Identification of key autophagy-related genes and pathways in spinal cord injury.

Spinal cord injury (SCI) can cause a range of functional impairments, and patients with SCI have limited potential for functional recovery. Previous studies have demonstrated that autophagy plays a role in the pathological process of SCI, but the specific mechanism of autophagy in this context remains unclear. Therefore, we explored the role of autophagy in SCI by identifying key autophagy-related genes and pathways. This study utilized the GSE132242 expression profile dataset, which consists of four control samples and four SCI samples; autophagy-related genes were sourced from GeneCards. R software was used to screen differentially expressed genes (DEGs) in the GSE132242 dataset, which were then intersected with autophagy-related genes to identify autophagy-related DEGs in SCI. Subsequently, the expression levels of these genes were confirmed and analyzed with gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). A protein-protein interaction (PPI) analysis was conducted to identify interaction genes, and the resulting network was visualized with Cytoscape. The MCODE plug-in was used to build gene cluster modules, and the cytoHubba plug-in was applied to screen for hub genes. Finally, the GSE5296 dataset was used to verify the reliability of the hub genes. We screened 129 autophagy-related DEGs, including 126 up-regulated and 3 down-regulated genes. GO and KEGG pathway enrichment analysis showed that these 129 genes were mainly involved in the process of cell apoptosis, angiogenesis, IL-1 production, and inflammatory reactions, the TNF signaling pathway and the p53 signaling pathway. PPI identified 10 hub genes, including CCL2, TGFB1, PTGS2, FN1, HGF, MYC, IGF1, CD44, CXCR4, and SERPINEL1. The GSE5296 dataset revealed that the control group exhibited lower expression levels than the SCI group, although only CD44 and TGFB1 showed significant differences. This study identified 129 autophagy-related genes that might play a role in SCI. CD44 and TGFB1 were identified as potentially important genes in the autophagy process after SCI. These findings provide new targets for future research and offer new perspectives on the pathogenesis of SCI.

Activated CD4 T cells/Tregs derived immune-metabolism signature provide precise prognosis assessment for gastric cancer and beneficial for treatment option.

Background: The prognostic significance of the ratio of activated CD4 T cells to Tregs infiltrating tumor tissues in gastric cancer (GC) remains unknown. Materials and methods: For the quantification of infiltration of immune cells, the ssGSEA algorithm, which is a single sample gene set enrichment analysis, was utilized. Group A was defined as having activated CD4 T cells/Tregs >1, while group B was defined as having activated CD4 T cells/Tregs <1. To compare the overall survival (OS) of the two groups, the Kaplan-Meier survival analysis was employed. The R package 'limma' was used to identify the immune and metabolism related genes that were expressed differentially between the two groups, with a false discovery rate (FDR) less than 0.05. The risk score (RS) was constructed by combining univariate Cox regression analysis, LASSO penalized Cox regression analysis, and multivariate Cox regression analysis. The median RS was used to classify high-risk (HR) and low-risk (LR) groups. Results: A predicted unfavorable outcome of GC was observed when the ratio of activated CD4 T cells to Tregs was less than 1. Our proposed RS was utilized for prognostic risk categorization in ten distinct independent cohorts (TCGA-STAD, n = 371; GSE84437, n = 433; GSE26253, n = 432; GSE13861, n = 65; GSE15459, n = 192; GSE26899, n = 93; GSE26901, n = 109; GSE28541, n = 40; GSE34942, n = 56; GSE62254, n = 300) and exhibited exceptional precision. In terms of tumor microenvironment (TME) and treatment strategies, compared to the LR group, the HR group was characterized by a higher infiltration levels of stromal cells, Tregs, macrophages, Tfh, mast cells, and NK cells, inclined to activated CD4 T cells/Tregs <1, and exhibited insensitivity to immunotherapy and multiple chemotherapy drugs. In relation to the potential molecular mechanism, the excessive activation of oncogenic pathways such as MAPK, hedgehog, WNT, calcium, and TGF-ß signaling pathways may accelerate the malignant progression of GC by stimulating angiogenesis, promoting EMT, and altering ECM. Conversely, the overactivation of the P53 pathway is likely to inhibit tumor proliferation by regulating the cell cycle. Conclusion: The immune-metabolism signature associated with the ratio of activated CD4 T cells and Tregs could be used to assess prognosis, TME, and treatment strategies in GC patients.

Case report: The utilization of crizotinib and brentuximab vedotin as a bridge to autologous stem cell transplantation and followed by CD30-directed CAR-T cell therapy in relapsed/refractory ALK+ ALCL.

Background: Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL) is a rare, mature T-cell non-Hodgkin lymphoma. The prognosis of patients with relapsed or refractory ALCL following first-line chemotherapy is extremely poor. NCCN guidelines recommend intensified chemotherapy with or without ASCT consolidation for r/r ALCL, however, this is not an effective treatment for all ALK+ALCL. Case report: Herein, we report a patient with relapsed/refractory ALK+ ALCL who received crizotinib and brentuximab vedotin as bridging therapy, followed by autologous stem cell transplantation and sequential anti-CD30 CAR T cell therapy. Conclusion: The patient achieved complete remission and long-term disease-free survival of months and continues to be followed up. The combination therapy model in this case may provide guidance for the management of relapsed/refractory ALK+ ALCL, and further prospective trials are needed to confirm its effectiveness.

Upper gastrointestinal tract immune-related adverse events: Two cases of obstructive complications occurred in immune consolidation therapy after sequential chimeric antigen receptor T cell therapy with autologous hematopoietic stem cell transplantation for refractory/relapsed diffuse large B cell lymphoma.

Key Clinical Message: Immune checkpoint inhibitors are a very popular method of treating malignant tumors. But its side effects cannot be ignored. This study revealed obstructive complications during immune consolidation therapy following sequential chimeric antigen receptor T cell therapy with autologous hematopoietic stem cell transplantation in two patients with diffuse large b cell lymphoma (DLBCL). Both our patients had the same symptoms of vomiting and inability to eat due to pyloric obstruction, it should be highlighted that this is a relatively rare and irreversible complication of upper gastrointestinal caused by immune consolidation therapy. Abstract: Immune checkpoint inhibitors (ICIs) have become the standard therapy for many malignant tumors.However, ICIs are associated with unique immune-related adverse events (irAEs) caused by dysregulated immune activation and associated complications have been observed in patients. Here, we report two cases of patients with pyloric obstruction and duodenal ulcers induced by the use of sintilimab, which provides some guidance for the widely used anti-programmed death-1 therapy. During the entire treatment progression for such patients, the correct differential diagnosis of adverse effects and the use of immunosuppressive agents such as glucocorticoids are essential to facilitate early prevention and intervention of irAEs.

Promoting Electromagnetic Wave Absorption Performance by Integrating MoS2@Gd2O3/MXene Multiple Hetero-Interfaces in Wood-Derived Carbon Aerogels.

Multi-component composite materials with a magnetic-dielectric synergistic effect exhibit satisfactory electromagnetic wave absorption performance. However, the effective construction of the structure for these multi-component materials to fully exploit the advantages of each component remains a challenge. Inspired by natural biomass, this study utilizes wood as the raw material and successfully prepares high-performance MoS2@Gd2O3/Mxene loaded porous carbon aerogel (MGMCA) composite material through a one-pot hydrothermal method and carbonization treatment process. With a delicate structural design, the MGMCA is endowed with abundant heterogeneous interface structures, favorable impedance matching characteristics, and a magnetic-dielectric synergistic system, thus demonstrating multiple electromagnetic wave loss mechanisms. Benefiting from these advantages, the obtained MGMCA exhibits outstanding electromagnetic wave absorption performance, with a minimum reflection loss of -57.5 dB at an ultra-thin thickness of only 1.9 mm. This research proposes a reliable strategy for the design of multi-component composite materials, providing valuable insight for the design of biomass-based materials as electromagnetic wave absorbers.

DNA damage repair molecular subtype derived immune signature applicable for the prognosis and immunotherapy response prediction in colon cancer.

Background: The DNA damage repair (DDR) pathway is one of the pathways of tumor pathogenesis, but its relationship with the immunophenotype has not been clarified in colon cancer (CC). Methods: We identified the differentially expressed immune-related genes (DEIRGs) between two DDR molecular subtypes, namely, C1 and C2, and used univariate Cox analysis and least absolute shrinkage and selection operator (LASSO) penalized Cox regression analysis to construct the risk score in the training cohort [n=1,009, a combination of The Cancer Genome Atlas (TCGA) and GSE39582]. Regarding the median risk score as the unified cutoff to classify the patients into high- and low-risk groups. Two independent cohorts (GSE17538, n=232; GSE38832, n=122) were used for external validation of the prognostic value of the risk score. The IMvigor210 cohort (n=348) was used to test the predictive value of the risk score for immunotherapy response. Gene set variation analysis (GSVA) and gene set enrichment analysis (GSEA) were performed to discover the underlying mechanism. Immune cell infiltration was quantified by the single sample gene set enrichment analysis (ssGSEA) algorithm. Results: The high-risk group showed significantly reduced overall survival (OS), disease-specific survival (DSS), disease-free survival (DFS), progression-free survival (PFS), and relapse-free survival (RFS) compared to the low-risk group, and the two groups differed significantly in lymphatic invasion, American Joint Committee on Cancer (AJCC) TNM stage, preoperative carcinoembryonic antigen (CEA) level, etc. The enrichment levels of pathways related to colorectal cancer, epithelial-mesenchymal transition (EMT), angiogenesis, hypoxia, P53, TGF-ß, KRAS signaling, etc., were upregulated in the high-risk group, but DDR-related pathways were defective in the high-risk group. The immunophenotypes of the high-risk group tended to be desert and excluded, and the risk score of patients who responded to immunotherapy was significantly lower than that of patients who did not respond to immunotherapy. The higher the infiltration levels of gamma delta T cells (γδ T cells), immature dendritic cells, and T follicular helper (Tfh) cells, the more significant adverse impact on the prognosis of CC patients was exhibited and an obviously positive correlation with the risk score was showed. Conclusions: An immune gene risk score associated with the DDR molecular subtype was built and verified herein; that is applicable to the prognosis and immunotherapy response prediction in CC.

Case Report: A recurrent case of ALK-ALCL after autologous transplantation was successfully treated with BV + a modified CHEP chemotherapy containing mitoxantrone hydrochloride liposome with the addition of chidamide maintenance therapy.

Background: ALK-negative anaplastic large cell lymphoma (ALK-ALCL) is a rare heterogeneous malignancy of T-cell origin.ALK- ALCL has a poor prognosis, with more patients experiencing relapses and refractory to treatment, and its treatment remains challenging. We report a case with bone involvement as the main clinical manifestation of recurrent, and the patient achieved significant partial remission after brentuximab vedotin(BV) combined with a modified CHEP chemotherapy containing mitoxantrone hydrochloride liposome (PLM60) with the addition of chidamide maintenance therapy and received regular follow-up, with a disease-free survival of 16 months to date. A literature review of the clinical presentation and treatment of ALCL was also conducted to identify strategies for its diagnosis and management. Conclusions: ALK-ALCL with bone involvement as the main manifestation of recurrent is relatively rare. Here, BV combined a modified CHEP chemotherapy containing mitoxantrone hydrochloride liposome was applied for the first time in a patient with relapsed ALK-ALCL, inducing remission and extending survival. However, further prospective studies with many patients are needed to determine the biological characteristics of this rare type of ALK-ALCL and relevant treatment strategies.

A double-decomposition based parallel exact algorithm for the feedback length minimization problem.

Product development projects usually contain many interrelated activities with complex information dependences, which induce activity rework, project delay and cost overrun. To reduce negative impacts, scheduling interrelated activities in an appropriate sequence is an important issue for project managers. This study develops a double-decomposition based parallel branch-and-prune algorithm, to determine the optimal activity sequence that minimizes the total feedback length (FLMP). This algorithm decomposes FLMP from two perspectives, which enables the use of all available computing resources to solve subproblems concurrently. In addition, we propose a result-compression strategy and a hash-address strategy to enhance this algorithm. Experimental results indicate that our algorithm can find the optimal sequence for FLMP up to 27 activities within 1 h, and outperforms state of the art exact algorithms.

Physicochemical characterization, digestion profile and gut microbiota regulation activity of intracellular polysaccharides from Chlorella zofingiensis.

A number of studies have shown that the polysaccharides from microalgae exhibit diverse biological activities, however, little is known about their digestibility and impact on human gut microbiota. In this study, a simulating digestion and fermentation system were established to investigate the digestibility and fermentation of intracellular polysaccharides from Chlorella zofingiensis (CZIP-S3). The results indicated that CZIP-S3 is a macromolecular polysaccharide composed of mannose, glucose, galactose and rhamnose, consisting of a main chain and two branched repeating units. CZIP-S3 could not be digested in the upper gastrointestinal tract. However, CZIP-S3 could be metabolized into smaller molecules by the gut microbiota. The pH values continuously decrease during fermentation, whereas, the amount of short-chain fatty acids steadily increase. Furthermore, CZIP-S3 could modulate the composition of gut microbiota, via lowering the ratio of Firmicutes/Bacteroidetes and increasing the relative abundance of Bacteroides, Bifidobacterium and Akkermansia. The data suggested that CZIP-S3 could potentially be used as an ingredient for functional foods or prebiotics to improve human health by promoting the relative abundances of beneficial bacteria.

Ring Finger Protein 146-mediated Long-chain Fatty-acid-Coenzyme a Ligase 4 Ubiquitination Regulates Ferroptosis-induced Neuronal Damage in Ischemic Stroke.

Ischemic stroke (IS) is one of the leading causes of disability and death worldwide. Long-chain fatty-acid-coenzyme A ligase 4 (ACSL4) is a critical isozyme for ferroptosis that participates in the progression of IS. RING finger protein 146 (RNF146) is an E3 ligase predicted to interact with ACSL4 and regulated by activating transcription factor 3 (ATF3). The molecular mechanism of the RNF146/ACSL4 axis in IS is still unclear. Oxygen-glucose deprivation/reperfusion (OGD/R) treatment was used as the in vitro model, and middle cerebral artery occlusion (MCAO) mice were established for the in vivo model for IS. The protein level of ACSL4 was monitored by Western blot during ischemic injury. RNF146 was overexpressed in vitro and in vivo. The interaction of RNF146 and ACSL4 was determined by co-immunoprecipitation (Co-IP) assay. Chromatin immunoprecipitation (ChIP) assay and luciferase assay were utilized to determine the regulation of ATF3 on RNF146. Ferroptosis was evaluated by the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), Fe2+, and protein levels of related genes including ACSL4, SLC7A11, and GPX4. ACSL4 was downregulated upon OGD treatment and then increased by re-oxygenation. RNF146 was responsible for the ubiquitination and degradation of ACSL4 protein. RNF146 overexpression could prevent the stimulation of OGD/R-induced LDH, MDA, and Fe2+ levels and ferroptosis-related gene expression. ATF3 could activate the transcription and expression of RNF146, leading to the inhibition of OGD/R-induced neuron ferroptosis. The ATF3-mediated RNF146 could alleviate neuronal damage in IS by regulating ACSL4 ubiquitination and ferroptosis, providing a novel theoretical basis for exploring therapeutic targets and strategies.

Nobiletin Ameliorates Nonalcoholic Fatty Liver Disease by Regulating Gut Microbiota and Myristoleic Acid Metabolism.

Disturbance of the gut microbiota plays a critical role in the development of nonalcoholic fatty liver disease (NAFLD). Increasing evidence supports that natural products may serve as prebiotics to regulate the gut microbiota in the treatment of NAFLD. In the present study, the effect of nobiletin, a naturally occurring polymethoxyflavone, on NAFLD was evaluated, and metabolomics, 16S rRNA gene sequencing, and transcriptomics analysis were performed to determine the underlying mechanism of nobiletin, and the key bacteria and metabolites screened were confirmed by in vivo experiment. Nobiletin treatment could significantly reduce lipid accumulation in high-fat/high-sucrose diet-fed mice. 16S rRNA analysis demonstrated that nobiletin could reverse the dysbiosis of gut microbiota in NAFLD mice and nobiletin could regulate myristoleic acid metabolism, as revealed by untargeted metabolomics analysis. Treatment with the bacteria Allobaculum stercoricanis, Lactobacillus casei, or the metabolite myristoleic acid displayed a protective effect on liver lipid accumulation under metabolic stress. These results indicated that nobiletin might target gut microbiota and myristoleic acid metabolism to ameliorate NAFLD.

Case report: Germline RECQL mutation potentially involved in hereditary predisposition to acute leukemia.

The pathogenesis of acute leukemia is still complex and vague. Most types of acute leukemia are related to somatic gene mutations, and familial incidence is rare. Here we report a case of familial leukemia. The proband presented to our hospital with vaginal bleeding and disseminated intravascular coagulation at the age of 42 and was diagnosed with acute promyelocytic leukemia with typical PML-RARα fusion gene caused by t(15;17)(q24;q21) translocation. By taking the history, we found that the patient's second daughter had been diagnosed with B-cell acute leukemia with ETV6-RUNX1 fusion gene at age 6. Then we performed whole exome sequencing in peripheral blood mononuclear cells from these two patients at remission status and identified 8 shared germline gene mutations. Using functional annotation and Sanger sequencing validation, we finally focused on a single nucleotide variant in RecQ like helicase (RECQL), rs146924988, which was negative in the proband's healthy eldest daughter. This gene variant potentially led to a relative lack of RECQL protein, disordered DNA repair and chromatin rearrangement, which may mediate the occurrence of fusion genes, as driving factors for leukemia. This study identified a novel possible leukemia-related germline gene variant and provided a new understanding for the screening and pathogenesis of hereditary predisposition syndromes.

Dendrobium huoshanense stem polysaccharide ameliorates alcohol-induced gastric ulcer in rats through Nrf2-mediated strengthening of gastric mucosal barrier.

This study aimed to explore whether Dendrobium huoshanense stem polysaccharide (cDHPS) ameliorates alcohol-induced gastric ulcer (GU) through the strengthening effect of the gastric mucosal barrier in rats and its potential mechanism. In normal rats, the pretreatment of cDHPS effectively strengthened gastric mucosal barrier by increasing mucus secretion and tight junction protein expression. In GU rats, cDHPS supplementation effectively alleviated alcohol-induced gastric mucosal injury and nuclear factor κB (NF-κB)-driven inflammation by strengthening gastric mucosal barrier. Moreover, cDHPS significantly activated nuclear factor E2-related factor 2 (Nrf2) signaling and promoted antioxidant enzymes activities in both normal and GU rats. These results suggested that the pretreatment of cDHPS could strengthen gastric mucosal barrier to inhibit oxidative stress and NF-κB-driven inflammation induced gastric mucosal injury, which was likely related to the activation of Nrf2 signaling.

Experiment investigation on effects of elastic modulus on cavitation erosion of silicone rubber.

Research into cavitation phenomena in various fields shows that the elastic modulus of a boundary has a potential impact on cavitation erosion. To obtain the direct relationship between the elastic modulus of the boundary and cavitiation erosion, single-layer samples with different chemical composition and moduli, and double-layer samples with different elastic moduli and the same surface layer material, were prepared with silicone rubber. The results of cavitation experiments on single-layer samples, show that the coating chemical composition and mechanical properties together affect the cavitation morphology of the coating, and dominant factors vary with erosion stage. Through the cavitation test of double-layer samples, it was found that there is a positive correlation between the elastic modulus of the coating and the degree of cavitation. This study helps us to understand the relationship between coating elastic modulus and cavitation more directly, and provides theoretical and technical guidance for the application of anti-cavitation for elastic coating in engineering.

Evolving interplay between natural products and gut microbiota.

Growing evidence suggests gut microbiota status affects human health, and microbiota imbalance will induce multiple disorders. Natural products are gaining increasing attention for their therapeutical effects and less side effects. The emerging studies support that the activities of many natural products are dependent on gut microbiota, meanwhile gut microbiota is modulated by natural products. In this review, we summarized the interplay between the gut microbiota and host disease, and the emerging molecular mechanisms of the interaction between natural products and gut microbiota. Focusing on gut microbiota metabolite of various natural products, and the effects of natural products on gut microbiota, we summarized the biotransformation pathways of natural products, and discussed the effect of natural products on the composition modulation of gut microbiota, protection of gut mucosal barrier and modulation of the gut microbiota metabolites. Dissecting the interplay between gut microbiota and natural products will help elucidate the therapeutic mechanisms of natural products.

Optimal dose of cefotaxime in neonates with early-onset sepsis: A developmental pharmacokinetic model-based evaluation.

Objective: The perspective of real-world study is especially relevant to newborns, enabling dosage regimen optimization and regulatory approval of medications for use in newborns. The aim of the present study was to conduct a pharmacokinetic analysis of cefotaxime and evaluate the dosage used in newborns with early-onset sepsis (EOS) using real-world data in order to support the rational use in the clinical practice. Methods: This prospective, open-label study was performed in newborns with EOS. A developmental pharmacokinetic-pharmacodynamic model of cefotaxime in EOS patients was established based on an opportunistic sampling method. Then, clinical evaluation of cefotaxime was conducted in newborns with EOS using real-world data. Results: A one-compartment model with first-order elimination was developed, using 101 cefotaxime concentrations derived from 51 neonates (30.1-41.3°C weeks postmenstrual age), combining current weight and postnatal age. The pharmacokinetic-pharmacodynamic target was defined as the free cefotaxime concentration above MIC during 70% of the dosing interval (70% fT > MIC), and 100% of neonates receiving the dose of 50 mg/kg, BID attained the target evaluated using the model. Additionally, only two newborns had adverse reactions possibly related to cefotaxime treatment, including diarrhea and feeding intolerance. Conclusion: This prospective real-world study demonstrated that cefotaxime (50 mg/kg, BID) had a favorable efficacy and an accepted safety profile for neonates with EOS.

Restorative therapy using microglial depletion and repopulation for central nervous system injuries and diseases.

Microglia are important resident immune cells in the central nervous system (CNS) and play an important role in its development, homeostasis, and disease treatments. Activated microglia perform diverse functions in mouse models of CNS neurodegenerative diseases or deficits. In humans, microglia have been linked to various neurodegenerative diseases. Following brain or spinal cord injury, microglia express pro- and anti-inflammatory phenotypes at different stages of recovery. With the development of pharmacological and genetic tools for microglial depletion, studies have demonstrated that microglial depletion exerts both positive and negative effects in the treatment of CNS diseases. Notably, microglial depletion provides an empty niche that stimulates production of new microglia. Microglial depletion and repopulation can not only treat diseases by eliminating dysfunctional microglia but can also provide an indication of the molecular mechanisms of diseases. Although this approach has shown impressive results, its use is still in its infancy. In this review, we summarize the current pharmacological and genetic tools for microglial depletion and highlight recent advances in microglial repopulation therapy for the treatment and functional recovery of neurological diseases and deficits. Finally, we briefly discuss the therapeutic challenges and prospective uses of microglial repopulation therapy.

CircPTK2 promotes cell viability, cell cycle process, and glycolysis and inhibits cell apoptosis in acute myeloid leukemia by regulating miR-582-3p/ALG3 axis.

BACKGROUND: Circular RNA (circRNA) regulates the pathogenesis of acute myeloid leukemia (AML). However, the mechanism of circRNA protein tyrosine kinase 2 (circPTK2) in AML remains unclear. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was adopted for circPTK2, miR-582-3p and alpha-1,3-mannosyltransferase (ALG3) mRNA levels. 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and 5'-ethynyl-2'-deoxyuridine (EdU) assay were conducted for cell proliferation. Flow cytometry analysis was employed for cell apoptosis and cell cycle process. The glycolysis level was estimated by specific commercial kits. Western blot assay was utilized for protein levels. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the interaction between miR-582-3p and circPTK2 or ALG3. RESULTS: CircPTK2 level was enhanced in AML peripheral blood samples and cells. CircPTK2 knockdown restrained AML cell proliferation and glycolysis and promoted cell apoptosis and cell cycle arrest. Mechanically, circPTK2 functioned as the sponge for miR-582-3p to positively ALG3 expression in AML cells. Moreover, miR-582-3p inhibition ameliorated the impacts of circPTK2 knockdown on AML cell processes. MiR-582-3p overexpression regulated cell phenotypes by targeting ALG3. CONCLUSION: CircPTK2 contributed to AML cell malignant behaviors by modulation of miR-582-3p/ALG3 axis, which might provide a potential target for AML therapy.

Comparison of different algorithms based on TKEO for EMG change point detection.

Objective.A significant challenge in surface electromyography (EMG) is the accurate identification of onset and offset of muscle activation while maintaining high real-time performance. Teager-Kaiser energy operator (TKEO) is widely used in muscle activity monitoring systems because of its computational simplicity and strong real-time performance. However, in contrast to TKEO ontology, few studies have examined how well the energy operator variants from multiple fields perform in conditioning EMG signals. This paper aims to investigate the role of the energy operator and its variants in EMG change point detection by a threshold detector.Approach.To compare the stability and accuracy of TKEO and its variants for EMG change point detection, the EMG data of extensor carpi radialis longus and flexor carpi radialis were acquired from twenty participants operating a controller under normal and disturbed conditions, and EMG change point detection was performed by four energy operators and their rectified versions.Main results.Based on the 'standard' change points collected by the controller, the detection results were evaluated by three evaluation indexes: detection rate,F1 Score, and accuracy. The experimental results show that the multiresolution energy operator and the TKEO with rectified (abs-TKEO) are more suitable for EMG change point detection.Significance.This paper compared the effect of the energy operator and its variants on a threshold-based EMG change point detector. The experimental results in this paper can provide a reference for the selection of EMG signal conditioning methods to improve the detection performance of the EMG change point detector.