Inflammatory response is a crucial factor that affects prognosis and therapeutic effect in tumor cells. Although some studies have shown that inflammation could make DNA more vulnerable to external attacks, resulting in serious DNA damage, the underlying mechanism remains unknown. Then, using tumor necrosis factor α (TNF-α) and lipopolysaccharide (LPS), this research elevated the level of inflammation in cancer cells, and hydrogen peroxide (H2O2) and ultraviolet (UV) were utilized as common reactive oxygen species (ROS)-induced DNA damage agents. We show that either H2O2 or UV achieved a more substantial antiproliferative effect in the inflammation environment compared with H2O2 or UV treatment alone. The inflammation environment enhanced H2O2- or UV-induced cell apoptosis and ROS production. Although the phenomenon that inflammation itself could trigger ROS-dependent DNA damage was well known, the underlying mechanism for the sensitization of inflammation to trigger intense DNA damage via ROS in cancer cells remains unclear. In this study, the inflammation-related genes and the corresponding expression information were obtained from the TCGA and fetched genes associated with inflammatory factors. Screening of thirteen inflammatory-related, including ATM, and prognostic genes. In addition, KEGG analysis of prognostic genes shows that biological processes such as DNA replication. ATM and ATR, which belong to the PI3/PI4-kinase family, can activate p53. Inflammation promotes the vulnerability of DNA by activating the ATM/ATR/p53 pathway, while not affecting the DNA damage repair pathway. In brief, this research suggested that inflammation made DNA vulnerable due to the amplifying H2O2- or UV-induced ROS production and the motoring ATM/ATR/p53 pathway. In addition, our findings revealed that inflammation's motoring of the ATM/ATR/p53 pathway plays a crucial role in DNA damage. Therefore, exploring the mechanism between inflammation and ROS-dependent DNA damage would be extremely valuable and innovative. This study would somewhat establish a better understanding of inflammation, DNA damage, and cancer.

Background: Pneumocystis jiroveci pneumonia (PJP) is one of the common opportunistic infectious diseases of thelungs in immunosuppressed populations. With the global epidemic of the Delta variant of the novel coronavirus (SARS-CoV-2), it has been found that patients with novel coronavirus pneumonia can have concurrent or subsequent co-infection with Pneumocystis jiroveci. The purpose of this paper was to investigate the clinical characteristics and diagnosis and treatment of patients with Pneumocystis jiroveci pneumonia (PJP) secondary to novel coronavirus (COVID-19) infection. Methods: Clinical data of 14 patients with Pneumocystis jiroveci pneumonia secondary to novel coronavirus infection diagnosed in the First Hospital of Wenzhou Medical University from September 2022 to May 2023 were collected, and their general conditions, laboratory tests, imaging data, and treatments and regressions were analyzed. Result: Secondary PJP occurs more often in patients with severe novel coronavirus infection with immunocompromised patients and manifests itself as dyspnea and a significant decrease in arterial oxygen saturation higher than that of the average COVID-19 patients. Laboratory tests suggest a decrease in lymphocyte subset counts, absolute CD4+ T-cell counts, and elevated differential partial pressure of alveolar arterial blood oxygen, lactate dehydrogenase (LDH), and serum (1,3)-β-D-glucan (BDG). Metagenomic Next-Generation Sequencing (mNGS) combined with serum (1,3)-β-D-glucan (BDG) has a higher sensitivity for screening PJP. On chest imaging, it is mostly characterized by the crescent sign, pleural effusion, and enlarged hilar and mediastinal lymph nodes. Conclusions: It is difficult to identify PJP in the early stage of COVID-19 infection, and the combination of respiratory symptoms with BDG, mNGS and imaging examination is of great value for the early diagnosis of PJP. SMZCO and respiratory support are the most important treatments.

AbstractEvidence for the treatment of patients with mild-to-moderate chronic obstructive pulmonary disease (COPD) is limited. The efficacy of N-acetylcysteine (an antioxidant and mucolytic agent) for patients with mild-to-moderate COPD is uncertain. In this multicentre, randomised, double-blind, placebo-controlled trial, we randomly assigned 968 patients with mild-to-moderate COPD to treatment with N-acetylcysteine (600 mg, twice daily) or matched placebo for two years. Eligible participants were 40-80 years of age and had mild-to-moderate COPD (forced expiratory volume in 1 second [FEV1] to forced vital capacity ratio <0.70 and an FEV1 ≥ 50% predicted value after bronchodilator use). The coprimary outcomes were the annual rate of total exacerbations and the between-group difference in the change from baseline to 24 months in FEV1 before bronchodilator use. COPD exacerbation was defined as the appearance or worsening of at least two major symptoms (cough, expectoration, purulent sputum, wheezing, or dyspnoea) persisting for at least 48 hours. Assessment of exacerbations was conducted every three months, and lung function was performed annually after enrolment. The difference between the N-acetylcysteine group and the placebo group in the annual rate of total exacerbation were not significant (0.65 vs. 0.72 per patient-year; relative risk [RR], 0.90; 95% confidence interval [CI], 0.80–1.02; P = 0.10). There was no significant difference in FEV1 before bronchodilator use at 24 months. Long-term treatment with high-dose N-acetylcysteine neither significantly reduced the annual rate of total exacerbations nor improved lung function in patients with mild-to-moderate COPD. Chinese Clinical Trial Registration: ChiCTR-IIR-17012604.

expression pattern of miR-627-5p, miR-128-3p, miR-101-3p, miR-129-5p (A), miR-1246 and miR-155-5p (C) in AC and health controls or miR-150-5p, miR-4459, miR-6873-3p, miR-9-3p (B), miR-149-5p and miR-1246 (D) in SCC and health controls comparison by evaluating threshold cycle number difference (A, B) or calculating 2ÃÆ'Ã,Æ'ÂÃ,â¢ÃƒÆ'Ã,‚-ÃÆ'Ã,‚ÂÃ,â³Ct(C, D).

Hypoxic pulmonary hypertension (HPH) is a life-threatening disease that occurs due to a lack of oxygen in the lungs, leading to an increase in pulmonary vascular resistance, right ventricular failure, and ultimately death. HPH is a multifactorial disorder that involves multiple molecular pathways, making it a challenge for clinicians to identify effective therapies. Pulmonary artery smooth muscle cells (PASMCs) play a crucial role in HPH pathogenesis by proliferating, resisting apoptosis, and promoting vascular remodelling. Curcumin, a natural polyphenolic compound, has shown potential as a therapeutic agent for HPH by reducing pulmonary vascular resistance, inhibiting vascular remodelling, and promoting apoptosis of PASMCs. Regulation of PASMCs could significantly inhibits HPH. However, curcumin has the disadvantages of poor solubility and low bioavailability, and its derivative WZ35 has better biosafety. Here, Cu-based metal organic frameworks (MOFCu ) was fabricated to encapsulate the curcumin analogue WZ35 (MOFCu @WZ35) for the inhibition of PASMCs proliferation. The authors found that the MOFCu @WZ35 could promote the death of PASMCs. Furthermore, the authors believed that this drug delivery system will effectively alleviate the HPH.

Copper-dependent cell death, called cuproptosis, is connected to tumor development, prognosis, and the immune response. Nevertheless, the function of cuproptosis-related genes (CRGs) in the tumor microenvironment (TME) of lung adenocarcinoma (LUAD) remains unknown. This work used R software packages to classify the raw data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases of LUAD patients. Afterward, the connections of the various subgroups, clinical pathological traits, and immune infiltration (IMIF) features with the TME mutation status were explored. Ultimately, a nomogram and calibration curve were developed, aiming at enhancing the clinical application of CRG scores and estimating the survival probability of patients. Moreover, the relationships between cuproptosis and the molecular traits, immune cell infiltration of tumor tissue, prognosis, and clinical treatment of patients were investigated in this work. Subsequently, the CRG score was established to predict overall survival (OS), and its credible predictive ability in LUAD patients was identified. Afterward, a highly credible nomogram was created to contribute to the clinical viability of the CRG score. Furthermore, as demonstrated, gene signatures could be applied in assessing tumor immune cell infiltration, clinical traits, and prognosis. In addition, high tumor mutation burden, immunological activity, and significant survival probability were characterized by low CRG scores, and high CRG scores were related to immunosuppression and stromal pathway activation. The current work also discovered a predictive CRG-related signature for LUAD patients, probably contributing to TME trait clarification and more potent immunotherapy strategy exploration.

Strategy for the evaluation of the early diagnostic accuracy of AC- and SCC-specific tumor-derived exosomal miRNAs in a symptomatic set

enrichment of selected miRNAs potential target genes in oncogenesis-related pathway

mappable miRNA was chosen for further analysis based on differentially expressed gene (DEG) analysis

Objective: To analyze the disease burden of pneumoconiosis globally and in China from 1990 to 2019 using Global Burden of Disease (GBD) 2019 data, and to provide a theoretical basis for prevention and control of pneumoconiosis. Methods: In September 2022, the data of incidence, prevalence, morality and disability-adjusted life years (DALY) of pneumoconiosis and its subtypes globally and in China from 1990 to 2019 were collected from GBD 2019, including absolute number and age-standardized rate (ASR). Joinpoint linear regression model was used to calculate average annual percent change (AAPC) and analyze the change trends of incidence, prevalence, mortality and DALY of pneumoconiosis and its subtypes. Results: From 1990 to 2019, the incident cases, prevalent cases and DALY value of pneumoconiosis showed upward trends, while the number of death cases showed downward trends. And the ASR of incidence (ASIR), the ASR of prevalence (ASPR), the ASR of mortality (ASMR) and the ASR of DALY (ASDR) showed downward trends globally and in China. China accounted for a large proportion of the global disease burden of penumoconiosis, accounting for more than 67% of the incident cases, more than 80% of the prevalent cases, more than 43% of the deaths cases and more than 60% of the absolute number of DALY in the world every year. Male were the main population of pneumoconiosis disease burden globally and in China, and the age of onset was earlier than that of female. The peak age periods of incidence, prevalence, mortality and DALY of pneumoconiosis globally and in China from 1990 to 2019 have increased. Silicosis was still the type with the highest disease burden of pneumoconiosis globally and in China. The disease burden of coal workers' pneumoconiosis had an overall improvement trend, but asbestosis had an increasing disease burden worldwide. Conclusion: The disease burden of pneumoconiosis is heavy globally and in China, which is necessary to strengthen the supervision and prevention measures according to gender, age and etiological types.

Background The burden of chronic respiratory diseases has changed over the three decades. This study aims to describe the spatiotemporal trends of prevalence, mortality, and disability-adjusted life years (DALY) due to chronic respiratory diseases (CRDs) worldwide during 1990–2019 using data from the Global Burden of Disease Study 2019 (GBD 2019). Methods The prevalence, mortality, and DALY attributable to CRDs and risk factors from 1990 to 2019 were estimated. We also assessed the driving factors and potentiality for improvement with decomposition and frontier analyses, respectively. Results In 2019, 454.56 [95% uncertainty interval (UI): 417.35–499.14] million individuals worldwide had a CRD, showing a 39·8% increase compared with 1990. Deaths due to CRDs were 3.97 (95%UI: 3.58–4.30) million, and DALY in 2019 was 103.53 (95%UI: 94.79–112.27) million. Declines by average annual percent change (AAPC) were observed in age-standardized prevalence rates (ASPR) (0.64% decrease), age-standardized mortality rates (ASMR) (1.92%), and age-standardized DALY rates (ASDR) (1.72%) globally and in 5 socio-demographic index (SDI) regions. Decomposition analyses represented that the increase in overall CRDs DALY was driven by aging and population growth. However, chronic obstructive pulmonary disease (COPD) was the leading driver of increased DALY worldwide. Frontier analyses witnessed significant improvement opportunities at all levels of the development spectrum. Smoking remained a leading risk factor (RF) for mortality and DALY, although it showed a downward trend. Air pollution, a growing factor especially in relatively low SDI regions, deserves our attention. Conclusion Our study clarified that CRDs remain the leading causes of prevalence, mortality, and DALY worldwide, with growth in absolute numbers but declines in several age-standardized estimators since 1990. The estimated contribution of risk factors to mortality and DALY demands the need for urgent measures to improve them. Systematic review registration http://ghdx.healthdata.org/gbd-results-tool.

Abstract Background The burden of chronic respiratory diseases has changed over three decades.To describe the spatiotemporal trends of prevalence, mortality and disability adjusted life years (DALY) due to chronic respiratory diseases(CRDs), across the globe during 1990–2019 using data from the Global Burden of Disease Study 2019(GBD 2019). Methods The prevalence, mortality and DALY attributable to CRDs, and risk factors from 1990 to 2019 were estimated. We also assessed the driving factors and potentiality for improvement by decomposition analyses and frontier analyses. Results In 2019, 454.56 (95% uncertainty interval(UI): 417.35-499.14) million individuals worldwide had a CRD, showing a 39·8% increase compared with 1990. Deaths due to CRDs numbered 3.97(95% UI: 3.58–4.30) million, and DALY in 2019 was 103.53 (95% UI:94.79-112.27) million. Declines by average annual percent change(AAPC) were observed in age-standardized prevalence rates(ASPR) (0.64% decrease), age-standardized mortality rates(ASMR) (1.92%), and age-standardized DALY rates(ASDR) (1.72%) globally and in 5 socio-demographic index (SDI) regions. Decomposition analyses represented that the increase in overall CRDs DALY was driven by aging and population growth. Chronic obstructive pulmonary disease (COPD) was the leading drivers globally. Frontier analyses witnessed significant improvement opportunities at all levels of the development spectrum. Smoking remained a leading risk factor(RF) for the mortality and DALY, although, it showed a downward trend. Air pollution, a growing factor especially in relatively low SDI regions, deserves our attention. Conclusion Our study clarified that CRDs remain a leading cause of prevalence, mortality and DALY worldwide, with growth in absolute numbers but declines in several age-standardized estimators since 1990. The estimated contribution of risk factors to mortality and DALY supports the need for urgent measures to improve them.

目的:利用客观结构化临床(OSCE)考核系统分析学生操作项目中的失分率,进行教学策略改进,探究教学质量提升方法.方法:研究选取临床医学五年制学生4个班级120人,在2022年3月-5月学习临床技能学,分为实验组和对照组,对照组按传统教学,实验组根据OSCE考核系统分析的数据,改进并实施教学,学习结束后利用OSCE对两组学生进行考核,分析其平均分,失分率,并实施学生满意度调查.结果:实验组学生的平均分明显高于对照组(P＜0.05),失分率明显下降,实验组学生对教学模型、教师与学生互动、教师示范这三方面满意度评分均高于对照组(P＜0.05),教学改进策略有效.结论:利用OSCE考核系统可以分析出教学薄弱点,制定相应的教学策略,有效提升教学质量.

Objective To analyze the disease burden of interstitial lung disease and pulmonary sarcoidosis （ILD＆） and its trend in China from 1990 to 2019， and provide theoretical evidence for the prevention and control of ILD＆PS. Methods Based on the data of Global Burden of Disease （GBD） Study 2019， the prevalence， mortality and absolute number of disability-adjusted life years （DALYs） of ILD＆PS in China from 1990 to 2019 were obtained， including age-standardized rate （ASR）. Joinpoint linear regression model was used to calculate average annual percent change （AAPC） and analyze the change trends of prevalence， mortality and DALYs of ILD＆PS. Age-period-cohort （APC） model was used to analyze the effects of age， period and cohort on changes in the mortality. Results The prevalence， mortality and absolute number of DALYs of ILD＆PS showed increasing trends in China from 1990 to 2019. In 2019， there were 722410 cases （95%UI 586951～872704），8181 deaths （95% UI 5796～10302） of ILD＆PS，and the absolute number of DALYs was 240576 person years （95% UI 189934～299740）. In general， the age-standardized prevalence rate （ASPR）（AAPC=0.58%，P＜0.05）showed an upward trend， while the age-standardized mortality rate （ASMR）（AAPC=-0.07%，P＞0.05）and age-standardized DALYs rate （ASDR） （AAPC=-0.20%，P＜0.05）showed downward trends， from 1990 to 2019. The trends in women were similar to the general trends， but the ASMR（AAPC=0.23%，P＜0.05）and ASDR（AAPC=0.04%，P＞0.05）in men showed upward trends. The prevalence， mortality and absolute number of DALYs of ILD＆PS generally increased first and then decreased with age， with the peaks at about 70 years old. Except for the sustained growth of ASMR， ASPR and ASDR increased first and then decreased with age. The mortality APC model suggested that the net drift value during 1990-2019 was negative （-0.50%，P＜0.05）， the death risk increased with age， and the risk of death decreased in the period after 2010 and in birth cohort after 1955. But the risk of death was higher in men. Conclusion Although the overall ASMR and ASDR of ILD＆PS showed downward trends in China from 1990 to 2019， and APC analysis also showed a downtrend in mortality rate， the prevalence， ASPR， mortality and absolute number of DALYs still showed gradual increase trends. The burden of ILD＆PS remains heavy， especially in men. So more works are need to do in the prevention and treatment of ILD＆PS in China.

Bleomycin (BLM), a frequently employed chemotherapeutic agent, exhibits restricted clinical utility owing to its pulmonary toxicity. Meanwhile, baicalin (BA)-an active ingredient extracted from the roots of Scutellaria baicalensis Georgi -has been shown to alleviate BLM-induced pulmonary fibrosis (PF). Hence, the objective of this study was to examine the protective effects of BA in the context of BLM-induced early PF in mice and elucidate the underlying mechanism(s). We established an in vivo BLM (3.5 mg/kg)-induced PF murine model and in vitro BLM (35 μM)-damaged MLE-12 cell model. On Day 14 of treatment, the levels of fibrosis and apoptosis were evaluated in mouse lungs via hydroxyproline analysis, western blotting (COL1A1, TGF-β, Bax, Bcl-2, cleaved caspase-3), and Masson, immunohistochemical (α-SMA, AIF, Cyto C), and TUNEL staining. Additionally, in vitro, apoptosis was assessed in MLE-12 cells exposed to BLM for 24 h using the Annexin V/PI assay and western blotting (Bax, Bcl-2, cleaved caspase-3, AIF, Cyto C). To elucidate the role of the mitochondrial ATP-sensitive potassium channel (mitoKATP) in the protective effect of BA, we utilised diazoxide (DZX)-a mitoKATP agonist-and 5-hydroxydecanoate sodium (5-HD)-a mitoKATP inhibitor. Results revealed the involvement of mitoKATP in the protective effect of BA in BLM-induced PF. More specifically, mitoKATP activation can attenuate BLM-induced PF progression and mitigate alveolar epithelial type II cell death by reducing mitochondrial ROS, maintaining the mitochondrial membrane potential, and impeding the mitochondrial apoptotic pathway. Collectively, the findings offer pharmacological support to use BA for the treatment or prevention of BLM-induced PF and suggest that mitoKATP might serve as an effective therapeutic target for this condition.

Introduction Pulmonary embolism (PE) is a common thrombotic disease and potentially deadly cardiovascular disorder. The ratio of clinical misdiagnosis and missed diagnosis of PE is very large because patients with PE are asymptomatic or non-specific. Methods Using the clinical data from the First Affiliated Hospital of Wenzhou Medical University (Wenzhou, China), we proposed a swarm intelligence algorithm-based kernel extreme learning machine model (SSACS-KELM) to recognize and discriminate the severity of the PE by patient’s basic information and serum biomarkers. First, an enhanced method (SSACS) is presented by combining the salp swarm algorithm (SSA) with the cuckoo search (CS). Then, the SSACS algorithm is introduced into the KELM classifier to propose the SSACS-KELM model to improve the accuracy and stability of the traditional classifier. Results In the experiments, the benchmark optimization performance of SSACS is confirmed by comparing SSACS with five original classical methods and five high-performance improved algorithms through benchmark function experiments. Then, the overall adaptability and accuracy of the SSACS-KELM model are tested using eight public data sets. Further, to highlight the superiority of SSACS-KELM on PE datasets, this paper conducts comparison experiments with other classical classifiers, swarm intelligence algorithms, and feature selection approaches. Discussion The experimental results show that high D-dimer concentration, hypoalbuminemia, and other indicators are important for the diagnosis of PE. The classification results showed that the accuracy of the prediction model was 99.33%. It is expected to be a new and accurate method to distinguish the severity of PE.

Background and objective The pulmonary embolism severity index (PESI) and simplified PESI (sPESI) are recommended to recognize patients with acute pulmonary thromboembolism (PTE) with low prognosis risk, which is of great significance for treatment. This study aims to verify the influence of hypocalcaemia on the prognosis of patients with PTE and to establish a new prognosis assessment model. Methods This is an observational, multicentre study enrolling patients with PTE from February 2010 to June 2020 across 12 Chinese hospitals. Variables in PESI, serum calcium levels and patient survival status as of 5 July 2020 were collected. The area under the curve of the receiver operating characteristic curve, sensitivity, specificity and Youden index were used to evaluate model performance. Results In the cohort of 4196 patients with PTE, independent associations existed between hypocalcaemia and mid- and long-term mortalities (p <0.05). By including hypocalcaemia, the new 30-day death risk prediction rule, Peking Union Medical College Hospital rule (PUMCH rule), showed significantly higher specificity (0.622 [0.582, 0.661]; p <0.001) than the PESI (0.514 [0.473, 0.554]) and sPESI (0.484 [0.444, 0.525]) and similar sensitivity (0.963 [0.810, 0.999]; p = 0.161) with PESI (0.889 [0.708, 0.976]) and sPESI (0.963 [0.810, 0.999]) in the internal validation cohort. Well-performing predictive validity was also verified on a constructed external validation cohort. Conclusion Hypocalcaemia is independently associated with mid- and long-term PTE mortalities. The PUMCH rule showed significantly higher specificity than the PESI and sPESI and similar sensitivity, which may be used as a prognostic assessment tool for patients with acute PTE.

Abstract Accumulating evidence links m6A modification with lung adenocarcinoma (LUAD) tumorigenesis development and tumor immune microenvironment. However, the deep impact of m6A modification in tumor-immune interactions of LUAD still remains largely unknown. In the present study, the landscape of m6A modification features were drawn by analyzing the multi-omics features of 20 m6A regulators from TCGA database. Many m6A regulators were aberrantly expressed in LUAD, whose mutations and copy number variation (CNV) frequency were difference. Besides, overall survival showed many m6A regulators are associated with LUAD prognosis. However, the three m6A modification clusters (m6ACluster) determined by unsupervised consensus clustering based on m6A regulators was hard to distinguish. And then the common intersection differentially expressed genes (inter-DEGs) with significant prognosis among m6AClusters were obtained by univariate cox regression analysis. Encouragingly, the m6A-related geneClusters based on significant inter-DEGs were distinguished from each other by PCA analysis. The three geneClusters were depicted the high-, middle- and low- immune cell infiltration subtypes by ssGSEA analysis. Specially, we established a scoring tool named genescore, which was negatively correlated with PD-1, PD-L1, and CTLA4 expression and could reflect both the tumor microenvironment characterization and prognosis of LUAD patients. Majority of the DEGs between high and low genescore group were closely related to the tumor immune response. Low genescore group associated with poor prognosis exhibited higher immuneScore and lower tumorPurity applied by the ESTIMATE algorithm. Application of genescore on estimation of drug sensitivity confirmed that low genescore was more sensitive to Cisplatin, Docetaxel, Gemcitabine, Paclitaxel and Vinblastine, while the high genescore group was more sensitive to Erlotinib. Our study indicated that m6A modification related classification closely associated with tumor microenvironment and will provide novel insights into the molecular mechanisms of LUAD and contribute to develop more effective personalized treatment decisions.

IntroductionPulmonary embolism (PE) is a cardiopulmonary condition that can be fatal. PE can lead to sudden cardiovascular collapse and is potentially life-threatening, necessitating risk classification to modify therapy following the diagnosis of PE. We collected clinical characteristics, routine blood data, and arterial blood gas analysis data from all 139 patients.MethodsCombining these data, this paper proposes a PE risk stratified prediction framework based on machine learning technology. An improved algorithm is proposed by adding sobol sequence and black hole mechanism to the cuckoo search algorithm (CS), called SBCS. Based on the coupling of the enhanced algorithm and the kernel extreme learning machine (KELM), a prediction framework is also proposed.ResultsTo confirm the overall performance of SBCS, we run benchmark function experiments in this work. The results demonstrate that SBCS has great convergence accuracy and speed. Then, tests based on seven open data sets are carried out in this study to verify the performance of SBCS on the feature selection problem. To further demonstrate the usefulness and applicability of the SBCS-KELM framework, this paper conducts aided diagnosis experiments on PE data collected from the hospital.DiscussionThe experiment findings show that the indicators chosen, such as syncope, systolic blood pressure (SBP), oxygen saturation (SaO2%), white blood cell (WBC), neutrophil percentage (NEUT%), and others, are crucial for the feature selection approach presented in this study to assess the severity of PE. The classification results reveal that the prediction model’s accuracy is 99.26% and its sensitivity is 98.57%. It is expected to become a new and accurate method to distinguish the severity of PE.

The proliferation, migration and apoptotic resistance of pulmonary artery smooth muscle cells (PASMCs) are central to the progression of pulmonary arterial hypertension (PAH). Our previous study identified that fibroblast growth factor 21 (FGF21) regulates signalling pathway molecules, such as peroxisome proliferator-activated receptor gamma (PPARγ), to play an important role in PAH treatment. However, the biological roles of miRNAs in these effects are not yet clear. In this study, using miRNA sequencing and real-time PCR, we found that FGF21 treatment inhibited miR-130 elevation in hypoxia-induced PAH in vitro and in vivo. Dual luciferase reporter gene assays showed that miR-130 directly negatively regulates PPARγ expression. Inhibition of miR-130 expression suppressed abnormal proliferation, migration and apoptotic resistance in hypoxic PASMCs, and this effect was corrected upon PPARγ knockdown. Both the ameliorative effect of FGF21 on pulmonary vascular remodelling and the inhibitory effect on proliferation, migration and apoptotic resistance in PASMCs were observed following exogenous administration of miR-130 agomir. In conclusion, this study revealed the protective effect and mechanism of FGF21 on PAH through regulation of the miR-130/PPARγ axis, providing new ideas for the development of potential drugs for PAH based on FGF21.