BACKGROUND:Studies have shown that irisin can delay joint degeneration by modulating the metabolic homeostasis of chondrocytes and inhibiting inflammatory responses and oxidative stress.OBJECTIVE:To further explore the mechanism by which irisin exerts therapeutic effects on osteoarthritis.METHODS:(1)Bioinformatics analysis:Gene expression data from cartilage tissues of patients with osteoarthritis and healthy controls were obtained from the GSE51588 and GSE207881 datasets.Gene set variation analysis assessed the activation of programmed cell death in osteoarthritis.Differential expression analysis identified differentially expressed genes between osteoarthritis and control samples,followed by pathway enrichment analysis.Ferroptosis-related differentially expressed genes were further identified,with those having an area under the receiver operating characteristic curve greater than 0.9 designated as core genes.(2)Cell experiment.Human articular chondrocytes were divided into four groups:control(chondrocytes),model(inflammatory models were established in chondrocytes induced by tumor necrosis factor α),model+Erastin(a ferroptosis inducer),and model+Erastin+irisin.ELISA measured glutathione,malondialdehyde and reactive oxygen species levels,while JC-1 assays assessed mitochondrial membrane potential.RT-qPCR quantified mRNA levels of core and ferroptosis-related genes,and western blot analyzed the expression of core genes,ferroptosis-related proteins,ERK pathway components,and apoptotic proteins.RESULTS AND CONCLUSION:(1)Gene set variation analysis indicated significant ferroptosis activation in osteoarthritis.(2)Differential expression analysis highlighted significant enrichment of differentially expressed genes in the ERK signaling pathway.Sixteen ferroptosis-related differentially expressed genes including HMOX1,G6PD,and ALOX5,were identified,all with the area under the curve values above 0.9.(3)In the human articular chondrocytes model+Erastin group,glutathione levels and mitochondrial membrane potential decreased significantly,while malondialdehyde and reactive oxygen species levels increased.The expression of HMOX1,G6PD,ALOX5,glutathione peroxidase 4,and SLC7A11 was significantly downregulated,while p-ERK and Bax levels rose,and Bcl2 decreased(all P＜0.05).Irisin treatment significantly improved ferroptosis-related markers(all P＜0.05).To conclude,HMOX1,G6PD,and ALOX5 may be potential therapeutic targets of osteoarthritis.Irisin offers protective effects in osteoarthritis by modulating ferroptosis-related genes and pathways.

BACKGROUND:Studies have shown that irisin can delay joint degeneration by modulating the metabolic homeostasis of chondrocytes and inhibiting inflammatory responses and oxidative stress.OBJECTIVE:To further explore the mechanism by which irisin exerts therapeutic effects on osteoarthritis.METHODS:(1)Bioinformatics analysis:Gene expression data from cartilage tissues of patients with osteoarthritis and healthy controls were obtained from the GSE51588 and GSE207881 datasets.Gene set variation analysis assessed the activation of programmed cell death in osteoarthritis.Differential expression analysis identified differentially expressed genes between osteoarthritis and control samples,followed by pathway enrichment analysis.Ferroptosis-related differentially expressed genes were further identified,with those having an area under the receiver operating characteristic curve greater than 0.9 designated as core genes.(2)Cell experiment.Human articular chondrocytes were divided into four groups:control(chondrocytes),model(inflammatory models were established in chondrocytes induced by tumor necrosis factor α),model+Erastin(a ferroptosis inducer),and model+Erastin+irisin.ELISA measured glutathione,malondialdehyde and reactive oxygen species levels,while JC-1 assays assessed mitochondrial membrane potential.RT-qPCR quantified mRNA levels of core and ferroptosis-related genes,and western blot analyzed the expression of core genes,ferroptosis-related proteins,ERK pathway components,and apoptotic proteins.RESULTS AND CONCLUSION:(1)Gene set variation analysis indicated significant ferroptosis activation in osteoarthritis.(2)Differential expression analysis highlighted significant enrichment of differentially expressed genes in the ERK signaling pathway.Sixteen ferroptosis-related differentially expressed genes including HMOX1,G6PD,and ALOX5,were identified,all with the area under the curve values above 0.9.(3)In the human articular chondrocytes model+Erastin group,glutathione levels and mitochondrial membrane potential decreased significantly,while malondialdehyde and reactive oxygen species levels increased.The expression of HMOX1,G6PD,ALOX5,glutathione peroxidase 4,and SLC7A11 was significantly downregulated,while p-ERK and Bax levels rose,and Bcl2 decreased(all P＜0.05).Irisin treatment significantly improved ferroptosis-related markers(all P＜0.05).To conclude,HMOX1,G6PD,and ALOX5 may be potential therapeutic targets of osteoarthritis.Irisin offers protective effects in osteoarthritis by modulating ferroptosis-related genes and pathways.

Non-specific low back pain is a major cause of productivity decline and disability worldwide.Its pathogenesis remains unclear,lacking significant organic lesions and imaging features.When the disease course persists for more than three months,it is referred to as chronic non-specific low back pain.Currently,rehabilita-tion for chronic non-specific low back pain often focuses on a single biomedical model and lacks multi-perspective analysis of its therapeutic mechanism.For such a complex condition with high prevalence and high recurrence rate,a multidimensional analysis of the mechanism of action and application of rehabilitation methods may contribute to more precise treatment.core training is an important method for the rehabilitation of chronic non-specific low back pain.This article reviews the mechanism of action of core training in treating chronic non-specific low back pain from the perspectives of biomechanics,neuromodulation,and psychological adaptation,and explores its combined application with emerging technologies such as virtual reality,thereby potentially improving treatment compliance and efficacy,aiming to provide insights for chronic non-specific low back pain precision rehabilitation and to facilitate the transition toward a multifactorial,multidisciplinary integrated model.

Non-specific low back pain is a major cause of productivity decline and disability worldwide.Its pathogenesis remains unclear,lacking significant organic lesions and imaging features.When the disease course persists for more than three months,it is referred to as chronic non-specific low back pain.Currently,rehabilita-tion for chronic non-specific low back pain often focuses on a single biomedical model and lacks multi-perspective analysis of its therapeutic mechanism.For such a complex condition with high prevalence and high recurrence rate,a multidimensional analysis of the mechanism of action and application of rehabilitation methods may contribute to more precise treatment.core training is an important method for the rehabilitation of chronic non-specific low back pain.This article reviews the mechanism of action of core training in treating chronic non-specific low back pain from the perspectives of biomechanics,neuromodulation,and psychological adaptation,and explores its combined application with emerging technologies such as virtual reality,thereby potentially improving treatment compliance and efficacy,aiming to provide insights for chronic non-specific low back pain precision rehabilitation and to facilitate the transition toward a multifactorial,multidisciplinary integrated model.

BACKGROUND:Whether continuous passive motion improves osteoarthritis by enhancing the proliferation ability of chondrocytes is rarely reported.
OBJECTIVE:To analyze the therapeutic outcomes of continuous passive motion in rabbits with osteoarthritis and the underlying mechanism.
METHODS:Thirty-six New Zealand white rabbits were randomly al otted into three groups (n=12 per group). Rabbits in control group only underwent capsulotomy with no harm to the cartilage;osteoarthritis models were established in the rabbits of model and treatment groups using Hulth method. At 1 day after modeling, the treatment group rabbits were treated with continuous passive motion, 8 hours daily for consecutive 8 weeks. Interleukin-1 and tumor necrosis factorαlevels in the synovial fluid were detected by ELISA;col agen type II expression and the proliferation ability of chondrocytes were detected by MTT assay;Erk signaling pathway activation was determined using western blot assay.
RESULTS AND CONCLUSION:In the model group, interleukin-1 and tumor necrosis factorαlevels in the synovial fluid were significantly increased, and the expression level of col agen type II mRNA was remarkablely down-regulated. Continuous passive motion significantly downregulated interleukin-1 and tumor necrosis factorαlevels and up-regulated the col agen type II mRNA level (P<0.01). The model group showed significantly decreased proliferation ability of chondrocytes and down-regulated Erk signaling pathway activation, while after continuous passive motion, al above indicators were significantly improved (P<0.01). These results indicate that the continuous passive motion can al eviate osteoarthritis probably by influencing interleukin-1 and tumor necrosis factorαlevels, proliferation ability of chondrocytes, and col agen type II expression, as wel as regulating Erk signaling pathway activation.

Aphasia is a common clinical manifestation after ischemic stroke.The therapeutic effect of low-frequency repetitive transcranial magnetic stimulation and mechanisms at different times after stroke are not exactly the same.This article reviews the advances in low-frequency repetitive transcranial magnetic stimulation for the treatment of aphasia after ischemic stroke.

Objective To study the effects of task-oriented training combined with electromyographic biofeedback on wrist and finger extension after stroke.Methods Thirty-eight stroke patients were assigned randomly into either an experimental group (18 cases) or a control group (18 cases).Both groups received routine rehabilitation treatment and electromyographic biofeedback training.In addition,the experimental group was given task-oriented training in wrist and finger extension.Myoelectricity values,the active range of wrist dorsiflexion and the FuglMeyer upper extremity assessment (FMA) were assessed before and after 8 weeks of training.Results All of the patients showed significant improvements after 8 weeks of training,but compared with the controls,the patients in the experimental group improved significantly more in terms of all of the measures.Conclusion Task-oriented training with electromyographic biofeedback can improve upper extremity function,particularly wrist extension,among hemiplegic stroke survivors.