New insights on COPD imaging via CT and MRI

Multidetector-row computed tomography (MDCT) can be used to quantify morphological features and investigate structure/function relationship in COPD. This approach allows a phenotypical definition of COPD patients, and might improve our understanding of disease pathogenesis and suggest new therapeutical options. In recent years, magnetic resonance imaging (MRI) has also become potentially suitable for the assessment of ventilation, perfusion and respiratory mechanics. This review focuses on the established clinical applications of CT, and novel CT and MRI techniques, which may prove valuable in evaluating the structural and functional damage in COPD

Serum Levels of Surfactant Proteins in Patients with Combined Pulmonary Fibrosis and Emphysema (CPFE)

Introduction Emphysema and idiopathic pulmonary fibrosis (IPF) present either per se or coexist in combined pulmonary fibrosis and emphysema (CPFE). Serum surfactant proteins (SPs) A, B, C and D levels may reflect lung damage. We evaluated serum SP levels in healthy controls, emphysema, IPF, and CPFE patients and their associations to disease severity and survival. Methods 122 consecutive patients (31 emphysema, 62 IPF, and 29 CPFE) and 25 healthy controls underwent PFTs, ABG-measurements, 6MWT and chest HRCT. Serum levels of SPs were measured. Patients were followed-up for 1-year. Results SP-A and SP-D levels differed between groups (p = 0.006 and p= 26 ng/mL) presented a weak association with reduced survival (p = 0.05). Conclusion In conclusion, serum SP-A and SP-D levels were higher where fibrosis exists or coexists and related to disease severity, suggesting that serum SPs relate to alveolar damage in fibrotic lungs and may reflect either local overproduction or overleakage. The weak association between high levels of SP-B and survival needs further validation in clinical trials

Occupational respiratory diseases

Shipping list no.: 87-222-P."September 1986."S/N 017-033-00425-1 Item 499-F-2Also available via the World Wide Web.Includes bibliographies and index

Alterations of CCSP expression and macrophages metabolism in the development of silica-induced pulmonary inflammation and fibrosis

Silicosis is a lethal pneumoconiosis, for which no therapy is available. Silicosis is a public health threat: more than 2.2 million people/year in the US and 230 million/year worldwide, are exposed to silica, and consequently are at increased risk of active mycobacterial tuberculosis (TB), and lung cancer. The initial response to silica is mediated by the innate immunity in a two-stage process: 1)injury of conducting epithelium at distal lung, loss of Club cells secretory protein (CCSP), and impairment of regenerative capacity; 2)phagocytosis of silica by macrophages, metabolic alterations, oxidative stress, and release of reactive-oxygen-species (ROS) and inflammatory cytokines, such as Interleukin-(IL-)1β, Tumor necrosis factor-(TNF-)α, Interferon-(IFN-)β. However, the specific role of airway epithelium and macrophage in the pathogenesis of silicosis in humans is poorly understood. This study focuses on whether silica-induced inflammation compromises the Club cells ability to regenerate bronchiolar and/or alveolar epithelium and on the macrophages metabolic alterations that occurs upon phagocytosis of silica, leading to chronic inflammation. Using wild-type and CCSP-deficient (CCSP-/-) mice we exhibit that the development of the silicotic nodules in the lung is characterized by peri-bronchiolar inflammatory cell recruitment and tissue fibrosis, that compromises the expression and proliferation of CCSP-expressing progenitor cells and limits the reparative properties of the distal airway epithelium, resulting in exacerbation of silicosis. We reveal an immunomodulatory role for CCSP in response to silica both in mice and in human lungs. Subsequently, using murine RAW 264.7 macrophage cell lines, and state- of- art techniques, such as high-resolution respirometer and liquid chromatography-high resolution mass spectrometry (LC-HRMS), to determine the effects of silica on mitochondrial respiration, and the changes in central carbon metabolism of silica-exposed macrophages, we demonstrate that in contrast to the prevalent view, crystalline silica alone induces an innate immune response without previous macrophage activation with LPS, and yet different from the one LPS-induced, since they affect differently the CII of ETC, which plays a crucial role in macrophages survival and silica-induced inflammation. Our data highlight the urgency to validate these concepts and elucidate the mechanisms underlying the silica-induced impairment of macrophages, development of inflammation and fibrosis, and consequent increased TB risk

Diseases of the Chest, Breast, Heart and Vessels 2019-2022

This open access book focuses on diagnostic and interventional imaging of the chest, breast, heart, and vessels. It consists of a remarkable collection of contributions authored by internationally respected experts, featuring the most recent diagnostic developments and technological advances with a highly didactical approach. The chapters are disease-oriented and cover all the relevant imaging modalities, including standard radiography, CT, nuclear medicine with PET, ultrasound and magnetic resonance imaging, as well as imaging-guided interventions. As such, it presents a comprehensive review of current knowledge on imaging of the heart and chest, as well as thoracic interventions and a selection of "hot topics". The book is intended for radiologists, however, it is also of interest to clinicians in oncology, cardiology, and pulmonology

Novel approaches to the assessment of patients with chest systoms in the acute medical and outpatient settings: the use of multislice computed tomography

This thesis evaluated the clinical utility of cardiopulmonary computed tomography (CT) in patients presenting with chest pain and dyspnoea. Studies within this thesis confirmed the following. Firstly, there is a requirement for improved diagnostic pathways to minimise patients being discharged without a diagnosis, which currently occurs in 30-40% of patients admitted with chest pain and dyspnoea. Historically, CT has been utilised in 32% of admissions with chest pain and 10% of admissions with dyspnoea. Secondly, challenges exist to the wider adoption of cardiopulmonary CT. These include patient-related factors, institutional capabilities and guideline restrictions. In acute admissions, 11% of patients with dyspnoea and 7% of patients with chest pain and a low to moderate likelihood of CAD are suitable for CT. In the RACPC setting, including patients across the entire spectrum of CAD likelihood, 18% of patients are suitable for CT. NICE CG95 would recommend only 1% of acute chest pain admissions and 2% of RACPC attenders for CT. Thirdly, NICE CG95 would recommend 51% of acute chest pain admissions and 66% of RACPC attenders for discharge without cardiac investigation. In the RACPC population, significant CAD is identified in 10% of these patients and a major adverse cardiac event in 2%. Fourthly, in selected patients with suspected cardiac chest pain, cardiac CT has a diagnostic yield of 21% in acute admissions and 13% in RACPC attenders for significant CAD. In acute admissions with dyspnoea, cardiopulmonary CT has a diagnostic yield of 20% for CAD, 20% for pulmonary embolism, nil for aortic dissection and 89% for non-vascular chest pathology. Fifthly, inclusion of CT in diagnostic pathways for chest pain result in fewer patients discharged without a diagnosis, fewer invasive angiography procedures and reduced diagnostic costs. In patients with dyspnoea, CT provides value to clinicians making diagnoses and supports early discharge without detrimental outcomes.Open Acces