Emphysema Group Research Articles

The severity assessment and nucleic acid turning-negative-time prediction in COVID-19 patients with COPD using a fused deep learning model

BackgroundPrevious studies have shown that patients with pre-existing chronic obstructive pulmonary diseases (COPD) were more likely to be infected with coronavirus disease (COVID-19) and lead to more severe lung lesions. However, few studies have explored the severity and prognosis of COVID-19 patients with different phenotypes of COPD.PurposeThe aim of this study is to investigate the value of the deep learning and radiomics features for the severity evaluation and the nucleic acid turning-negative time prediction in COVID-19 patients with COPD including two phenotypes of chronic bronchitis predominant patients and emphysema predominant patients.MethodsA total of 281 patients were retrospectively collected from Hohhot First Hospital between October 2022 and January 2023. They were divided to three groups: COVID-19 group of 95 patients, COVID-19 with emphysema group of 94 patients, COVID-19 with chronic bronchitis group of 92 patients. All patients underwent chest computed tomography (CT) scans and recorded clinical data. The U-net model was pretrained to segment the pulmonary involvement area on CT images and the severity of pneumonia were evaluated by the percentage of pulmonary involvement volume to lung volume. The 107 radiomics features were extracted by pyradiomics package. The Spearman method was employed to analyze the correlation of the data and visualize it through a heatmap. Then we establish a deep learning model (model 1) and a fusion model (model 2) combined deep learning with radiomics features to predict nucleic acid turning-negative time.ResultsCOVID-19 patients with emphysema was lowest in the lymphocyte count compared to COVID-19 patients and COVID-19 companied with chronic bronchitis, and they have the most extensive range of pulmonary inflammation. The lymphocyte count was significantly correlated with pulmonary involvement and the time for nucleic acid turning negative (r=-0.145, P < 0.05). Importantly, our results demonstrated that model 2 achieved an accuracy of 80.9% in predicting nucleic acid turning-negative time.ConclusionThe pre-existing emphysema phenotype of COPD severely aggravated the pulmonary involvement of COVID-19 patients. Deep learning and radiomics features may provide more information to accurately predict the nucleic acid turning-negative time, which is expected to play an important role in clinical practice.

The Role of Emphysema on Postoperative Prognosis in Early-Stage Nonsmall Cell Lung Cancer

BackgroundEmphysema is generally considered a poor prognostic factor for patients with nonsmall cell lung cancer; however, whether the poor prognosis is due to highly malignant tumors or emphysema itself remains unclear. This study was designed to determine the prognostic value of emphysema in patients with early-stage nonsmall cell lung cancer.MethodsA total of 721 patients with clinical stage IA nonsmall cell lung cancer who underwent complete resection between April 2007 and December 2018 were retrospectively analyzed regarding clinicopathological findings and prognosis related to emphysema.ResultsThe emphysematous and normal lung groups comprised 197 and 524 patients, respectively. Compared with the normal lung group, lymphatic invasion (23.9% vs. 14.1%, P = 0.003), vascular invasion (37.6% vs. 17.2%, P < 0.001), and pleural invasion (18.8% vs. 10.9%, P = 0.006) were observed more frequently in the emphysema group. Additionally, the 5-year overall survival rate was lower (77.1% vs. 91.4%, P < 0.001), and the cumulative incidence of other causes of death was higher in the emphysema group (14.0% vs. 3.50%, P < 0.001). Multivariable Cox regression analysis of overall survival revealed that emphysema (vs. normal lung, hazard ratio 2.02, P = 0.0052), age > 70 years (vs. < 70 years, hazard ratio 4.03, P < 0.001), and SUVmax > 1.8 (vs. ≤ 1.8, hazard ratio 2.20, P = 0.0043) were independent prognostic factors.ConclusionsEarly-stage nonsmall cell lung cancer with emphysema has a tendency for the development of highly malignant tumors. Additionally, emphysema itself may have an impact on poor prognosis.

Contribution of small airway inflammation to the development of COPD

BackgroundLittle attention has been paid to the pathophysiological changes in the natural history of chronic obstructive pulmonary disease (COPD). The destructions of the small airways were visualized on thoracic micro-computed tomography scan. We investigated whether small airway inflammation (SAI) was the risk for the development of COPD.MethodsA total of 1062 patients were enrolled and analyzed in the study. The partitioned airway inflammation was determined by exhaled nitric oxide (NO) of FnNO, FeNO50, FeNO200, and calculated CaNOdual. Both FeNO200 and CaNOdual were compared to detect the promising predictor for peripheral airway/alveolar inflammation in COPD. The correlation between exhaled NO and white cell classification was evaluated to determine the inflammation type during the development of COPD.ResultsExhaled NO levels (FnNO, FeNO50, FeNO200, and CaNOdual) were the highest in the COPD group compared with all other groups. Furthermore, compared with controls, exhaled NO levels (FeNO50, FeNO200, and CaNOdual) were also significantly higher in the emphysema, chronic bronchitis, and smoking groups. FeNO200 was found to be a promising predictor for peripheral airway/alveolar inflammation (area under the curve [AUC] of the receiver operating characteristic [ROC] curve, area under the curve [AUC] = 0.841) compared with CaNOdual (AUC ROC = 0.707) in COPD. FeNO200 was the main risk factor (adjusted odds ratio, 2.191; 95% CI, 1.797–2.671; p = 0.002) for the development of COPD. The blood eosinophil and basophil levels were correlated with FeNO50 and FeNO200.ConclusionThe complete airway inflammations were shown in COPD, whereas SAI was the main risk factor for the development of COPD, which might relate to eosinophil and basophil levels.

Subtypes of Patients with Mild to Moderate Airflow Limitation as Predictors of Chronic Obstructive Pulmonary Disease Exacerbation.

COPD is a heterogeneous disease, and its acute exacerbation is a major prognostic factor. We used cluster analysis to predict COPD exacerbation due to subtypes of mild-moderate airflow limitation. In all, 924 patients from the Korea COPD Subgroup Study cohort, with a forced expiratory volume (FEV1) ≥ 50% and documented age, body mass index (BMI), smoking status, smoking pack-years, COPD assessment test (CAT) score, predicted post-bronchodilator FEV1, were enrolled. Four groups, putative chronic bronchitis (n = 224), emphysema (n = 235), young smokers (n = 248), and near normal (n = 217), were identified. The chronic bronchitis group had the highest BMI, and the one with emphysema had the oldest age, lowest BMI, and highest smoking pack-years. The young smokers group had the youngest age and the highest proportion of current smokers. The near-normal group had the highest proportion of never-smokers and near-normal lung function. When compared with the near-normal group, the emphysema group had a higher risk of acute exacerbation (OR: 1.93, 95% CI: 1.29-2.88). However, multiple logistic regression showed that chronic bronchitis (OR: 2.887, 95% CI: 1.065-8.192), predicted functional residual capacity (OR: 1.023, 95% CI: 1.007-1.040), fibrinogen (OR: 1.004, 95% CI: 1.001-1.008), and gastroesophageal reflux disease were independent predictors of exacerbation (OR: 2.646, 95% CI: 1.142-6.181). The exacerbation-susceptible subtypes require more aggressive prevention strategies.

Gut microbiota composition and metabolite profiling in smokers: a comparative study between emphysema and asymptomatic individuals with therapeutic implications

BackgroundDiet has a crucial role in the gut microbiota, and dysbiosis in the gut and lungs has been suggested to be associated with chronic obstructive pulmonary disease. We compared the...

PDK1 inhibition reduces autophagy and cell senescence through the PI3K/AKT signalling pathway in a cigarette smoke mouse emphysema model.

A number of previous studies have demonstrated the pivotal role of PI3K/AKT signalling in cigarette smoke (CS)-induced emphysema, where phosphoinositide dependent protein kinase 1 (PDK1) is a critical component of this pathway. Therefore, the present study aimed to investigate the effects of a PDK1 inhibitor (GSK-2334470) on the expression levels of PI3K, AKT, cyclin-dependent kinase inhibitor 2A (p16) and LC3B in a CS + CS extract (CSE)-induced mouse emphysema model. CS exposure and intraperitoneal injections of CSE were combined for 4 weeks to establish an emphysema model. Mice (n=35) were randomly divided into the normal control, emphysema (CS), PI3K inhibitor (CS3) and PDK1 inhibitor (CS1) groups. Immunohistochemistry staining of lung tissues was used to measure the expression of the PI3K, PDK1 and AKT proteins in airway epithelial tissues. Immunofluorescence staining was also used to measure the levels of p16 and LC3BII protein expression in the airway epithelial tissues. In addition, PI3K, PDK1, AKT, p16 and LC3B protein expression was semi-quantified using western blotting. The expression of PDK1, PI3K and AKT proteins in the airway epithelial tissues was significantly increased in the CS + CSE group compared with that in the control group. The expression levels of p16 and LC3B were also increased as well in the CS + CSE group compared with those in the control group. The expression levels of PI3K, PDK1, AKT, LC3B and p16 in the airway epithelial tissues of the CS3 group were lower compared with those in the CS + CSE group. A decrease in the expression levels of PDK1, AKT, p16 and LC3B in the airway epithelial tissues of the CS1 group compared with those in the CS + CSE group was also observed. However, there were no significant differences in the expression levels of PI3K between the CS1 and the CS groups. The present study concluded that the inhibition of PDK1 can potentially reduce autophagy and cell senescence by downregulating the expression of PI3K/AKT pathway related proteins in airway epithelial cells, thereby protecting against CS + CSE-induced emphysema in mice.

Clinical outcome and risk factors for subcutaneous emphysema in patients with lung cancer after video-assisted thorascopic surgery.

Background and purposeWith the clinical application of minimally invasive surgery and concept of enhanced recovery after surgery, the incidence of postoperative complications in lung cancer patients has been significantly reduced. However, postoperative subcutaneous emphysema (SE) becomes the main factor affecting the early discharge of patients. The aim of this study was to analyze the clinical outcome and risk factors for postoperative SE in lung cancer patients.MethodsThe clinical data of 414 lung cancer patients who were admitted to the Department of Thoracic Surgery, West China Hospital, Sichuan University from September 2021 to December 2021 were prospectively collected. The incidence, severity and treatment of patients who had SE, surgery approach, application of drainage tube and clinical information were analyzed.ResultsThe incidence rate of postoperative SE in patients with lung cancer was 33.09% (137/414) and mild cases accounted for the vast majority (30.19%, 125/414). Multivariate analysis indicated that male [odds ratio (OR) = 2.247, P = .014] and advanced age (OR = 1.021, P = .043) were main risk factors for postoperative SE in patients with lung cancer. Conservative treatment was the main treatment option for SE (98.5%, 135/137). The average hospital stay in the subcutaneous emphysema group (5.49 ± 4.41 days) was significantly longer than that in the non-subcutaneous emphysema group (4.44 ± 3.32 days) (P = .014) and no significant statistical difference in the average total hospital cost between the two groups (7,798.31 ± 1,414.85$ vs. 7,501.14 ± 1,605.18$, P = .072).ConclusionPostoperative SE in patients with minimally invasive lung cancer is mainly mild, and conservative treatment is appropriate for most cases.

Effect and Mechanism of Running on Mouse Emphysema Model Induced by Cigarette Extract

<bold>Objective</bold> To observe the effect of running on mouse emphysema model induced by cigarette extract, and to explore its mechanism based on signal transducer and activator of transcription 3 (STAT3). <bold>Methods</bold> A total of 40 male C57BL/6 mice were randomly divided into control group, exercise group, emphysema group and emphysema + exercise group, with 10 mice in each group. The control group and the exercise group were intraperitoneally injected with 0.3 mL phosphate buffer saline (PBS) at the 0, 11th and 22th day in the experiment; the emphysema group and the emphysema + exercise group were intraperitoneally injected with 0.3 mL cigarette extract at the 0, 11th and 22th day in the experiment. The control group and the emphysema group were free to move in the cage from the 23rd to 29th day; the exercise group and the emphysema + exercise group received aerobic running training from the 23rd day to the 29th day (15 m/min, 30 minutes a day). Hematoxylin eosin (HE) staining was used to observe the pathological changes of lung tissue and evaluate the severity of emphysema in the four groups; the expression levels of inflammatory cells and cytokines in bronchoalveolar lavage fluid (BAL) and serum were analyzed to evaluate the pulmonary and systemic inflammation of the four groups; Western blot method was used to analyze the expression of STAT3 in lung tissues. <bold>Results</bold> 1) Severity of emphysema: compared with the control group, the alveolar chord length of mice in the emphysema group and the emphysema + exercise group significantly increased, the difference was statistically significant (<italic>P</italic>&lt;0.05). Compared with the emphysema group, the alveolar chord length in the emphysema + exercise group significantly decreased，the difference was statistically significant (<italic>P</italic>&lt;0.05). 2) Lung inflammation: compared with the control group, the contents of white blood cells, neutrophils and lymphocytes and the expression levels of IL-1β, IL-6, and IL-17 in BAL of the emphysema group and the emphysema + exercise group significantly increased, while the IL-10 level significantly decreased (<italic>P</italic>&lt;0.05). Compared with the emphysema group, the counts of white blood cells, neutrophils and lymphocytes and the expression levels of IL-1β, IL-6, and IL-17 in BAL of the emphysema + exercise group were statistically lower, and the IL-10 level was statistically higher, the difference was statistically significant (<italic>P</italic>&lt;0.05). 3) Systemic inflammation: compared with the control group, the counts of white blood cells, neutrophils and lymphocytes in the emphysema group statistically increased (<italic>P</italic>&lt;0.05), the expression levels of IL-1β, IL-17, and TNF-α in the emphysema group and the emphysema + exercise group statistically increased, and the IL-10 level statistically decreased (<italic>P</italic>&lt;0.05). Compared with emphysema group, the counts of white blood cells, neutrophils and lymphocytes and the expression levels of IL-1β, IL-17, and TNF-α in the emphysema + exercise group were lower, and the IL-10 level was statistically higher, the difference was statistically significant (<italic>P</italic>&lt;0.05). 4) STAT3 expression level in lung tissues: compared with the control group, p-STAT3 expression level in lung tissues of the emphysema group and the emphysema + exercise group statistically increased (<italic>P</italic>&lt;0.05). Compared with the emphysema group, the expression level of p-STAT3 in lung tissues of the emphysema + exercise group statistically decreased, the difference was statistically significant (<italic>P</italic>&lt;0.05). <bold>Conclusion</bold> Running could reduce the pulmonary and systemic inflammation, and alleviate the pathological manifestations of emphysema in the mice model of emphysema, and its mechanism may be related to the inhibition of STAT 3 activation.

Subtyping emphysematous COPD by respiratory volume change distributions on CT

BackgroundThere is considerable heterogeneity among patients with emphysematous chronic obstructive pulmonary disease (COPD). We hypothesised that in addition to emphysema severity, ventilation distribution in emphysematous regions would be associated with...

Quantitative evaluation of emphysema for predicting immunotherapy response in patients with advanced non-small-cell lung cancer

The efficacy of immune checkpoint inhibitors (ICIs) in patients with advanced non-small-cell lung cancer (NSCLC) might depend on the presence of emphysema, but this association is not established. We aimed to investigate if quantitively and automatically measuring emphysema can predict the effect of ICIs. We retrospectively analyzed 56 patients with NSCLC who underwent immunotherapy at our hospital. We used the Goddard scoring system (GS) to evaluate the severity of emphysema on baseline CT scans using three-dimensional image analysis software. The emphysema group (GS ≥ 1) showed better progression-free survival (PFS) than the non-emphysema group (GS = 0) (6.5 vs. 2.3 months, respectively, p < 0.01). Multivariate analyses revealed that good performance status, GS of ≥ 1, and high expression of PD-L1 were independently associated with better PFS, while smoking status was not. In conclusion, quantitative evaluation of emphysema can be an objective parameter for predicting the therapeutic effects of ICIs in patients with NSCLC. Our findings can be used to generate hypotheses for future studies.

Regeneration of emphysematous lungs using gelatin sheets that release basic fibroblast growth factor.

Basic fibroblast growth factor (bFGF) induces regeneration and neovascularization of the lungs. We conducted this study to demonstrate the regeneration of emphysematous lungs achieved by gelatin sheets that slowly release bFGF into the visceral pleura in a canine model. Porcine pancreatic elastase was used to induce bilateral lower lobe pulmonary emphysema in dogs. Slow-release bFGF gelatin sheets were attached to the visceral pleura of the left lower lobe via thoracotomy. The subjects were divided into two groups: one treated with gelatin sheets containing slow-release bFGF (bFGF+ group, n = 5), and the other, treated with only gelatin sheets (bFGF- group, n = 5). The subjects were euthanized after 28days and histologic lung assessment was performed. The results were evaluated in terms of the mean linear intercept (MLI) and microvessel count. The MLI was significantly shorter in the bFGF+ group than in the bFGF- group; (110.0 ± 24.38 vs. 208.9 ± 33.08μm; P = 0.0006). The microvessel count was not significantly different between the bFGF+ and bFGF- groups (12.20 ± 3.007 vs. 5.35 ± 2.3425; P = 0.075); however, it was significantly higher in the bFGF-attached lungs than in the emphysema group (12.20 ± 3.007 vs. 4.57 ± 0.8896; P = 0.012). Attaching gelatin sheets with slow-release bFGF to the visceral pleura induced lung regeneration and vascularization in a canine pulmonary emphysema model.

Radiofrequency therapy improves exercise capacity of mice with emphysema

Emphysema is a common phenotype of chronic obstructive pulmonary disease (COPD). Although resection of emphysematous tissue can improve lung mechanics, it is invasive and fraught with adverse effects. Meanwhile, radiofrequency (RF) treatment is an extracorporeal method that leads to tissue destruction and remodeling, resulting in “volume reduction” and overall improvement in lung compliance of emphysematous lungs. Whether these changes lead to improved exercise tolerance is unknown. Here, we investigated the effectiveness of RF treatment to improve the exercise capacity of mice with emphysema. Fifty-two mice (7 weeks of age) were used in this experiment. A bilateral emphysema model was created by intratracheally instilling porcine pancreatic elastase (PPE) (1.5U/100 g body weight). RF treatment (0.5 W/ g body weight) was administered extracorporeally 14 days later and mice were sacrificed after another 21 days. The exercise capacity of mice was measured using a treadmill. Treadmill runs were performed just before PPE instillation (baseline), before RF treatment and before sacrifice. Following sacrifice, lung compliance and mean linear intercept (Lm) were measured and fibrosis was assessed using a modified Ashcroft score. There were 3 experimental groups: controls (instilled with saline, n = 12), emphysema (instilled with porcine pancreatic elastase, PPE, n = 11) and emphysema + treatment (instilled with PPE and given RF, n = 9). At endpoint, the maximum velocity of the emphysema + treatment group was significantly higher than that of the emphysema group, indicating improved exercise tolerance (86.29% of baseline vs 61.69% of baseline, p = 0.01). Histological analysis revealed a significant reduction in emphysema as denoted by Lm between the two groups (median 29.60 µm vs 35.68 µm, p = 0.03). The emphysema + treatment group also demonstrated a higher prevalence of lung fibrosis (≧Grade 3) compared with the emphysema group (11.7% vs 5.4%, p < 0.01). No severe adverse events from RF were observed. RF treatment improved the exercise capacity of mice with emphysema. These data highlight the therapeutic potential of RF treatment in improving the functional status of patients with COPD.

Tumor size in patients with severe pulmonary emphysema might be underestimated on preoperative CT

To evaluate the effect of emphysema on tumor diameter measured on preoperative computed tomography (CT) images versus pathological specimens. We investigated patients who underwent primary lung cancer surgery: 55 patients (57 tumors) with severe emphysema and 57 patients (57 tumors) without emphysema. The tumor diameters measured in the postoperative pathological specimens were compared with those measured on the axial CT images and on multiplanar reconstruction (MPR) CT images by two independent radiologists; a subgroup analysis according to tumor size was also performed. A paired or unpaired t test was performed, depending on the tested subjects. In the emphysema group, the mean axial CT diameter was significantly smaller than the mean pathological diameter (p = 0.025/0.001 for reader 1/2), whereas in the non-emphysema group, the mean axial CT diameter was not significantly different from the pathological one for both readers. The difference between CT axial diameter and pathological diameter (= CT diameter - pathological diameter) was significantly smaller (i.e., had a stronger tendency toward underestimation on radiological measurements) in the emphysema group compared with the non-emphysema group (p = 0.014/0.008 for reader 1/2), and the difference was significantly smaller in tumors sized > 30 mm than tumors sized ≤ 20 mm in both groups. Tumor size is significantly smaller on preoperative CT in patients with severe emphysema compared to patients without emphysema, especially in the case of large tumors. MPR measurement using the widest of three dimensions should be used to select T-stage for patients with severe emphysema. • The presence of emphysema affects the accuracy of tumor size measurements on CT. • Compared to patients without emphysema, the tumor size in severe emphysema patients tends to be measured smaller in preoperative CT than the pathological specimen. • This trend is more evident when large tumors are measured on axial CT images alone.

Combined Pulmonary Fibrosis Emphysema: Role of Cigarette Smoking and Pulmonary Hypertension in a Rural Cohort.

BackgroundDisease heterogeneity in idiopathic pulmonary fibrosis (IPF) often complicates the systematic study of disease, management of patients and clinical investigations.ObjectiveTo describe combined pulmonary fibrosis emphysema (CPFE) phenotype in a rural Appalachian IPF cohort with the highest smoking rates in the United States.MethodsCPFE patients (n = 60) in a developed IPF cohort (n = 153) were characterized. Groups (CPFE vs IPF without emphysema) were categorized based on the predominant HRCT patterns of UIP (n = 109). Demographics, clinical variables, and treatment details were recorded. Kaplan–Meier survival and multivariate logistic regression analysis were performed.ResultsThe prevalence of CPFE in our IPF cohort was 45% (n = 49). The CPFE group was younger (73.9 vs 78.2), had a more extensive smoking history (93.9% vs 53.3%) with greater mean smoking pack years (49.09 vs 15.39) and had lower percentage predicted DLCO on presentation (38.35 vs 51.09) compared to IPF without emphysema group. Both groups shared equivalent higher burden of comorbidities, including pulmonary hypertension (PH) (46.9% vs 33.3%). One-fifth of patients were prescribed antifibrotics and only a subset (5%) of patients underwent lung transplantation. There was a non-significant trend towards reduced survival in CPFE (p = 0.076). Smoking status and DLCO predicted CPFE in our cohort. Body mass index (BMI), PH, and pirfenidone use were significant predictors of mortality.ConclusionCPFE was highly prevalent in our rural IPF cohort. In contrast to previous studies, CPFE group was older and had higher female (approx. 30%) occurrence. A greater exposure to cigarette smoke and reduced DLCO at diagnosis predicted CPFE. Lower BMI and PH predicted higher mortality whereas use of pirfenidone improved survival in our cohort. This study highlights a complex interaction of cigarette smoking, advanced fibrosis of UIP, PH and potential utility of antifibrotic agents in CPFE phenotype. Substantial burden of comorbidities, older age, and the limited utilization of advanced therapeutics in the cohort emphasize the challenges faced by rural Appalachian patients.

Clinical relevance of emphysema in patients hospitalized with community-acquired pneumonia: Clinical features and prognosis.

Few studies have investigated the influence of emphysema on clinical features of patients presenting with community-acquired pneumonia (CAP). The aim of this study was to examine the clinical and microbiological features of patients with both CAP and emphysema. This retrospective study included patients with CAP who underwent computed tomography (CT) scan at the time of presentation. Patients were allocated into emphysema and control groups, and clinical variables were compared between the two groups. The emphysema group was further divided into three subgroups (mild, moderate, and severe) according to the extent of emphysema on CT scan. The clinical variables of each subgroup were compared with the control group. Of 1676 patients, 431 patients (25.7%) were classified into the emphysema group. CAP patients with emphysema were more likely to have a high CURB-65 score and pneumonia severity index and a lower incidence of complicated parapneumonic effusion or empyema. The emphysema group exhibited longer hospital stay. In addition, 30-day mortality in the severe emphysema group was significantly higher compared with the control group. As etiological agents, Streptococcus pneumoniae, Pseudomonas aeruginosa, Enterobacteriaceae, and multidrug-resistant pathogens were significantly more common in the emphysema group compared with the control group. The presence of emphysema in CAP patients was associated with a more severe form of CAP, a longer hospital stay, and a lower incidence of complicated parapneumonic effusion or empyema. Moreover, CAP patients with severe emphysema exhibited higher 30-day mortality than those without emphysema.

Correlation between systemic inflammation level and emphysema degree and bone mineral density in chronic obstructive pulmonary disease patients and its mechanism

Objective: To study the correlation between systemic inflammation level and emphysema degree and bone mineral density in chronic obstructive pulmonary disease (COPD) patients and its possible mechanism. Methods: 90 patients with stable COPD who met the inclusion criteria and 50 controls in the physical examination center during the same period were recruited. All the enrolled objects have collected general clinical data, analyzed peripheral blood samples, measuring the Low-attenuation area of lung and CT value of lumbar 1 vertebra (L1-CT) by chest spiral CT. According to LAA%, COPD patients were divided into 36 cases of the non-emphysema group, 32cases of mild to moderate emphysema group, and 22 cases of severe emphysema group. The correlation between L1-CT value, LAA%, peripheral blood inflammatory factors, and pulmonary function indices in each group was analyzed and compared. Results: The HU value of L1-CT (107±32) in the COPD group was significantly lower than that in the control group (153±30), and the difference was statistically significant (P<0.05). The higher the LAA% in COPD patients was, the lower the value of L1-CT was, and the difference between groups was statistically significant. Compared with COPD patients in the non-emphysema group, peripheral blood neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and C-reactive protein (CRP) were all increased in the emphysema group, and the differences were statistically significant (P<0.05). L1-CT was negatively correlated with LAA, PLR, NLR, and CRP while uncorrelated with serum concentration of calcium and phosphorus. Conclusion: The decrease in bone density in COPD patients is closely related to the degree of emphysema. It is associated with increased levels of systemic inflammation caused by COPD itself. Early and timely broad-spectrum anti-inflammatory treatment may have certain clinical significance for the prevention and treatment of comorbidity with osteoporosis.

CT Assessment of Subtypes of Pulmonary Emphysema in Mongolian Miners

Objectives: To determine the incidence of subtypes of pulmonary emphysema identified by LDCT imaging and the relationship between emphysema subtypes with smoking and pulmonary function in miners. Methods: We reviewed 329 miners (245 men and 84 women). Each miner had a low dose (LD) chest CT. Among them 75 miners had a standard chest CT. The images were reconstructed using contemporary iterative reconstruction. Lung volumes and emphysema severity was calculated using automated densitometry segmentation software and qualitative visual analyses.There were two subtypes of pulmonary emphysema found: centrilobular emphysema (CLE) and paraseptal emphysema (PSE). Based on these subtypes, CLE was divided into the following five categories: trace, mild, moderate, confluent, and advanced CLE. PSE was divided into the following two catergories: mild and substantial PSE. Results: Pulmonary emphysema was found in 89 (27.1%) of 329 miners. According to the survey, 73 (82.0%) miners had centrilobulor emphysema, and 17 (18.0%) had a paraseptal emphysema. The emphysema group was a lower Gensler index than thenon-emphysema group. The smoker group had higher emphysematous changes than the non-smoker groups (p &lt; 0.05). Conclusions: Dose reduced CT isauseful study for the assessment of emphysema.

Distinguishing Smoking-Related Lung Disease Phenotypes Via Imaging and Molecular Features

Chronic tobacco smoke exposure results in a broad range of lung pathologies including emphysema, airway disease and parenchymal fibrosis as well as a multitude of extra-pulmonary comorbidities. Prior work using CT imaging has identified several clinically relevant subgroups of smoking related lung disease, but these investigations have generally lacked organ specific molecular correlates. Can CT imaging be used to identify clinical phenotypes of smoking related lung disease that have specific bronchial epithelial gene expression patterns to better understand disease pathogenesis? Using K-means clustering, we clustered participants from the COPDGene study (n= 5,273) based on CT imaging characteristics and then evaluated their clinical phenotypes. These clusters were replicated in the Detection of Early Lung Cancer Among Military Personnel (DECAMP) cohort (n= 360), and were further characterized using bronchial epithelial gene expression. Three clusters (preserved, interstitial predominant and emphysema predominant) were identified. Compared to the preserved cluster, the interstitial and emphysema clusters had worse lung function, exercise capacity and quality of life. In longitudinal follow-up, individuals from the emphysema group had greater declines in exercise capacity and lung function, more emphysema, more exacerbations, and higher mortality. Similarly, genes involved in inflammatory pathways (tumor necrosis factor-α, interferon-β) are more highly expressed in bronchial epithelial cells from individuals in the emphysema cluster, while genes associated with T-cell related biology are decreased in these samples. Samples from individuals in the interstitial cluster generally had intermediate levels of expression of these genes. Using quantitative CT imaging, we identified three groups of individuals in older ever-smokers that replicate in two cohorts. Airway gene expression differences between the three groups suggests increased levels of inflammation in the most severe clinical phenotype, possibly mediated by the tumor necrosis factor-α and interferon-β pathways. COPDGene (NCT00608764), DECAMP-1 (NCT01785342), DECAMP-2 (NCT02504697).

All Trans Retinoic Acid (ATRA) progresses alveolar epithelium regeneration by involving diverse signalling pathways in emphysematous rat

IntroductionPulmonary emphysema is characterized by destruction of alveoli leading to inadequate oxygenation, disability and frequently death. This destruction was understood so far as irreversible. Published data has shown that ATRA (All Trans Retinoic Acid) reverses elastase-induced emphysema in rats. However, the molecular mechanisms governing regeneration process are so far unknown. ObjectiveTo examine the therapeutic potential of ATRA on various molecular pathways and their coordination towards governance of alveolar epithelial regeneration in emphysematous rats. MethodsEmphysema was induced by elastase versus saline in Sprague-Dawley rats. On days 26–37, rats received daily intraperitoneal injections with ATRA (500 μg/kg b.w.) versus olive-oil. Lungs were removed at day 38 for histopathology and investigation of relative mRNA and protein expressions. ResultsHistopathological analysis has shown that losses of alveoli were recovered in therapy (EA) group. Moreover, expressions of markers genes for alveolar cell proliferation, differentiation and EMT events at mRNA and protein levels were significantly increased in EA group than emphysema group (ES). Upon validation at genomics level, expressions of components of Notch, Hedgehog, Wnt, BMP and TGFβ pathways were significantly attenuated in EA group when compared with ES and were well comparable with the healthy group. ConclusionTherapeutic supplementation of ATRA rectifies the deregulated Notch, Hedgehog, Wnt, BMP and TGFβ pathways in emphysema condition, resulting in alveolar epithelium regeneration. Hence, ATRA may prove to be a potential drug in the treatment of emphysema. Nevertheless, elaborated studies are to be conducted.

Pulmonary Emphysema Impairs Male Reproductive Physiology Due To Testosterone and Oxidative Stress Imbalance in Mesocricetus auratus.

This study evaluated whether pulmonary emphysema affects sperm quality, male reproductive organs, and testosterone levels in adult male hamsters. Mesocricetus auratus males (130-150g) were subdivided into a control group (C group) and an emphysema group (E group). The C group received an intratracheal instillation of saline solution (0.3mL/100g of body weight), and the E group received papain (40mg/100g of body weight). After 60days, the biometric, pulmonary, and reproductive parameters of each group were evaluated. The E group developed pulmonary emphysema, which decreased body weight and sperm quality compared to the C group. In oxidative stress-related assays, lipid peroxidation was increased in the testis and epididymis (caput and cauda) in the E group compared with the C group. However, only the caput epididymis showed a reduction in glutathione levels. Pulmonary emphysema also affected the testicle by inducing an increase in abnormal seminiferous tubules, accompanied by a decrease in seminiferous epithelium height. Spermatogenesis kinetics were also modified by pulmonary emphysema. The number of Leydig and Sertoli cells decreased in the E group, accompanied by an increase in the nuclear volume of Leydig cells. Testosterone concentration was increased in the E group. Similarly, pulmonary emphysema altered epididymal components in all regions. In conclusion, pulmonary emphysema affected the reproductive system in this experimental model, as shown by testicular and epididymal morphophysiology changes, hormonal alteration, and oxidative stress imbalance, inducing the loss of correct function in the male reproductive system.