At present, fatigue state monitoring of upper limb movement generally relies solely on surface electromyographic signal (sEMG) to identify and classify fatigue, resulting in unstable results and certain limitations. This paper introduces the sEMG signal recognition and motion capture technology into the fatigue state monitoring process and proposes a fatigue analysis method combining an improved EMG fatigue threshold algorithm and biomechanical analysis. In this study, the right upper limb load elbow flexion test was used to simultaneously collect the biceps brachii sEMG signal and upper limb motion capture data, and at the same time the Borg Fatigue Subjective and Self-awareness Scale were used to record the fatigue feelings of the subjects. Then, the fatigue analysis method combining the EMG fatigue threshold algorithm and the biomechanical analysis was combined with four single types: mean power frequency (MPF), spectral moments ratio (SMR), fuzzy approximate entropy (fApEn) and Lempel-Ziv complexity (LZC). The test results of the evaluation index fatigue evaluation method were compared. The test results show that the method in this paper has a recognition rate of 98.6% for the overall fatigue state and 97%, 100%, and 99% for the three states of ease, transition and fatigue, which are more advantageous than other methods. The research results of this paper prove that the method in this paper can effectively prevent secondary injury caused by overtraining during upper limb exercises, and is of great significance for fatigue monitoring.
【Abstract】 Objective To review the progress in the treatment of bone defect by porous tantalum implant. Methods Recent l iterature was extensively reviewed and summarized, concerning the treatment method of bonedefect by porous tantalum implant. Results By right of their unique properties, porous tantalum implants have achievedvery good results in the treatment of certain types of bone defects. Conclusion Porous tantalum implants have their ownadvantages and disadvantages. If the case is meet to its indications, this method can obtain a good effect. Porous tantalum implants provide a new way for the cl inical treatment of bone defects.
ObjectiveTo systematically summarize the role and molecular basis of lactylation modification in gastric cancer progression (including tumor initiation, development, and drug resistance), and to explore its potential clinical translational value. MethodThe literature published in recent years, both domestically and internationally, focusing on the regulatory mechanisms and clinical applications of lactylation modification in gastric cancer progression was reviewed. ResultsA substantial number of lysine lactylation sites have been systematically identified in gastric cancer. Lactylation modification dynamically regulates the functions of histones (e.g., H3K18la) and non-histone proteins (e.g., PKM2, CPT2) through the “writer–reader–eraser” enzymatic mechanism. It drives cancer cell proliferation, invasion, and metastasis via the NLRP12/HK2 axis and the H3K18la/METTL14/ATF5 pathway. Furthermore, lactylation mediates immune escape by upregulating programmed death-ligand 1 and inducing M2 polarization of macrophages. It also confers resistance to treatments such as oxaliplatin and anlotinib through the BASP1-AS1/LDHA/PCBP2 positive feedback loop and lactate dehydrogenase (LDH) B delactylation. Preclinical studies have demonstrated that targeting glycolysis (inhibiting LDHA), restoring delactylase (SIRT1/2) activity, precisely intervening in the lactylation levels of specific proteins (such as LDHBK58 and TRIM29), or combining with cuproptosis inducers can effectively inhibit tumor growth and sensitize therapeutic responses. Additionally, prognostic models based on lactylation-related genes (e.g., NLRP12) have shown significant potential for clinical outcome assessment. ConclusionsLactylation modification synergistically promotes the malignant progression and multidrug resistance of gastric cancer by integrating metabolic reprogramming with epigenetic regulation. Interventions targeting key components of this modification demonstrate promising therapeutic prospects. However, there is currently a lack of highly specific targeting tools. Future research should focus on deeply deciphering the regulatory networks of lactylation, developing selective inhibitors, and establishing reliable prognostic evaluation models to facilitate clinical translation.
