OBJECTIVE To investigate the role of clinical pharmacists in the individualized treatment of a rare case of diffuse pulmonary microabscesses caused by Streptococcus constellatus complicated with organizing pneumonia （OP） in a non-immunocompromised patient. METHODS For a middle-aged， non-immunocompromised patient with a one-year disease course， whose imaging findings showed the coexistence of diffuse microabscesses and OP caused by S. constellatus pulmonary abscess， the clinical pharmacist， based on pharmacokinetics/pharmacodynamics characteristics， assisted the physician in optimizing the previously ineffective anti-infective regimen to Ceftriaxone sodium for injection combined with Metronidazole and sodium chloride injection， so as to enhance coverage of mixed anaerobes and lesion penetration. After the patient’s hemoptysis ceased， the clinical pharmacist recommended timely initiation of low-dose Methylprednisolone sodium succinate for injection to manage OP. Upon discharge， sequential oral therapy with Linezolid tablets， Metronidazole tablets， Methylprednisolone tablets and Omeprazole enteric-coated tablets was prescribed. RESULTS After implementation of the individualized treatment regimen， the patient’s hemoptysis resolved， pulmonary lesions significantly regressed， and the patient was discharged in a stable condition. At the three-month follow-up， the patient remained stable. CONCLUSIONS For chronic persistent pulmonary infection complicated with OP in a non-immunocompromised host， clinical pharmacists assist clinicians in optimizing anti-infective regimens and recommend the timely initiation of anti-inflammatory therapy after infection control， thereby contributing to favorable clinical outcomes. Individualized treatment of such complex cases requires comprehensive consideration of pathogen coverage， pathological barriers， and the timing of anti-inflammatory intervention.

With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

Organophosphorus pesticide(OP)is one of the most widely used pesticides in the world with the largest dosage.Acute organophosphorus pesticide poisoning(AOPP)is a common clinical disease,and AOPP accounts for 20%-50%of poisoning cases in China every year,with case fatality rate of 3%-40%.Bromophos(BDF)is a long-acting anticoagulant rodenticide,which inhibits vitamin K epoxide reductase and interferes with the synthesis of coagulation factorsⅡ,Ⅶ,Ⅸ and Ⅹ,leading to coagulation dysfunction.This article discusses the multidisciplinary diagnosis and treatment(MDT)process of a patient with combined poisoning of dichlorvos and bromadiolone.The article explores blood purification,management of coagulation abnormalities,secondary infection,atropinization and altered consciousnes in patients with organophosphorus poisoning and anticoagulant rodenticide compound poisoning,with the aim of providing clinicians with references for early diagnosis and treatment.

Objective To observe the clinical and echocardiographic manifestations of Williams syndrome(WS).Methods Two children with WS were retrospectively enrolled,and 21 cases of WS in literature were reviewed,and clinical and echocardiographic manifestations of WS were observed.Results Clinical manifestations of 23 cases including 21 cases of"elf"face,8 cases of intellectual disability,7 cases of developmental delay,7 cases of inguinal hernia,6 cases of hypothyroidism,4 cases of hypercalcemia,3 cases of urinary system abnormalities(1 case of hydrocele,1 case of ureteral dilation and tortuosity,and 1 case of kidney stones),2 cases of behavioral abnormalities,2 cases of feeding difficulties,1 case of congenital hypertrophic pyloric stenosis,1 case of binocular esotropia,1 case of hyperbilirubinemia,and 1 case of corpus callosum dysplasia.Echocardiography showed cardiovascular malformations in all 23 cases,including 20 cases of supravalvular aortic stenosis(SVAS),18 cases of pulmonary artery stenosis(PAS)and 10 cases of other cardiovascular malformations.Conclusion WS presented multiple system abnormalities in clinic,and cardiovascular malformations,especially SVAS and PAS could often be detected with echocardiography.

Objective:To analyze the genetic characteristics of the prevalent strains of Varicella-Zoster virus (VZV) in the population of Dali, Yunnan, and to understand its evolutionary status in the population of Dali.Methods:Herpes fluid and 163 sera were collected from 249 patients clinically suspected to have varicella or herpes zoster in the Department of Dermatology of the Second People′s Hospital of Dali city, Yunnan province, China, from 2023 to 2024. The levels of VZV-specific IgG and IgM antibodies in serum were detected using enzyme-linked immunoassay. Viral DNA was extracted from the herpes fluid, and the cycle threshold ( Ct) of the samples was detected using quantitative real-time polymerase chain reaction (qPCR), and some samples with Ct ≦ 22 were selected for sequencing by next-generation sequencing technology (next-generation sequencing). Next-generation sequencing (NGS) was used to obtain 90 whole genome sequences of VZV, and the sequencing result were compared with the sequences of reference strains for multiple sequence comparison and evolutionary analysis. Snapgene was used to translate the nucleotides into amino acids, and the result were compared with the amino acid sequences of the reference strain. Results:Of the 90 VZV whole-genome sequences, one whole-genome sequence was from an adult varicella patient, and the remaining 89 whole-genome sequences were from herpes zoster patients. The serum-specific IgG antibody positivity rate was 99.4%, and the IgM antibody positivity rate was 52.8%. The result of both single nucleotide polymorphism (SNPs) site typing and genome-wide phylogenetic tree analysis showed that 83 of the 90 VZV whole-genome sequences in this study were on the same branch as Clade 2, and 7 VZV whole-genome sequences were on the branch of Clade 9.Conclusions:The main endemic branch in Dali region in 2023-2024 was Clade 2, with the emergence of Clade 9 branch; there were amino acid mutations in the proteins encoded by ORF22 and ORF68 in 83 VZV whole genome sequences of Clade 2 branch, and the mutations did not cause significant changes to the protein structure.

Objective:To investigate the clinical characteristics and independent risk factors of severe disease in patients with anti-nuclear matrix protein (NXP) 2 antibody-positive juvenile dermatomyositis (JDM).Methods:A retrospective cohort study was conducted, including 219 anti-NXP2 antibody-positive JDM patients admitted to 23 children′s hospitals across China from July 2011 to July 2023. Patients were classified into severe and non-severe groups based on classification criteria for severe dermatomyositis. Demographic characteristics, clinical manifestations, and laboratory parameters were compared between the 2 groups using independent sample t-test, Mann-Whitney U test, or χ2 test. Univariate and multivariate Logistic regression analyses were performed to identify risk factors for severe disease. The receiver operating characteristic curve was employed to calculate optimal cut-off values. Results:Among the 219 patients, 108 were male and 111 were female, with an age at onset of 6.3 (3.5, 9.4) years. The severe group comprised 69 patients, and the non-severe group 150 patients. The severe group had significantly higher rates of fever, heliotrope rash, subcutaneous edema, periorbital edema, anti-Ro52 antibody positivity, as well as elevated levels of ferritin-to-albumin ratio (FAR), creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) (all P<0.05). Multivariate analysis identified anti-Ro52 antibody positivity ( OR=13.26, 95% CI 1.37-128.29) and elevated FAR ( OR=1.90, 95% CI 1.09-2.31) as independent risk factors for severe anti-NXP2 antibody-positive JDM (both P<0.05). Receiver operating characteristic curve analysis revealed that a FAR cutoff value of 6.82 predicted severe disease with an area under the curve of 0.87 (95% CI 0.81-0.94, P<0.001), sensitivity of 0.85, and specificity of 0.70. All patients received glucocorticoid therapy, and the severe group received higher proportions of steroid pulse therapy, cyclophosphamide, mycophenolate mofetil, intravenous immunoglobulin, biologics, and adjuvant treatments compared to the non-severe group (all P<0.05). In terms of outcomes, 2 patients (2.9%) in the severe group died (due to neurological involvement and intestinal perforation, respectively), while the remaining patients achieved complete clinical response or remission. All patients in the non-severe group achieved remission. Conclusions:The primary clinical features of anti-NXP2 antibody-positive JDM included fever, heliotrope rash, subcutaneous edema, periorbital edema, anti-Ro52 antibody positivity, and elevated levels of CK, AST, LDH, and FAR. Furthermore, anti-Ro52 antibody positivity and a FAR>6.82 were identified as independent risk factors.

Objectives:Comparative analysis of the beagles acute-phase electrocardiographic,hemodynamic,left ventricular flow field status,and energy consumption characteristics of pacing at different sites of conduction system may help to elucidate the scientific mechanism of left bundle branch pacing(LBBP)as a option of physiological pacing therapy.Methods:Eight healthy adult beagles were used in this study.Initially,an active fixation lead was implanted in the right atrial appendage,followed by implantation of another active fixation lead at the right ventricular apex,distal His bundle,and left bundle septal branch,respectively.After connecting a dual-chamber pacemaker,electrocardiographic and acute phase hemodynamic parameters under sinus rhythm,right ventricular apex pacing(RVAP),distal His bundle pacing(DHBP),and LBBP states were collected and analyzed.Three complete cardiac cycles of standard apical three-chamber color Doppler dynamic images were acquired under vector flow mapping(VFM)mode.Offline analysis was performed on obtained parameters including isovolumic contraction period,rapid ejection period,isovolumic relaxation period,rapid filling period,atrial contraction period,and left ventricular intracavitary energy consumption.These parameters were compared under pacing at different sites and the linear correlations of major parameters were analyzed.Results:The QRS duration of baseline intrinsic sinus rhythm,RVAP,DHBP and LBBP were(45.0±4.0)ms,(98.4±6.2)ms,(50.0±4.5)ms and(62.0±4.7)ms,respectively.The LBBP-QRS duration was significantly wider than intrinsic sinus rhythm and DHBP,but significantly narrower than RVAP(all P<0.01).Compared with baseline AOO mode(the pacing rate was performed at 10 beats/min above the intrinsic heart rate),the change of acute phase maximum left ventricular pressure rise rate(LVdP/dtmax)in RVAP,DHBP and LBBP was([-7.89±5.67]% ),([0.74±2.05]% )and([-0.14±3.59]% ),respectively.There was no significant difference in LVdP/dtmax changes between DHBP and LBBP(P=0.667),but both pacing modalities were significantly better than RVAP(all P<0.01).The average energy consumption of the left ventricle under RVAP was significantly higher than that of intrinsic sinus rhythm,DHBP,and LBBP in isovolumic contraction period,rapid ejection period,isovolumic relaxation period,rapid filling period,and atrial contraction period(all P<0.01).However,there was no statistically significant difference in energy consumption among intrinsic sinus rhythm,DHBP,and LBBP during the above five phases(all P>0.05).DHBP and LBBP did not show a significant increase in the number of left ventricular vortices,vortex area,and circulation intensity compared to intrinsic sinus rhythm,and LBBP did not show a significant increase in vortex area and circulation intensity compared to DHBP.Conclusions:Although LBBP canines significantly prolonged the paced QRS duration,it showed no significant differences in acute phase left ventricular hemodynamics,left ventricular flow field status,and energy consumption compared to intrinsic sinus rhythm and DHBP.Performance of LBBP was superior to RVAP.This study may contribute to revealing the theoretical basis of LBBP as a feasible physiological pacing therapy.

Objective:To analyze the etiological characteristics, serotype distribution, drug resistance and molecular typing characteristics based on data collected by active surveillance of foodborne diseases in Shanxi Province from 2021 to 2022.Methods:Fecal and anal swabs for foodborne disease tests were collected from 17 sentinel hospitals in Shanxi Province from 2021 to 2022. The pathogens included Shigella, Salmonella, Vibrio parahaemolyticus and 5 types of diarrheagenic Escherichia coli ( E. coli). The positive strains were identified by mass spectrometry or systematic biochemistry. Salmonella and Shigella were serotyped by slide agglutination, and diarrheagenic E. coli was typed by multiplex fluorescence PCR. Vibrio parahaemolyticus was tested for tlh/ tdh/ trh virulence genes by multiplex fluorescent PCR. All strains were also tested for drug resistance by the microbroth dilution method. Molecular typing was performed by pulsed-field gel electrophoresis (PFGE). Results:A total of 4 481 samples were collected from patients with diarrhea, and 555 target strains were detected, with a detection rate of 12.39%(555/4 481). Among them, there were 365 strains of Salmonella, 175 strains of diarrheagenic E. coli, 15 strains of Vibrio parahaemolyticus, and no Shigella. There were 32 serotypes of Salmonella, and the dominant serotypes were 158 strains of Salmonella senteritidis and 124 strains of Salmonella typhimurium. diarrheagenic E. coli classification: 79 strains of enteroaggregative E. coli, 72 strains of enteropathogenic E. coli, 23 strains of enterotoxic E. coli, 1 strain of enterohemorrhagic E. coli, and none of enteroinvasive E. coli. For Vibrio parahaemolyticus virulence gene carriage, all strains carried tlh; 11 strains (73.33%, 11/15) carried tdh only; 2 strains (13.33%, 2/15) carried trh; 1 strain (6.67%, 1/15) carried both tdh and trh genes; 1 strain (6.67%, 1/15) did not carry these two virulence genes. Antimicrobial resistance tests presented that Salmonella had the highest resistance rate to ampicillin (85.21%, 311/365), followed by naphridic acid (66.58%, 243/365), and multi-drug resistance (78.63%, 287/365), resulting in 135 drug resistance spectrums. The resistance rate of diarrheagenic E. coli to ampicillin was the highest (81.71%, 143/175), followed by tetracycline (67.43%, 118/175), and multi-drug resistance (72.57%, 127/175), resulting in 81 drug resistance spectrums. Vibrio parahaemolyticus had the highest resistance rate to cefazolin (93.33%, 14/15), followed by tetracycline (26.67%, 4/15) and multi-drug resistance (20.00%, 3/15), resulting in 3 drug resistance spectrums. A total of 158 strains of Salmonella enteritidi, 124 strains of Salmonella typhimurium, 13 strains of Salmonella london and 175 strains of DEC were typed by PFGE. Among 470 strains of PFGE typing, 6 strains of DEC were degraded by DNA, while the remaining strains obtained effective PFGE band. Salmonella enteritidi were divided into 64 PFGE band types, Salmonella typhimurium were divided into 115 PFGE band types, Salmonella london were divided into 13 PFGE band types and diarrheagenic E. coli were divided into 165 PFGE band types. Conclusions:Shigella is not detected in the active surveillance, and Salmonella is detected most frequently. Salmonella and diarrheagenic E. coli have the highest resistance rates to ampicillin, and Vibrio parahaemolyticus has the highest resistance rates to cefazolin. The PFGE classification is polymorphic, and the dominant band type is not obvious. The evidence of multi-drug resistance suggests further strengthening monitoring and management of drug resistance.

ObjectiveTo investigate the mechanism of Huangqi Gegentang （HGT） in the treatment of type 2 diabetes mellitus （T2DM） through the application of proteomic techniques. MethodsThe rat model of T2DM was established by streptozotocin combined with a high-fat， high-sugar diet. Thirty-two male SD rats were randomized into four groups： blank， model， HGT （8.10 g·kg^-1·d^-1）， and positive control （metformin hydrochloride， 76.5 mg·kg^-1·d^-1）. After 6 weeks of drug intervention， the fasting blood glucose level was measured， and an oral glucose tolerance test （OGTT） was performed. The area under the curve （AUC） was calculated. Enzyme-linked immunosorbent assay was performed to assess the level of glycated hemoglobin （GHbA1c） in the serum. The limulus amebocyte lysate assay was employed to measure the serum level of lipopolysaccharide （LPS）. Pathological changes in the colon were observed by hematoxylin-eosin staining. The mRNA levels of pro-inflammatory cytokines including tumor necrosis factor （TNF）-α， interleukin （IL）-6， and IL-1β in the colon tissue were quantified via Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. Additionally， the protein and mRNA levels of zonula occludens-1 （ZO-1）， Occludin， and Claudin-1 in the colon tissue were assessed by Western blot and Real-time PCR， respectively. Label-free quantitative proteomics was employed to identify the differentially expressed proteins between the colon tissue samples from the blank， model， and HGT groups. Key proteins identified were subsequently validated by Western blot and Real-time PCR. Finally， bioinformatics analysis was conducted on the differentially expressed proteins. ResultsCompared with the blank group， the model group exhibited increased fasting blood glucose， AUC， and GHbA1c levels （P<0.01）， damaged colonic mucosal epithelial structure and inflammatory cell infiltration， up-regulated mRNA levels of TNF-α， IL-6， and IL-1β in the colon and an increase in serum LPS content （P<0.05， P<0.01）， and down-regulated protein and mRNA levels of ZO-1， Occludin， and Claudin-1 in the colon （P<0.01）. Compared with the model group， the HGT group showed reductions in fasting blood glucose， AUC， and GHbA1c （P<0.01）， alleviated damage to the colonic mucosal epithelium， down-regulated mRNA levels of TNF-α， IL-6， and IL-1β in the colon， a reduction in serum LPS content （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of ZO-1， Occludin， and Claudin-1 in the colon （P<0.05， P<0.01）. Proteomics analysis identified 70 differentially expressed proteins that exhibited a downward trend in the model group relative to the blank group and an upward trend in the HGT group relative to the model group. These findings were corroborated by Western blot and Real-time PCR， which confirmed that the protein and mRNA levels of mucin 2 （Muc2） and transforming growth factor （TGF）-beta receptor 1 （Tgfbr1） in the colon tissue were consistent with the proteomic data. Bioinformatics analysis showed that these 70 differentially expressed proteins identified were significantly enriched in multiple signaling pathways， among which the TGF-β and advanced glycation endproduct （AGE）/receptor for advanced glycation endproduct （RAGE） signaling pathways were closely associated with damage to the intestinal mucosal barrier. This suggests that HGT may ameliorate intestinal mucosal barrier damage by regulating these pathways. ConclusionHGT potentially exerts anti-T2DM effects by influencing AGE/RAGE and TGF-β signaling pathways， thereby contributing to the restoration of the intestinal mucosal barrier.

Objective:To investigate the mechanism of microRNA-597-3p ( miR-579-3p) in improving hypoxic-ischemic encephalopathy (HIE) by regulating the interleukin-1 receptor-associated kinase 1 (IRAK1)/tumor necrosis factor receptor-associated factor 6 (TRAF6)/transforming growth factor-β-activated kinase 1 (TAK1)/nuclear factor-κB (NF-κB) signaling pathway. Methods:Peripheral blood of healthy neonates ( n=5) and HIE newborns ( n=5) from June 2023 to June 2024 in the No.215 Hospital of Shaanxi Nuclear Industry were collected. The differential expression of miRNA in peripheral blood of neonates with HIE was analyzed by next-generation sequencing. The oxygen-glucose deprivation (OGD) method was used to establish the HIE cell model, which was designated as the OGD group, while cells without OGD treatment served as the control group. Rat adrenal pheochromocytoma PC12 cells were transfected with miR-579-3p mimic (mimic), mimic negative control (mimic-NC), miR-579-3p inhibitor (inhibitor), inhibitor negative control (inhibitor-NC), respectively, and divided into the mimic group, mimic-NC group, inhibitor group, inhibitor-NC group. On the basis of mimic group and inhibitor group, IRAK1 overexpression plasmid ( oeIRAK1) and IRAK1 small interfering RNA plasmid ( siIRAK1) were transfected respectively, which were divided into oeIRAK1 group and siIRAK1 group. The relative expression level of mRNA was detected by real-time reverse transcription-PCR. The absorbance ( A) value was detected by cell counting kit-8 assay. The apoptosis rate was detected by Annexin Ⅴ-fluorescein isothiocyanate/propidium iodide double staining. The relative expression of protein was detected by Western blotting. The levels of pro-inflammatory factors and anti-oxidative stress factors were detected by enzyme-linked immunosorbent assay. Bioinformatics analysis was used to predict the binding site between miR-579-3p and IRAK1, and the dual-luciferase reporter assay was performed to validate their targeting relationship. A total of 12 7-day-old SD rats were selected and randomly divided into the HIE group and the sham group by the random number table method. In the HIE group, the right common carotid artery of rats was permanently occluded, followed by hypoxia exposure, whereas rats in the sham group only underwent common carotid artery exposure without ligation or hypoxia treatment. Immunohistochemical staining was used to detect the expression of protein in brain tissue of HIE rats. The least significant difference t-test was used for comparison between the two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with the healthy neonates, a total of 278 differentially expressed miRNAs were detected in the peripheral blood of neonates with HIE, among which miR-579-3p showed the most significant downregulation. The relative expression level of miR-579-3p in the mimic group (15.78±1.93) was significantly higher than that in the mimic-NC group (1.00±0.14) ( P<0.01), and in the inhibitor group (0.29±0.14) was significantly lower than that in inhibitor-NC group (1.00±0.14) ( P<0.01). The A value in the mimic group (0.89±0.09) was significantly higher than that in the mimic-NC group (0.52±0.08) ( P<0.01), and in the inhibitor group (0.30±0.05 ) was significantly lower than that in the inhibitor-NC group (0.56±0.07) ( P<0.05). The apoptosis rate of mimic group [(7.47±1.53)%] was significantly lower than that in the mimic-NC group [(30.97±3.47)%] ( P<0.05), and in the inhibitor group [(49.05±4.21)%] was significantly lower than that in the inhibitor-NC group [(35.51±3.64)%] ( P<0.01). The relative expression level of cysteine aspartic acid specific protease-3 ( Caspase-3) and B-cell lymphoma-2 (Bcl-2) associated X protein ( Bax) (1.21±0.10, 1.40±0.13), the relative expression of cleaved Caspase-3 and Bax (1.00±0.13, 1.13±0.09), the levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α [(45.15±5.14, 38.34±5.69) pg/mg] in the mimic group were significantly lower than those in the mimic-NC group [2.10±0.14, 2.37±0.16, 2.29±0.09, 2.27±0.12, (95.67±9.05, 63.99±5.24) pg/mg] (all P<0.01). The relative expression level of Bcl-2 and Claspin (1.03±0.09, 1.00±0.04), the relative expression of Bcl-2 and Claspin (1.21±0.06, 0.94±0.09), the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) [(67.65±6.86, 58.07±5.20) U/mg] in the mimic group were significantly higher than those in the mimic-NC group [(0.51±0.05, 0.52±0.02, 0.58±0.05, 0.46±0.07, 42.08±5.86, 29.80±4.85) U/mg] ( P<0.05, 0.01). The relative expression level of Caspase-3 and Bax (2.72±0.16, 2.97±0.10), the relative expression of cleaved Caspase-3 and Bax (3.25±0.17, 2.76±0.16), the levels of IL-6 and TNF-α [(122.80±11.59, 92.58±7.56) pg/mg] in the inhibitor group were significantly higher than those in the inhibitor-NC group [(1.86±0.14, 2.12±0.10, 2.35±0.15, 1.82±0.15, (88.13±8.59, 68.61±6.17) pg/mg] ( P<0.05, 0.01). The relative expression levels of Bcl-2 and Claspin mRNA (0.17±0.04, 0.20±0.06), the relative expression of Bcl-2 and Claspin proteins (0.11±0.03, 0.13±0.05), the levels of SOD and GSH-Px [(16.62±3.19, 12.01±1.92) U/mg] in the inhibitor group were significantly lower than those in the inhibitor-NC group [0.54±0.05, 0.54±0.05, 0.53±0.10, 0.45±0.07, (38.09±5.47, 30.90±3.87) U/mg] ( P<0.05, 0.01). IRAK1 was identified as a putative target of miR-579-3p. The relative luciferase activity of wild-type IRAK1 in the mimic group (0.45±0.05) was significantly lower than that in the mimic-NC group (1.00±0.08) ( P<0.01). The relative expression levels of IRAK1, TRAF6, TAK1 and NF-κB mRNA in the mimic group (0.96±0.09, 0.96±0.11, 1.34±0.16, 1.74±0.20), the relative expression of IRAK1, TRAF6, TAK1, and phosphorylated NF-κB (p-NF-κB) proteins (0.96±0.20, 1.27±0.19, 1.34±0.18, 1.16±0.19) were all lower than those in the mimic-NC group (1.96±0.17, 1.88±0.24, 2.39±0.23, 2.44±0.20, 2.33±0.22, 2.17±0.24, 2.25±0.28, 2.06±0.28) (all P<0.01). The relative expression levels of IRAK1, TRAF6, TAK1 and NF-κB mRNA in the inhibitor group (2.54±0.15, 2.61±0.13, 2.97±0.15, 2.99±0.20), the relative expression of IRAK1, TRAF6, TAK1 and p-NF-κB proteins (3.73±0.34, 3.17±0.25, 3.68±0.22, 3.29±0.20) were all higher than those in the inhibitor-NC group (1.87±0.18, 1.84±0.19, 2.15±0.24, 2.24±0.26, 2.35±0.23, 1.94±0.25, 2.05±0.27, 2.17±0.29) (all P<0.01). The A value in the oeIRAK1 group (0.66±0.07) was significantly lower than that in the mimic group (0.94±0.10) ( P<0.05), and in the siIRAK1 group (0.51±0.08) was significantly higher than that in the inhibitor group (0.23±0.05) ( P<0.05). The apoptosis rate in the oeIRAK1 group [(23.32±2.40)%] was significantly higher than that in the mimic group [(9.02±1.23)%] ( P<0.05), and in the siIRAK1 group [(28.27±2.57)%] was significantly lower than that in the inhibitor group [(48.96±4.60)%] ( P<0.01). The levels of IL-6 and TNF-α in the oeIRAK1 group [(85.10±6.98, 59.49±5.78) pg/mg] were significantly higher than those in the mimic group [(47.51±8.87, 23.65±3.75) pg/mg], and the levels of SOD and GSH-Px [(49.58±5.63, 41.31±6.21) U/mg] were significantly lower than those in the mimic group [(81.22±6.94, 62.26±5.44) U/mg] ( P<0.05, 0.01). The levels of IL-6 and TNF-α in the siIRAK1 group [(108.25±9.47, 74.87±8.71) pg/mg] were significantly lower than those in the inhibitor group [(142.65±13.88, 104.49±9.18) pg/mg], and the levels of SOD and GSH-Px [(35.87±3.69, 34.89±4.96) U/mg] were significantly higher than those in the inhibitor group [(15.55±3.70, 15.62±3.30) U/mg] ( P<0.05, 0.01). The relative expression level of miR-579-3p in the HIE group (0.47±0.11) was significantly lower than that in the sham group (1.00±0.09) ( P<0.01). The levels of IL-6 and TNF-α in the HIE group [(62.18±6.42, 68.42±4.91) pg/mg] were significantly higher than those in the sham group [(20.77±4.68, 31.16±4.95) pg/mg], and the levels of SOD and GSH-Px [(22.63±3.33, 19.07±2.86) U/mg] were significantly lower than those in the sham group [(47.89±4.58, 56.55±4.45) U/mg] (all P<0.01). The relative levels of TLR4, IRAK1, TRAF6, TAK1, NF-κB, and Caspase-3 mRNA, TLR4, IRAK1, TRAF6, TAK1, p-NF-κB, and cleaved Caspase-3 proteins in the HIE group (1.87±0.24, 2.03±0.21, 2.23±0.20, 1.85±0.18, 1.91±0.20, 2.36±0.20, 2.36±0.28, 2.16±0.28, 1.95±0.27, 2.05±0.26, 2.34±0.24, and 2.72±0.23) were all higher than those in the sham group (1.00±0.15, 1.00±0.11, 1.00±0.09, 1.00±0.05, 1.00±0.12, 1.00±0.15, 1.00±0.15, 1.00±0.21, 1.00±0.10, 1.00±0.14, 1.00±0.19, 1.00±0.16) (all P<0.01), which were consistent with the immunohistochemical staining results. Conclusions:miR-579-3p might alleviate HIE-induced neuronal damage by regulating the IRAK1/TRAF6/TAK1/NF-κB signaling pathway.