ObjectiveTo observe the effects of Yifei Tongluo prescription on the NOD-like receptor protein 3 （NLRP3）/Caspase-1/gasdermin D （GSDMD） pathway and epithelial-mesenchymal transition （EMT） in rats with pulmonary fibrosis. MethodsTracheal instillation of bleomycin was conducted to establish a rat model of pulmonary fibrosis. Thirty Sprague-Dawley （SD） rats were randomly divided into a blank group， a model group， a prednisone acetate group （1.17 mg·kg^-1）， and low- and high-dose Yifei Tongluo prescription groups （10.62 and 21.24 g·kg^-1， respectively）. Administration started on the 7th day after modeling， once a day for 28 consecutive days. The lung coefficient of each group was calculated. The pathological changes of lung tissues in each group were observed by hematoxylin-eosin （HE） staining and Masson staining. The expression of α-smooth muscle actin （α-SMA） and vimentin in rat lung tissues was detected by immunohistochemistry. The expression of NLRP3 inflammasome， E-cadherin （E-cad）， and typeⅠ collagen （ColⅠ） in lung tissues was detected by immunofluorescence. The content of hydroxyproline （HYP）， tumor necrosis factor （TNF）-α， interleukin （IL）-18， and IL-1β in rat serum was detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expression levels of NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， IL-1β， and transforming growth factor （TGF）-β₁ in rat lung tissues were determined by real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression levels of NLRP3， GSDMD， ASC， and Caspase-1 in rat lung tissues were determined by Western blot. ResultsCompared with the blank group， the model group exhibited a significantly increased lung coefficient （P<0.01） and significantly increased range of pulmonary interstitial inflammation and collagen deposition. In addition， the levels of α-SMA， Vimentin， E-cad， and ColⅠ in lung tissues were significantly increased （P<0.01）. The levels of fibrosis- and inflammation-related factors HYP， TNF-α， IL-18， and IL-1β in serum were significantly upregulated （P<0.01）. The levels of factors related to the activation of NLRP3 inflammasome in lung tissues， including NLRP3， GSDMD， ASC， Caspase-1， IL-1β， and TGF-β₁， were significantly upregulated （P<0.01）. Compared with the model group， the Yifei Tongluo prescription groups showed improved lung coefficients. Additionally， the extent of lung inflammation and collagen deposition was significantly reduced. The expression of α-SMA， Vimentin， E-cad， and ColⅠ in lung tissue was significantly decreased （P<0.01）. The levels of HYP， TNF-α， IL-18， and IL-1β in serum were significantly reduced （P<0.01）. The expression levels of NLRP3， GSDMD， ASC， Caspase-1， IL-1β， and TGF-β₁ in lung tissue were also significantly decreased （P<0.01）. ConclusionYifei Tongluo prescription can regulate the NLRP3/Caspase-1/GSDMD pathway， down-regulate release of pro-inflammatory and pro-fibrotic cytokines， alleviate NLRP3 inflammasome-mediated pyroptosis and EMT， and thereby improve pulmonary fibrosis in rats.

OBJECTIVE To predict and validate the mechanisms of Chaiqi yigan granules （CQYG） improving hepatocellular carcinoma （HCC）. METHODS The signaling pathways of CQYG intervention in HCC were predicted using network pharmacology. A mice model of transplanted hepatocellular carcinoma was established by injecting H22 hepatoma cells into the axilla. Successfully modeled mice were randomly divided into model group （normal saline）， sorafenib group （positive control， 50 mg/kg）， and CQYG low-， medium- and high-dose groups （24.83， 49.66， 99.32 g/kg）， with 10 mice in each group. Mice in each group were administered the corresponding drug solution or normal saline intragastrically， once a day， for 14 consecutive days. After last administration， pathological morphological changes in the tumor tissues of mice were observed in each group. Immunohistochemical staining was performed to detect the expression of the nuclear proliferation antigen Ki-67 in tumor tissues of mice. Western blot assay was used to measure the expression of proteins related to epithelial-mesenchymal transition （EMT） [N-cadherin， E-cadherin， Vimentin， matrix metalloproteinase 7 （MMP7）] and the mitogen-activated protein kinase （MAPK） signaling pathway [p38 MAPK， phosphorylated p38 MAPK， c-Jun N-terminal kinase （JNK）， phosphorylated JNK， extracellular regulated protein kinase 1/2 （ERK1/2）， phosphorylated ERK1/2] in tumor tissue of mice. RESULTS Network pharmacology analysis revealed that metabolic pathways， pathways in cancer， and the MAPK signaling pathway were key signaling pathways through which CQYG exert their anti-hepatocellular carcinoma effects. In animal experiments， the tumor tissues of mice in the model group exhibited dense tumor cells and vigorous growth. Compared with model group， CQYG high-dose group showed a decreased density of tumor cells in the tumor tissues of mice. Moreover， the expression levels of Ki-67， N-cadherin， MMP7 and Vimentin proteins， along with the phosphorylation levels of ERK1/2 and JNK proteins， were all significantly reduced （ P ＜0.05）. The expression level of E-cadherin protein was significantly increased （ P ＜0.05）， the phosphorylation level of p38 MAPK protein was increased， the difference was not statistically significant （ P ＞0.05）. CONCLUSIONS CQYG can inhibit EMT by regulating the MAPK signaling pathway， thereby suppressing tumor cell invasion and metastasis and ultimately exerting a therapeutic effect in improving HCC.

OBJECTIVE To explore the mechanism of Chaiqi yigan granules （CQYG） against liver cancer through the ferroptosis pathway. METHODS Network pharmacology combined with ferroptosis-related database was used to screen key targets and main effective components of CQYG against liver cancer via regulating ferroptosis； molecular docking technology was employed to analyze the binding ability of main active components to key targets. Human liver Huh-7 cells were divided into blank serum control （CON） group， CQYG drug-containing serum （CQYGKL） group， ferroptosis inducer （RSL3） group， mammalian target of rapamycin complex 1 （mTORC1） inhibitor （RMC-5552） group， mTORC1 agonist （CCT007093） group， and CCT007093+CQYGKL group. The levels of Fe 2+ ， malondialdehyde （MDA）， and glutathione （GSH） in the cells were detected in the former three groups； mRNA expressions of mammalian target of rapamycin （mTOR）， sterol regulatory element-binding protein 1 （SREBP1）， and stearoyl-CoA desaturase 1 （SCD1）， protein expressions of SREBP1 and SCD1 as well as phosphorylation levels of mTOR and ribosomal S6 kinase （S6K） proteins were detected in all groups. RESULTS Key targets of CQYG for anti-liver cancer through the ferroptosis pathway were mTOR， SREBP1， SCD1，etc. The main active components included quercetin， tanshinone Ⅱ A ， baicalein， etc. The binding energies of main active components to key targets were all less than －5 kJ/mol. Compared with CON group， the levels of Fe 2+ and MDA in the cells in CQYGKL group and RSL3 group were significantly increased， while the levels of GSH were significantly decreased （ P ＜0.05）. mRNA expressions of mTOR， SREBP1 and SCD1， protein expressions of SREBP1 and SCD1， as well as the phosphorylation levels of mTOR and S6K proteins were significantly decreased in the CQYGKL group， RSL3 group， and RMC-5552 group， whereas all the above indicators were significantly increased in the CCT007093 group （ P ＜0.05）. Compared with CCT007093 group， the changes in all the above indicators were significantly suppressed in the CCT007093+CQYGKL group （ P ＜0.05）. CONCLUSIONS CQYG may induce ferroptosis by inhibiting mTORC1/SREBP1/SCD1 axis， thereby exerting anti-liver cancer effects.

ObjectiveTo characterize the features of the gut microbiome and its association with clinical prognosis in patients with intermediate and advanced hepatocellular carcinoma （HCC） treated with transcatheter arterial chemoembolization （TACE） combined with targeted therapy and immunotherapy. MethodsThis retrospective study enrolled patients with intermediate and advanced HCC who received TACE combined with targeted therapy and immunotherapy at the First Affiliated Hospital of Sun Yat-sen University from February 2025 to July 2025. Baseline clinical data and fecal samples were collected from all enrolled patients before the index hospitalization and treatment. Patients were stratified using two independent criteria： ① a good-prognosis group and a poor-prognosis group， based on whether progression-free survival （PFS） reached 6 months； ② a response group and a non-response group， based on tumor response to the first TACE assessed by the modified Response Evaluation Criteria in Solid Tumors （mRECIST）. Metagenomic sequencing was performed on fecal samples. Bioinformatic analysis was conducted to evaluate the diversity and compositional differences of intestinal bacterial and fungal communities between groups in each stratification， and to screen for prognosis-associated characteristic microbial taxa. ResultsA total of 61 patients met the inclusion criteria. Analysis of α-diversity and β-diversity showed no statistically significant differences in bacterial and fungal diversity between groups under either stratification strategy （P＞ 0.05）. At the bacterial level， Lactobacillus johnsonii （prognosis stratification： P=0.048； response stratification： P=0.043）， Bifidobacterium dentium （prognosis stratification： P=0.004； response stratification： P=0.030） and Clostridioides difficile （prognosis stratification： P=0.017； response stratification： P=0.016） were significantly enriched in both the good prognosis group and the response group. At the fungal level， Cryptococcus decaguttatus （P=0.045）， Puccinia striiformis （P=0.002）， and Kwoniella quercicola （P=0.015） were enriched in the good‑prognosis group； Kwoniella bestiolae （P=0.037） was enriched in the response group； and Akanthomyces muscarius （P=0.024） was enriched in the non-response group. Survival analysis based on the common differential bacterial abundance in both groupings showed a significant correlation between the abundance of Bifidobacterium dentium and patient prognosis. ConclusionDifferences in the gut microbiota are associated with the prognosis of patients with intermediate and advanced HCC treated with TACE combined with targeted therapy and immunotherapy. Bifidobacterium dentium may serve as a potential predictive biomarker for the efficacy of this combination regimen， and represents a potential intervention target to modulate treatment response. Differences in gut fungal communities are also potentially associated with the prognosis of intermediate and advanced HCC patients receiving TACE combined with targeted therapy and immunotherapy.

Background Patients with pneumoconiosis often have limited disease-related knowledge, insufficient access to health education, and substantial health management needs. Health education may help improve rehabilitation outcomes and quality of life in this population. Objective To evaluate the effects of health education based on the Listen-Establish-Adopt-Reinforce-Name-Strength (LEARNS) model on rehabilitation outcomes, health-related behaviors, and quality of life among pneumoconiosis patients, and provide effective intervention strategies for the rehabilitation management of patients with pneumoconiosis. Methods A randomized controlled trial was conducted. A total of 120 pneumoconiosis patients treated in the Department of Occupational Diseases, Beijing Emergency General Hospital, from November 2024 to February 2025 were enrolled. Participants were randomly assigned to a control group or an intervention group using a random number table method, with 60 patients in each group. The control group received routine pharmacotherapy, whereas the intervention group received a 12-week LEARNS model-based health-education intervention in addition to routine treatment. The 6-Minute Walk Test (6MWT) was used to assess exercise tolerance, and the modified Medical Research Council dyspnoea scale (mMRC) was used to evaluate dyspnoea. The Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS) were applied for psychological status assessment. Pulmonary function, including forced expiratory volume in one second (FEV₁) and forced vital capacity (FVC), was measured using spirometry. A self-designed scale was used to evaluate eight health-related behaviors targeted by the health education program. The 36-Item Short-Form Health Survey (SF-36) and Chronic Obstructive Pulmonary Disease (COPD) Assessment Test (CAT) were used to assess quality of life, and the Pittsburgh Sleep Quality Index (PSQI) was adopted to evaluate sleep quality. Results After the 12-week intervention, the control group showed no statistically significant changes from baseline in the measured outcomes(P＞0.05). In the intervention group, exercise tolerance improved significantly, with the 6-minute walking distance increasing from (382.55±19.52) m to (426.84±33.59) m (P＜0.001). Dyspnoea was also alleviated, with the mMRC score decreasing from 1.37±0.66 to 0.96±0.54 (P＜0.001). The CAT score decreased from 18.95±7.03 to 10.67±3.64 (P＜0.001). Significant improvements were observed in anxiety and depression symptoms (P＜0.001), with the SAS score decreasing from 38.85±6.24 to 34.27±2.27, and the SDS score decreasing from 49.01±3.25 to 45.49±3.44. Sleep quality improved significantly, with the PSQI score dropping from 7.89±4.35 to 4.05±2.31 (P＜0.001). All eight health-related behaviors in the intervention group improved significantly after the intervention (P＜0.001), including acquisition of disease-related knowledge (1.87±0.34 vs. 3.13±0.45), participation in health education activities (1.89±0.52 vs. 3.61±0.38), and regular physical exercise (2.37±0.41 vs. 4.17±0.33). All SF-36 domain scores increased significantly (P＜0.05), with the most prominent improvements observed in physical functioning, general health, and vitality. At week 12, all SF-36 domain scores were significantly higher in the intervention group than in the control group (P＜0.05). No statistically significant between-group differences were detected in pulmonary function parameters (P＞0.05). Conclusion LEARNS model-based health education could improve exercise tolerance, dyspnea, psychological status, sleep quality, health-related behaviors, and quality of life among patients with pneumoconiosis, and therefore may be a useful adjunctive strategy for rehabilitation management in patients with pneumoconiosis.

ObjectiveTo combine metabolomics， proteomics， and transcriptomics to analyze the biological characteristics of damp-heat toxin accumulation syndrome and damp-heat accumulation syndrome in acute gout. MethodsBlood samples were collected from 15 patients with damp-heat toxin accumulation syndrome and 15 patients with damp-heat accumulation syndrome in acute gout in clinical practice. Metabolomics technology was applied to detect serum metabolites， and an orthogonal partial sample least squares discriminant analysis model was constructed to screen for metabolites with significant intergroup changes， and enrichment pathway analysis and receiver operating characteristic （ROC） curve analysis were performed. Astral data independence acquisition （DIA） was used to detect serum proteins， perform principal component analysis and screen differential proteins， demonstrate differential ploidy by radargram， apply subcellular localisation to analyse protein sources， and finally apply weighted gene co-expression network analysis （WGCNA） to find key proteins. Transcriptome sequencing technology was also applied to detect whole blood mRNA， screen differential genes and perform WGCNA， and construct machine learning models to screen key genes. ResultsMetabolome differential analysis revealed 62 differential metabolites in positive ion mode and 26 in negative ion mode. These differential metabolites were mainly enriched in the mTOR signaling pathway and FoxO signaling pathway， with trans-3,5-dimethoxy-4-hydroxycinnamaldehyde， guanabenz， 4-aminophenyl-1-thio-beta-d-galactopyranoside showing the highest diagnostic efficacy. The proteome differential analysis found that 55 proteins up-regulated and 20 proteins down-regulated in the samples of damp-heat toxin accumulation syndrome. Notably， myelin basic protein （MBP）， transferrin （TF）， DKFZp686N02209， and apolipoprotein B （APOB） showed the most significant differences in expression. Differential proteins were mainly enriched in pathways related to fat digestion and absorption， lipid and atherosclerosis， and cholesterol metabolism. WGCNA showed the highest correlation between damp-heat toxin accumulation syndrome and the brown module， with proteins in this module primarily enriched in the hypoxia-inducible factor 1 （HIF-1） signaling pathway and lipid and atherosclerosis. Transcriptomic differential analysis identified 252 differentially expressed genes， with WGCNA indicating the highest correlation between damp-heat toxin accumulation syndrome and the midnight blue module. The random forest （RF） model was identified as the optimal machine learning model， predicting apolipoprotein B receptor （APOBR）， far upstream element-binding protein 2 （KHSRP）， POU domain class 2 transcription factor 2 （POU2F2）， EH domain-containing protein 1 （EHD1）， and family with sequence similarity 110A （FAM110A） as key genes. Integrated multi-omics analysis suggested that damp-heat toxin accumulation syndrome in the acute phase of gout is closely associated with lipid metabolism， particularly APOB. ConclusionCompared to damp-heat accumulation syndrome in the acute phase of gout， damp-heat toxin accumulation syndrome is more closely associated with lipid metabolism， particularly APOB， and lipid metabolism disorders contribute to the development of damp-heat toxin accumulation syndrome in patients with acute gout.

Objective:To explore of auditory-vestibular function and inner ear imaging features of patients with Meniere's disease（MD） at different clinical stages. Methods:The clinical data of 110 patients with unilateral MD who were admitted from January 2023 to March 2024 were collected, and all patients were staged according to the results of pure tone hearing threshold test, including 13 patients with stage Ⅰ, 18 cases with stage Ⅱ, 65 cases with stage Ⅲ, and 14 cases with stage Ⅳ. All patients were tested for vestibular function, including caloric tests, vestibular evoked myogenic potentials（VEMPs）, vHIT and sensory integration tests（SOT）. The sites of endolymphatic hydrops were evaluated by intravenous endotogidolinium-based MRI, twenty-seven patients completed electrocochleography. Results:①The disease course time of patients with different stages was different, and the disease course time of stage Ⅰ and Ⅱ was shorter than that of stage Ⅲ and Ⅳpatients（P<0.05）. ②No statistical differences were found in clinical data or vestibular function between normal and abnormal ECochG groups（P>0.05）. ③The results of caloric tests showed that the UW% values of stage Ⅲ（45.5±14.79） and stage Ⅳ （51.57±22.44） were higher than those of stageⅠ（31.2±14.9） and stage Ⅱ（33.5±13.31）, there were statistically significant differences between stage Ⅰ and stage Ⅱ with stage Ⅲ and Ⅳ groups（P<0.05）, the total abnormal rate of cVEMP was 62.72%, there was a statistically significant difference between stageⅠand stage Ⅲ with the stage Ⅳ group（P<0.05）, the total abnormal rate of oVEMP was 71.82%, the difference between stage Ⅰ and stage Ⅳ group was statistically significant（P<0.05）. The total score of SOT comprehensive balance gradually decreased with the increase of clinical stage, and there was a significant difference between the stage Ⅰ and Ⅳ groups（H=26.08, P<0.01）, and there was a statistically significant difference in the rate of vestibular dysfunction of SOT between the two groups（χ²=6.7, P<0.05）. ④Patients with vestibular and cochlear endolymphatic hydrops, and patients with simple cochlear or vestibular had significantly differences in disease course time, clinical stages, UW% value of caloric test, abnormal rate of cVEMP and oVEMP, total SOT balance score, the rate of vestibular abnormality（P<0.01）. Among them, when the vestibular and cochlear endolymphatic hydrops are at the same time, the clinical stage of the patient is mainly stage Ⅲand Ⅳ. Conclusion:Auditory-vestibular and inner ear gadolinium-contrasted MRI examinations in clinical practice provide a supplementary reference for judging vestibular function and the type of endolymphatic hydrops.
Humans ; Meniere Disease/diagnostic imaging* ; Ear, Inner/physiopathology* ; Male ; Magnetic Resonance Imaging ; Female ; Middle Aged ; Vestibule, Labyrinth/diagnostic imaging* ; Adult ; Vestibular Evoked Myogenic Potentials ; Aged ; Audiometry, Pure-Tone ; Caloric Tests ; Vestibular Function Tests

Cardiac fibrosis is characterized by an elevated amount of extracellular matrix (ECM) within the heart. However, the persistence of cardiac fibrosis ultimately diminishes contractility and precipitates cardiac dysfunction. Circular RNAs (circRNAs) are emerging as important regulators of cardiac fibrosis. Here, we elucidate the functional role of a specific circular RNA CELF1 in cardiac fibrosis and delineate a novel feedback loop mechanism. Functionally, circ-CELF1 was involved in enhancing fibrosis-related markers' expression and promoting the proliferation of cardiac fibroblasts (CFs), thereby exacerbating cardiac fibrosis. Mechanistically, circ-CELF1 reduced the ubiquitination-degradation rate of BRPF3, leading to an elevation of BRPF3 protein levels. Additionally, BRPF3 acted as a modular scaffold for the recruitment of histone acetyltransferase KAT7 to facilitate the induction of H3K14 acetylation within the promoters of the Celf1 gene. Thus, the transcription of Celf1 was dramatically activated, thereby inhibiting the subsequent response of their downstream target gene Smad7 expression to promote cardiac fibrosis. Moreover, Celf1 further promoted Celf1 pre-mRNA transcription and back-splicing, thereby establishing a feedback loop for circ-CELF1 production. Consequently, a novel feedback loop involving CELF1/circ-CELF1/BRPF3/KAT7 was established, suggesting that circ-CELF1 may serve as a potential novel therapeutic target for cardiac fibrosis.

Local anesthetics (LAs), such as articaine (AT), exhibit limited efficacy in inflammatory environments, which constitutes a significant limitation in their clinical application within oral medicine. In our prior research, we developed AT-17, which demonstrated effective properties in chronic inflammatory conditions and appears to function as a novel oral LA that could address this challenge. In the present study, we further elucidated the beneficial effects of AT-17 in acute inflammation, particularly in oral acute inflammation, where mitochondrial-related apoptosis played a crucial role. Our findings indicated that AT-17 effectively inhibited lipopolysaccharide (LPS)-induced nerve cell apoptosis by ameliorating mitochondrial dysfunction in vitro. This process involved the inhibition of mitochondrial reactive oxygen species (mtROS) production and the subsequent activation of the NRF2 pathway. Most notably, improvements in mitochondria-related apoptosis were key contributors to AT-17's inhibition of voltage-gated sodium channels. Additionally, AT-17 was shown to reduce mtROS production in nerve cells through the Na⁺/NCLX/ETC signaling axis. In conclusion, we have developed a novel local anesthetic that exhibits pronounced anesthetic functionality under inflammatory conditions by enhancing mitochondria-related apoptosis. This advancement holds considerable promise for future drug development and deepening our understanding of the underlying mechanisms of action.

OBJECTIVE: To investigate the relationship between peripheral blood circular RNA Bardet-Biedl syndrome 9 (circBBS9) and circRNA catenin beta 1 (circCTNNB1) and weaning failure of mechanical ventilation in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). METHODS: A prospective, observational cohort study was conducted. The patients with AECOPD who received invasive mechanical ventilation and passed the spontaneous breathing test (SBT) admitted to the First Affiliated Hospital of Hebei North University from January 2022 to February 2024 were selected as the study subjects. According to the outcome of weaning, the patients were divided into failed weaning group and successful weaning group. At admission and before SBT, the expression levels of circBBS9 and circCTNNB1 in peripheral blood were detected by fluorescence quantitative polymerase chain reaction (PCR). General information, acute physiology and chronic health evaluation II (APACHEII) score within 24 hours of admission, vital signs before SBT and the most recent laboratory indicators before SBT of the patients were collected. The differences in circBBS9 and circCTNNB1 expression levels and clinical data between the two groups were compared. Multivariate Logistic regression was used to analyze the influencing factors of the weaning failure. Receiver operator characteristic curve (ROC curve) was used to analyze the predictive value of each index on weaning failure. RESULTS: Ultimately, 132 patients with AECOPD who underwent invasive mechanical ventilation and passed the SBT were enrolled in the study. Among them, 82 patients were successfully weaned from mechanical ventilation, while 50 patients failed to be weaned, resulting in a weaning failure rate of 37.88%. There was no statistically significant difference in the expression levels of circBBS9 and circCTNNB1 in the peripheral blood at admission of patients between the two groups. The expression level of circBBS9 in the peripheral blood before SBT of patients in the failed weaning group was significantly higher than that in the successful weaning group (2^-ΔΔCt: 131.64±30.24 vs. 100.00±21.32), and the expression level of circCTNNB1 was significantly lower than that in the successful weaning group (2^-ΔΔCt: 79.90±16.82 vs. 100.00±26.43), and the differences were statistically significant (both P < 0.05). The APACHEII score within 24 hours of admission and the levels of RSBI, SCr, and PCT before SBT in the failed weaning group were significantly higher than those in the successful weaning group [APACHEII score: 22.54±4.62 vs. 16.56±4.58, RSBI: 81.90±16.56 vs. 63.25±17.00, SCr (μmol/L): 100.20±17.27 vs. 89.93±26.29, PCT (μg/L): 1.08±0.18 vs. 0.87±0.22], and the Alb level before SBT was significantly lower than that in the successful weaning group (g/L: 29.71±2.73 vs. 33.93±2.89), and the differences were statistically significant (all P < 0.05). There was no statistically significant difference in other clinical data between the two groups. Multivariate Logistic regression analysis showed that circBBS9 [odds ratio (OR) = 1.291, 95% confidence interval (95%CI) was 1.049-1.588] and APACHEII score (OR = 2.897, 95%CI was 1.004-8.353), RSBI (OR = 1.413, 95%CI was 1.057-1.890) were independent risk factors for weaning failure (all P < 0.05), and circCTNNB1 (OR = 0.812, 95%CI was 0.688-0.959) and Alb (OR = 0.149, 95%CI was 0.036-0.614) were protective factors (both P < 0.05). ROC curve analysis showed that circBBS9, circCTNNB1, APACHEII score, RSBI, and Alb all had certain value for predicting weaning failure. The area under the ROC curve (AUC) and 95%CI were 0.820 (0.750-0.890), 0.755 (0.674-0.835), 0.827 (0.757-0.897), 0.795 (0.715-0.876), and 0.854 (0.791-0.919), respectively. Using the multivariate Logistic regression equation as the combined indicator, the AUC for predicting weaning failure reached 0.997 (95%CI was 0.993-1.000), which was significantly higher than that of the single indicators including circBBS9, circCTNNB1, APACHEII score, RSBI, and Alb (the Z value was 5.582, 6.093, 5.771, 5.932, and 5.182, respectively, all P < 0.05). CONCLUSIONS High expression of circBBS9 and low expression of circCTNNB1 in the peripheral blood of AECOPD patients receiving invasive mechanical ventilation before SBT are associated with weaning failure. circBBS9, circCTNNB1 combined with APACHEII score, RSBI and Alb are helpful for predicting the failure of weaning in these patients.
Humans ; Pulmonary Disease, Chronic Obstructive/blood* ; Prospective Studies ; Ventilator Weaning ; RNA, Circular/blood* ; Respiration, Artificial ; Male ; Female ; Aged