Environmental factors such as air pollutants,plastic micro-particles,ionizing radiation,and traffic noise promote the onset and progression of atherosclerotic cardiovascular disease(CVD)through mechanisms including inducing inflammatory responses,promoting oxidative stress,and accelerating lipid deposition.Notably,the modification of apoli-poprotein(Apo)by reactive oxygen species(ROS)accelerates this process.On one hand,ROS can oxidize key amino acid residues in Apo,altering its structure and thereby impairing its normal physiological function.On the other hand,ROS can induce lipid peroxidation of Apo,rendering the oxidized Apo more susceptible to recognition and uptake by macro-phages.This accelerates foam cell formation and drives the progression of atherosclerotic(As)plaques.This review summarizes recent research advances on the role of ROS-induced modification of Apo by environmental factors in atheroscle-rotic CVD.

Environmental factors such as air pollutants,plastic micro-particles,ionizing radiation,and traffic noise promote the onset and progression of atherosclerotic cardiovascular disease(CVD)through mechanisms including inducing inflammatory responses,promoting oxidative stress,and accelerating lipid deposition.Notably,the modification of apoli-poprotein(Apo)by reactive oxygen species(ROS)accelerates this process.On one hand,ROS can oxidize key amino acid residues in Apo,altering its structure and thereby impairing its normal physiological function.On the other hand,ROS can induce lipid peroxidation of Apo,rendering the oxidized Apo more susceptible to recognition and uptake by macro-phages.This accelerates foam cell formation and drives the progression of atherosclerotic(As)plaques.This review summarizes recent research advances on the role of ROS-induced modification of Apo by environmental factors in atheroscle-rotic CVD.

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Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Objective:To explore any effect of intermittent theta burst stimulation (iTBS) and of different sequencing of rehabilitation training on upper limb dysfunction after a stroke.Methods:Thirty-six patients with upper limb motor dysfunction after subacute subcortical cerebral infarction were divided at random into a control group, an experimental group 1, and an experimental group 2, each of 12. The control group was given prosthetic stimulation and upper limb function rehabilitation training. Experimental group l received focal iTBS stimulation on M1 immediately followed by upper limb rehabilitation training. Experimental group 2 received the same treatment but in reverse order. The experiment lasted four weeks. Upper limb functioning and ability in the activities of daily living (ADL) were quantified before and after the interventions using the Fugl-Meyer upper extremity assessment (FMA-UE) and the modified Barthel index (MBI). Cortical latency (CL) was also recorded.Results:Before the treatment there were no significant differences among the three groups, but afterward a significant increase was observed in the average FMA-UE and MBI scores of both experimental groups accompanied by a significant decrease in CL. There was no significant difference between the two experimental groups′ results, on average.Conclusion:Supplementing upper limb rehabilitation training with iTBS can significantly improve the upper limb functioning of ischemic stroke survivors, and the sequencing of the training has no effect on the therapeutic results.

Background and objective The pathological types of lung ground glass nodules(GGNs)show great significance to the clinical treatment.This study was aimed to predict pathological types of GGNs based on computed tomog-raphy(CT)quantitative parameters.Methods 389 GGNs confirmed by postoperative pathology were selected,including 138 cases of precursor glandular lesions[atypical adenomatous hyperplasia(AAH)and adenocarcinoma in situ(AIS)],109 cases of microinvasive adenocarcinoma(MIA)and 142 cases of invasive adenocarcinoma(IAC).The morphological characteristics of nodules were evaluated subjectively by radiologist,as well as artificial intelligence(AI).Results In the subjective CT signs,the maximum diameter of nodule and the frequency of spiculation,lobulation and pleural traction increased from AAH+AIS,MIA to IAC.In the AI quantitative parameters,parameters related to size and CT value,proportion of solid component,energy and entropy increased from AAH+AIS,MIA to IAC.There was no significant difference between AI quantitative parameters and the subjective CT signs for distinguishing the pathological types of GGNs.Conclusion AI quantitative parameters were valu-able in distinguishing the pathological types of GGNs.

Background::Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer associated with poor prognosis and limited treatment options. The androgen receptor (AR) has emerged as a potential therapeutic target for luminal androgen receptor (LAR) TNBC. However, multiple studies have claimed that anti-androgen therapy for AR-positive TNBC only has limited clinical benefits. This study aimed to investigate the role of AR in TNBC and its detailed mechanism.Methods::Immunohistochemistry and TNBC tissue sections were applied to investigate AR and nectin cell adhesion molecule 4 (NECTIN4) expression in TNBC tissues. Then, in vitro and in vivo assays were used to explore the function of AR and estrogen receptor beta (ERβ) in TNBC. Chromatin immunoprecipitation sequencing (ChIP-seq), co-immunoprecipitation (co-IP), molecular docking method, and luciferase reporter assay were performed to identify key molecules that affect the function of AR. Results::Based on the TNBC tissue array analysis, we revealed that ERβ and AR were positive in 21.92% (32/146) and 24.66% (36/146) of 146 TNBC samples, respectively, and about 13.70% (20/146) of TNBC patients were ERβ positive and AR positive. We further demonstrated the pro-tumoral effects of AR on TNBC cells, however, the oncogenic biology was significantly suppressed when ERβ transfection in LAR TNBC cell lines but not in AR-negative TNBC. Mechanistically, we identified that NECTIN4 promoter –42 bp to –28 bp was an AR response element, and that ERβ interacted with AR thus impeding the AR-mediated NECTIN4 transcription which promoted epithelial–mesenchymal transition in tumor progression. Conclusions::This study suggests that ERβ functions as a suppressor mediating the effect of AR in TNBC prognosis and cell proliferation. Therefore, our current research facilitates a better understanding of the role and mechanisms of AR in TNBC carcinogenesis.

Objective:To investigate the relationship between family functioning and self-injurious behavior among primary school children, as well as the effects of teacher-student relationship and friendship quality.Methods:A questionnaire survey was conducted with 1 033 primary school children from grade four to six in Hunan province from March to April 2024, using the family APGAR index scale, the deliberate self-injury inventory, the teacher-student relationship subscale of the my class questionnaire, and the friendship quality questionnaire. Data were analyzed using SPSS 26.0 software for normality tests, descriptive statistics, chi-square tests, and Pearson correlation analyses. Confirmatory factor analysis was performed with AMOS 24.0, and moderated mediating effects were examined using the PROCESS 3.5 macro program.Results:(1) The prevalence of self-injurious behavior among the sampled children was 37.4% (359/958), with no significant gender difference ( χ2=0.01, P>0.05). However, the detection rate among grades was significantly different ( χ2=8.25, P<0.05, Cramer's V=0.09). (2) Self-injurious behavior was negatively correlated with family functioning, teacher-student relationship, and friendship quality ( r=-0.29, -0.25, -0.18, P<0.01). Among family functioning, teacher-student relationship and friendship quality, there was positive correlations between each other ( r=0.33-0.40, all P<0.01). (3) Teacher-student relationship partially mediated the relationship between family functioning and self-injurious behavior, with the mediating effect value accounting for 20%(-0.06/-0.30) of the total effect. (4) Friendship quality moderated the first stage of the mediating effect of teacher-student relationship on the relationship between family functioning and self-injurious behavior ( β=0.08, P<0.01). When children's friendship quality was higher, the predictive effect of family functioning on teacher-student relationship was significantly strengthened ( βsimple=0.30, P<0.001, 95% CI=0.21~0.38). Conclusion:Effective family functioning promotes positive teacher-student relationship in children, thereby reducing the risk of self-injurious behavior. This effect is notably stronger among children with higher-quality friendships.

【Objective】 To clarify the role and molecular mechanism of Tanshinone ⅡA (TanⅡA) in the pathological integration of granule cells in the dentate gyrus (DG) by using the mouse model of temporal lobe epilepsy (TLE). 【Methods】 Status epilepticus (SE) was induced in the mice with pilocarpine and treated with TanⅡA 5 mg/kg. After two months, Morris water maze was used to examine the spatial learning and memory ability and video surveillance was used to monitor spontaneous seizures. The DG was removed for staining of Timm, Prox-1, DCX and SynⅠ. PTEN, p-AKT, and p-S6 expressions were observed by Western blotting. 【Results】 TanⅡA decreased Timm score, SynⅠ, PSD-95 and pS6 levels, and increased the level of PTEN in the DG, and attenuated the formation of mossy fiber sproutings and basal dendrites of the granule cells. Video surveillance showed that TanⅡA reduced the frequency of Racine’ grade 5 seizures. 【Conclusion】 TanⅡA can effectively attenuate the abnormal integration of the granule cells in the DG by regulating PTEN/AKT/mTOR pathway and thus plays an anti-epileptic role.