Brain maintenance(BM)refers to the process of preserving the structural and functional integrity of the brain by reducing age-related brain tissue alterations and pathological brain changes caused by genetic factors or lifestyle. This process encompasses multiple complex physiological mechanisms, including neurogenesis, regulation of cerebral microenvironment homeostasis, and neural compensation. Currently, the most widely recognized method for measuring BM is the analysis of relative structural brain changes based on longitudinal observational data. Various modifiable factors can effectively maintain a youthful brain state by slowing physiological or pathological decline and promoting neural repair processes. Studies indicate that the primary mechanism underlying preserved cognitive function in older adults lies in the relative delay of age-related brain changes. Maintaining optimal brain structure and function in older populations contri-butes to improving quality of life and alleviating family caregiving burdens. This review summarizes research progress in BM from three perspectives-measurement methods, influencing factors, and mechanisms-to provide a theoretical basis for developing intervention strategies against brain aging.

Sleep disorders and cognitive dysfunction are common comorbid conditions in modern society, with a close association in their pathological mechanisms. The phosphatidylinositol 3-kinase(PI3K)-protein kinase B(AKT)signaling pathway plays a central role in neuroprotection, metabolic regulation, and synaptic plasticity, thus being regarded as a key target for the intervention in such diseases. In recent years, studies have demonstrated that traditional Chinese medicine monomers, extracts, and their compound preparations can improve sleep and cognitive impairments by activating the PI3K/AKT pathway. On the basis of outlining the functions and regulatory mechanisms of the PI33K/AKT pathway, this paper systematically summarizes the research progress of traditional Chinese medicine monomers, extracts, and compound preparations in improving sleep disorders and cognitive impairments by regulating this signaling pathway, reveals their potential role in the treatment of comorbidities, and provides a theoretical basis for the development of combined therapies for neuropsychiatric diseases and the research and development of new Chinese medicines based on traditional medicine.

Objective To investigate the association between excessive daytime sleepiness(EDS)severity and anxiety/depression symptoms in obstructive sleep apnea(OSA)patients, and to evaluate the clinical value of EDS stratification in psychiatric risk assessment. Methods A total of 1,185 OSA patients diagnosed by polysomnography(PSG)at the Sleep Medicine Center of the Second Affiliated Hospital of Xian Jiaotong University(January 2022-December 2024)were enrolled. Participants were categorized using the Epworth Sleepiness Scale(ESS)into non-EDS and EDS groups. Psychological symptoms were assessed using the Self-Rating Anxiety Scale(SAS)and Self-Rating Depression Scale(SDS). Statistical analyses included χ2 test, Fishers exact test, Mann-Whitney U test, Pearson correlation, and multivariate logistic regression to examine relationships between EDS levels, PSG parameters, and psychiatric symptoms. Results The EDS group(n=498)showed significantly higher prevalence rates of depression(36.35% vs 27.94%, P<0.01)and anxiety(17.07% vs 8.15%, P<0.01)compared to non-EDS group(n=687). A dose-dependent relationship was observed: depression prevalence increased from 26.79%(mild), 39.45%(moderate)to 54.03%(severe EDS); anxiety rates progressed from 12.45% to 21.10% and 23.39% respectively. Multivariate regression analysis revealed that moderate EDS(OR=1.894, 95%CI: 1.170-3.067)and severe EDS(OR=3.184, 95%CI: 1.974-5.137)significantly increased depressive symptom risk. Similarly, anxiety risk increased with EDS severity(moderate: OR=2.032, 95%CI: 1.114-3.705; severe: OR=2.435, 95%CI: 1.340-4.425). Conclusion EDS severity independently predicts anxiety and depression risks in OSA patients, demonstrating clinically significant dose-response effects. Stratified EDS assessment should be incorporated into personalized therapeutic strategies for comprehensive OSA management.

Objective To explore the causal relationship between obstructive sleep apnea(OSA)and depression and to find potential targets for the treatment of OSA with depression from the targets of antidepressant drugs. Methods Data on genetic variants associated with depression and OSA were obtained from genome-wide association studies(GWAS). The coding gene data of antidepressant drug targets were obtained from eQTLGen Consortium website. TSMR analysis was performed with depression and antidepressant drug targets as exposure and OSA as outcome. Single nucleotide polymorphisms(SNPS)strongly associated with exposure variables were used as instrumental variables, and inverse-variance weighted(IVW)was used as the main analysis method while MR-Egger, weighted median(WME), simple mode(SM)and weighted mode(WM)were used as supplementary evidence for TSMR analysis. Sensitivity analysis was performed with MR-PRESSO and leave-one-out method, excluding each instrumental variable to observe its influence on the overall estimation. Cochrans Q test and MR-Egger intercept test were used to determine heterogeneity and horizontal pleiotropy. Funnel plot was used to assess potential bias. Results IVW analysis showed that there was a causal relationship between genetic prediction of depression and increased risk of OSA(OR=1.180, 95%CI=1.065-1.306, P=0.001). Cochrans Q test and MR-Egger intercept test showed no heterogeneity and horizontal pleiotropy. MR-PRESSO test and leave-one-out test indicated that the effect of excluding any SNP on causality was not significant, and the funnel plot showed that the left and right distribution was roughly uniform. The expression of antidepressant drug targets HTR3A(OR=1.174,95%CI= 1.022-1.350,P=0.024)and GRIN3A(OR=1.227,95%CI= 1.126-1.338,P<0.001)had a causal relationship with increased risk of OSA. Conclusion Depression can increase the risk of OSA, and the antidepressant drug targets HTR3A and GRIN3A may be candidate drug targets for the treatment of depression with OSA.

Objective To explore the relationship between serum levels of thyroxine(T₄), triiodothyronine(T₃), cortisol(Cor), and the insight of patients with bipolar disorder(BD), and to analyze their predictive value for aggressive behavior in patients. Methods A total of 184 BD patients admitted to Jiangxi Mental Hospital from June 2021 to June 2024 were selected and divided into an aggressive behavior group(71 cases)and a non-aggressive behavior group(113 cases)based on the presence or absence of aggressive behavior. Additionally, 70 healthy individuals were selected as a control group during the same period. Serum levels of T₄, T₃, and Cor were measured. The insight and treatment attitudes questionnaires(ITAQ)were used to assess the patients insight. Pearson correlation analysis was used to analyze the correlation between serum levels of T₄, T₃, Cor, and insight in BD patients. Logistic regression analysis was used to analyze the risk factors for aggressive behavior in BD patients. The predictive value of serum T₄, T₃, and Cor levels for aggressive behavior in BD patients was analyzed by receiver operating characteristic(ROC)curves. Results The serum levels of T₄, T₃, and Cor in the aggressive behavior group were higher than those in the non-aggressive behavior group, and the ITAQ score was lower than that in the non-aggressive behavior group, with statistically significant differences(P<0.05). Serum levels of T₄, T₃, and Cor in BD patients were negatively correlated with insight(r=-0.443, -0.364, -0.461, P<0.001). Serum T₄(OR=1.192, 95%CI=1.052-1.352), T₃(OR=1.177, 95%CI=1.036-1.337), Cor levels(OR=1.196, 95%CI=1.059-1.351), marital status(OR=1.175, 95%CI=1.010-1.366), and stress events(OR=1.183, 95%CI=1.043-1.341)were risk factors for aggressive behavior in BD patients, and ITAQ score(OR=0.781, 95%CI=0.663-0.921)was negatively correlated with the risk of aggressive behavior(P<0.05). The AUCs of serum T₄ and Cor levels for predicting aggressive behavior were 0.755 and 0.725, respectively. Conclusion Serum levels of T₄, T₃, and Cor are negatively correlated with the insight of BD patients, and serum levels of T₄ and Cor have certain predictive value for aggressive behavior in BD patients.

Objective To explore the effects of intraperitoneal epigallocatechin-3-gallate(EGCG)on cerebellar Purkinje cell morphology and autism-like behaviors in valproic acid-induced autistic offspring mice. Methods A valproic acid(VPA)-induced mouse model of autism spectrum disorder(ASD)was established. Following intraperitoneal injection of epigallocatechin-3-gallate(EGCG), hematoxylin and eosin(H&E)staining and immunofluorescence were performed to evaluate the effects of EGCG on VPA-induced pathological changes in cerebellar Purkinje cells. Behavioral tests including the three-chamber social interaction test, open field test, elevated plus maze test, novel object recognition test, and Morris water maze test were performed to assess differences in social behavior, spontaneous locomotor activity, anxiety-like behaviors, and learning/memory performance among control mice, VPA-exposed mice, and VPA+ EGCG-treated mice. Results H&E staining and immunofluorescence analyses revealed that intraperitoneal administration of EGCG reversed VPA-induced reductions in cerebellar Purkinje cell density and ameliorated pathological alterations in offspring ASD model mice. In the three-chamber social test, EGCG administration improved social preference deficits and restored novelty-induced social interaction in VPA-exposed mice. Behavioral assessments further demonstrated that EGCG significantly reduced hyperactivity in novel environments(open field test)and alleviated anxiety-like behaviors(elevated plus maze test)in VPA-induced offspring. Additionally, EGCG enhanced novel object recognition memory in the novel object recognition test and mitigated spatial learning and memory impairments in the Morris water maze. Conclusion EGCG treatment ameliorates the VPA-induced reduction in the number of cerebellar Purkinje cells and the associated pathological changes in the cerebellum of offspring autistic mice, resulting in an improvement in ASD-like behavioral abnormalities.

Objective To explore the mediating roles of childrens difficulties and prosocial behaviour in the relationship between family resilience and grandparenting stress. Methods A total of 247 grandparents involved in co-parenting were surveyed using the Family Resilience Assessment Scale, the Grandparenting Stress Scale, and the Strengths and Difficulties Questionnaire(parental version). Structural equation modeling was conducted using AMOS 24.0, and the Bootstrap method was employed to test the mediating effects. Results Family resilience was negatively correlated with both grandparenting stress and childrens difficulties(r=-0.22, r=-0.26; both P<0.01), and positively correlated with childrens prosocial behaviour(r=0.16, P<0.05). Childrens difficulties were positively correlated with grandparenting stress(r=0.39, P<0.01), whereas childrens prosocial behaviour was negatively correlated with grandparenting stress(r=-0.32, P<0.01). Childrens difficulties mediated the relationship between family resilience and grandparenting stress, with a mediation effect of -0.668, accounting for 48.94% of the total effect. Childrens prosocial behavior partially mediated the relationship between family resilience and grandparenting stress, with a mediation effect of -0.268, accounting for 19.43% of the total effect. Conclusion Family resilience can directly reduce grandparenting stress, and also indirectly alleviate it by decreasing childrens difficulties and enhancing childrens prosocial behaviour.

Objective To investigate the expression characteristics, subcellular localization of glutathione peroxidase-1(GPX1)in different pathological types of lung cancer cell lines and the influence on the biological functions of lung adenocarcinoma cell lines. Methods The expressions of GPX1 at mRNA and protein levels in normal lung epithelial cells HPAEpic, lung adenocarcinoma cell line A549 and H292, lung squamous cell carcinoma cell line Calu1, large cell lung cancer cell line 95D, and small cell lung cancer cell line H446 were detected by quantitative real-time PCR and Western blotting, respectively. The expression differences of GPX1 between different pathological types of lung cancer cell lines and normal lung epithelial cells were compared through analysis of variance. The subcellular localization of GPX1 in lung adenocarcinoma cell lines was clarified by immunofluorescence staining. The lung adenocarcinoma cell lines H292 and A549 GPX1 stably knocked down cell strains were constructed, and the knockdown efficiency was verified at mRNA and protein levels, respectively. The proliferation, migration, invasion abilities and apoptosis of H292 and A549 cell strains were detected by CCK-8 assay, wound healing assay, Transwell assay and flow cytometry, respectively. Results The quantitative real-time PCR results showed that the expression of GPX1 was upregulated in lung adenocarcinoma cell line H292 compared with the normal lung epithelial cells HPAEpic(P=0.006). The results of Western blotting showed that compared with the normal lung epithelial cells HPAEpic, expression of GPX1 was upregulated in multiple lung cancer cell lines(A549, H292, Calu1, 95D, and H446)(P<0.001). The results of CCK-8, wound healing assay, Transwell assay and flow cytometry showed that after knockdown of GPX1, the proliferation(P<0.001), migration(P<0.001, P=0.002)and invasion abilities(P=0.039, P=0.014)of H292 and A549 cell strains were all weakened, while apoptosis rate increased(P=0.008, P=0.040). Conclusion The expression of GPX1 is highly upregulated in various pathological types of lung cancer cell lines, and its expression level is the highest among lung adenocarcinoma cell lines. GPX1 is mainly located in cytoplasm. Down-regulation of GPX1 expression can significantly inhibit the proliferation, migration and invasion abilities of A549 and H292 lung adenocarcinoma cell strains, and promote cell apoptosis.

Objective To identify the common asthma genes involved in autophagy and ferroptosis processes using bioinformatics analysis methods. Methods The asthma-related GSE74986 dataset were obtained from the Gene Expre-ssion Omnibus(GEO)database and analyzed using the GEO2R web tool. The differentially expressed genes(DEGs)were screened by setting the criteria of |log₂ FC| ≥ 1 and a corrected P-value <0.05. Ferroptosis- and autophagy-related DEGs were intersected with Venn diagrams. Hub genes were further identified with functional and pathway enrichment analysis, protein-protein interaction network analysis, and algorithms in Cytoscape software, followed by the construction of a transcription factor-miRNA-hub gene interaction network. Hub genes were subjected to immune cell infiltration analysis in asthmatic patients. In addition, the diagnostic value of hub genes was assessed with receiver opera-ting characteristic(ROC)curves analyses. Animal experiments were conducted to validate hub genes. Results A total of 105 autophagy-related DEGs and 37 ferroptosis-related DEGs were identified, which were involved in autophagy-animal, PI3K-Akt pathway, ferroptosis, and PPAR pathway. Ten hub genes were yielded, including HSPA8, NPM1, HNRNPA2B1, HNRNPA1, HSPA5, EEF1A1, G3BP1, TFRC, GABARAPL1, and XBP1 targeting a total of 61 miRNAs and 17 TFs. Immune cell infiltration analysis showed that these hub genes were closely related to macrophages M0, activated NK cells, and macrophages M1. ROC curve analyses indicated the high diagnostic value of the hub genes for asthma. Animal experiments confirmed that the protein expression levels of HSPA8, NPM1, HNRNPA2B1, HNRNPA1, and HSPA5 in the lung tissue of the model group were significantly lower than those in the normal group. Conclusion The screened hub genes,including HSPA8, NPM1, HNRNPA2B1, HNRNPA1, HSPA5, EEF1A1, G3BP1, TFRC, GABARAPL1, and XBP1, may be potential therapeutic targets for asthma.

Objective To investigate how cigarette smoke accelerates skin aging by focusing on the interaction between the anti-aging protein Klotho and the tobacco-associated receptor CHRNA5, and explore potential targets for skin rejuvenation strategies. Methods HaCaT cells were treated with CSE(cigarette smoke extract). Cellular senescence and the expression of CHRNA5 and Klotho proteins were assessed by β-galactosidase staining and Western blotting. Subsequently, skin samples from mice aged 3-5, 6-7, and 14 months were analyzed using H&E staining, immunohistochemistry, Western blotting, and RT-qPCR to determine age-dependent changes in CHRNA5, Klotho and senescence-associated markers. Furthermore, in Klotho-knockdown mice, we assessed the efficiency of Klotho silencing and the effects of Klotho on both CHRNA5 expression and senescence markers using immunohistochemistry, Western blotting and RT-qPCR. Finally, HaCaT cells were transfected with siRNAs targeting Klotho or CHRNA5, and the expression of both genes and related senescence markers was measured by Western blotting and RT-qPCR to verify their regulatory relationship. Results CSE exposure induced senescence in HaCaT cells, as evidenced by a significant increase in β-galactosidase-positive cells(P=0.000 4), accompanied by the upregulation of CHRNA5(P=0.000 2)and the downregulation of Klotho(P=0.002 5). In 14-month-old mice, compared with 3-5-month-old controls, the epidermis was thinner(P<0.000 1), CHRNA5 was elevated(P=0.000 9), and Klotho was markedly decreased(P=0.000 1). In Klotho-knockdown mice, accelerated skin aging phenotypes were observed along with increased CHRNA5 expression(P=0.010 7). Similarly, Klotho-knockdown HaCaT cells exhibited enhanced senescence markers and elevated CHRNA5 expression(P=0.034 7). In contrast, CHRNA5 knockdown significantly reduced the expression of senescence-associated markers p16 and p21 in HaCaT cells(P=0.002 3; P=0.005 4). Conclusion CSE downregulates Klotho and upregulates CHRNA5, thereby promoting keratinocyte senescence andaccelerating skin aging.

Objective To explore the mechanism of Suanzaoren-Yuanzhi drug pair in the treatment of breast cancer related insomnia(BCRI)based on network pharmacology and animal experiments. Methods The core targets of Suanzaoren-Yuanzhi drug pair for treating BCRI were screened through TCMSP database, HERB database, and DisGeNET database. The STRING database was applied to construct an interaction network diagram of the core target proteins for the treatment of BCRI with Suanzaoren-Yuanzhi drug pair. The core targets were subjected to GO and KEGG enrichment analysis through the Metascape platform. Sixty mice were divided into control group, BCRI group, Suanzaoren-Yuanzhi drug pair group, diazepam group, Suanzaoren-Yuanzhi drug pair+LY294002(PI3K inhibitor)group, with 12 mice in each group. The control group mice were only used to establish a breast cancer model, without undergoing chronic unpredictable stress or intraperitoneal injection of cyclophosphamide. In other groups, the BCRI models were established using the method of breast cancer modeling + chronic unpredictable stress + intraperitoneal injection of cyclophosphamide. After successful modeling, administration was performed once daily for 7 consecutive days. The latency and duration of sleep in mice were detected. HE staining was used to detect hypothalamic pathology. ELISA was used to detect the levels of 4-aminobutyric acid(GABA)and 5-hydroxytryptamine(5-HT)in the hypotha-lamus. QRT-PCR was used to detect the mRNA expressions of brain and muscle arnt-like 1(BMAL1)and circadian locomotor output cycles kaput(CLOCK)in the hypothalamus. The phosphorylated phosphatidylinositol 3-kinase(p-PI3K)and phosphorylated protein kinase B(p-AKT)proteins in the hypothalamus were detected. Results The core targets for the treatment of BCRI using Suanzaoren-Yuanzhi drug pair were AKT1, TP53, TNF, ALB, HIF1A, STAT3, ESR1, BCL2, HSP90AA1, CASP3, PPARG, HSP90AB1, MAPK3, TGFB1, MMP9, MTOR, and CCND1. GO enrichment analysis for the aforementioned 17 core targets revealed that the cellular component(CC)of Suanzaoren-Yuanzhi drug pair for treating BCRI comprised 23 entries, the molecular function(MF)comprised 47 entries, and the biological process(BP)comprised 211 entries. KEGG enrichment analysis identified 116 pathways, predicting that the PI3K/AKT signaling pathway might be a crucial mechanism for Suanzaoren-Yuanzhi drug pair in the treatment of BCRI. Animal experiments indicated that, compared with the control group, the pathological damage to the hypothalamus of mice in the BCRI group was severe, the sleep latency extended, the duration of sleep decreased, the levels of GABA and 5-HT decreased, the expressions of BMAL1 and CLOCK mRNA, and p-PI3K and p-AKT proteins in the hypothalamus were reduced(all P<0.05). Compared with the BCRI group, the pathological damage to the hypothalamus of mice in the Suanzaoren-Yuanzhi drug pair group and diazepam group was reduced, the sleep latency shor-tened, the duration of sleep increased, the levels of GABA and 5-HT incresed, the expressions of BMAL1 and CLOCK mRNA, and p-PI3K and p-AKT proteins in the hypothalamus were elevated(all P<0.05). LY294002 reversed the effects of Suanzaoren-Yuanzhi drug pair on hypothalamus pathology, neurotransmitter and circadian rhythm in BCRI mice. Conclusion Suanzaoren-Yuanzhi drug pair can improve the hypothalamic pathology of BCRI mice, promote neurotransmitter balance, restore circadian rhythm, and improve sleep. Its mechanism of action may be related to the regulation of the PI3K/AKT pathway.

Objective To explore the learning curve and clinical efficacy of modified single-port axillary approach non-liposuction endoscopic gland excision for the treatment of gynecomastia. Methods Clinical data from 68 gynecomastia patients who underwent modified single-port axillary non-liposuction endoscopic gland excision were retrospectively reviewed. All procedures were performed between March 2023 and February 2025. Parameters recorded included unila-teral incision length, operative time, intraoperative blood loss, postoperative drainage duration, postoperative drainage volume, surgical complications, and patient satisfaction. The cumulative sum method was used to plot the learning curve. Differences in related indicators between the growth level group and the master level group were compared. Results All 123 breasts in 68 patients underwent successful surgery. The median unilateral incision length was 5 cm(range: 4-6 cm). The unilateral operative time was(96.46±21.81)min(range: 50-135 min). The median unilateral intraoperative blood loss was 25 mL(range: 5-75 mL). The median unilateral postoperative drainage duration was 7 days(range: 4-12 days). The median unilateral postoperative drainage volume was 216.5 mL(range: 52.0-450.0 mL). All postoperative incisions achieved grade A healing without complications such as infection, fat liquefaction, or nipple and skin necrosis. Ischemic changes of the nipple were noted in 2 patients, subcutaneous hemorrhage occurred in 3 patients, and subcutaneous seroma developed in 5 patients. Patient satisfaction at 3 months postoperatively was 91.2%(62/68). The learning curve was constructed by plotting the cumulative sum analysis of operative times. The inflection point of the curve, which corresponded to 32 cases, was used as the threshold to define two distinct periods: the growth level group(patient IDs: 1-32)and the master level group(patient IDs: 33-68). During the growth level group, the mean unilateral operative time was(106.27±19.36)min(range: 65-135 min)and the median unilateral postoperative drainage duration was 8.25 days(range: 4.50-12.00 days). During the master level group the unilateral operative time was(87.75±20.32)min(range: 50-127.50 min)and the median unilateral postoperative drainage duration was 7 days(range: 4-11.50 days). Statistically significant differences between the two groups were observed in unilateral operative time and postoperative drainage duration(P<0.05). No statistically significant differences were found between the groups regarding age, BMI, incision length, unilateral intraoperative blood loss, unilateral postoperative drainage volume, or complication rates(P>0.05). Conclusion The modified single-port axillary approach non-liposuction endoscopic subcutaneous gland excision is safe and feasible, and the surgeon requires a learning curve of 32 cases to achieve proficiency. This surgical approach significantly reduces operative time, minimizes visible scarring, and is associated with a low rate of postoperative complications while offering superior cosmetic outcomes.

Objective To investigate the epidemiological characteristics and influencing factors of hand, foot and mouth disease(HFMD)at the county level in Binzhou City, Shandong Province, in order to provide a scientific basis for health administrative departments in developing prevention and control strategies. Methods A total of 24,147 reported cases of HFMD in Binzhou City, Shandong Province, were collected from January 1,2015 to December 31,2019, along with meteorological, pollutant and socio-economic data. The temporal, spatial and population distribution characteristics of HFMD were described. Spatial clustering was assessed using the global Morans I index. Bayesian spatio-temporal model was used to identify influencing factors associated with HFMD incidence. Results HFMD incidence in Binzhou City showed a fluctuating downward trend from 2015 to 2019, with an average annual reported incidence rate of 122.57/100,000. The incidence exhibited distinct seasonality characterized by a primary peak from May to July and a secondary autumn peak. Spatial autocorrelation analysis revealed a distinct pattern of incidence, with the central region exhibiting the highest rates and the northern area the lowest. The population distribution showed that the sex ratio was 1.55:1, with HFMD cases was mainly concentrated in children aged 1-3 years, while the number of cases among scattered children was higher than that among kiudergarten children. Bayesian spatio-temporal modeling identified positive associations for mean temperature(RR=1.146; 95%CI: 1.102-1.193)and gross domestic product(GDP)(RR=1.001; 95%CI: 1.000-1.003), and a negative association for mean wind speed(RR=0.593; 95%CI: 0.360-0.976). Temperature had a stronger effect on 0-2 years old, and wind speed had a stronger effect on 0-2 years old and males. Conclusion The incidence of HFMD in Binzhou City shows a fluctuating downward trend, with distinct spatial clustering. High temperature and low wind speed are risk factors for HFMD occurrence, with high GDP levels showing a positive correlation with its incidence. It is recommended that health departments enhance monitoring in high-risk areas and vulnerable populations during seasonal epidemic peaks and periods of high temperature, and optimize the allocation of medical resources to reduce the risk of transmission.

Objective To explore the clinical characteristics, diagnostic difficulties, and treatment strategies of a case of Q fever with fever of unknown origin as the main manifestation, which was complicated by an infection following the implantation of a thoracoabdominal aortic aneurysm stent. Methods Anti-infective treatments involving ceftriaxone, ornidazole, moxifloxacin, meropenem, daptomycin, etc., were administered successively. Q fever was confirmed when Coxiella burnetii(7 sequences)was detected by blood metagenomic next-generation sequencing(mNGS). During this period, SARS-CoV-2 infection was diagnosed in the patient(positive nucleic acid test on 29 May 2025). After confirmation, the treatment was adjusted to triple therapy with piperacillin-tazobactam(4.5 g q8h)combined with levofloxacin(0.5 g qd)and minocycline(100 mg q12h), alongside thoracic drainage and supportive and symptomatic treatment. Results After the triple anti-infective therapy, the patients body temperature returned to normal, but the thoracic drainage fluid remained bloody. Anti-infective therapy was continued with minocycline(100 mg q12h)combined with levofloxacin(0.5 g qd), and body temperature remained normal without any recurrence of fever. Conclusion For patients with a long-term fever and coagulopathy after the implantation of a vascular device, rare pathogens such as C. burnetii should be considered even in the absence of typical epidemiological exposure. mNGS is crucial for identifying the pathogen. Multidisciplinary management, which combining antimicrobial therapy with surgical intervention, is often essential to cure biofilm-associated infections.