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Abstract This study was performed to investigate the diagnostic value of radiomics models constructed by fat suppressed T2-weighted imaging (T2WI-FS) and contrast-enhanced T1-weighted imaging (CET1) based on magnetic resonance imaging (MRI) for differentiation of osteosarcoma (OS) and chondrosarcoma (CS). In this retrospective cohort study, we included all inpatients with pathologically confirmed OS or CS from Second Xiangya Hospital of Central South University (Hunan, China) as of October 2020. Demographic and imaging variables were extracted from electronic medical records and compared between OS and CS group. Totals of 530 radiomics features were extracted from CET1 and T2WI-FS sequences based on MRI. The least absolute shrinkage and selection operator (LASSO) method was used for screening and dimensionality reduction of the radiomics model. Multivariate logistic regression analysis was performed to construct the radiomics model, and receiver operating characteristic curve (ROC) was generated to evaluate the diagnostic accuracy of the radiomics model. The training cohort and validation cohort included 87 and 29 patients, respectively. 8 CET1 features and 15 T2WI-FS features were screened based on the radiomics features. In the training group, the area under the receiver-operator characteristic curve (AUC) value for CET1 and T2WI-FS sequences in the radiomics model was 0.894 (95% CI 0.817–0.970) and 0.970 (95% CI 0.940–0.999), respectively. In the validation group, the AUC value for CET1 and T2WI-FS sequences in the radiomics model was 0.821 (95% CI 0.642–1.000) and 0.899 (95% CI 0.785–1.000), respectively. In this study, we developed a radiomics model based on T2WI-FS and CET1 sequences to differentiate between OS and CS. This model exhibits good performance and can help clinicians make decisions and optimize the use of healthcare resources.

Introduction The aim of the study is the regulatory effect of MicroRNA-210 (MiR- 210) on cigarette smoke extract (CSE)-induced mouse lung epithelial type II cells (MLE-12) apoptosis and determine whether the MiR-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via Shh signaling pathway. Methods Expression of MiR-210 in CSE-induced MLE-12 was assessed by qRTPCR. The emphysema mouse model and MiR-210 knockdown mice were each established by inhaling cigarette smoke or intratracheal lentiviral vector instillation. The Sonic hedgehog (Shh), Ptch1, Gli1, B-cell lymphoma-2 (Bcl-2), and Caspase 3 protein expressions were detected by Western blotting. mRNA expressions of MiR-210, Shh, Ptch1, and Gli1 were measured using quantitative real-time polymerase chain reaction (qRT-PCR). Apoptotic ratios in mice and CSE-induced HPVEC were assessed using TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assays and flow cytometry. Results Our results showed that MiR-210 mRNA levels were significantly downregulated in the CSE-induced MLE 12. MLE 12 apoptosis with down-regulated Shh, Ptch1, Gli1, and Bcl-2 expression, increased Caspase 3 expression in the emphysema mouse model and CSE-induced MLE 12. Knockdown MiR-210 can facilitate cell apoptosis and emphysema via the Shh signaling pathway in mice. In vitro , MiR-210 can attenuate the apoptosis of CSE-exposed MLE 12. Moreover, MiR-210 regulated the Shh pathway and promoted its expression. Conclusions MiRNA-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via the Shh signaling pathway. The present study reveals that MiRNA-210 may be a key regulator of cellular apoptosis and could be explored as a potential therapeutic target in the future.

ObjectiveAlthough the mechanism is unclear, Pseudomonas aeruginosa (PA) infection directly affects the frequency of acute exacerbations in patients with bronchiectasis. The aims of this article are to analyze the genetic mutation characteristics of the algUmucABD operon in PA, isolated from hospitalized patients with bronchiectasis, and to explore independent risk factors for frequent acute exacerbations of bronchiectasis.MethodsBased on the number of acute exacerbations that occurred in the past year, these patients with bronchiectasis were divided into those with frequent acute exacerbations (Group A) and those with non-frequent acute exacerbations (Group B). We identified the distribution of mucoid phenotypes (MPs) and alginate morphotypes (AMs) in PA, and classified them into I–IV categories based on their different AMs; otherwise, the gene mutation types (GMTs) of the algUmucABD operon were tested. Subsequently, the relationship between GMT, MP, and AM and the independent risk factors for frequent acute exacerbations in patients with bronchiectasis were explored.ResultsA total of 93 patients and 75 PA strains, from January 2019 to August 2023, were included in this study. The MP and AM distributions of PA were as follows: 64 strains (85.33%) of mucoid (the AMs were 38 strains of type I, 3 strains of type II, and 23 strains of type IV) and 11 strains of non-mucoid (the AM was type III only). Mucoid PA with algU, mucA, mucB, and mucD mutations accounted for 19.61%, 74.51%, 31.37%, and 50.98%, respectively. GMT was divided into the following: mucA mutations only, mucA combined with other gene mutations, other gene mutations without mucA mutations, and without gene mutations. In 91.7% of PA with type I of AM, only mucA mutations occurred, and in both separate MP and AM, the GMT differences were statistically significant. Lastly, the number of lung lobes with bronchiectasis and the number of PA with mucA mutations only were the independent risk factors for frequent acute exacerbations.ConclusionThe mucA mutation was primarily responsible for the mucoid of MP and type I of AM in PA, and it was also an independent risk factor for frequent exacerbations of bronchiectasis.

Abstract. Background:. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 proposed a new classification that reclassified many chronic obstructive pulmonary disease (COPD) patients from group D to B. However, there is a paucity of data related to the comparison between reclassified and non-reclassified COPD patients in terms of long-term prognosis. This study aimed to investigate long-term outcomes of them and determine whether the GOLD 2017 revision improved the assessment of COPD patients. Methods:. This observational, multicenter, prospective study recruited outpatients at 12 tertiary hospitals in China from November 2016 to February 2018 and followed them up until February 2022. All enrolled patients were classified into groups A to D based on GOLD 2017, and the subjects in group B included patients reclassified from group D to B (group DB) and those remaining in group B (group BB). Incidence rates and hazard ratios (HRs) were calculated for the exacerbation of COPD and hospitalization in each group. Results:. We included and followed up 845 patients. During the first year of follow-up, the GOLD 2017 classification had a better discrimination ability for different risks of COPD exacerbation and hospitalization than GOLD 2013. Group DB was associated with a higher risk of moderate-to-severe exacerbation (HR = 1.88, 95% confidence interval [CI] = 1.37–2.59, P

Abstract Background To study the regulatory effect of Long non-coding RNA (LncRNA) HOX transcript antisense RNA (HOTAIR) on pulmonary vascular endothelial cell (HPVEC) apoptosis and determine whether the HOTAIR facilitate HPVEC apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in chronic obstructive pulmonary disease (COPD). Methods LncRNA array was used to measure the differentially expressed lncRNAs in COPD and non-COPD lung tissues. Expression of HOTAIR in COPD patient lungs and cigarette smoke extract (CSE)-induced HPVEC was assessed by qRT-PCR. The location of HOTAIR was determined in COPD patient lungs and HPVEC by RNA in situ hybridization (RNA-ISH). The emphysema mouse model and HOTAIR knockdown mice were each established by inhaling cigarette smoke or intratracheal lentiviral vectors instillation. The dysregulation of DNA methyltransferase enzyme 1 (DNMT1), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax) and Cleaved-caspase 3 protein expression were detected by Western blotting. HOTAIR, DNMT1, Bcl-2 and Bax mRNA expression were measured by quantitative real-time polymerase chain reaction. TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assays were used to assess apoptotic ratio in mice and CSE-induced HPVEC. Methylation-specific PCR (MSP) assay was conducted to observe the alterations in the methylation of the Bcl-2 promoter in specimens. RNA pull-down assay was used for analysis of the correlation between HOTAIR and DNMT1. Results The expression levels of the HOTAIR were up-regulated in COPD patient lungs and CSE-induced HPVEC. HPVEC apoptosis with down-regulated Bcl-2 expression, increased promoter methylation, DNMT1, Bax and Cleaved-caspase 3 expression was found in emphysema mouse model and CSE-induced HPVEC. Knockdown HOTAIR can attenuate cell apoptosis and emphysema via DNMT1 mediated hypermethylation of Bcl-2 promoter in mice. In vitro, HOTAIR can aggravate the apoptosis of CSE-exposed HPVEC. DNMT1 was a target of HOTAIR and had a positive correlation with HOTAIR. Conclusion HOTAIR facilitates HPVEC apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD, and attenuating the expression of HOTAIR may be a new therapy to prevent COPD.

Abstract To estimate the severity of the disease in outpatients with chronic obstructive pulmonary disease (COPD) in Hunan Province, China and use the subgroup analysis to evaluate the reliability of the new comprehensive evaluation of Global Initiative for Chronic Obstructive Lung Disease (GOLD). COPD outpatients from 12 medical centers in Hunan Province, China were stratified into groups A–D, and group D patients were further stratified into subgroups D1–D3 according to the GOLD 2016 and 2019 comprehensive assessment. Demography, clinical characteristics and medications were compared among groups. In 1017 COPD outpatients, the distribution from group A to D and subgroup D1 to D3 was 41 (4.0%), 249 (24.5%), 17 (1.7%), 710 (69.8%) and 214 (30.2%), 204 (28.7%), 292 (41.1%), according to GOLD 2016. In terms of demographic and clinical characteristics related to A–D groups, there was a significant difference in COPD assessment test (CAT), modified Medical British Research Council (mMRC), the clinical COPD questionnaire(CCQ), age, BMI, education level, smoking history, comorbidities, the course of chronic bronchitis/emphysema, number of exacerbations/hospitalisations in the previous year, treatment protocols, forced expiratory volume in one second (FEV1) % predicted, and FEV1/forced vital capacity (FVC) (p

Abstract To explore the status of diagnostic delay and to clarify its potentially influencing factors in patients with chronic obstructive pulmonary disease (COPD). A cross-sectional study was conducted in a Chinese tertiary hospital between July 2019 and February 2020. A total of 408 eligible outpatients with COPD were recruited, and relevant data were collected in the form of questionnaires. Diagnostic delay was compared among different characteristics using the Wilcoxon test and Kruskal–Wallis H test. Multivariable linear regression analysis was performed to determine the factors related to diagnostic delay. The median (interquartile range [IQR]) duration of diagnostic delay was 230 (50–720) days. The proportions of COPD patients who chose tertiary, secondary, and first-level hospitals for the first visit were 53.7%, 29.9%, and 16.4%, respectively. Additionally, the proportions of patients who underwent pulmonary function tests for the first visit in tertiary, secondary, and first-level hospitals were 74.0%, 24.6%, and 1.5% (p

Abstract Obstructive sleep apnea syndrome (OSAS), a state of sleep disorder, is characterized by repetitive apnea, chronic hypoxia, oxygen desaturation, and hypercapnia. Previous studies have revealed that intermittent hypoxia (IH) conditions in OSAS patients elicited neuron injury (especially in the hippocampus and cortex), leading to cognitive dysfunction, a significant and extraordinary complication of OSAS patients. The repeated courses of airway collapse and obstruction in OSAS patients resulted in apnea and arousal during sleep, leading to IH and excessive daytime sleepiness (EDS) and subsequently contributing to the development of inflammation. IH-mediated inflammation could further trigger various types of cognitive dysfunction. Many researchers have found that, besides continuous positive airway pressure (CPAP) treatment and surgery, anti-inflammatory substances might alleviate IH-induced neurocognitive dysfunction. Clarifying the role of inflammation in IH-mediated cognitive impairment is crucial for potentially valuable therapies and future research in the related domain. The objective of this article was to critically review the relationship between inflammation and cognitive deficits in OSAS.

Objective To evaluate the feasibility of mean platelet volume (MPV) as a biomarker for chronic obstructive pulmonary disease (COPD). Methods A systematic search for studies published up to March 2019 was performed in the PubMed and Web of Science databases. Three independent investigators screened the titles and abstracts of including studies according to eligibility criteria. The Newcastle–Ottawa Scale was used to assess the quality of eligible studies, and statistical analyses were performed using Review Manager version 5.3. Results A total of eight studies with 1230 COPD patients and 443 healthy controls were included in our meta-analysis. No significant differences in MPV level were identified in pairwise comparisons of the acute exacerbations of COPD (AECOPD), stable COPD, and control groups. Furthermore, no significant correlation was observed between MPV level and systemic inflammatory biomarkers. Conclusions MPV does not appear to represent a suitable biomarker of disease phase or inflammatory burden in COPD. However, future large-scale studies should be performed to further investigate the relationship between MPV and COPD.