Objective Using event-related potentials(ERPs)technology to study the effect of long term emotional distress on selective attention distraction inhibition function in college students and its neuroelectrophysiological mechanism.Methods The Eysenck personality questionnaire(EPQ)adult version was used to screen the high and low neuroticism groups among college students,and 35 subjects in each group were included in the long term emotional distress group and the emotional smoothness control group,respectively,and the response time,correct rate,N2 and P3 amplitude and latency results of the participants to complete the negative priming paradigm task were collected and analyzed.Results Compared with the control group,① the long term emotional distress group showed a prolonged response trend(P=0.072).② the long term emotional distress group had a prolonged N2 and P3 latency(P<0.05).Conclusion Selective attention distraction inhibition in college students with long term emotional distress decreased,and the decline mechanism may be related to the decline of inhibition processing and attention resource allocation ability.

Objective To investigate the effect of Qi stagnation on inhibitory control function and its neuroelectrophysiological mechanism in college students.Methods The population of peace and Qi depression was screened from college students through the scale of"Classification and Judgment Criteria of Traditional Chinese Medicine Constitution",and 35 subjects were included in each group.Combined with event-related potential technology,the two groups were collected to complete the Flanker paradigm behavioral indicators(accuracy,response time)and EEG data indicators(amplitude and latency of N2 and P3 components),and the behavioral differences and neuroelectrophysiological mechanisms between the two groups under the Flanker paradigm were explored.Results Compared with the flat group,the reaction time of the gas depression group was longer(P=0.07).Compared with the consistent dondition,the reaction time was longer under the inconsistent condition(P<0.001),and the accuracy rate was lower under the inconsistent condition significantly(P<0.001).Compared with the peaceful group,the N2 amplitude of the air depression group was higher(P<0.05).There was a statistically significant difference in the main effect of brain regions in the N2 latency period(P<0.001).Frontal lobe zero(Fz)in frontal region was greater than Frontal lobe central zero(FCz)in frontal region and greater than Central zero(Cz)in central region(P<0.05).There was a statistically significant difference in the main effect of brain region(P<0.001).FCz in the frontal central region was significantly greater than that in the frontal region Fz(P<0.001),and the difference was statistically significant in the central region Cz was significantly greater than that in the frontal region(P<0.001).The incubation period of P3 component was significantly smaller than that of inconsistent stimulation(P<0.001).Conclusion Qi stagnation has a negative effect on the inhibitory control function of college students,and the decline of conflict monitoring and control ability is one of the possible mechanisms.

Family with sequence similarity 3 member A(FAM3A),a novel mitochondrial protein,plays a pivotal role in hepatic glucose and lipid metabolism by enhancing ATP synthesis and secretion and mod-ulating the ATP-P2 receptor-Akt signaling pathway.Dysregulation of FAM3A is closely associated with the pathogenesis of non-alcoholic fatty liver disease(NAFLD)and type 2 diabetes mellitus(T2DM).In this study,targeting FAM3A as a therapeutic candidate,we conducted virtual screening to identify 47 small-molecule compounds with potential binding activity.Surface plasmon resonance(SPR)analysis re-vealed three compounds exhibiting high binding affinity to FAM3 A.Further structural characterization of the FAM3A-compound complexes,combined with intermolecular interaction analysis,elucidated the binding mode of the lead compound Index 2(taxifolin)to FAM3A at atomic resolution.These findings provide critical insights into the molecular mechanisms underlying ligand-FAM3A interactions and deliver valuable chemical scaffolds for the development of therapeutics targeting NAFLD and T2DM.This work establishes a foundation for advancing drug discovery efforts focused on FAM3A-mediated metabolic disor-ders.

BACKGROUND:Mitophagy is closely associated with the development of idiopathic pulmonary fibrosis,but its mechanism remains unclear.OBJECTIVE:To investigate the biological mechanism of mitophagy in idiopathic pulmonary fibrosis and provide ideas for the risk prediction of idiopathic pulmonary fibrosis and subtype differentiation.METHODS:The mitophagy-related genes in idiopathic pulmonary fibrosis were obtained through GEO and Reactome Pathway databases.The mitophagy-related characteristic genes in idiopathic pulmonary fibrosis were screened based on intergroup differences and random forest model.GO functional enrichment analysis and KEGG,Reactome with WIKI pathway enrichment analyses were performed by g:Profiler database.Mitophagy subtypes in idiopathic pulmonary fibrosis were distinguished by consensus clustering method and immune infiltration analysis was performed.The mitophagy-related key gene was screened.Finally,the predictive value of mitophagy-related key gene for the risk of idiopathic pulmonary fibrosis was quantified by alignment diagram and the correlation between mitophagy-related key gene and clinical characteristics of idiopathic pulmonary fibrosis was explored.RESULTS AND CONCLUSION:(1)A total of 13 genes related to mitophagy in idiopathic pulmonary fibrosis were identified and 5 characteristic genes were screened,containing PINK1,RPS27A,SRC,HIF1A,and CDH6.(2)GO analysis was mainly involved in ubiquitin protein ligase binding,and cellular response to hypoxia.Pathway enrichment analysis was mainly involved in PINK1-PRKN mediated mitophagy,NOTCH signaling pathway,signaling by EGFR and angiogenesis.(3)HIF1A had significant expression differences between subtypes,which might serve as a key gene for the differentiation of mitophagy subtypes of idiopathic pulmonary fibrosis.(4)Immune infiltration analysis suggested that myeloid-derived suppressor cell,neutrophil and type 1 T helper cell might have infiltration differences between subtypes,while HIF1A was positively correlated with multiple immune cells.(5)Alignment diagram suggested that the risk of idiopathic pulmonary fibrosis might be predicted by the expression level of HIF1A.(6)Clinical characteristics analysis indicated patients with high expression of HIF1A might have poorer lung function and more severe fibrosis.It is concluded that PINK1,RPS27A,SRC,HIF1A,and CDH6 may influence the development of idiopathic pulmonary fibrosis through mitophagy,in which HIF1A may serve as a key gene for risk prediction with clinical subtype differentiation and HIF1A is strongly associated with the lung function of patients.

Aim To reveal the mechanism of CIP4 homologs protein 1(RICH1)are involved in the regu-lation of myocardial fibrosis.Methods Mouse cardiac fibroblasts(MCFs)cells were treated with transforming growth factor-β(TGF-β1)to induce the formation of a myocardial fibrosis cell model;the level of the target protein was detected by Western blotting;and the RICH1 gene was detected by transfection of the cells with plasmid.The RICH1 gene was overexpressed(RICH 1 OE)using plasmid transfection;the RICH1 gene was silenced using siRNA fragment(siRICH1);and the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3 a1,and Acta2,were de-tected using RT-qPCR.Results RICH1 was signifi-cantly down-regulated in TGF-β1-treated MCFs;the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3a1,and Acta2,were down-regu-lated in the RICH1 OE+TGF-β1 group;and in the siRICH1+TGF-β1 group,myocardial fibrosis marker genes,such as Col1 a1,Col3a1 and Acta2 were up-regulated at the expression level;phosphorylated SMAD2(p-SMAD2)and phosphorylated SMAD3(p-SMAD3)levels were down-regulated in the siRICH1 OE+TGF-β1 group.p-SMAD2 and P-SMAD3 levels were upregulated in the siRICH1+TGF-β1 group.Conclusion RICH1 inhibits TGF-β1-induced myo-cardial fibrosis;RICH1 inhibits TGF-β1-induced myo-cardial fibrosis by negatively regulating the SMAD2/3 signaling pathway.

Aim To reveal the mechanism of CIP4 homologs protein 1(RICH1)are involved in the regu-lation of myocardial fibrosis.Methods Mouse cardiac fibroblasts(MCFs)cells were treated with transforming growth factor-β(TGF-β1)to induce the formation of a myocardial fibrosis cell model;the level of the target protein was detected by Western blotting;and the RICH1 gene was detected by transfection of the cells with plasmid.The RICH1 gene was overexpressed(RICH 1 OE)using plasmid transfection;the RICH1 gene was silenced using siRNA fragment(siRICH1);and the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3 a1,and Acta2,were de-tected using RT-qPCR.Results RICH1 was signifi-cantly down-regulated in TGF-β1-treated MCFs;the expression levels of myocardial fibrosis marker genes,such as Col1 a1,Col3a1,and Acta2,were down-regu-lated in the RICH1 OE+TGF-β1 group;and in the siRICH1+TGF-β1 group,myocardial fibrosis marker genes,such as Col1 a1,Col3a1 and Acta2 were up-regulated at the expression level;phosphorylated SMAD2(p-SMAD2)and phosphorylated SMAD3(p-SMAD3)levels were down-regulated in the siRICH1 OE+TGF-β1 group.p-SMAD2 and P-SMAD3 levels were upregulated in the siRICH1+TGF-β1 group.Conclusion RICH1 inhibits TGF-β1-induced myo-cardial fibrosis;RICH1 inhibits TGF-β1-induced myo-cardial fibrosis by negatively regulating the SMAD2/3 signaling pathway.

Objective:To comprehensively evaluate the application of Common Data Model (CDM) of Observational Medical Outcomes Partnership (OMOP) in China, and provide reference for the implementation of data standardization and evidence sharing in China.Methods:PubMed, Embase, Web of Science, CNKI, VIP, WanFang and SinoMed databases were used for literature retrieval to collect the research papers of OMOP CDM application for data standardization in China until March 15, 2023. The information about institutions, types and numbers of patients were extracted.Results:A total of 14 research papers, including 9 in English and 5 in Chinese, were selected. The research papers published since 2018 were collected, which focused on patients with hypertension, diabetes, and depression. A total of 12 institutions or platforms transformed data into OMOP CDM. Jiangsu Provincial People's Hospital was the first one to apply the CDM and demonstrated its feasibility in China. Additionally, the regional information system in Yinzhou District of Ningbo, Zhejiang Province, standardized the multi-dimensional data of patients with diabetes and hypertension. Based on this platform, a series of prediction models for complications in patients with diabetes were constructed. Another major database in Beijing Anding Hospital applied OMOP CDM to analyze the characteristics of patients with late-life depression and dementia.Conclusions:This study analyzed the application of OMOP CDM in China. Through in-depth analysis of specific cases, the study provided guidance for the future cross-regional evidence sharing and collaboration.

Objective To investigate the influence of the liver failing to convey and disperse on space navigation aging.Methods High and low neuroticism subjects screened by Eysenck personality questionnaire were included in liver failing to convey and disperse group and liver controlling conveyance and dispersion group,respectively.The two groups were then divided into youth and elderly groups based on age.Finally,spatial navigation task was conducted to record and analyze behavioral(reaction time and accuracy)and EEG data(amplitude and latency of P2 and N2 components)of all the four groups(30 subjects each group).Results Compared with liver controlling conveyance and dispersion group,the accuracy in subjects with liver failing to convey and disperse decreased significantly(P<0.001)and reaction time was prolonged significantly(P<0.05).The interaction effect between age and liver regulation status showed a marginal significant difference(P=0.078).The accuracy of elderly people was lower than that of youth people(P=0.002)for liver failing to convey and disperse subjects,while there was no significant difference between the two groups for subjects with liver controlling conveyance and dispersion.The P2 amplitude in the elderly group was significantly smaller than that in the youth group(P=0.027).The amplitude of P2 in group of liver failing to convey and disperse was significantly smaller than that in group of liver controlling conveyance and dispersion(P=0.042).The interaction effect of P2 amplitude between age and liver regulation status showed a marginal significance(P=0.073).For youth subjects,the P2 amplitude in group of liver controlling conveyance and dispersion was significantly larger than that in group of liver failing to convey and disperse(P=0.007),while there was no significant difference in P2 amplitude between the two groups for the elderly subjects.The N2 amplitude for tasks of allocentric frames of reference was significantly greater than that of egocentric frames of reference(P=0.024).Conclusion Liver failing to convey and disperse caused by long-term emotional disturbance accelerates spatial navigation aging,and selective attention feature inhibition disorder may be the underlying ERPs neuroelectrophysiological mechanism.

Objective To investigate the influence of the and mechanism of liver failing to convey and disperse on age-related changes in attentional search based on ERPs.Methods oddball attention search task was administrated to record and analyze behavioral and EEG data(N2pc、SPCN、N2pc-Ptc components)of 120 subjects.Results Compared with liver controlling conveyance and dispersion group,the accuracy in subjects with liver failing to convey and disperse decreased significantly(P<0.05).The elderly group had a lower accuracy(P<0.001)and a longer reaction time(P<0.001)compared to the young group.The N2pc amplitude in subjects with liver failing to convey and disperse was significantly greater than that in subjects with liver controlling conveyance and dispersion(P<0.05).The interaction effect of SPCN amplitude between age and liver failing to convey and disperse status was significant(P=0.024).And in the elderly group,SPCN amplitude in subjects with liver dysregulation was significantly smaller than that of liver controlling conveyance and dispersion(P=0.042).The N2pc-Ptc peak to peak amplitude interaction effect between age and liver regulation status was marginal significant(P=0.087),and in liver failing to convey and disperse group,N2pc-Ptc peak to peak amplitude of the elderly was significantly smaller than that of the young(P=0.008).Conclusion Attention search ability is impaired in the elderly with liver failing to convey and disperse,and the electrophysiological abnormalities,such as directed attention allocation,spatiotemporal dynamic cohesion and short-term memory maintenance,may be part of the mechanism.

With the deepening of molecular biology and cell biology research,the regulatory mechanism of autophagy has been gradually revealed,providing new ideas for the treatment of numerous diseases.Autophagy may be closely related to pathological changes such as apoptosis resistance of fibroblast-like synoviocytes,disturbances in bone metabolic homeostasis,and antigen presentation,the regulation of autophagy homeostasis may be an important approach for the treatment of rheumatoid arthritis(RA).In this paper,we provide a review on the pathological mechanism of autophagy in RA,with a view to providing a theoretical basis for later studies.