PURPOSE:The Fugl-Meyer assessment (FMA) is the gold standard for evaluating sensorimotor-impairment after stroke, yet no validated Chinese translation exists despite China's large stroke burden. This study aimed to develop and validate a Chinese version of the FMA for use in Chinese-speaking stroke populations. METHODS:We followed internationally accepted guidelines for translation and cross-cultural adaptation to ensure conceptual, semantic, and cultural equivalence. The process involved forward and backward translation, expert team review, and cognitive pretesting. The finalized Simplified Chinese FMA was administered to 60 adult stroke survivors (subacute and chronic) from rehabilitation centers in Chongqing, China. Psychometric evaluation was cross-sectional and included internal consistency (Cronbach's α), inter-rater reliability (ICC), item-level agreement, concurrent validity (NIHSS, mRS, FIM), and construct validity using factor analysis. RESULTS:The Chinese FMA showed excellent internal consistency (α = 0.770-0.970) and outstanding inter-rater reliability (ICC = 0.99 for both extremities), with item-level agreement of 95% (upper limb) and 93.33% (lower limb). Concurrent validity was confirmed via strong correlations with the mRS (r=-0.534), NIHSS (r=-0.856), and FIM (r = 0.867). Factor analysis supported its theoretical structure, with no ceiling or floor effects observed. CONCLUSIONS:The Chinese FMA demonstrates robust psychometric properties comparable to the original English version and other validated translations.

The International Classification of Functioning, Disability and Health (ICF), developed by the World Health Organization, provides a biopsychosocial framework for describing health and health-related states. This short review explores ICF's evolution, current applications, and future directions in rehabilitation medicine. We highlight how the ICF bridges traditional biomedical diagnoses and patient-centered outcomes, promotes multidisciplinary collaboration, and supports functional and policy-level integration in healthcare systems. With the rise of digital health technologies, the ICF is poised to play a transformative role in redefining rehabilitation goals and practices.

Regeneration of the corticospinal tract (CST) is considered a therapeutic target to achieve improved recovery of motor function after spinal cord injury (SCI), which is an incurable CNS damage that affects millions of people. Exercise training is effective in improving multiple functions in spinal cord-injured patients. However, the effects of exercise training on axon regeneration have not been sufficiently reported. Osteopontin (OPN) has great potential application as a neuroprotective agent for the repair of the nervous system. Studies have shown that the extent of axon regeneration strongly correlates with the expression of OPN. Our previous studies demonstrated that treadmill exercise supplemented by OPN enhances motor function recovery, but axon regeneration is still limited. Extending the treadmill exercise for 12 weeks, we observed promoted axon regeneration, motor function improvement, and signaling pathway activation in mice with SCI after supplementing OPN. Axon regeneration was observed with an anterograde tracer, motor function recovery was evaluated by animal ethology and electrophysiology, and the levels of IGF-1R/Akt/mTOR signaling pathway were evaluated. The results showed that the CST of C5 crushed mice regenerated and formed synaptic connections with neurons after treadmill exercise supplemented by OPN, the horizontal ladder and cylinder rearing test of injured limbs were improved, motor evoked potential also suggested enhanced nerve conduction, and the expression of p-IR, p-Akt, and p-S6 were increased. And the improvements were more obvious than that of the exercise group. Collectively, our study found that treadmill exercise supplemented by OPN promote axon regeneration and motor function through the IGF-1R/Akt/mTOR signaling pathways, and these improvements can be inhibited by rapamycin and Methyl-beta-CD (M-B-CD).

BackgroundThe optimal treatment methods for delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) were not identified. Thus, this study was conducted to compare the efficacies of intermittent theta burst stimulation (iTBS) and short-chain fatty acids (SCFAs) in treating cognitive dysfunction and anxiety symptoms of DEACMP rat.MethodsIn phase I, a DEACMP rat model was built to assess the inflammation levels in the hippocampus and levels of SCFAs in the serum of DEACMP rats. In phase II, DEACMP rats were randomly assigned into four groups: DEACMP + placebo, DEACMP + SCFAs, DEACMP + sham iTBS, and DEACMP + iTBS. The intervention was continued for 2 weeks. A Morris water maze and open field tests were used to assess cognitive function and anxiety symptoms, respectively.ResultsThe levels of three inflammatory factors (IL-1β, IL-6, and TNF-α) and two SCFAs (acetate and propionate) were significantly increased and decreased, respectively, in DEACMP rats. After treatment, cognitive dysfunction and anxiety symptoms were significantly improved in the DEACMP + iTBS group and the DEACMP + SCFAs (consisting of acetate and propionate) group. Both SCFAs and iTBS could significantly improve the increased levels of IL-1β, IL-6, and TNF-α in the hippocampus, and SCFAs could also improve the decreased levels of GPR41, GPR43, dopamine, and norepinephrine in the hippocampus of DEACMP rats.ConclusionThese results indicate that both iTBS and SCFA solutions consisting of acetate and propionate produced good effects on DEACMP rats by regulating inflammation levels in the hippocampus, and acetate/propionate–GPR41/GPR43–IL-1β/IL-6/TNF-α–dopamine/norepinephrine may be a potential pathway in SCFAs for the treatment of DEACMP.

Regulatory T (Treg) cells contribute to white matter repair following ischemic stroke, but their limited availability in circulation restricts their therapeutic potential. Exercise, as a non-invasive and effective rehabilitation method, has been shown to restore Treg balance in diseases. This study explores the effects of treadmill training on Treg upregulation and its influence on myelin repair and functional recovery in rats with middle cerebral artery occlusion (MCAO). After four weeks of treadmill training, we analyzed the proportion of Treg cells (Tregs), FOXP3 expression, and oligodendrocyte-related protein levels using flow cytometry, immunofluorescence, and Western blotting. Myelin structure was examined with transmission electron microscopy (TEM), while motor coordination and balance were assessed using the fatigue rotarod and CatWalk analysis systems. To further explore the role of Tregs, the FOXP3 inhibitor P60 was used to inhibit Treg activity. The findings of our study indicate that training on a treadmill supports the maturation of oligodendrocytes, leads to an increase in myelin-associated proteins and the thickness of myelin, and promotes the recovery of motor function. Inhibition of Treg activity diminished these benefits, highlighting Tregs’ key role in exercise-induced remyelination. These findings suggest that treadmill training facilitates myelin regeneration and functional recovery by upregulating Tregs, offering potential new strategies for stroke treatment.

Regenerative rehabilitation is an evolving discipline that strategically unites regenerative medicine with rehabilitation science to enhance functional recovery through synergistic biological and physical interventions. Integrating stem cell therapies, tissue engineering, and bioactive factors with tailored rehabilitation modalities amplifies innate regenerative mechanisms while directing tissue remodeling toward functional outcomes. This review outlines the foundational principles, developmental milestones, and mechanistic insights of regenerative rehabilitation, emphasizing its application across neurological, musculoskeletal, and integumentary injuries. In neurological disorders, stem cell-derived therapies and task-specific training foster neuroplasticity and circuit reorganization. Scaffold-based strategies paired with progressive loading optimize cartilage regeneration and biomechanical resilience for musculoskeletal repair. In burn injuries, engineered skin substitutes integrated with early mobilization mitigate fibrosis and restore mobility. Across these domains, rehabilitation is a dynamic guide for regenerative processes—modulating the fate of the stem cells, enhancing tissue integration, and translating structural repair into functional gains. These advances underscore a paradigm in which regenerative technologies and rehabilitative protocols are codependent, ensuring cellular and tissue-level regeneration aligns with holistic functional restoration.

This article offers a comprehensive review of research progress in the field of artificial intelligence and stroke rehabilitation. It begins by exploring its historical development, which has progressed through the stages of germination, technological integration, and initial application, marked by ongoing innovation. The article then delves into the current research landscape, addressing core technological support, the expansion of application scenarios, and the verification of clinical effects that showcase the pivotal role of artificial intelligence in enhancing the efficiency and effectiveness of rehabilitation. Subsequently, future development trends are analyzed, including the move toward personalization and precision, the widespread adoption of remote and home-based rehabilitation, and the integration of multi-technology approaches alongside cross-disciplinary innovation. Concurrently, challenges facing the field—such as technological bottlenecks, the absence of ethical guidelines, and difficulties in adapting healthcare systems—are examined, with corresponding strategies and recommendations proposed. Lastly, the article highlights the reshaping of the stroke rehabilitation paradigm through artificial intelligence, discussing future research directions, social impacts, and visionary goals. It underscores the global importance of artificial intelligence in advancing stroke rehabilitation and fostering its development worldwide.

Pain is a widespread motivation for seeking healthcare and stands as a substantial global public health concern. Despite comprehensive investigations into the mechanisms of pain sensitization induced by inflammation, efficacious treatments options remain scarce . Neutrophil extracellular traps (NETs) have been associated with the progression and tissue damage of diverse inflammatory diseases. This study aims to explore the impact of NETs on the progression of inflammatory pain and explore potential therapeutic approaches. Initially, we observed neutrophil infiltration and the formation of NETs in the left hind paw of mice with inflammatory pain induced by complete Freund 's adjuvant (CFA). Furthermore, we employed the peptidyl arginine deiminase 4 (PAD4) inhibitor Cl-amidine (diluted at 50 mg/kg in saline, administered via tail vein injection once daily for three days) to impede NETs formation and administered DNase1 (diluted at 10 mg/kg in saline, once daily for three days) to break down NETs. We investigated the pathological importance of peripheral NETs formation in inflammatory pain and its influence on the activation of spinal dorsal horn microglia. The findings indicate that neutrophils infiltrating locally generate NETs, leading to an increased release of inflammatory mediators that worsen peripheral inflammatory reactions. Consequently, this results in the transmission of more harmful peripheral stimuli to the spinal cord, triggering microglial activation and NF- kappa B phosphorylation, thereby escalating neuroinflammation and fostering pain sensitization. Suppression of peripheral NETs can mitigate peripheral inflammation in mice with inflammatory pain, reverse mechanical and thermal hypersensitivity by suppressing microglial activation in the spinal cord, ultimately diminishing inflammatory pain. In conclusion, these discoveries propose that obstructing or intervening with NETs introduces a novel therapeutic avenue for addressing inflammatory pain.

Previous studies reported that the codeletion of PTEN and SOCS3 can greatly enhance the capacity of axon regeneration after central nervous system (CNS) injury. Moreover, the promotion of functional recovery can be improved by rehabilitative training under a use-dependent plasticity mechanism after CNS injury. However, few studies have reported the interaction between these mechanisms after spinal cord injury (SCI). Therefore, we investigated the combined effects of PTEN/SOCS3 coinhibition and rehabilitative training on axon regeneration and upper extremity motor functional improvement after cervical SCI in mice. In this study, we used RNA interference viruses to coinhibit PTEN and SOCS3 and induced a C5 crush injury on the side of preference. The injured upper extremity was trained by single pellet grasping for 4 weeks. We found that the coinjection of viruses significantly increased the expression of p-S6 and p-STAT in the cortex, reduced the dieback pattern of injured axons and promoted traced axon regeneration. More importantly, combination therapy further enhanced axon regeneration compared with PTEN/SOCS3 coinhibition alone. In behavioral tests, the motor performance of the mice in the PTEN/SOCS3 + Training group was better than that of the mice in the other groups. These results indicate that combining task-based rehabilitative training with PTEN/SOCS3 coinhibition further promotes axon regeneration and significant improvement in forelimb skilled motor function after cervical SCI. Our findings provide new therapeutic insights into SCI treatment.

[This corrects the article DOI: 10.3892/ol.2016.4709.].

Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) is a pivotal regulatory protein in energy metabolism. In a pilot study, we found that AMPK-associated energy metabolism imbalance in neurons contributes to the occurrence and maintenance of neuropathic pain (NeP). This study aimed to explore the relationship between genetic polymorphisms of AMPK gene (Rs13361707, rs3792822, and rs10074991) in PRKAA1 and postherpetic neuralgia (PHN) in Chinese individuals. Hundred and thirty two patients with PHN and 118 control individuals were enrolled in this study. All blood samples were shuffled and blinded to the person performing the haplotype analysis. Rs13361707, rs3792822, and rs10074991 PRKAA1 genotypes were identified in all participants. Dominant and recessive models were used for evaluating the association between these nucleotide polymorphisms and PHN susceptibility. A haplotype analysis of PHN patients and healthy controls was performed. Clinical characteristics between the two groups were not significantly different ( p > 0.05) except that the ages in control subjects were younger than the PHN patients ( p < 0.05). Genotypes and allele frequencies are significantly different between the PHN patients and control subjects for the rs13361707 and rs10074991 polymorphisms ( p < 0.05), but not for rs3792822 ( p > 0.05). In addition, the CCG haplotype of rs13361707-rs3792822-rs10074991 correlated negatively with PHN occurrence, but TCA was positively correlated with PHN ( p < 0.05). Our results indicate that PRKAA1 gene polymorphisms rs13361707 and rs10074991 were associated with a risk of PHN, and that the CCG haplotype of rs13361707-rs3792822-rs10074991 correlated negatively with PHN occurrence in haplotype analysis. TCA was positively associated with PHN in Chinese individuals.

Mitophagy is critical for maintaining proper cellular functions, and it contributes to the onset and progression of osteoarthritis (OA). A recent study showed that focused low-intensity pulsed ultrasound (FLIPUS) could activate mitophagy, but the molecular mechanism remains unclear. This study aimed to elucidate the chondroprotective effects of FLIPUS in OA and the regulatory effects on FUN14-domain containing 1 (FUNDC1-mediated mitophagy. In vitro, FLIPUS improved inflammatory response, anabolism, and catabolism in interleukin (IL)-1 beta-induced OA chondrocytes. The chondroprotective effects of FLIPUS were attributed to promoting the expression of phosphoglycerate mutase 5 (PGAM5) and the dephosphorylation of FUNDC1 at serine 13 (Ser13), as well as promoting the mitophagy process. In vivo, FLIPUS reduced the cartilage degeneration and apoptosis and reversed the change of anabolic-and catabolic-related proteins in destabilized medial meniscus (DMM)-induced mouse model. Thus, the study indicates that FLIPUS exhibits a chondroprotective effect via activating impaired FUNDC1-mediated mitophagy.

基于响应曲面法的中心复合设计(CCD)法设计了3D打印石膏粉末流动性优化试验,考察疏水性纳米二氧化硅和可溶性淀粉掺量对3D打印石膏粉末流动性的影响,并对优化效果下制备的3D打印粉末进行打印机铺粉、表面形貌和流速的分析、验证.结果表明:在疏水性纳米SiO2掺量为1％(质量分数)、可溶性淀粉掺量为3％(质量分数)的条件下,石膏流动性能改善效果最佳,相较于未改性的石膏提高了38％,得到了响应变量粉末流动性与疏水性纳米二氧化硅和可溶性淀粉掺量的非线性回归方程,流动性最佳优化预测值与实测值相对误差仅为0.31％;最佳优化条件下,改性石膏粉末流速为3.16 g/s,可连续流动,粉层表面均匀无明显缺陷.本研究提高了石膏基粉末3D打印的精确度,有利于石膏材料在3D打印中的应用.

Abstract Treadmill exercise is beneficial for spinal cord injury (SCI) both in bench and in bedside, but the most effective treadmill exercise intensity and mechanisms underlying the treadmill exercise on skilled motor function recovery remain elusive. Here, the improved skilled motor function recovery, enhanced nerve conduction capability, neuroplasticity, and axonal sprouting were observed in the SCI mice after training for 4 weeks. However, high exercise intensity (HEI) leads to vulnerability and impaired exercise tolerance during training. We further found that in the moderate exercise intensity (MEI) and HEI groups showed elevated expression of brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1). Meanwhile, elevated phosphorylated levels of ribosomal protein S6 (p-S6) and protein kinase B (p-AKT) in mouse motor cortex were also observed, indicating the cortical mechanistic target of rapamycin (mTOR) pathway activation. To investigate the role of the cortical mTOR activation, we performed a rapamycin assay. After using rapamycin, the exercise-induced activation of the cortical mTOR pathway and the exercise-enhanced effects were inhibited. Together, the expression of neurotrophic factors and the activation of the cortical mTOR pathway are in an intensity-dependent manner. And the MEI is safer and more beneficial than the LEI and HEI. Based on the rapamycin assay, the exercise-induced activation of mTOR pathway is necessary for the enhanced motor cortex and spine remodeling, all of which further contribute to better-skilled motor function recovery. These dates may provide a new window to further understand the mechanisms underlying exercise training effects on the skilled motor function recovery following SCI.

Exercise has been reported to elicit a transient suppression of appetite. Plasma lactate, which is produced by exercising muscle, is believed to have a critical effect on exercise-induced anorexia. However, some other underlying mechanisms and signaling steps remain unexplored. By using a chemical lactate inhibition model via central oxamate administration, we investigated the impact of central lactate metabolism on food intake and appetite-regulating neuropeptide expression in mice following an acute bout of treadmill running. Downstream molecules of the leptin signaling pathway, including janus kinase 2 (Jak2) and signal transducer and activator of transcription 3 (STAT3), were also determined by Western blot. In addition, hypoxia-inducible factor-1α (HIF-1α), peroxisome proliferator-activated receptor-γ coactivator 1-alpha (PGC-1α), and mitochondria-related proteins, including mitochondrial fusion related protein 1 (MFN1) and mitochondrial fusion related protein 2 (MFN2), were investigated to explore the effect of central lactate metabolism on appetite. We found that central oxamate administration reversed exercise-induced suppression of food intake and as well as changes in neuropeptide expression. Moreover, acute exercise led to an increase in the phosphorylation of Jak2 and STAT3 in the hypothalamus, while central lactate inhibition significantly blunted this effect. In addition, HIF-1α expression increased obviously after exercise, while it was attenuated by central oxamate administration. However, hypothalamic mitochondria-related protein levels were not improved after only one acute bout of exercise. Collectively, our data reveal that central lactate metabolism mediates exercise-induced suppression of appetite and changes in neuropeptides, possibly through enhanced Jak2-STAT3 signaling.Funding Information: This study was funded by the Natural Science Foundation Project (No. 82072543) and Natural Science Foundation Project of Chongqing (No.cstc2021jcyj-msxmX0076). Declaration of Interests: The authors declare that they have no conflict of interest. Ethical Approval Statement: All animal protocols were approved by the Institutional Animal Care and Use Committee of Chongqing Medical University.

Electroacupuncture (EA), as a particular type of electrostimulation treatment, has an extensive application in the field of biomedicine. Triboelectric nanogenerator (TENG) has sparked significant concern attributed to the high electrical output with low cost, whose electrical signals can also be directly usable for electrical stimulation. Here we propose a Chinese medicine EA treatment with the assistance of TENG technology, in which a bidirectional continuous current from a soft-contact freestanding rotary TENG (FR-TENG) is applied to two effective acupoints of rats by inserting electric needles. The TENG-driven EA treatment promotes the performance of gait 2 weeks after as well as the Basso-Beattie-Bresnahan (BBB) score. This elevation last as long as 4 weeks post injury. Moreover, the TENG-driven EA treatment enhances neuron survival in the ventral horn and inhibits astrocyte activation in the lesion site. Therefore, the TENG-driven EA treatment provides a significant neuroprotection effect on spinal cord contusion in rats. Our studies not only demonstrate the possibility of the TENG-driven EA treatment for traumatic central nervous system injuries but also provide an experimental basis for the prevention and treatment of diseases by traditional Chinese medicine treatment.

This study aimed to investigate the prevalence of and risk factors for multidrug-resistant organism (MDRO) infection in the rehabilitation ward of a general hospital in Southwest China. We analyzed rehabilitation patients with nosocomial infections caused by MDROs from June 2016 to June 2020. MDRO infection pathogens and associated antibiotic resistance were calculated. Possible risk factors for MDRO-related infection in the neurorehabilitation ward were analyzed using chi-square, and logistic regression. A total of 112 strains of MDRO were found positive from 96 patients. The MDRO test-positive rate was 16.70% (96/575). Ninety-five MDRO strains were detected in sputum, of which 84.82% (95/112) were gram-negative bacteria. Acinetobacter baumannii (A. Baumannii), Pseudomonas aeruginosa (P. aeruginosa), and Klebsiella pneumonia (K. pneumonia) were the most frequently isolated MDRO strains. The logistic regression model and multifactorial analysis showed that long-term (≥ 7 days) antibiotic use (OR 6.901), history of tracheotomy (OR 4.458), and a low albumin level (< 40 g/L) (OR 2.749) were independent risk factors for the development of MDRO infection in patients in the rehabilitation ward (all P < 0.05). Gram-negative MRDOs were dominant in rehabilitation ward patients. Low albumin, history of a tracheostomy, and long-term use of antibiotics were independent risk factors for MRDO infection and are worthy of attention.

Introduction Adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK) can influence energy metabolism. Energy metabolism imbalance is closely associated with the occurrence of neuropathic pain (NeP). Rs10789038 and rs2796498 are genetic polymorphisms of PRKAA2, the gene encoding AMPK, which is closely related to energy metabolism imbalance. This study aimed to explore the relationship between PRKAA2 and postherpetic neuralgia (PHN) in the southwestern Chinese Han population. Methods This study enrolled 132 PHN patients and 118 healthy subjects. The rs10789038 and rs2796498 PRKAA2 genotypes were identified in all participants. The association between these single nucleotide polymorphisms and PHN susceptibility was evaluated in the dominant and recessive models. Haplotype analysis of patients with PHN and healthy controls was performed. Results The PHN patients were older than the healthy subjects (P < 0.05); however, the other clinical characteristics between two groups were not significantly different (all P >0.05). Genotypes and allele frequencies differed significantly between PHN patients and healthy subjects in the rs10789038 polymorphism (P < 0.05), but not in rs2796498 (P > 0.05). In addition, the GG haplotype of rs10789038-rs2796498 correlated negatively with PHN occurrence in haplotype analysis (P < 0.05). Conclusion PHN occurrence may be related to the PRKAA2 rs10789038 A>G genetic polymorphism in the southwestern Chinese Han population.