Background: Visceral white adipose tissue (vWAT) inflammation is a critical pathology of obesity-caused heart damage and is closely associated with adipocyte endoplasmic reticulum (ER) dysfunction. Serine (or cysteine) peptidase inhibitor, clade A, member 3C (Serpina3c) has been identified as an adipokine with anti-vWAT inflammatory effects. However, it remains unclear whether Serpina3c deficiency promotion of vWAT inflammation involves adipocyte ER dysfunction and whether it further contributes to heart damage in obesity. Methods: Wild type and Serpina3c knockout (Serpina3c–/–) mice were fed a high-fat diet (HFD) for 12 weeks. An adeno-associated virus (AAV) was injected locally into epididymal white adipose tissue (eWAT) of Serpina3c–/– mice to induce eWAT-adipocyte- specific overexpression of Serpina3c (AAV-Serpina3c) or knockdown of hypoxia-inducible factor 1α (AAV-shHIF1α). In vitro experiments were performed in 3T3-L1 adipocytes. Results: Serpina3c–/– mice exhibited more severe eWAT, serum and heart inflammation after HFD feeding. Consistently, these adverse phenotypes were mitigated in AAV-Serpina3c and AAV-shHIF1α mice. Mechanistically, ER oxidoreductase 1α (Ero1α) and protein disulfide isomerase (PDI) family members PDIA3 and PDIA4 were found to be target genes of HIF1α. In the obese mice, Serpina3c deficiency caused adipocyte more hypertrophy, and activated HIF1α-Ero1α/PDI mediated ER overoxidation and ER stress in eWAT. Subsequently, this led to increased adipocyte apoptosis and chemokine production and decreased adiponectin expression, which promoted macrophage infiltration and M1 polarization in eWAT, thus exacerbating eWAT inflammation and ultimately facilitating serum and distal heart inflammation. Conclusion These findings indicate that Serpina3c is a significant regulator of adipocyte ER redox homeostasis, thus highlighting Serpina3c as a potential therapeutic target for obesity-related eWAT inflammation and heart damage.

Objective To investigate the association of serum total testosterone(TT),free testosterone(FT),sex hormone-binding globulin(SHBG),and estradiol(E_2)with all-cause mortality rate(AMR)in males and to evaluate their predictive value. Methods Based on data from the National Health and Nutrition Examination Survey(NHANES)cycles(1999—2004 and 2013—2016),the relationships between different sex hormones and AMR was analyzed with Cox proportional hazards regression models. The dose-response relationships between different sex hormones and male AMR were assessed with restricted cubic splines(RCS). The predictive performances of different sex hormones for male AMR were compared with receiver operating characteristic(ROC)curves and the area under the curve(AUC). The survival differences across varying sex hormone levels were evaluated with Kaplan-Meier survival curves and log-rank tests. Results This study involved 3632 adult male participants with a median follow-up of 6.5 years,during which 320 AMR occurred(8.8%). Cox univariate analysis indicated that TT,FT and SHBG were risk factors for AMR(P＜0.001). Cox multivariate analysis revealed that FT and SHBG were independent risk factors for AMR(FT:HR=0.90,95%CI:0.86-0.94; SHBG:HR=1.01,95%CI:1.01-1.02). RCS revealed a U-shaped nonlinear relationship between TT,FT and AMR(P＜0.001); SHBG showed a positive dose-response relationship with AMR(P＜0.001). The AUCs of FT predicting the 5-year,10-year,and 15-year AMR were 0.78(95%CI:0.73-0.82),0.80(95%CI:0.76-0.84),and 0.84(95%CI: 0.80-0.88),respectively,significantly outperforming other indicators. Subgroup analysis revealed that FT was negatively correlated with male AMR,but this association was modulated by age,race,smoking status and diabetes status(P_(interaction)＜0.05). Kaplan-Meier survival analysis showed that different levels of TT and FT(Q1-Q4)were significantly positively correlated with survival rate(P＜0.001),while different levels of SHBG were significantly negatively correlated with survival rate,with patients in the Q4 group having the highest risk of death(P＜0.001). Conclusion Based on US NHANES,studies have shown that the FT and SHBG are independent risk factors for male AMR,and FT demonstrates greater predictive value for male AMR than TT.

Electroencephalography (EEG) is a non-invasive neurophysiological monitoring technique. It records the electrical activity of the cerebral cortex using electrodes placed on the scalp surface. Owing to its high safety, portability, and millisecond-level temporal resolution, EEG has been widely utilized in a variety of fields, including clinical diagnosis, brain-computer interfaces (BCIs), and cognitive neuroscience research. However, due to its microvolt-level amplitude, EEG is highly susceptible to various artifacts, including electrooculographic (EOG), electrocardiographic (ECG), electromyographic (EMG), and power line interference (PLI). These artifacts can obscure genuine neural activity and introduce spurious electrophysiological features. Consequently, they may compromise EEG signal quality, thereby reducing the reliability of downstream analyses. To address this issue, numerous EEG artifact removal methods have been developed, including both traditional denoising techniques and deep learning-based approaches. Traditional EEG denoising methods have long served as the primary solutions for artifact removal. Representative approaches include filtering, regression, and blind source separation. Although these methods have demonstrated effectiveness in specific scenarios, they suffer from several inherent limitations. Filtering assumes that artifacts and EEG signals can be separated in the frequency domain, but many artifacts, such as EOG and EMG, overlap with EEG spectra, which may lead to the loss of valuable neural information. Regression methods require high-quality artifact references to estimate and subtract contaminations, limiting their effectiveness in reference-free scenarios. Blind source separation can remove artifacts without external references, but it typically requires the number of EEG channels to exceed the number of sources, restricting its application in single- or low-channel EEG recordings. Deep learning-based EEG denoising methods address these limitations effectively. First, they learn the nonlinear mapping between contaminated and clean EEG directly from data in an end-to-end manner. This approach does not rely on assumptions about spectral separability, thereby preserving neural activity more completely. Second, the reference information is incorporated during the training phase, allowing the trained model to perform artifact removal independently without external references. Third, deep learning models can be flexibly designed to accommodate various recording setups, achieving robust denoising for both high-density and single-channel EEG. Collectively, these advantages enable deep learning-based methods to overcome the main challenges of traditional approaches, providing more accurate and reliable EEG signal recovery. The superior denoising performance of deep learning-based EEG denoising methods has attracted increasing attention in EEG artifact removal research. As a result, many deep learning-based denoising methods have been developed and successfully applied in neural engineering areas. However, a systematic review of the techniques and applications in this field is still lacking. To address this gap, this paper reviews recent advances in deep learning-based EEG denoising from four perspectives: technical principle, benchmark dataset, denoising model, and evaluation method. Representative applications in neural signal analysis and BCI decoding are also summarized. Furthermore, the advantage, existing challenge, and future research direction of deep learning-based EEG denoising are discussed. This review aims to provide valuable theoretical insights and technical guidance for researchers. It is also expected to promote further advances and broader applications of deep learning-based EEG denoising techniques.

ObjectiveTo explore the long-term dynamic trajectories of fasting blood glucose （FBG） and insulin resistance （IR） in patients with type 2 diabetes mellitus （T2DM） and their influencing factors. MethodsThis retrospective cohort study included 1 896 T2DM patients registered at Tongren Hospital from May 2020 to May 2025. Based on longitudinal follow-up data of FBG and fasting insulin， joint latent class mixed models （JLMM） were applied to identify FBG-IR trajectories. Univariate and multinomial logistic regression was used to examine demographic characteristics， lifestyle， and clinical determinants of trajectory type. ResultsFour distinct FBG-IR trajectories were identified： stable FBG-IR （9.76%）， rising FBG-stable IR （5.01%）， stable FBG-elevated IR （75.90%）， and elevated FBG-IR （9.34%）. Compared with the stable FBG-IR group， age ≥60 years was protective against the elevated FBG-stable IR trajectory （OR=0.55， 95%CI：0.33-0.92， P=0.023）. Highereducation increased the risk of stable FBG-elevated IR （OR=1.40， 95%CI：1.01-1.94， P=0.046）. Abnormal blood pressure was associated with lower risks of stable FBG-elevated IR （OR=0.66， 95%CI：0.48-0.92， P=0.013） and elevated FBG-IR （OR=0.48， 95%CI：0.31-0.74， P=0.001）. Non-drinkers were less likely to belong to the stable FBG-elevated IR trajectory （OR=0.39， 95%CI：0.16-0.95， P=0.038）. ConclusionsThe evolution trajectory of FBG and IR in T2DM patients shows significant heterogeneity. The majority of patients have a deterioration of IR first. Age， education level， blood pressure， and alcohol consumption are the main influencing factors. Joint assessment of FBG and IR is helpful for early identification of high-risk individuals and guiding individualized intervention.

ObjectiveThis study aimed to investigate whether dexmedetomidine （Dex） alleviates stress-induced mammary tumor progression in mice by inhibiting the TLR4/NF‑κB signaling pathway， and to examine its effects on anxiety‑depression‑like behaviors and stress hormone levels. MethodsAn orthotopic EMT6 mammary tumor model was established in mice， and chronic mild stress （CMS） was applied to induce anxiety‑depression‑like states. The mice were divided into six groups： naive， tumor， CMS， CMS+tumor， CMS+tumor+Dex， and CMS+tumor+Vehicle groups. Behavioral changes were evaluated using the open field test and tail suspension test. Plasma stress hormone levels were measured by high‑performance liquid chromatography. Western blot and RT‑qPCR were performed to detect the expression of TLR4， p‑NF‑κB p65， p‑IκBα， and inflammatory cytokines （IL‑6， IL‑1β， TNF‑α） in tumor tissues. In vitro， EMT6 cells were treated with cortisol to mimic the stress-related microenvironment， and the effects of Dex on the TLR4/NF‑κB pathway were assessed by CCK‑8， Western blot， and RT-qPCR. ResultsTumor‑bearing mice exhibited significant anxiety‑depression‑like behaviors （P＜0.05）， along with markedly elevated plasma levels of norepinephrine， epinephrine， and cortisol （P＜0.05）. Chronic stress further aggravated these behavioral abnormalities and promoted tumor growth （P＜0.05）. Dexmedetomidine intervention significantly improved anxiety‑depression‑like behaviors （P＜0.05） and lowered peripheral stress hormone levels （P＜0.05） in stress‑exposed tumor‑bearing mice. In vitro experiments demonstrated that cortisol treatment activated the TLR4/NF‑κB pathway （P＜0.001） and upregulated the expression of inflammatory cytokines （P＜0.05 in EMT6 cells， whereas dexmedetomidine effectively suppressed this activation （P＜0.001）. In the in vivo model， dexmedetomidine treatment downregulated the expression of TLR4， p‑NF‑κB p65， p‑IκBα， and pro‑inflammatory cytokines in tumor tissues （P＜0.001） and significantly inhibited tumor growth （P＜0.05）. ConclusionDexmedetomidine inhibits the TLR4/NF‑κB signaling pathway， alleviates stress‑induced inflammatory responses， improves anxiety- and depression‑ like behaviors， reduces stress hormone levels， and suppresses mammary tumor progression. These findings provide an experimental basis for understanding anxiety- and depression- associated breast tumor progression and suggest that Dexmedetomidine and the TLR4/NF-κB pathway may serve as potential therapeutic targets.

Objective To investigate the effects of Duzhi Pills combined with MOTOmed training on limb function and activities of daily living in patients with cerebral infarction of qi deficiency and blood stasis type.Methods A prospective randomized controlled trial enrolled 98 cerebral infarction patients with qi deficiency and blood stasis treated at Qinhuangdao Hospital,Oriental Hospital of Beijing University of Chinese Medicine(Qinhuangdao Hospital of Traditional Chinese Medicine)from June 2022 to December 2024.Participants were randomized into control group(n=49,receiving conventional rehabilitation)and observation group(n=49,receiving additional Duzhi Pills+MOTOmed training)for 8 weeks.All patients received standard medication.Limb motor function and activities of daily living,and quality of life were assessed before and after treatment.Results(1)After treatment,both groups showed significant increases in Carroll Hand Function Test for Upper Extremity(CHFT-UE)scores,Fugl-Meyer Assessment Scale for Upper Extremity(FMA-UE)scores,and Simple Test for Evaluating Hand Function(STEF)scores compared to baseline(P＜0.05),with significantly greater improvements observed in the observation group(P＜0.01).(2)After treatment,both groups exhibited significant increases in Barthel Index scores for daily activity(P＜0.05),with the observation group demonstrating significantly greater improvement(P＜0.01).(3)After treatment,all subscale scores of the 36-Item Short-Form Health Survey(SF-36),including physical function,bodily pain,mental health,vitality,social functioning,emotional role,and general health,were significantly increased in both groups(P＜0.05),with significantly greater improvements in the observation group,the difference being statistically significant(P＜0.01).Conclusion The combined regimen of Duzhi Pills and MOTOmed training significantly enhances limb function,daily activity,and quality of life in cerebral infarction patients with qi deficiency and blood stasis syndrome,demonstrating clinical value for rehabilitation.

Objective To investigate the efficacy and safety of transcutaneous electrical acupoint stimulation(TEAS)in reducing the consumption of analgesics after total knee arthroplasty(TKA).Methods Totally 124 patients undergoing unilateral TKA were included and divided into an intervention group and a control group according to random number table method,with 62 cases in each group.Both groups received routine postoperative analgesic protocols,with the intervention group additionally receiving TEAS treatment,30 min per time,twice a day.The additional doses of intravenous patient-controlled analgesia pumps and opioid analgesic consumption in two groups of patients after surgery were analyzed,as well as the adverse events and laboratory test results(WBC,PLT,SCr,BUN,ALT and AST)in both groups.Results The number of additional doses in the intervention group with the patient-controlled analgesia pump and the consumption of opioid analgesic were both lower than those in the control group(P<0.05);the incidence of postoperative nausea symptoms in the intervention group was lower than that in the control group,while other adverse reactions showed no significant difference(P>0.05).There was no significant difference in laboratory test results(WBC,PLT,SCr,BUN,ALT and AST)between the two groups on the day before surgery and on the 1st and 7th days after surgery(P>0.05).Conclusion TEAS can reduce the consumption of analgesics after TKA,decrease some adverse reactions associated with the use of analgesics,and has good safety.

AIM To study the chemical constituents from the buds of Aralia chinensis L.var.nuda Nakai and their in vitro anti-inflammatory activities.METHODS The 70％ethanol extract from the buds of A.chinensis var.nuda was isolated and purified by silica gel,Sephadex LH-20,ODS and semi-preparative HPLC,then the structures of compounds were identified by physicochemical properties and spectral data.Their anti-inflammatory activities in vitro were evaluated by RAW264.7 model.RESULTS Sixteen compounds were isolated and identified as 4-(2,2-dibutoxyethyl)phenol(1),trans-linalool-3,7-oxide-6-O-β-D-glucopyranoside(2),2'-O-(9Z,12Z,15Z-octadecatrienoyl)glyceryl β-D-galactopyranoside(3),quercetin-3-O-β-D-glucopyranoside(3'→ O-3''')quercetin-3-O-β-D-galactopyranoside(4),syringaresinol-4'-O-β-D-glucopyranoside(5),p-hydroxybenzaldehyde(6),7α-hydroxystigmasterol 3-O-β-D-glucopyranoside(7),trans-p-hydroxy cinnamic acid methyl ester(8),funingensin A(9),3,4-dihydroxy-acetophenone(10),N-acetyltyramine(11),3,4-di-O-caffeoyl quinic acid(12),chlorogenic acid(13),aralia cerebroside(14),caffeic acid methyl ester(15),tetradecanoic acid(16).The IC50values of compounds 8,10,12 and 13 were(22.19±1.59),(35.25±1.30),(13.38±0.72),(15.73±1.16)μmol/L,respectively.CONCLUSION Compound 1 is a new compound,2-13 are isolated from genus Aralia for the first time.Compounds 8,10,12,13 exhibit significant in vitro anti-inflammatory activities.

Objective To investigate the current situation of frailty in patients with home peritoneal dialysis and analyze its influencing factors,so as to provide bases for early identification of high-risk groups and targeted clinical intervention.Methods From October to December 2024,205 home-based peritoneal dialysis patients under long-term follow-up at a tertiary A hospital in Zhongshan,Guangdong Province,were selected by convenience sampling.The General Information Questionnaire,Fried Phenotype Scale,Nutritional Risk Screening Tool,Exercise Self-Efficacy Scale,and Social Support Rating Scale were used to investigate the influencing factors of frailty in home-based peritoneal dialysis patients by ordinal logistic regression analysis.Results A total of 201 valid questionnaires were collected.The prevalence of frailty among home-based peritoneal dialysis patients was 24.3％,while 39.3％were in the pre-frailty stage,and 36.3％showed no frailty.0rdinal logistic regression analysis revealed that age,residence location,primary disease,sleep status,serum albumin concentration,and exercise self-efficacy level were influencing factors of frailty in the home peritoneal dialysis patients(P＜0.05).Conclusion The incidence of frailty in patients with home peritoneal dialysis is higher,and patients with advanced age,living in rural areas,other types of primary diseases,insomnia,low serum albumin concentration and low exercise self-efficacy are more likely to develop frailty.Specialist doctors and nurses of peritoneal dialysis should pay attention to the early screening of frailty in patients with peritoneal dialysis at home,and take personalized intervention measures to prevent or delay the occurrence of frailty according to the relevant risk factors.

A mounting body of research suggests that circRNAs significantly contribute to the develop-ment of myocardial fibrosis.The microarray results of human circular RNA expression profile indicated that circHERC4_041 expression increased in the myocardium of patients with heart failure,RT-qPCR a-nalysis confirmed that the myocardial expression level of circHERC4_041 in individuals with heart failure were considerably elevated compared to that in healthy organ donors.Fluorescence in situ hybridization(FISH)confirmed that circHERC4_041 was abundant in the cytoplasm of human cardiomyocyte AC16.Overexpression of circHERC4_041 in mouse myocardial fibroblasts(mCFs)mediated by adenovirus in-hibited the expression of fibrosis-related proteins in mCFs.Experiments involving cell proliferation,wound healing,and Transwell assays demonstrated that overexpression of circHERC4_041 suppressed the growth and mobility of mCFs(P＜0.001).Sequence analysis results suggested that circHERC4_041 con-tains potential ribosome entry sequence(IRES)and open reading frame(ORF).Western blot confirmed that circHERC4_041 could translate the 516 amino acid HERC4-516aa protein,which was mainly located in the cytoplasm of the cell.Cell functional experiments confirmed that circHERC4_041 inhibited the fi-brotic phenotype of mCFs by specifically translating HERC4-516aa(P＜0.05).The specific interaction between HERC4-516aa and transglutaminase 2(TGM2)was confirmed by IP-MS screening and Co-IP i-dentification.Further results found that the degradation of TGM2 was promoted through proteasome path-way.The overexpression of TGM2 in mCFs facilitated by adenoviral vectors could counteract the suppres-sive effects of HERC4-516aa on the fibrotic phenotype of mCFs.Therefore,this study confirmed that the HERC4-516aa protein translated by circHERC4_041 can specifically bind to TGM2 to inhibit the fibrotic phenotype of myocardial fibroblasts.