovered that EVs can carry multiple biological cargos, such as DNA, non-coding RNAs (ncRNAs), proteins, cytokines, and lipids, and mediate intercellular signal transduction. Bone is a connective tissue with a nerve supply and high vascularization. The repair process after injury is highly complex, involving interactions among multiple cell types and biological signaling pathways. Bone regeneration consists of a series of coordinated osteoconductive and osteoinductive biological processes. As mediators of intercellular communication, EVs can promote bone regeneration by regulating osteoblast-mediated bone formation, osteoclast-mediated bone resorption, and other pathways. This review summarizes the biogenesis of EVs and the mechanisms by which EV-mediated intercellular communication promotes bone regeneration. Additionally, we focus on the research progress of EVs in various diseases related to bone regeneration. Finally, based on the above research, we explore the clinical applications of engineered EVs in the diagnosis and treatment of bone regeneration-related diseases.

1、The article mentions the evaluation and classification of images by three experts, but lacks statistical analysis of the results of the assessments by these three experts. Is there a statistical difference in the assessments among the various expe...