Objective:To investigate the role of heat shock transcription factor 1(HSF1)in hepatitis B virus X protein(HBx)-driven migration and invasion of hepatocellular carcinoma(HCC)cells,and to preliminarily explore the mechanism of HSF1 mediating HBx-driven HCC progression.Methods:4D label-free quantitative proteomics and Western blot were used to analyze the effect of HBx on HSF1 expression.HBx was overexpressed in the HCC cell lines Huh7 and MHCC97H,and its impact on the mRNA and protein levels and stability of HSF1 was assessed by RT-PCR and Western blot.The Cancer Genome Atlas database was used to analyze the expres-sion of HSF1 in hepatitis B virus(HBV)-associated HCC tissues and its relationship with tumor stage/grade and patient prognosis,and Western blot was used to measure the expression of HSF1 in HBV-associated HCC tissues.HBx was overexpressed in HCC cells,fol-lowed by HSF1 knockdown or cell treatment with the HSF1 inhibitor KRIBB11,and Transwell migration and invasion assay,scratch as-say,and F-actin staining experiment were performed to analyze the role of HSF1 in HBx-driven HCC cell migration and invasion.GEO and HCMDB datasets were used to identify the downstream target of HSF1,and the role of downstream target c-Myb in HSF1-me-diated HBx-driven HCC progression.Results:HBx upregulated HSF1 protein levels without significantly affecting its mRNA expres-sion,through enhancing HSF1 protein stability.HSF1 was highly ex-pressed in HBV-associated HCC tissues,and its elevated expres-sion correlated with tumor stage/grade and poor prognosis.HBx overexpression significantly promoted the migration,invasion,wound-healing capacity,and pseudopodia formation capacity of Huh7 and MHCC97H cells,while HSF1 knockdown or KRIBB11 treatment significantly attenuated the HBx-driven migration and in-vasion of HCC.HSF1 promoted the expression of the metastasis-associated protein c-Myb,and c-Myb overexpression in HSF1-knock-down HCC cells restored the promotive effect of HBx on HCC cell migration and invasion.Conclusion:HBx enhances HSF1 protein stability to promote its expression.Upregulation of c-Myb by HSF1 plays a pivotal role in HBx-driven HCC cell migration and inva-sion.Targeting HSF1 may help to delay the progression of HBV-associated HCC.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Objective The Hybrid Education Competence Instrument(HybridEduCom)was sinicized,and its reliability and validity were tested.Methods The translation,cultural adjustment and pre-investigation of HybridEduCom were followed by the Brislin translation model.The reliability and validity of the HybridEduCom was tested by surveying 553 educators in medical and nursing related fields by convenience sampling from March to April 2024.Results The Chinese version of HybridEduCom consisted of 46 items in 5 dimensions:planning and resourcing competence,technology competence,interaction competence,digital pedagogy competence,and ethical competence in the hybrid education.The confirmatory factor analysis resulted in the second-order five-factor model,with the chi-square and degree of freedom ratio being 1.274,approximate root mean square error being 0.022,goodness of fit index being 0.913,and standard fit index(NFI)being 0.934,and Tucker-Lewis and comparative fit index being 0.985.All main evaluation indexes were within the acceptable range of the judgment criteria.The item-content validity index was 0.833-1.000,and the scale-content validity index was 0.968.The Cronbach's α for the whole scale was 0.982,while varied from 0.892 to 0.936 for each dimension.The test-retest reliability of the scale was 0.978.Conclusion The reliability and validity of the Chinese version of HybridEduCom were satisfactory,and it can serve as a valid assessment instrument for the implementation of hybrid education competence of Chinese higher medical and nursing educators.

Parkinson's disease(PD),the second most common neurodegenerative disorder,involves dopaminergic neuron degeneration,abnormal α-synuclein aggregation,and energy metabolic disruption.AMP-activated protein kinase(AMPK),a key cellular energy metabolic regulator,has multiple roles in PD progression.This paper explores the structure and function of AMPK and its regulatory mechanisms in PD,including its roles in modulating neuronal energy metabolism,mediating mitochondrial function,inhibiting oxidative stress,inducing autophagy,and regulating neuroinflammation and apoptosis.Potential AMPK-based PD therapies are also reviewed,including natural products(e.g.,resveratrol,curcumin),gene therapy,and targeted delivery systems,while noting the need to precisely control the dual effects of AMPK(e.g.,overactivation causes energy stress).Future research should focus on clarifying interactions between AMPK and other pathways(e.g.,SIRT1 and NF-κB)and improving the spatiotemporal specificity of targeted treatments for clinical translation.This study offers crucial theoretical support for understanding mechanisms underlying PD and developing AMPK-targeted therapies.

Parkinson's disease(PD),the second most common neurodegenerative disorder,involves dopaminergic neuron degeneration,abnormal α-synuclein aggregation,and energy metabolic disruption.AMP-activated protein kinase(AMPK),a key cellular energy metabolic regulator,has multiple roles in PD progression.This paper explores the structure and function of AMPK and its regulatory mechanisms in PD,including its roles in modulating neuronal energy metabolism,mediating mitochondrial function,inhibiting oxidative stress,inducing autophagy,and regulating neuroinflammation and apoptosis.Potential AMPK-based PD therapies are also reviewed,including natural products(e.g.,resveratrol,curcumin),gene therapy,and targeted delivery systems,while noting the need to precisely control the dual effects of AMPK(e.g.,overactivation causes energy stress).Future research should focus on clarifying interactions between AMPK and other pathways(e.g.,SIRT1 and NF-κB)and improving the spatiotemporal specificity of targeted treatments for clinical translation.This study offers crucial theoretical support for understanding mechanisms underlying PD and developing AMPK-targeted therapies.

BACKGROUND:The immune response is strongly associated with the pathological development of Parkinson's disease.Studies have shown that the major histocompatibility complex plays a key role in immune response.OBJECTIVE:To summarize the mechanism of major histocompatibility complex regulation of immune response and the effect on the pathological markerα-synuclein of Parkinson's disease.METHODS:"Parkinson's disease,the major histocompatibility complex,innate immunity,adaptive immunity,microglia,T cell,B cell,α-syn,inflammation,MHC-Ⅰ,MHC-Ⅱ"were used as search terms to search the literature in PubMed database.Finally,92 articles were included for reading analysis.RESULTS AND CONCLUSION:(1)Congenital immune response is involved in the occurrence and development of Parkinson's disease,and the change of microglia's pro-inflammatory and anti-inflammatory phenotypes may aggravate the degenerative changes of Parkinson's disease.(2)The phenotype and function of T cells are related to the progression of Parkinson's disease.Regulatory T cells promote the activation of anti-inflammatory microglia and inhibit Th subgroup.B-cell-mediated humoral immunity can clear pathological α-synuclein,and its specific mechanism needs further study.(3)The major histocompatibility complex is closely related to the occurrence of innate and adaptive immunity,and thus affects the inflammation of Parkinson's disease.(4)α-Synuclein can regulate the activation of microglia and the expression of major histocompatibility complex,which leads to inflammatory changes in Parkinson's disease.(5)α-Synuclein is closely related to the immune response of Parkinson's disease and has become an important target for the treatment of Parkinson's disease.

Alzheimer's disease(AD)is a neurodegenerative disorder associated with aging,characterized by neurofibrillary tangles,accumulation of amyloid-β(Aβ)plaques,and neuronal death.These pathological changes lead to a gradual decline in cognitive function,ultimately impairing the ability to perform daily activities.Currently,treatment options for AD are limited,with pharmacological interventions often being ineffective and frequently accompanied by side effects.Therefore,the study of non-pharmacological therapies,especially nutritional interventions,has become particularly important.Omega-3 polyunsaturated fatty acids(ω-3PUFAs)are essential fatty acids crucial for health,primarily found in fish oil and certain plant oils.They play a key role in anti-inflammatory,antioxidant,neuroprotective,and immunomodulatory activities.Epidemiological evidence and clinical trials have shown that supplementation with ω-3PUFAs is associated with improved cognitive function,with particularly positive effects demonstrated in the use of docosahexaenoic acid(DHA)and eicosapentaenoic acid(EPA).This article reviews the role of ω-3PUFAs in AD and the latest advances in their mechanism of action,with a particular focus on their ability to reduce brain Aβ deposition and Tau protein phosphorylation,inhibit oxidative stress and neuroinflammation,maintain the integrity of the blood-brain barrier,and regulate energy metabolism.However,current research findings remain inconsistent,especially regarding the significant differences in effects among individuals with different genotypes.Therefore,future studies need to further explore the role of ω-3PUFAs in early intervention and optimize their dosage and formulations to achieve the best neuroprotective effects.Additionally,this article provides dietary recommendations and dosage suggestions based on existing research,hoping to offer new directions for the prevention and treatment of AD.

BACKGROUND:The immune response is strongly associated with the pathological development of Parkinson's disease.Studies have shown that the major histocompatibility complex plays a key role in immune response.OBJECTIVE:To summarize the mechanism of major histocompatibility complex regulation of immune response and the effect on the pathological markerα-synuclein of Parkinson's disease.METHODS:"Parkinson's disease,the major histocompatibility complex,innate immunity,adaptive immunity,microglia,T cell,B cell,α-syn,inflammation,MHC-Ⅰ,MHC-Ⅱ"were used as search terms to search the literature in PubMed database.Finally,92 articles were included for reading analysis.RESULTS AND CONCLUSION:(1)Congenital immune response is involved in the occurrence and development of Parkinson's disease,and the change of microglia's pro-inflammatory and anti-inflammatory phenotypes may aggravate the degenerative changes of Parkinson's disease.(2)The phenotype and function of T cells are related to the progression of Parkinson's disease.Regulatory T cells promote the activation of anti-inflammatory microglia and inhibit Th subgroup.B-cell-mediated humoral immunity can clear pathological α-synuclein,and its specific mechanism needs further study.(3)The major histocompatibility complex is closely related to the occurrence of innate and adaptive immunity,and thus affects the inflammation of Parkinson's disease.(4)α-Synuclein can regulate the activation of microglia and the expression of major histocompatibility complex,which leads to inflammatory changes in Parkinson's disease.(5)α-Synuclein is closely related to the immune response of Parkinson's disease and has become an important target for the treatment of Parkinson's disease.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Objective The Hybrid Education Competence Instrument(HybridEduCom)was sinicized,and its reliability and validity were tested.Methods The translation,cultural adjustment and pre-investigation of HybridEduCom were followed by the Brislin translation model.The reliability and validity of the HybridEduCom was tested by surveying 553 educators in medical and nursing related fields by convenience sampling from March to April 2024.Results The Chinese version of HybridEduCom consisted of 46 items in 5 dimensions:planning and resourcing competence,technology competence,interaction competence,digital pedagogy competence,and ethical competence in the hybrid education.The confirmatory factor analysis resulted in the second-order five-factor model,with the chi-square and degree of freedom ratio being 1.274,approximate root mean square error being 0.022,goodness of fit index being 0.913,and standard fit index(NFI)being 0.934,and Tucker-Lewis and comparative fit index being 0.985.All main evaluation indexes were within the acceptable range of the judgment criteria.The item-content validity index was 0.833-1.000,and the scale-content validity index was 0.968.The Cronbach's α for the whole scale was 0.982,while varied from 0.892 to 0.936 for each dimension.The test-retest reliability of the scale was 0.978.Conclusion The reliability and validity of the Chinese version of HybridEduCom were satisfactory,and it can serve as a valid assessment instrument for the implementation of hybrid education competence of Chinese higher medical and nursing educators.