clinical-effects-ultrasound-guided-acupotomy-knee-osteoarthritis

Clinical Effects of Ultrasound-Guided Acupotomy in Knee Osteoarthritis Treatment

The protocol presented here demonstrates the operation method of ultrasound-guided acupotomy for knee osteoarthritis (KOA), including patient recruitment, ...

Longhua Hospital affiliated to Shanghai University of Traditional Chinese Medicine

The treatment of spinal cord injury is always a stubborn problem for neurosurgeons because nerve cell cannot regenerate and the glia scar can prevent the axonal regeneration. Olfactory ensheathing cells (OECs) is a kind of especial glia cell, which possesses the character of horizontal cell of central nervous system and schwann cell. Many foundational and clinical studies showed that the olfactory ensheathing cellscan promote axonal regeneration and prove axonal growth, some progress is made and this is bringing hope for treatment of spine injury.

[An update of repairing spinal cord injury by olfactory ensheathing cells].

The aim of this study was to investigate whether miR-490 was involved in the regulation of angiogenesis after cerebral infarction by regulating vascular endothelial growth factor (VEGF) expression.

MiR-940 regulates angiogenesis after cerebral infarction through VEGF.

Osteoporosis (OP) is a prevalent metabolic disease, with aging and menopause being the major risk factors. Studies have shown that nearly one-third of postmenopausal women suffer from osteoporosis. However, there is a scarcity of research on antioxidant systems for the prevention and treatment of postmenopausal osteoporosis (PM-OP). To address this gap, we performed differential analysis using Limma to identify differentially expressed genes (DEGs) in PM-OP samples. We employed weighted correlation network analysis (WGCNA) to identify oxidative stress (OS)-related genes (OSRGs) highly correlated with PM-OP. The intersection of key modular genes and DEGs yielded differentially expressed OSRGs (DE-OSRGs) specific to PM-OP. We conducted GO and KEGG functional enrichment analyses on these genes. Additionally, we constructed a protein-protein interaction (PPI) network and utilized support vector machine recursive feature elimination (SVM-RFE) and random forest (RF) algorithms to identify signature genes. The diagnostic value of the signature genes was evaluated and validated using ROC curves. GSEA enrichment analysis was employed to explore the potential mechanisms associated with the signature genes. Finally, we constructed a regulatory network involving TF-miRNA-mRNA interactions for the signature genes and verified the biological roles of FOXO3 and DDIT3 in PM-OP and healthy groups using quantitative real-time PCR (qRT-PCR). Our analysis revealed 20 DE-OSRGs specific to PM-OP, obtained by intersecting modular and differential genes. The PPI network identified central genes (DDIT3, MAPK8, CDK2, SIRT1, and FOXO3) with more than 3 nodes. Through integration with machine learning algorithms, we identified DDIT3 and FOXO3 as signature genes. The ROC curve analysis indicated that the AUC value was greater than 0.7, suggesting the potential diagnostic value of these signature genes. Furthermore, GSEA results revealed their involvement in pathways related to the regulation of neutrophil activation, oxidative phosphorylation, MAPK signaling, mitochondrial matrix, and phagocytosis. Lastly, we constructed a regulatory network comprising 27 nodes (22 TFs, 3 miRNAs, and 2 mRNAs) and 28 edges. Additionally, qRT-PCR confirmed the significant up-regulation of FOXO3 and DDIT3 expressions in the PM-OP group compared to the healthy control group. In summary, this study employed bioinformatics analysis to identify OS-related biomarkers (DDIT3 and FOXO3) in PM-OP, providing new biological targets for clinical treatment.

Identification of biomarkers associated with oxidative stress-related genes in postmenopausal osteoporosis.

Osteoarthritis (OA) is a degenerative bone disease associated with aging. The rising global aging population has led to a surge in OA cases, thereby imposing a significant socioeconomic burden. Researchers have been keenly investigating the mechanisms underlying OA. Previous studies have suggested that the disease starts with synovial inflammation and hyperplasia, advancing toward cartilage degradation. Ultimately, subchondral-bone collapse, sclerosis, and osteophyte formation occur. This progression is deemed as "top to bottom." However, recent research is challenging this perspective by indicating that initial changes occur in subchondral bone, precipitating cartilage breakdown. In this review, we elucidate the epidemiology of OA and present an in-depth overview of the subchondral bone's physiological state, functions, and the varied pathological shifts during OA progression. We also introduce the role of multifunctional signal pathways (including osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B ligand (RANKL)/receptor activator of nuclear factor-kappa B (RANK), and chemokine (CXC motif) ligand 12 (CXCL12)/CXC motif chemokine receptor 4 (CXCR4)) in the pathology of subchondral bone and their role in the "bottom-up" progression of OA. Using vivid pattern maps and clinical images, this review highlights the crucial role of subchondral bone in driving OA progression, illuminating its interplay with the condition.

Zhi Jun Hu

Longhua Hospital affiliated to Shanghai University of Traditional Chinese Medicine

Clinical Effects of Ultrasound-Guided Acupotomy in Knee Osteoarthritis Treatment