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.

Sarcopenia, an age-related degenerative skeletal muscle disorder characterized by progressive loss of muscle mass, diminished strength, and impaired physical function, poses substantial challenges to global healthy aging initiatives. The pathogenesis of this condition is fundamentally rooted in mitochondrial dysfunction, manifested through defective energy metabolism, disrupted redox equilibrium, imbalanced dynamics, and compromised organelle quality control. This comprehensive review elucidates the central role of exercise-induced mitochondrial hormesis as a critical adaptive mechanism counteracting sarcopenia. Mitohormesis represents an evolutionarily conserved stress response wherein sublethal mitochondrial perturbations, particularly transient low-dose reactive oxygen species (ROS) generated during muscle contraction, activate cytoprotective signaling cascades rather than inflicting macromolecular damage. The mechanistic foundation of this process involves ROS functioning as essential signaling molecules that activate the Keap1 nuclear factor erythroid 2 related factor 2 (Nrf2) antioxidant response element pathway. This activation drives transcriptional upregulation of phase II detoxifying enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GPx), thereby enhancing cellular redox buffering capacity. Crucially, Nrf2 engages in bidirectional molecular crosstalk with peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC-1α), the principal regulator orchestrating mitochondrial biogenesis through coordinated induction of nuclear respiratory factors 1 and 2 (NRF1/2) along with mitochondrial transcription factor A (Tfam), collectively facilitating mitochondrial DNA replication and respiratory complex assembly. Concurrently, exercise-induced alterations in cellular energy status, specifically diminished ATP to AMP ratios, potently activate AMP activated protein kinase (AMPK). This energy-sensing kinase phosphorylates PGC-1α while concomitantly stimulating NAD dependent deacetylase sirtuin 1 (SIRT1) activity, which further potentiates PGC-1α function through post-translational deacetylation. The integrated AMPK/PGC-1α/SIRT1 axis coordinates mitochondrial biogenesis, optimizes network architecture through regulation of fusion proteins mitofusin 1 (Mfn1), mitofusin 2 (Mfn2) and optic atrophy protein 1 (OPA1), and enhances clearance of damaged organelles via selective activation of mitophagy receptors BCL2 interacting protein 3 (Bnip1) and FUN14 domain containing 1 (FNDC1). Exercise further stimulates the mitochondrial unfolded protein response (UPRmt), increasing molecular chaperones such as heat shock protein 60 (HSP60) and HSP10 to preserve proteostasis. Within the mitochondrial matrix, SIRT3 fine-tunes metabolic flux through deacetylation of electron transport chain components, improving phosphorylation efficiency while attenuating pathological ROS emission. Distinct exercise modalities differentially engage these pathways. Aerobic endurance training primarily activates AMPK/PGC-1α signaling and UPRmt to expand mitochondrial volume and oxidative capacity. Resistance training exploits mechanical tension to acutely stimulate mechanistic target of rapamycin complex 1 (mTORC1) mediated protein synthesis while modulating dynamin related protein 1 (Drp1) phosphorylation dynamics to support mitochondrial network reorganization. High intensity interval training generates potent metabolic oscillations that rapidly amplify AMPK/PGC-1α and Nrf2 activation, demonstrating particular efficacy in insulin-resistant phenotypes. Strategically designed concurrent training regimens synergistically integrate these adaptations. Mitochondrial-nuclear communication through tricarboxylic acid cycle metabolites and mitochondrially derived peptides such as mitochondrial open reading frame of 12s rRNA-c (MOTS-c) coordinates systemic metabolic reprogramming, with exercise-responsive myokines including fibroblast growth factor 21 (FGF-21) mediating inter-tissue signaling to reduce inflammation and enhance insulin sensitivity. This integrated framework provides the scientific foundation for precision exercise interventions targeting mitochondrial pathophysiology in sarcopenia, incorporating biomarker monitoring and exploring pharmacological potentiators including nicotinamide riboside and MOTS-c mimetics. Future investigations should delineate temporal dynamics of mitohormesis signaling and epigenetic regulation to optimize therapeutic approaches for age-related muscle decline.

Aim To investigate the effect of total glu-cosides of paeony on inflammatory injury and TLR4/NF-κB/NLRP3 pathway in autoimmune thyroiditis(AIT)rats.Methods The experiment was divided into control group,model group,total glucosides of pae-ony(TGP),TLR4 inhibitor group and TGP+TLR4 ag-onist group,with 10 animals in each group.Except for the control group,the rats in other groups were subcu-taneously injected with thyroglobulin and Freund's ad-juvant to induce the AIT rat model.After six weeks of administration,thyroid histopathological changes were observed using hematoxylin-eosin(HE)staining;ser-um levels of TPOAb,TgAb,TSH,T3,T4,TNF-α,INF-γ,IL-1 β and IL-1 β were detected by enzyme-linked immunosorbent assay(ELISA);TLR4/NF-κB/NLRP3 pathway mRNAs and proteins expression in thyroid tis-sues were detected by RT-qPCR and Western blot.Re-sults Compared with the control group,the thyroid follicular epithelium of rats was significantly damaged,and the serum levels of TPOAb,TgAb,TSH,T3,T4,TNF-α,INF-γ,IL-1 β and IL-1 β increased(P＜0.01).The expression of TLR4/NF-κB/NLRP3 path-way mRNAs and proteins increased in the model group(P＜0.01).Compared with the model group,the damage of thyroid follicular epithelium was alleviated,and the serum levels of TPOAb,TgAb,TSH,T3,T4,TNF-α,INF-γ,IL-1 β and IL-1 β were reduced(P＜0.01),the expression of TLR4/NF-κB/NLRP3 path-way mRNAs and proteins were down-regulated in the TGP group and TLR4 inhibitor group(P＜0.01).Compared with TGP group,the damage of thyroid follic-ular epithelium was aggravated,and the levels of serum TPOAb,TgAb,TSH,T3,T4,TNF-α,INF-γ,IL-1 β and IL-1 β were elevated(P＜0.05 or P＜0.01),the pro-tein expressions of TLR4/NF-κB/NLRP3 pathway mR-NAs and proteins were up-regulated in TGP+TLR4 ag-onist group(P＜0.05 or P＜0.01).Conclusions TGP may play a protective role in thyroid by inhibiting the TLR4/NF-κB/NLRP3 pathway and improving the inflammatory injury of thyroid tissues.

Objective To compare the clinical outcomes of using elastic intramedullary nail and plate to fix fibular frac-ture.Methods The 60 patients with tibiofibular fractures admitted from January 2015 to December 2022 were divided into two groups:intramedullary nail group and plate group,30 cases each,intramedullary nail group was treated with elastic in-tramedullary nail fixation group,plate group was treated with steel plate and screw fixation group.Intramedullary nail group,there were 18 males and 12 females,aged from 22 to 75 years old with an average of(39.4±9.8)years old,including 24 cases of traffic accidents injury,6 cases of falling injury,23 cases of closed fractures,7 cases of open fractures.Steel plate group,there were 15 males and 15 females,aged from 24 to 78 years old with an average of(38.6±10.2)years old.The 22 cases were injured by traffic accident,8 cases were injured by falling.The 24 cases were closed fractures and 6 cases were open fractures.The operation time,intraoperative bleeding,American Orthopedic Foot and Ankle Society(AOFAS)ankle and hind foot scores,clinical healing time of fibula and the incidence of wound complications were compared between the two groups.Re-sults The patients in both groups were followed up for 6 to 21 months,with an average of(14.0±2.8)months.Compared with plate group,intramedullary nail group had shorter operative time,less bleeding,shorter clinical healing time of fibula,and low-er infection rate of incision,and the difference was statistically significant(P＜0.05).There were 2 cases of delayed healing in intramedullary nail group,1 case of nonunion in plate group,and 2 cases of delayed healing in plate group,and there was no statistically significant difference between the two groups(P＞0.05).In the last follow-up,according to the AOFAS scoring standard,the ankle function in intramedullary nail group was excellent in 17 cases,good in 12 cases,fair in 1 case,with an av-erage of(88.33±4.57)points,while in plate group,excellent in 16 cases,good in 10 cases,fair in 4 cases,with an average of(87.00±4.14)points;There was no statistical difference between the two groups(P＞0.05).Conclusion Elastic intramedullary nail has the advantages of short operation time,less intraoperative bleeding,short fracture healing time and less incision com-plications in the treatment of fibular fracture,which is worthy of clinical application.

Objective To explore the risk factors for bile leakage after laparoscopic common bile duct exploration(LCBDE)with primary closure.Methods The clinical data of 560 patients with choledocholithiasis who underwent LCBDE with primary closure in Tianjin Hospital of Integrated Traditional Chinese and Western Medicine from September 2021 to September 2023 were retrospectively analyzed,and the patients were divided into the bile leak group and the non-bile leak group according to the occurrence of postoperative bile leakage.The risk factors affecting the occurrence of postoperative bile leakage were analyzed by multivariate analysis.Results A total of 64 cases(11.4% )experienced varying degrees of bile leakage,including 55 cases of grade A bile leakage,7 cases of grade B,and 2 cases of grade C.The thin common bile duct(OR=0.07,P<0.001),history of hypertension(OR=4.56,P<0.001),and high BMI(OR=1.17,P=0.002)were the risk factors for postoperative bile leakage in patients with choledocholithiasis.Conclusion Patients with thin common bile duct,hypertension and obesity are more likely to occur postoperative bile leakage.Patients with choledocholithiasis who have the above high-risk factors should be cautious in choosing LCBDE with primary closure.

Objective To investigate the effects of luteolin on brain injury and Toll like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)signaling pathway in rats with hypoxia-ischemia encephalopathy(HIE).Methods A total of 60 male rats were randomly divided into the normal control(NC)group,the model group,the low-dose group(25 mg/kg luteolin),the high-dose group(50 mg/kg luteolin),and the high-dose+lipopolysaccharide(LPS)group(50 mg/kg luteolin+0.5 mg/kg TLR4 agonist LPS),with 12 rats in each group.HIE model was constructed by ligation of common carotid artery and hypoxia.Neurological severity score(NSS)was used to detect the cerebral nerve function of rats in each group.Serum tumor necrosis factor-α(TNF-α)and brain-derived neurotrophic factor(BDNF)levels were detected by ELISA assay.HE staining was used to detect the pathological changes of brain tissue.The levels of malondialdehyde(MDA)and superoxide dismutase(SOD)in brain tissue of rats were detected by kit.TTC staining was used to detect cerebral infarction in rats.Western blot was used to detect the expression of TLR4,nuclear factor-kappa B(NF-κB),p-NF-κB,activated cleaved cysteine aspartate proteinase 3(Cleaved Caspase-3)protein in brain tissue.Results Compared with the model group,the NSS,levels of TNF-α and MDA,volume of cerebral infarction,and expression of TLR4,p-NF-κB/NF-κB and Cleaved Caspase-3 in low-dose group and high-dose group were decreased(P<0.05),BDNF and SOD levels were increased(P<0.05),the histopathological damage of hippocampus was obviously alleviated,the structure was gradually clear,and the number of nerve cells was normal.Compared with the high-dose group,the levels of the above indexes were inversely expressed in the high-dose+LPS group(P<0.05),and the histopathological damage in the hippocampus was aggravated.Conclusion Luteolin can improve brain injury and inhibit TLR4/NF-κB signaling pathway in HIE rats,and the inhibition of TLR4/NF-κB signaling pathway may be the mechanism of luteolin in improving brain injury.

This study was aimed at investigating the pathogenic and molecular characteristics of Klebsiella pneumoniae(KP)in fecal samples of diarrhea cases in a district of Beijing.Fecal samples from diarrhea cases in an outpatient department in a district of Beijing from 2018 to 2021 were collected,and used for isolation and culture of KP.The KP strains isolated strains were subjected to drug resistance phenotype testing and whole-genome sequencing.Multilocus sequence typing and whole-genome phyletic evolution analysis were performed on the sequencing results.The cases'epidemiological and clinical characteristics were analyzed.From 2018 to 2021,1 103 fecal samples were collected and detected.The total detection rate of KP was 10.43％(115/1 103),and the infection rate of KP mixed with other diarrhea-causing pathogens was 42.61％(49/115).The positivity rate was slightly high(12.47％,61/489)a-mong females and was highest in young adults 16-45 years of age.Small peaks were observed in January,April to May,and August to September.The gastrointestinal symptoms in cases were mainly nausea and watery stool,and the suspicious food was unknown.Ampicillin,tetracycline,and sulfafurazole were the top three antibiotics to which these 115 KP strains showed resistance,and 29 strains were resistant to multiple antibiotics.The strains were divided into 72 sequence types,among which ST23 was dominant.According to the phylogenetic tree,the strains were divided into four main branches,among which 14 ST23 strains had a very close genetic relationship with the highly virulent NTUH-K2044 reference strain.KP infection persisted in fecal samples from diarrhea cases in the district of Beijing.Women and young adults were particularly susceptible.The drug resistance of KP strains in this region was very serious,and the ST types were diverse.Moreover,the ST23 pathogenic strains were closely related to high virulence strains.

Objective:To understand the serological characteristics of irregular antibodies in pregnant women and explore their clinical significance.Methods:From January 2017 to March 2022,151 471 pregnant women in Women and Children's Hospital of Chongqing Medical University were enrolled in this study,microcolumn gel card test was used for irregular antibody screening,and antibody specificity identification was further performed in some antibody-positive subjects.Results:The positive rate of irregular antibody screening in the enrolled pregnant women was 0.91％(1 375/151 471),0.23％(355/151 471)was detected in the first trimester,0.05％(71/151 471)in the second trimester,and 0.63％(949/151 471)in the third trimester.The positive rate of irregular antibody screening in the third trimester was significantly higher than that in the first and second trimester,and a significant increase in the number of positive cases was found in the third trimester than that in the second trimester.The analysis of agglutination intensity of 1 375 irregular antibody screening positive results showed that the weakly positive agglutination intensity accounted for 50.11％(689/1 375),which was the highest,the suspicious positive was 18.69％(257/1 375),and the positive was 31.20％(429/1 375).The significant difference in distribution of agglutination intensity was not observed between the first trimester group and the second trimester group,however,in the third trimester,the proportion of suspicious positive and weakly positive was lower than the first trimester,while,the proportion of positive was higher than the first trimester,and the difference was statistically significant(P＜0.001).Among the irregular antibody screening positive pregnant women,the proportion of pregnant women with pregnancy number ≥ 2 was significantly higher than that with pregnancy≤1.Among 60 pregnant women who underwent antibody identification,the distributions of the antibodies were as follows:Rh blood group system accounted for 23.33％(14/60),Lewis system 43.33％(26/60),Kidd system 3.33％(2/60),MNS system 16.67％(10/60),P1PK system 1.67％(1/60),autoantibodies 1.67％(1/60),and 4 cases was unable to identify(6.67％,4/60).Among specific antibodies,the anti-Lea was the most common(30.00％),followed by anti-E(16.67％)and anti-M(16.67％).Conclusion:The differences of irregular antibody serological characteristics exist in pregnant women from different regions with different genetic backgrounds,understanding the characteristics of irregular antibody in local pregnant women is of great significance for ensuring transfusion safety in pregnant women and preventing hemolytic disease of newborn.

The incidence of male infertility has been increasing year by year,and one of the major causes is testicular spermato-genic epithelial injury,which affects the spermatogenic function of the testis.Ferroptosis is a novel mode of cell death and plays an im-portant role in testicular cell injury.Some traditional Chinese medicines can intervene in the progression of testicular injury by regula-ting the ferroptosis pathway in testicular spermatogenic epithelia.This paper focuses on the effect of traditional Chinese drugs in regula-ting the ferroptosis pathway in testicular cells,and summarizes the advances in the studies of traditional Chinese medicines in the treat-ment of testicular spermatogenic epithelial injury,aiming to provide a theoretical basis for the selection of relevant medicines and their clinical application.

Objective:To study the mechanism of icariin inhibiting the proliferation of human PCa PC-3 cells based on cell metabolomics technology.Methods:We determined the proliferation activity of human PC-3 cells by methyl thiazolyl tetrazolium(MTT)assay,and compared the proliferation of the PC-3 cells among the control,5-fluorouracil and icariin intervention groups.Using the Bligh Dyer method,we extracted endogenous metabolites from the cells,analyzed the metabolic profile by ultra-high pressure liquid chromatography tandem quadrupole time-of-flight mass spectrometry,identified the differential metabolites by principal component anal-ysis and orthogonal partial least-squares discrimination analysis,and enriched the metabolic pathways based on the MetaboAnalyst data-base.Results:Icariin significantly inhibited the proliferation of human PCa PC-3 cells.A total of 89 differential metabolites were i-dentified,mainly including amino acids,phosphatidylcholine,phosphatidylethanolamine,lysophosphatidylcholine,and lysophosphati-dylethanolamine,all with the tendency to return to the normal level after icariin intervention.Icariin significantly downregulated the metabolic levels of the glycerophospholipid metabolites phosphatidylcholine,phosphatidylethanolamine,lysophosphatidylcholine and ly-sophosphatidylethanolamine,and upregulated those of amino acid metabolites tryptophan,leucine,and proline in the PC-3 cells.Conclusion:Icariin inhibits the proliferation of human PCa PC-3 cells,which may be closely related to its regulatory effect on lipid metabolism(glycerophospholipid metabolism)and amino acid metabolism.