Brain’s neural activities encompass both periodic rhythmic oscillations and aperiodic neural fluctuations. Rhythmic oscillations manifest as spectral peaks of neural signals, directly reflecting the synchronized activities of neural populations and closely tied to cognitive and behavioral states. In contrast, aperiodic fluctuations exhibit a power-law decaying spectral trend, revealing the multiscale dynamics of brain neural activity. In recent years, researchers have made notable progress in studying brain aperiodic dynamics. These studies demonstrate that aperiodic activity holds significant physiological relevance, correlating with various physiological states such as external stimuli, drug induction, sleep states, and aging. Aperiodic activity serves as a reflection of the brain’s sensory capacity, consciousness level, and cognitive ability. In clinical research, the aperiodic exponent has emerged as a significant potential biomarker, capable of reflecting the progression and trends of brain diseases while being intricately intertwined with the excitation-inhibition balance of neural system. The physiological mechanisms underlying aperiodic dynamics span multiple neural scales, with activities at the levels of individual neurons, neuronal ensembles, and neural networks collectively influencing the frequency, oscillatory patterns, and spatiotemporal characteristics of aperiodic signals. Aperiodic dynamics currently boasts broad application prospects. It not only provides a novel perspective for investigating brain neural dynamics but also holds immense potential as a neural marker in neuromodulation or brain-computer interface technologies. This paper summarizes methods for extracting characteristic parameters of aperiodic activity, analyzes its physiological relevance and potential as a biomarker in brain diseases, summarizes its physiological mechanisms, and based on these findings, elaborates on the research prospects of aperiodic dynamics.

ObjectiveTo investigate the effect of Danggui Shaoyaosan on ferroptosis in the rat model of non-alcoholic fatty liver disease （NAFLD） and explore the underlying mechanism based on the nuclear factor E₂-related factor 2 （Nrf2）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） signaling pathway. MethodsThe sixty SD rats were randomly grouped as follows： control， model， Yishanfu （0.144 g·kg^-1）， and low-， medium-， and high-dose （2.44， 4.88， and 9.76 g·kg^-1， respectively） Danggui Shaoyaosan. A high-fat diet was used to establish the rat model of NAFLD. After 12 weeks of modeling， rats were treated with corresponding agents for 4 weeks. Then， the body weight and liver weight were measured， and the liver index was calculated. At the same time， serum and liver samples were collected. The levels or activities of total cholesterol （TC）， triglycerides （TG）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， and Fe²⁺ in the serum and TC， TG， free fatty acids （FFA）， malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione peroxidase （GPX）， and Fe²⁺ in the liver were measured. Hematoxylin-eosin staining and oil red O staining were employed to observe the pathological changes in the liver. Immunofluorescence was used to assess the reactive oxygen species （ROS） content in the liver. Mitochondrial morphology was observed by transmission electron microscopy. The protein levels of Nrf2， SLC7A11， GPX4， transferrin receptor 1 （TFR1）， and divalent metal transporter 1 （DMT1） in the liver were determined by Western blot. ResultsCompared with the control group， the model group showed increases in the body weight， liver weight， liver index， levels or activities of TC， TG， ALT， AST， and Fe²⁺ in the serum， levels of TC， TG， FFA， MDA， Fe²⁺， and ROS in the liver， and protein levels of TFR1 and DMT1 in the liver （P<0.01）， and decreases in the activities of SOD， GPX and the protein levels of Nrf2， SLC7A11， and GPX4 in the liver （P<0.05， P<0.01）. Meanwhile， the liver tissue in the model group presented steatosis， iron deposition， mitochondrial shrinkage， and blurred or swollen mitochondrial cristae. Compared with the model group， all doses of Danggui Shaoyaosan reduced the body weight， liver weight， liver index， levels or activities of TC， TG， ALT， AST， and Fe²⁺ in the serum， levels of TC， TG， FFA， MDA， Fe²⁺， and ROS in the liver， and protein levels of TFR1 and DMT1 in the liver （P<0.01）， while increasing the activities of SOD and GPX and the protein levels of Nrf2， SLC7A11， and GPX4 in the liver （P<0.01）. Furthermore， Danggui Shaoyaosan alleviated steatosis， iron deposition， and mitochondrial damage in the liver. ConclusionDanggui Shaoyaosan may inhibit lipid peroxidation and ferroptosis by activating the Nrf2/SLC7A11/GPX4 signaling pathway to treat NAFLD.

Objective:To investigate the effects of ATG5 and ATG7 genes on the sensitivity of multiple myeloma(MM)cell line RPMI-8226 cells to ferroptosis.Methods:CRISPR/Cas9 technology was used to knock out the autophagy key genes ATG5 and ATG7 in RPMI-8226 cells.Western blot was used to identify gene knockout cells,and detect the expression changes of autophagy-related proteins P62 and LC3B.Flow cytometry was used to detect the change of sensitivity of gene knockout cells to RSL3.The content of intracellular ferrous ions and reactive oxygen species(ROS)level in gene knockout cells were detected.Results:Western blot result confirmed that ATG5 and ATG7 genes were knocked out successfully in RPMI-8226 cells.The result of flow cytometry showed that the cell viability of RPMI-8226 cells was dose-dependent on different concentrations of RSL3(r=-0.969).RSL3(10 μmol/L)was used to induce ferroptosis in cells of control group and gene knockout groups,then the cell viability in gene knockout groups were both higher than control group after 48 hours(both P＜0.001).After knocking out the ATG5 and ATG7 genes,the content of intracellular Fe2+decreased significantly compared with control group(both P＜0.01),and the ROS level also decreased(both P＜0.001).Conclusion:Knockout of ATG5 and ATG7 genes can inhibit the ferroptosis of MM cells,and LAP pathway may be involved in the regulation.

Objective:To study the molecular mechanism of functional defect of protein C (PC) caused by point mutations of human protein C gene (PROC) N355S,G392E and T314A. Methods:The wild-type and mutant plasmids (PCWT,PCN355S,PCG392E,PCT314A) of PROC gene were constructed and transiently transfected into HEK293 cells. The expression of mutant proteins in vitro were tested. The mRNA level changes of wild-type and mutant PC after 24 h of transfection were detected by real-time PCR. Western blot and ELISA were used to detect the changes of intracellular and extracellular protein levels of wild-type and mutant PC. The supernatant of cells transfected for 24-48 h was concentrated by ultrafiltration. The protein in the concentrated solution was quantified,and PC activation and enzyme kinetics tests were performed. Clustal Omega multiple sequence alignment was used to analyze the conservation of amino acid mutation sites. The effect of mutation on PC protein structure was analyzed by PyMOL software. Results:The relative expression abundances of PROC mRNA in PCN355S,PCG392E and PCT314A groups were 1.14±0.46,0.96±0.08 and 1.08±0.17,respectively,and there were no significant differences compared with 1.02±0.24 in PCWT group (P>0.05). Western blot analysis of the lysates of transfected cells showed that the content of PCT314A recombinant protein slightly decreased and the band became relatively lighter. The ELISA results of the concentrated cell culture supernatants showed that the PC:Ag levels of PCN355S and PCG392E were 98.8％±2.4％ and 101.4％±3.1％,respectively,with no significant differences compared with PCWT,while PCT314A decreased compared with PCWT (PC:Ag:88.6％±3.2％) (P<0.05). The results of enzyme kinetics test showed that APCN355S (Km=338.3±43.2,Vmax=2.015±0.12),APCG392E (Km=292.2±28.4,Vmax=1.893±0.07) and APCT314A (Km=299.5±24.6,Vmax=1.775±0.06) showed an increase in Km and a decrease in Vmax compared with APCWT (Km=238.2±4.58,Vmax=3.205±0.06). Multiple sequence alignment suggested that the three mutations be highly conservative in different species. The structural model suggested that the amino acid substitutions of N355S,G392E and T314A mutations collide with the surrounding amino acid groups,causing distortion of the surrounding structure,which may have adverse effects on the folding and biological function of PC. Conclusion:The N355S,G392E and T314A mutations in the PROC gene cause functional defects in PC by weakening the binding between PC and substrate. These three mutations have caused serious spatial collisions in the protein structure,affecting the folding of PC and the reactivity of active sites.

Objective:To investigate the impact of daily activities on cognitive function in retired elderly people in Changsha.Methods:A study was conducted on retired individuals aged 60 years or older who participated in our hospital's community free clinic from January 2021 to October 2021.A total of 325 elderly people were surveyed.After obtaining their informed consent, they were evaluated in a relatively quiet environment using the Mini-Mental State Examination(MMSE), the Athens Insomnia Scale, and a self-made questionnaire.Multifactorial logistic regression analysis was used to analyze the factors influencing cognitive function.Results:A total of 304 valid questionnaires were collected, consisting of 180 individuals in the normal cognition group and 124 in the cognitive impairment group.The cognition scores for the two groups were(25.77±2.08)and(18.86±3.74), respectively.Comparisons were made between the two groups in terms of general information, sleep conditions, and daily activities.Multifactorial regression analysis revealed that engaging in labor before retirement( OR, 2.105; 95% CI: 1.040-4.262)higher education levels( OR, 0.416; 95% CI: 0.182-0.950), maintaining contact with relatives and friends( OR, 0.205; 95% CI: 0.080-0.529), nurturing plants or pets( OR, 0.264; 95% CI: 0.124-0.563), and caring for grandchildren( OR, 0.325; 95% CI: 0.158-0.665)were identified as protective factors against cognitive impairment( P<0.05). Conclusions:Encouraging active participation of elderly individuals in beneficial community activities is crucial, while also emphasizing the importance of social relationships among retired individuals to mitigate the onset of cognitive impairment.

Objective:To investigate the effect of sertraline hydrochloride combined with compound chamomile lidocaine gel in the treatment of premature ejaculation(PE).Methods:We selected 80 cases of PE treated in our hospital from June 2021 to May 2023 and equally randomized them into a control and an observation group,the former medicated with compound chamomile lidocaine gel while the latter with sertraline hydrochloride in addition,both for 6 weeks.We recorded and compared the intravaginal ejaculation latency time(IELT),the number of successful sexual intercourses per week,the Premature Ejaculation Diagnostic Tool(PEDT)scores,and the incidence of adverse reactions between the two groups of patients.Results:After the treatment,the IELT was signif-icantly longer([5.39±1.17]vs[2.49±0.73]min,P＜0.05),the weekly number of successful sexual intercourses remarkably higher(1.82±0.45 vs 0.93±0.19,P＜0.05)and the PEDT scores markedly lower(7.42±2.04 vs 9.85±2.36,P＜0.05)in the observation than in the control group,but no statistically significant differences were observed in the baseline PEDT scores or the incidence of adverse reactions between the two groups(P＞0.05).Conclusion:Sertraline hydrochloride combined with com-pound chamomile lidocaine gel is definitely effective in the treatment of PE,which can significantly improve the patients'quality of sexual life,with a high safety and low incidence of adverse reactions.

AIM To study the chemical constituents from n-butanol fraction of Corydalis impatiens(Pall.)Fisch.and their antioxidant activities.METHODS The n-butanol fraction was isolated and purified by silica gel,MCI,ODS,Sephadex LH-20 and semi-preparative HPLC,then the structures of obtained compounds were identified by physicochemical properties and spectral data.The antioxidant activities were determined by DPPH method and tyrosinase method.RESULTS Fourteen compounds were isolated and identified as nicotinamide(1),methyl L-pyroglutamate(2),bungeanoline F(3),monomethyl fumarate(4),5-hydroxymethylfurfural(5),4-hydroxybenzoic acid(6),hydroxybenzoate(7),methyl 3,4-dihydroxybenzoate(8),methyl ferulate(9),dimethylcaffeic acid(10),dimethyl feruloyl malate(11),(-)-4-O-feruloylquinic acid(12),syringaresinol(13)and(-)-loliolide(14).Compounds 1,8,11 and 13 showed strong antioxidant activites on DPPH free radicals,with IC50 values ranging from 54.47 to 97.4 μmol/L.Compound 13 had potential inhibitory effect on tyrosinase.CONCLUSION Compounds 4-14 are first isolated from Corydalis genus,and 3 is isolated from this plant for the first time.Compounds 1,8,11 and 13 have strong antioxidant activities.

Objective To assess the safety of transeptal puncture(TSP)guided by transthoracic echocardiography(TEE)in percutaneous transcatheter closure of patent foramen ovale(PFO).Methods From March 2022 to December 2022,our department performed TSP guided by TEE in 45 patients with PFO who were unable to pass through the PFO with transcatheter standard technique.After guiding the delivery of the sheath,the foramen ovale was occluded.Results PFO closure with TSP technique guided by transthoracic echocardiography was successfully finished in all the 45 patients,with an operative time of(15.0±3.7)min.No complications such as arrhythmia or cardiac perforation happened immediately and at 12 h after surgery.All the patients recovered and were discharged on the next day after surgery.All the 45 patients were followed up by outpatient echocardiography and dynamic electrocardiogram at 3 months after surgery,and no complications such as intracardiac shunt,pericardial effusion,atrial fibrillation,aortic regurgitation,or arrhythmia were observed.Conclusion TSP guided by TEE is safe and feasible,and it can be used as a supplementary method for complex PFO.

Objective To propose a YOLOv5 lightweight network-based face mask recognition method to solve the problems due to limited storage and computation resources of edge and mobile devices.Methods A YOLOv5 model composed of a backbone network(Backbone),a neck module(Neck)and a head module(Head)was selected as the base framework.Firstly,the Backbone part was modified and replaced using the ShuffleNetv2 lightweight network;secondly,a Ghost module and a C3_S module were introduced in the Neck part;finally,a Shuffle_Yolo_GS_CBAM model was formed by incorporating a convolutional block attention module(CBAM)to improve the detection accuracy.The model was trained and verified with the AIZOO dataset,which was evaluated for face mask recognition by mean average precision(mAP),frames per second(FPS),giga floating-point operations per second(GFLOPS)and parameters.Results The model proposed recognized face masks with the mAP being 89.5％,FPS being 158.7 frames/s,parameters being 2.38 M and and GFLOPS being 4.5 GFLOPS,which had the detection speed enhanced by 39.7％,parameters decreased by 67.3％and operations reduced by73.8％when compared with the YOLOv5s model.Conclusion The method proposed behaves well in increasing detection speed,decreasing parameters and operations and ensuring detection precision,and thus is worthy promoting for face mask recognition on edge and mobile devices.[Chinese Medical Equipment Journal,2024,45(9):7-13]

Benign prostatic hyperplasia(BPH)is one of the major chronic complications of type 2 diabetes mellitus(T2DM),and sex steroid hormones are common risk factors for the occurrence of T2DM and BPH.The profiles of sex steroid hormones are simultaneously quantified by LC-MS/MS in the clinical serum of patients,including simple BPH patients,newly diagnosed T2DM patients,T2DM complicated with BPH patients and matched healthy individuals.The G protein-coupled estrogen receptor(GPER)inhibitor G15,GPER knockdown lentivirus,the YAP1 inhibitor verteporfin,YAP1 knockdown/overexpression lentivirus,targeted metabolomics analysis,and Co-IP assays are used to investigate the molecular mechanisms of the disrupted sex steroid hormones homeostasis in the pathological process of T2DM complicated with BPH.The homeostasis of sex steroid hormone is disrupted in the serum of patients,accompanying with the proliferated prostatic epithelial cells(PECs).The sex steroid hormone metabolic profiles of T2DM patients complicated with BPH have the greatest degrees of separation from those of healthy individuals.Elevated 17β-estradiol(E2)is the key contributor to the disrupted sex steroid hormone homeostasis,and is significantly positively related to the clinical characteristics of T2DM patients complicated with BPH.Activating GPER by E2 via Hippo-YAP1 signaling exacerbates high glucose(HG)-induced PECs prolifer-ation through the formation of the YAP1-TEAD4 heterodimer.Knockdown or inhibition of GPER-mediated Hippo-YAP1 signaling suppresses PECs proliferation in HG and E2 co-treated BPH-1 cells.The anti-proliferative effects of verteporfin,an inhibitor of YAP1,are blocked by YAP1 overexpression in HG and E2 co-treated BPH-1 cells.Inactivating E2/GPER/Hippo/YAP1 signaling may be effective at delaying the progression of T2DM complicated with BPH by inhibiting PECs proliferation.