Background: Cerebral ischemia–reperfusion (I/R) injury can lead to severe dysfunction, and its treatment is difficult. It is reported that nucleotide-binding domain and leucine-rich repeat family protein 3 (NLRP3) inflammasome-mediated cell pyroptosis is an important part of cerebral I/R injury and the activation of autophagy can inhibit pyroptosis in some tissue injury. Our previous study found that the protective effects of bone marrow mesenchymal stem cells (BMSCs) in cerebral I/R injury may be associated with the regulation of autophagy. Recent studies have demonstrated that exosomes secreted from BMSCs (BMSC-Exos) may play an essential role in the effective biological performance of BMSCs and the protective mechanism of BMSC-Exos is associated with the activation of autophagy and the remission of inflammation, but it has not been reported in studies of cerebral I/R injury. We aimed to investigate the effects of BMSC-Exos on cerebral I/R injury and determine if the mechanism is associated with the regulation of pyroptosis and autophagic flux. Method: PC12 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to induce cerebral I/R in vitro and were cocultured with BMSC-Exos. Cell viability was determined with CCK-8 and lactate dehydrogenase (LDH) detection kits. Scanning electron microscopy (SEM), Hoechst 33342/propidium iodide (PI) double staining, 2′,7′-dichlorodihydrofluorescein diacetate assay, immunofluorescence, Western blot, and Enzyme-linked immunosorbent assay (ELISA) were used to detect cell pyroptosis. Furthermore, transmission electron microscopy (TEM), GFP-RFP-LC3 adenovirus transfection, and Western blot were used to detect autophagic flux and its influence on pyroptosis. Finally, coimmunoprecipitation was used to detect the binding interaction between NLRP3 and LC3. Results: BMSC-Exos increased cell viability in OGD/R. The inhibitory effect of BMSC-Exos on pyroptosis was comparable to the NLRP3 inhibitor MCC950 and was reversed by NLRP3 overexpression. Furthermore, BMSC-Exos promoted autophagic flux through the AMP-activated kinase (AMPK)/mammalian target of the rapamycin pathway, whereas chloroquine, AMPK silencing, and compound C blocked the inhibitory effect on pyroptosis. Conclusions: BMSC-Exos can protect PC12 cells against OGD/R injury via attenuation of NLRP3 inflammasome-mediated pyroptosis by promoting AMPK-dependent autophagic flux.

The aim of present study is to investigate the feasibility of patient-specific ankle-foot orthoses fabricated using additive manufacturing (AM) techniques. Then, clinical performance of the AFOs manufactured using material PA12 was evaluated in stroke survivors based on gait analysis data. The ankle and foot were scanned by EinScan-Pro 3D scanner. The software Geomagic Studio was used for modifying the AFO model. After processing the original AFO model into the final required model, material PA12 were used to fabricate the AFOs by Multi Jet Fusion (MJF) technique. Finally, gait analysis of 12 stroke patients was conducted to compare the effects with and without AFO. It took 2 hours from processing the initial AFO model to the completion of final model, and the printing time was 8 hours. The printing thickness of the AFO was 1.2 mm. With respect to the temporal-spatial parameters, the velocity and stride length in the gait with AFO increased significantly as compared to the gait without AFO (P = 0.001, P = 0.002). The cadence increased, double limb support phase decreased, and the step length difference decreased in the gait with AFO; however, the difference was not statistically significant (P = 0.117, P = 0.075, P = 0.051).This study confirmed the feasibility of patient-specific AFO fabricated by AM techniques, and demonstrated the process of modifying AFO models successfully. The specific ankle-foot orthoses fabricated by material PA12 have a significant effect on the improvement of velocity and stride length in people with stroke.

Individuals with amnestic mild cognitive impairment (aMCI) have a high risk of developing Alzheimer’s disease. Although repetitive transcranial magnetic stimulation (rTMS) is considered a potentially effective treatment for cognitive impairment in patients with aMCI, the neuroimaging mechanisms are poorly understood. Therefore, we performed a double-blind randomized sham-controlled trial in which rTMS was applied to the left dorsolateral prefrontal cortex of aMCI patients recruited from a community near the Third Hospital Affiliated to Sun Yat-sen University, China. Twenty-four patients with aMCI were randomly assigned to receive true rTMS (treatment group, n = 12, 6 men and 6 women; age 65.08 ± 4.89 years) or sham stimulation (sham group, n = 12, 5 men and 7 women; age 64.67 ± 4.77 years). rTMS parameters included a stimulation frequency of 10 Hz, stimulation duration of 2 seconds, stimulation interval of 8 seconds, 20 repetitions at 80% of the motor threshold, and 400 pulses per session. rTMS/sham stimulation was performed five times per week over a period of 4 consecutive weeks. Our results showed that compared with baseline, Montreal Cognitive Assessment scores were significantly increased and the value of the amplitude of low-frequency fluctuation (ALFF) was significantly increased at the end of treatment and 1 month after treatment. Compared with the sham group, the ALFF values in the right inferior frontal gyrus, triangular part of the inferior frontal gyrus, right precuneus, left angular gyrus, and right supramarginal gyrus were significantly increased, and the ALFF values in the right superior frontal gyrus were significantly decreased in the treatment group. These findings suggest that high-frequency rTMS can effectively improve cognitive function in aMCI patients and alter spontaneous brain activity in cognitive-related brain areas. This study was approved by the Ethics Committee of Shenzhen Baoan Hospital of Southern Medical University, China (approval No. BYL20190901) on September 3, 2019, and registered in the Chinese Clinical Trials Registry (registration No. ChiCTR1900028180) on December 14, 2019.

Background and aims: The mortality rate of stroke has been increasing worldwide. Poststroke somatic dysfunctions are common. Motor function rehabilitation of patients with such somatic dysfunctions enhances the quality of life and has long been the primary practice to achieve functional recovery. In this regard, we aimed to delineate the new trends and frontiers in stroke motor function rehabilitation literature published from 2004 to 2022 using a bibliometric software.Methods: All documents related to stroke rehabilitation and published from 2004 to 2022 were retrieved from the Web of Science Core Collection. Publication output, research categories, countries/institutions, authors/cocited authors, journals/cocited journals, cocited references, and keywords were assessed using VOSviewer v.1.6.15.0 and CiteSpace version 5.8. The cocitation map was plotted according to the analysis results to intuitively observe the research hotspots.Results: Overall, 3,302 articles were retrieved from 78 countries or regions and 564 institutions. Over time, the publication outputs increased annually. In terms of national contribution, the United States published the most papers, followed by China, Japan, South Korea, and Canada. Yeungnam University had the most articles among all institutions, followed by Emory University, Fudan University, and National Taiwan University. Jang Sung Ho and Wolf S.L. were the most productive (56 published articles) and influential (cited 1,121 times) authors, respectively. “Effect of constraint-induced movement therapy on upper extremity function 3–9 months after stroke: the Extremity Constraint Induced Therapy Evaluation randomized clinical trial” was the most frequently cited reference. Analysis of keywords showed that upper limbs, Fugl–Meyer assessment, electromyography, virtual reality, telerehabilitation, exoskeleton, and brain–computer interface were the research development trends and focus areas for this topic.Conclusion: Publications regarding motor function rehabilitation following stroke are likely to continuously increase. Research on virtual reality, telemedicine, electroacupuncture, the brain–computer interface, and rehabilitation robots has attracted increasing attention, with these topics becoming the hotspots of present research and the trends of future research.

Background. Electroacupuncture (EA) pretreatment plays a protective role in myocardial infarction injury. However, the mechanism of electroacupuncture remains unknown. The aim of this study was to confirm the protective effects of electroacupuncture (EA) on myocardial infarction injury and the possible mechanism. Methods. Sprague-Dawley (SD) rats, used to serve as acute myocardial infarction (AMI) model, were divided into sham group, model (M) group, M+EA group, AMPK inhibitor Compound C (M+EA+CC), and AMPK inhibitor solvent control (M+EA+DMSO) group, respectively. Rats in EA group were pretreated with EA and those in M+EA+CC group with intravenous AMPK inhibitor Compound C. The myocardial morphological changes and infarct size were observed through HE staining and TTC staining, and the concentrations of CK-MB and LDH were detected using ELISA kits. Transmission electron microscopy was employed to observe the autophagosome formation, and the AMPK-dependent autophagy-related protein expression was detected by immunohistochemistry and western blot. Results. EA could alleviate myocardial infarction injury and decrease the concentrations of CK-MB and LDH. Transmission electron microscopy showed that EA could also regulate the AMPK-dependent autophagosome formation and the AMPK-dependent autophagy-related protein expression. AMPK inhibitor Compound C could impair the effect of EA through regulating the concentrations of CK-MB and LDH, autophagosome formation, and autophagy-related protein expression. Conclusion. These results indicated that electroacupuncture could improve myocardial infarction injury and induce autophagy, and AMPK-dependent autophagy might be involved in this process.