Aiming at the problem that the existing ankle rehabilitation robot is difficult to fully fit the complex motion of human ankle joint and has poor human-machine motion compatibility, a equivalent series mechanism model which is highly matched with the actual bone structure of the human ankle joint is proposed and mapped into a parallel rehabilitation mechanism. And the parallel rehabilitation mechanism has two virtual motion centers(VMCs), which can simulate the complex motion of the ankle joint, adapt to the individual differences of various patients, and can meet the rehabilitation needs of both left and right feet of patients. Firstly, based on the motion properties and physiological structure of the human ankle joint, the mapping relationship between the rehabilitation mechanism and ankle joint is determined, and the series equivalent model of the ankle joint is established. According to the kinematic and constraint properties of the ankle equivalent model, the configuration design of the parallel ankle rehabilitation robot is carried out. Secondly, according to the intersecting motion planes theory, the full-cycle mobility of the mechanism is proved, and the continuous axis of the mechanism is judged based on the constraint power and its derivative. Then, the kinematics of the parallel ankle rehabilitation robot is analyzed. Finally, based on the OpenSim biomechanical software, a human-machine coupling rehabilitation simulation model is established to evaluate the rehabilitation effect, which lay the foundation for the formulation of a rehabilitation strategy for the later prototype.

Among arrhythmias, atrial fibrillation is one of the most prevalent. The most popular procedure for treating atrial fibrillation is now surgery. The prognosis is significantly impacted by postoperative atrial fibrillation recurrence, regardless of whether it is treated with maze or radiofrequency ablation. Genes are linked to the onset, progression of AF, as well as to individual variability in recurrence. Through bioinformatics analysis of open data sets, we sought to uncover probable important genes associated with AF recurrence in the current study. Differentially expressed genes (DEGs) were found using the GSE176166 microarray data set that was downloaded from the Gene Expression Omnibus (GEO) database. Based on the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Disease Ontology (DO) resources, functional enrichment studies were conducted. Using the STRING database, a protein-protein interaction (PPI) network was created. Possible essential genes were then chosen using the important bioinformatics data given before. The association of possible key genes with AF recurrence (AFR) was investigated using the comparative toxicogenomics database (CTD). In comparison to controls with sinus rhythm, we discovered 27 DEGs with |log2 FC|≥1 and 7 with |log2 FC|≥3.5 fold changes in gene expression in AFR patients. The probable bringing great were TNNC1, GABARAPL1, GNAS, PHLPP1, ELL2, SNORD108 and miR-548v. With AF, CTD revealed that TNNC1, GABARAPL1, GNAS,PHLPP1, and ELL2 had increased scores. The 4 possible risk factors for AFR, TNNC1, GABARAPL1, GNAS and PHLPP1 may be connected. Our research revealed novel genetic, molecular etiology, and treatment targets of AFR.

Dilated cardiomyopathy (DCM) is a myocardial disease characterized by bilateral or left ventricular cardiac dilation and systolic dysfunction leading to heart failure and sudden cardiac death in children. Most studies focus on the genetic alterations in DCM-related genes in adult populations; however, it remains enigmatic about the mutational landscape in pediatric DCM patients, especially in the Chinese population. We exploited the next-generation sequencing (NGS) technologies to genetically analyze 46 pediatric patients and to decipher the genotype-phenotype correlation in these patients’ clinical outcomes. Our results indicated DCM-associated pathogenic mutations in 10 genes related to the structure or function of the sarcomere, desmosomal and cytoskeletal proteins. We also identified 6 pathogenic mutations (5 novel) in the titin (TTN) gene leading to the formation of truncated TTN protein variants in 6 (13%) out of 46 patients each. Furthermore, we investigated the correlations between TTN gene mutation and clinical outcomes in these patients. Conclusion: Our data suggest that one-third of cases of pediatric DCM are caused by genetic mutations. The role of TTN variants should not be underestimated in pediatric DCM and age-dependent pathogenic penetrance of these genetic mutations needs to be considered in the case of familial DCM. Thus, NGS analysis can be applied to decode the yet unknown DCM etiological genetic factors in pediatric as well as adult patients.

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