Chronic obstructive pulmonary disease (COPD) and asthma are common diseases with a heterogeneous distribution worldwide. Here, we present methods and disease and risk estimates for COPD and asthma from the Global Burden of Diseases, Injuries, and Risk Factors (GBD) 2015 study. The GBD study provides annual updates on estimates of deaths, prevalence, and disability-adjusted life years (DALYs), a summary measure of fatal and non-fatal disease outcomes, for over 300 diseases and injuries, for 188 countries from 1990 to the most recent year.We estimated numbers of deaths due to COPD and asthma using the GBD Cause of Death Ensemble modelling (CODEm) tool. First, we analysed data from vital registration and verbal autopsy for the aggregate category of all chronic respiratory diseases. Subsequently, models were run for asthma and COPD relying on covariates to predict rates in countries that have incomplete or no vital registration data. Disease estimates for COPD and asthma were based on systematic reviews of published papers, unpublished reports, surveys, and health service encounter data from the USA. We used the Global Initiative of Chronic Obstructive Lung Disease spirometry-based definition as the reference for COPD and a reported diagnosis of asthma with current wheeze as the definition of asthma. We used a Bayesian meta-regression tool, DisMod-MR 2.1, to derive estimates of prevalence and incidence. We estimated population-attributable fractions for risk factors for COPD and asthma from exposure data, relative risks, and a theoretical minimum exposure level. Results were stratified by Socio-demographic Index (SDI), a composite measure of income per capita, mean years of education over the age of 15 years, and total fertility rate.In 2015, 3·2 million people (95% uncertainty interval [UI] 3·1 million to 3·3 million) died from COPD worldwide, an increase of 11·6% (95% UI 5·3 to 19·8) compared with 1990. There was a decrease in age-standardised death rate of 41·9% (37·7 to 45·1) but this was counteracted by population growth and ageing of the global population. From 1990 to 2015, the prevalence of COPD increased by 44·2% (41·7 to 46·6), whereas age-standardised prevalence decreased by 14·7% (13·5 to 15·9). In 2015, 0·40 million people (0·36 million to 0·44 million) died from asthma, a decrease of 26·7% (-7·2 to 43·7) from 1990, and the age-standardised death rate decreased by 58·8% (39·0 to 69·0). The prevalence of asthma increased by 12·6% (9·0 to 16·4), whereas the age-standardised prevalence decreased by 17·7% (15·1 to 19·9). Age-standardised DALY rates due to COPD increased until the middle range of the SDI before reducing sharply. Age-standardised DALY rates due to asthma in both sexes decreased monotonically with rising SDI. The relation between with SDI and DALY rates due to asthma was attributed to variation in years of life lost (YLLs), whereas DALY rates due to COPD varied similarly for YLLs and years lived with disability across the SDI continuum. Smoking and ambient particulate matter were the main risk factors for COPD followed by household air pollution, occupational particulates, ozone, and secondhand smoke. Together, these risks explained 73·3% (95% UI 65·8 to 80·1) of DALYs due to COPD. Smoking and occupational asthmagens were the only risks quantified for asthma in GBD, accounting for 16·5% (14·6 to 18·7) of DALYs due to asthma.Asthma was the most prevalent chronic respiratory disease worldwide in 2015, with twice the number of cases of COPD. Deaths from COPD were eight times more common than deaths from asthma. In 2015, COPD caused 2·6% of global DALYs and asthma 1·1% of global DALYs. Although there are laudable international collaborative efforts to make surveys of asthma and COPD more comparable, no consensus exists on case definitions and how to measure disease severity for population health measurements like GBD. Comparisons between countries and over time are important, as much of the chronic respiratory burden is either preventable or treatable with affordable interventions.Bill & Melinda Gates Foundation.Copyright © 2017 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) have considerably high mortality and re-hospitalisation rate. Diaphragmatic dysfunction (DD) is common in COPD patients. However, whether diaphragmatic dysfunction is related to acute exacerbation is yet to be elucidated. This study aimed to evaluate the diaphragm function by magnetic resonance imaging (MRI) in COPD patients and assess whether the impact of DD may help predict AECOPD.20 healthy adult volunteers and 80 COPD patients were enrolled. The diaphragms function parameters were accessed by MRI. Patients were guided to start self-management by the Telehealth-based monitoring system following the enrolment. Events of acute exacerbation of COPD were recorded by the system and confirmed by healthcare providers. Binary univariate and multivariate logistic regression analyses were performed to investigate the factors associated with the frequency of AECOPD. Receiver operating characteristic (ROC) curves were further used to assess the value of prediction indexes.Fifty-nine COPD patients completed a one-year follow-up based on the Telehealth-based monitoring system. The clinical outcomes showed that the diaphragm function parameters at the end of maximal breathing were lower in the COPD group than in the healthy control group (P < 0.05). ANOVA showed significant differences among Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages for diaphragm function parameters, including chest wall motion, lung area, upper-lower diameter, and the diaphragm thickening fraction at the end of maximal breathing (P < 0.05). Moreover, significant differences in diaphragm function parameters were observed between patients with infrequent AECOPD (n = 28) and frequent AECOPD (n = 31) based on the frequency of AECOPD (P < 0.05). The diaphragm thickening fraction and the chest wall motion were associated with AECOPD after adjusting for age, sex, BMI, and lung functions, and the combination of predictions showed better accuracy in predicting the frequency of AECOPD.In COPD patients, diaphragm function parameters correlate with the severity of airflow limitation. The diaphragm thickening fraction and the chest wall motion were associated with the frequency of AECOPD and can predict it.© 2022. The Author(s).

磁共振成像(MRI)技术具有非侵入、无放射性的特点，在临床疾病诊断中具有独特的优势，但是肺部空腔的特殊结构使传统质子MRI 无法对其直接成像．自旋交换光抽运(SEOP)方法可以使惰性气体原子的极化度增强4 个量级以上，从而使肺部的气体MRI 成为可能．该文介绍了超极化惰性气体肺部MRI 的最新研究进展，包括超极化气体磁共振相关参数的测量方法、肺部通气结构成像、肺部气体交换功能成像，同时比较了常用于肺部MRI气体的优点和缺点．

To demonstrate the feasibility to quantify the lung respiratory airway in vivo with hyperpolarized xenon diffusion magnetic resonance imaging (MRI), which is able to detect mild emphysema in the rat model.The lung respiratory airways were quantified in vivo using hyperpolarized xenon diffusion MRI (7T) with eight b values (5, 10, 15, 20, 25, 30, 35, 40 s/cm ) in five control rats and five mild emphysematous rats, which were induced by elastase. The morphological results from histology were acquired and used for comparison.The parameters D (longitudinal diffusion coefficient), r (internal radius), h (alveolar sleeve depth), Lm (mean linear intercept), and S/V (surface area to lung volume ratio) derived from the hyperpolarized xenon diffusion MRI in the emphysematous group showed significant differences from those in the control group (P < 0.05). Additionally, these parameters correlated well with the Lm obtained by the traditional histological sections (Pearson's correlation coefficients >0.8).The lung respiratory airways can be quantified by hyperpolarized xenon diffusion MRI, showing the potential for mild emphysema diagnosis. Also, the study suggested that the hyperpolarized xenon D is more sensitive than D (transverse diffusion coefficient) to detect mild emphysema.1 J. Magn. Reson. Imaging 2017;45:879-888.© 2016 International Society for Magnetic Resonance in Medicine.

: COPD biomarkers are urgently required for clinical trials of new therapies. We evaluated the longitudinal change and relationship of MRI and CT biomarkers of COPD with St. George's Respiratory Questionnaire (SGRO) and FEV worsening over 30 months. Among imaging biomarkers, only the longitudinal change in MRI ventilation defect percent (VDP) was greater in ever-smoker (n=34/p<0.05) and COPD (n=48/p<0.0001) subgroups compared with never-smokers (n=42). Only the longitudinal change in VDP was correlated with change in SGRQ (r=0.26/p=0.03), and only baseline VDP predicted longitudinal change in SGRQ>minimum clinically important difference (p=0.047) in mild-to-moderate COPD. These data strongly support the use of MRI intermediate endpoints in COPD studies.NCT02723474; Status: Recruiting.Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

因其较高的核自旋极化度所提供的探测灵敏度，超极化¹²⁹Xe气体已被成功应用于动物和人体磁共振成像（MRI）.但是，在超极化¹²⁹Xe的收集-升华过程中，多种因素会导致¹²⁹Xe核自旋弛豫，进而限制其应用范围.本文通过理论模型分析和实验测量，验证了温度、磁场、螺旋冷阱材质等对冷冻恢复过程中超极化¹²⁹Xe弛豫的影响；同时，测量了自动收集-升华装置的稳定性.研究结果表明，升华方式和冷阱材质对¹²⁹Xe极化度损耗的影响显著；自制收集-升华装置的自动化程度高、长时间稳定，¹²⁹Xe极化度的恢复率可达到85.6% ± 4.7%.本研究非常有助于提升超极化¹²⁹Xe在动物和人体MRI中的使用效率.

Chronic obstructive pulmonary disease (COPD) is a progressive disorder of the lung parenchyma which also involves extrapulmonary manifestations, such as cardiovascular impairment, diaphragm dysfunction, and frequent exacerbations. The development of animal models is important to elucidate the pathophysiology of COPD exacerbations and enable analysis of possible therapeutic approaches. We aimed to characterize a model of acute emphysema exacerbation and evaluate its consequences on the lung, heart, and diaphragm. Twenty-four Wistar rats were randomly assigned into one of two groups: control (C) or emphysema (ELA). In ELA group, animals received four intratracheal instillations of pancreatic porcine elastase (PPE) at 1-week intervals. The C group received saline under the same protocol. Five weeks after the last instillation, C and ELA animals received saline (SAL) or lipopolysaccharide (LPS) (200 μg in 200 μl) intratracheally. Twenty-four hours after saline or endotoxin administration, arterial blood gases, lung inflammation and morphometry, collagen fiber content, and lung mechanics were analyzed. Echocardiography, diaphragm ultrasonography (US), and computed tomography (CT) of the chest were done. ELA-LPS animals, compared to ELA-SAL, exhibited decreased arterial oxygenation; increases in alveolar collapse (< 0.0001), relative neutrophil counts ( = 0.007), levels of cytokine-induced neutrophil chemoattractant-1, interleukin (IL)-1β, tumor necrosis factor-α, IL-6, and vascular endothelial growth factor in lung tissue, collagen fiber deposition in alveolar septa, airways, and pulmonary vessel walls, and dynamic lung elastance (< 0.0001); reduced pulmonary acceleration time/ejection time ratio, (an indirect index of pulmonary arterial hypertension); decreased diaphragm thickening fraction and excursion; and areas of emphysema associated with heterogeneous alveolar opacities on chest CT. In conclusion, we developed a model of endotoxin-induced emphysema exacerbation that affected not only the lungs but also the heart and diaphragm, thus resembling several features of human disease. This model of emphysema should allow preclinical testing of novel therapies with potential for translation into clinical practice.