Academic literature on the topic 'Diffuse parenchymal lung diseases'

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Journal articles on the topic "Diffuse parenchymal lung diseases"

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Tomassetti, Sara, Claudia Ravaglia, and Venerino Poletti. "Diffuse parenchymal lung disease." European Respiratory Review 26, no. 144 (April 26, 2017): 170004. http://dx.doi.org/10.1183/16000617.0004-2017.

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Between September 2015 and August 2016 there were >1500 publications in the field of diffuse parenchymal lung diseases (DPLDs). For the Clinical Year in Review session at the European Respiratory Society Congress that was held in London, UK, in September 2016, we selected only five articles. This selection, made from the enormous number of published papers, does not include all the relevant studies that will significantly impact our knowledge in the field of DPLDs in the near future. This review article provides our personal view on the following topics: early diagnosis of idiopathic pulmonary fibrosis, current knowledge on the multidisciplinary team diagnosis of DPLDs and the diagnostic role of transbronchial cryobiopsy in this diagnostic setting, insights on the new entity of interstitial pneumonia with autoimmune features, and new therapeutic approaches for scleroderma-related interstitial lung disease.
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Poletti, Venerino, Claudia Ravaglia, and Sara Tomassetti. "Transbronchial cryobiopsy in diffuse parenchymal lung diseases." Current Opinion in Pulmonary Medicine 22, no. 3 (May 2016): 289–96. http://dx.doi.org/10.1097/mcp.0000000000000272.

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Martinez, Fernando J., and Michael P. Keane. "Update in Diffuse Parenchymal Lung Diseases 2005." American Journal of Respiratory and Critical Care Medicine 173, no. 10 (May 15, 2006): 1066–71. http://dx.doi.org/10.1164/rccm.2601011.

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Raghunath, Sushravya, Srinivasan Rajagopalan, Ronald A. Karwoski, Fabien Maldonado, Tobias Peikert, Teng Moua, Jay H. Ryu, Brian J. Bartholmai, and Richard A. Robb. "Quantitative Stratification of Diffuse Parenchymal Lung Diseases." PLoS ONE 9, no. 3 (March 27, 2014): e93229. http://dx.doi.org/10.1371/journal.pone.0093229.

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Walsh, Sinead M., and Anthony W. O’Regan. "Diffuse Parenchymal Lung Diseases in the Elderly." Current Geriatrics Reports 7, no. 3 (July 13, 2018): 174–80. http://dx.doi.org/10.1007/s13670-018-0249-x.

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Shlobin, Oksana A., A. Whitney Brown, and Steven D. Nathan. "Pulmonary Hypertension in Diffuse Parenchymal Lung Diseases." Chest 151, no. 1 (January 2017): 204–14. http://dx.doi.org/10.1016/j.chest.2016.08.002.

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Farag, TaghreedS, ZeinabR Adawy, LobnaK Sakr, and HanaaS Abdellateef. "Transthoracic ultrasonographic features of diffuse parenchymal lung diseases." Egyptian Journal of Bronchology 11, no. 3 (2017): 179. http://dx.doi.org/10.4103/ejb.ejb_3_17.

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Tsangaris, Iraklis, Georgios Tsaknis, Anastasia Anthi, and Stylianos E. Orfanos. "Pulmonary Hypertension in Parenchymal Lung Disease." Pulmonary Medicine 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/684781.

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Idiopathic pulmonary arterial hypertension (IPAH) has been extensively investigated, although it represents a less common form of the pulmonary hypertension (PH) family, as shown by international registries. Interestingly, in types of PH that are encountered in parenchymal lung diseases such as interstitial lung diseases (ILDs), chronic obstructive pulmonary disease (COPD), and many other diffuse parenchymal lung diseases, some of which are very common, the available data is limited. In this paper, we try to browse in the latest available data regarding the occurrence, pathogenesis, and treatment of PH in chronic parenchymal lung diseases.
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Braun, Sarah, Marion Ferner, Kai Kronfeld, and Matthias Griese. "Hydroxychloroquine in children with interstitial (diffuse parenchymal) lung diseases." Pediatric Pulmonology 50, no. 4 (December 9, 2014): 410–19. http://dx.doi.org/10.1002/ppul.23133.

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Pulagam, Ammi Reddy, Giri Babu Kande, Venkata Krishna Rao Ede, and Ramesh Babu Inampudi. "Automated Lung Segmentation from HRCT Scans with Diffuse Parenchymal Lung Diseases." Journal of Digital Imaging 29, no. 4 (March 9, 2016): 507–19. http://dx.doi.org/10.1007/s10278-016-9875-z.

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Dissertations / Theses on the topic "Diffuse parenchymal lung diseases"

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Sharp, Charles Michael Francis. "Clinical outcomes in diffuse parenchymal lung disease." Thesis, University of Bristol, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723507.

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Merola, Pietro Krauspenhar. "Avaliação funcional da musculatura respiratória e periférica e sua relação com a capacidade de exercício e dispneia em pacientes com pneumonias intersticiais fibrosantes." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/143039.

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Introdução: A área do músculo peitoral (AMP) é uma avaliação facilmente derivada da tomografia computadorizada do tórax com potencial de fornecer informações relevantes sobre outros músculos esqueléticos. A Disfunção muscular respiratória e periférica é cada vez mais reconhecida em pacientes com doença pulmonar intersticial (DPI). A sua relação com a capacidade de exercício tem sido controversa. Nosso objetivo foi investigar se AMP está relacionada com a força muscular esquelética respiratória e periférica em pacientes com DPI, e se a função dos músculos esqueléticos estaria reduzida e independentemente relacionada com a capacidade de exercício e dispneia nesses pacientes. Métodos: Estudo transversal onde foi realizado teste de exercício cardiopulmonar incremental em cicloergômetro com mensuração de pressão inspiratória máxima (PImax), pressão expiratória máxima (PEmax) e contração voluntária máxima (CVM) do quadríceps, antes e após o exercício. Os testes de função pulmonar em repouso e TC de tórax foram obtidos da rotina assistencial dos pacientes.
Background: Pectoralis muscle area (PMA) is an easily derived computed tomography-based assessment that can provide insight into clinical features of other skeletal muscles. Respiratory and locomotor muscle dysfunction has been increasingly recognized in patients with interstitial lung disease (ILD). Its contribution to exercise performance has been controversial. We aimed investigate if PMA is related with respiratory and locomotor skeletal muscle strength in ILD patients, and if skeletal muscle function is compromised and independently related with exercise capacity and dyspnea in these patients. Methods: Cross-sectional study where subjects performed incremental cycling cardiopulmonary exercise testing with maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), and quadriceps maximal voluntary contraction (MVC) before and after exercise.
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Jacob, Joseph. "Computer based analysis of diffuse fibrosing lung diseases." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/52803.

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Computer based CT analysis of interstitial lung disease (ILD) may finally have come of age with sophisticated new software algorithms that can analyse CTs of patients with idiopathic pulmonary fibrosis (IPF) with similar, or superior, precision to visual scoring by radiologists. However, the latest iterations of such tools have not been evaluated in large populations or in fibrosing lung diseases (FLD) other than IPF. The investigations in this thesis aimed to identify the role of a computer-based tool CALIPER, compared to visual CT scoring and pulmonary function indices, in predicting prognosis at baseline in a large IPF cohort and across a range of FLDs. A second line of enquiry was exploration of the utility of serial CT as a prognosticator in IPF patients. Visual scores for these investigations were provided by four experienced sub-specialty thoracic radiologists. Baseline CT analysis in IPF demonstrated that CALIPER parameters, particularly the percentage of the lung occupied by vessels (parenchymal vascular percentage - PVP), were strong predictors of pulmonary function indices as well as mortality. CALIPER variables were the strongest predictors of mortality in patients with hypersensitivity pneumonitis and connective tissue disease-related-ILD and were one of the strongest predictors of mortality in an “all-comers” cohort of FLD. Serial evaluation of CT scans demonstrated that change in CALIPER variables, specifically change in PVP, was a stronger and more sensitive predictor of survival than the best available measure of disease worsening in IPF, namely change in forced vital capacity (FVC). It is concluded that CALIPER is a viable complementary tool in the baseline and serial evaluation of IPF and the baseline analysis of the majority of FLDs. Change in PVP, in particular, may represent a new index in the clinical evaluation of disease progression in IPF and could represent a co-endpoint alongside FVC change in clinical trials.
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Abdallah, Atiyeh Mahmoud. "The genetics of co-stimulation in diffuse (pro-fibrotic) lung diseases." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439005.

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Camargo, Leandro do Nascimento. "O efeito do anti-IL-17 na inflama~ção, remodelamento e estresse oxidativo em modelo experimental de inflamação pulmonar alérgica crônica exacerbado por LPS." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-15082018-082634/.

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INTRODUÇÃO: A inflamação desempenha um papel central no desenvolvimento da asma, que é considerada uma doença alérgica com um perfil inflamatório clássico Th2. No entanto, as citocinas de perfil IL-17 tem sido estudadas para melhor compreender sua participação na fisiopatologia desta doença. Pacientes asmáticos graves apresentam exacerbações freqüentes, sendo a causa infecciosa um dos principais desencadeantes e que podem perpetuar as respostas inflamatórias. A resposta Th17 pode estar claramente associada a esses eventos. OBJETIVO: Este estudo avaliou os efeitos da terapia com anticorpo monoclonal anti-IL-17 nas alterações presentes nos septos alveolares em um modelo experimental de inflamação pulmonar alérgica crônica exacerbado por LPS. MÉTODOS: Foram utilizados 60 camundongos macho da espécie BALB/c, sendo sensibilizados com ovoalbumina intraperitoneal e repetidamente expostos à inalação com ovoalbumina, seguidos por tratamento com ou sem anti-IL-17. Vinte e quatro horas antes do final do protocolo experimental de 29 dias, dois grupos receberam LPS intratraqueal (0,1 mg/ml, sendo os grupos OVA-LPS e OVA-LPS anti-IL-17). Posteriormente, avaliamos o fluido do lavado broncoalveolar (FLBA), por morfometria quantificamos o recrutamento das células apresentadoras de antígenos (FOXP3 e células dendríticas), de eosinófilos, a expressão celular de citocinas próinflamatórias (TNF-alfa, IL-2, IL-4, IL-5, IL-6, IL13 e IL-17), anti-inflamatórias (IL-10), quimiocina (TARC), além da quantificação de IL-6 por RT-PCR. Avaliamos também elementos da matriz extracelular (fibras colágenas tipo I e III, MMP-9, MMP-12, TIMP-1, TGF-beta, actina, decorina, lumicam, biglicano, fibronectina e integrina), edema dos septos alveolares, resposta das vias de estresse oxidativo através dos marcadores iNOS e 8-iso-PGF2alfa e as vias sinalizadoras NF-kB e Rho quinase, além da avaliação do diâmetro alveolar médio. RESULTADOS: Os animais do grupo OVA-LPS apresentaram uma potencialização de todas as respostas (p < 0,05) comparativamente ao grupo OVA, exceto para: expressão de IL-17, TNF-alfa, NF-kB, TIMP-1 e na fração de volume de fibras colágenas tipo I, decorina, lumicam e actina. No grupo OVA-anti-IL17 houve atenuação de todos os parâmetros quando comparado ao grupo OVA (p < 0,05). Nos animais do modelo de inflamação alérgica crônica exacerbado pelo LPS e tratado com anti-IL-17 (grupo OVA-LPS anti-IL-17) houve diminuição comparativamente ao grupo OVA-LPS dos seguintes parâmetros: número de células totais do lavado broncoalveolar, de células positivas para FOXP3 e células dendríticas, número de CD4+ e CD8+, de células positivas para IL-10 anti-inflamatória e citocinas pró-inflamatórias (TNF-alfa, IL-2, IL-4, IL-5, IL-6, IL-13 e IL-17); quimiocinas (TARC), expressão gênica de IL-6, edema nos septos alveolares; elementos da matriz extracelular (fração de volume de fibras colágenas tipo I e III, actina, decorina, biglicano, lumicam, fibronectina, integrina e expressão de células positivas para TGF-beta, MMP-9, MMP-12 e TIMP-1), da resposta das vias de estresse oxidativo: (células positivas para iNOS e fração de volume de isoprostano PGF-2alfa; da expressão celular de NF-kB, e das proteínas Rho quinase 1 e 2 (p < 0,05). Não houve diferenças no diâmetro alveolar médio entre todos os grupos experimentais. CONCLUSÃO: Esses dados sugerem que a inibição da IL-17 pode ser uma via terapêutica promissora para o tratamento da inflamação alérgica crônica, mesmo durante uma exacerbação e pode contribuir para o controle da inflamação Th1/ Th2/Th17, da expressão de quimiocinas, do remodelamento da matriz extracelular e do estresse oxidativo. As vias sinalizadoras de NF-kB e Rho-quinase estão envolvidas no controle dessas respostas neste modelo de inflamação alérgica crônica exacerbado pelo LPS
INTRODUCTION: Inflammation plays a central role in the development of asthma, which is considered an allergic disease with a classic Th2 inflammatory profile. However, IL-17 profile cytokines have been studied to better understand their involvement in the pathophysiology of this disease. Severe asthmatic patients have frequent exacerbations, the infectious cause being one of the main triggers and that can perpetuate the inflammatory responses. The Th17 response may be clearly associated with these events. OBJECTIVE: This study evaluates the effects of anti-IL-17 monoclonal antibody therapy on alveolar septa in an experimental model of chronic allergic lung inflammation of asthma exacerbated by LPS. METHODS: Sixty male BALB / c mice were used, being sensitized with intraperitoneal ovalbumin and repeatedly exposed to inhalation with ovalbumin, followed by treatment with or without anti-IL-17. Twenty-four hours before the end of the 29-day experimental protocol, two groups received intratracheal LPS (0.1 mg / ml, OVA-LPS and anti-IL-17 OVA-LPS groups). Afterwards, we evaluated bronchoalveolar lavage fluid (BALF), by morphometry we quantified the recruitment of antigen-presenting cells (FOXP3 and dendritic cells), eosinophils, the cellular expression of proinflammatory cytokines (TNF-alpha, IL-2, IL IL-5, IL-6, IL-13 and IL-17), anti-inflammatory cytokines (IL-10), chemokine (TARC), and quantification of IL6 by RT-PCR. We also evaluated elements of the extracellular matrix (collagen fibers type I and III, MMP-9, MMP-12, TIMP-1, TGF-beta, actin, decorin, lumicam, biglican and fibronectin), alveolar septum edema, oxidative stress through the marker iNOS and 8-iso-PGF2? and the signaling pathways NF-kB and Rho kinase. In addition, we evaluated of the mean alveolar diameter. RESULTS: The animals of the OVA-LPS group presented a potentiation of the all responses compared to OVA (p < 0.05), except for: expression of IL-17, TNFalpha, NF-kB, TIMP-1 and in the volume fraction of type I collagen fibers, decorin, lumicam and actin. Treatment with anti-IL-17 (OVA-anti-IL17 group) attenuated all parameters compared to OVA group (p < 0.05). The animals of the chronic allergic inflammation model exacerbated by LPS and treated with anti-IL-17 (OVA-LPS anti-IL-17 group) had a decreased of the following parameters compared to OVA-LPS: total bronchoalveolar lavage cells number, FOXP3 and dendritic positive cells, CD4 + and CD8 + numbers, of cells positive for IL-10 antiinflammatory, and pro-inflammatory cytokines (TNF-alfa, IL-2, IL-4, IL-5, IL-6, IL- 13 and IL-17); chemokine (TARC), genic expression IL6; edema in the alveolar septum; extracellular matrix elements (volume fraction of collagen fibers type I and III, actin, decorin, biglican, lumicam, fibronectin, and expression of TGF-beta, MMP-9, MMP-12 and TIMP-1 positive cells) of the oxidative stress pathways response (iNOS positive cells and isoprostane volume fraction 8-isoPGF-2alfa) NFkB and Rho kinase 1 and 2 positive cells (p < 0.05). There were no differences in mean alveolar diameter among all experimental groups. CONCLUSION: These data suggest that inhibition of IL-17 may be a promising therapeutic pathway for the treatment of chronic allergic inflammation, even during an exacerbation, and may contribute to the control of Th1 / Th2 / Th17 inflammation, chemokine expression, extracellular matrix remodeling and oxidative stress. Signaling pathways of NF-kB and Rho-kinase are involved in the control of these responses in this model of chronic allergic inflammation exacerbated by LPS
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Tarando, Sebastian Roberto. "Quantitative follow-up of pulmonary diseases using deep learning models." Thesis, Evry, Institut national des télécommunications, 2018. http://www.theses.fr/2018TELE0008/document.

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Les pathologies infiltrantes diffuses recensent un large groupe de désordres pulmonaires et nécessitent un suivi régulier en imagerie tomodensitométrique (TDM). Une évaluation quantitative est nécessaire pour établir la progression (régionale) de la maladie et/ou l’impact thérapeutique. Cela implique le développement d’outils automatiques de diagnostic assisté par ordinateur (DAO) pour la segmentation du tissu pathologique dans les images TDM, problème adressé comme classification de texture. Traditionnellement, une telle classification repose sur une analyse des caractéristiques texturales 2D dans les images TDM axiales selon des critères définis par l’utilisateur. Récemment, des techniques d’intelligence artificielle fondées sur l’apprentissage profond, notamment les réseaux neuronaux convolutionnels (CNN), ont démontré des performances meilleures pour résoudre des tâches visuelles. Toutefois, pour les architectures CNN « classiques » il a été prouvé que les performances étaient moins bonnes en classification de texture par rapport à la reconnaissance d’objets, en raison de la dimensionnalité intrinsèque élevée des données texturales. Dans ce contexte, ce travail propose un système automatique pour l’analyse quantitative des pathologies infiltrantes diffuses du poumon fondé sur une architecture CNN en cascade (conçue spécialement pour l’analyse de texture) et sur un prétraitement spécifique des données d’entrée par filtrage localement connexe (permettant d’atténuer l’intensité des vaisseaux pulmonaires et d’augmenter ainsi le contraste des régions pathologiques). La classification, s’appliquant à l’ensemble du volume pulmonaire, atteint une précision moyenne de 84% (75.8% pour le tissu normal, 90% pour l’emphysème et la fibrose, 81.5% pour le verre dépoli)
Infiltrative lung diseases (ILDs) enclose a large group of irreversible lung disorders which require regular follow-up with computed tomography (CT) imaging. A quantitative assessment is mandatory to establish the (regional) disease progression and/or the therapeutic impact. This implies the development of automated computer-aided diagnosis (CAD) tools for pathological lung tissue segmentation, problem addressed as pixel-based texture classification. Traditionally, such classification relies on a two-dimensional analysis of axial CT images by means of handcrafted features. Recently, the use of deep learning techniques, especially Convolutional Neural Networks (CNNs) for visual tasks, has shown great improvements with respect to handcrafted heuristics-based methods. However, it has been demonstrated the limitations of "classic" CNN architectures when applied to texture-based datasets, due to their inherently higher dimension compared to handwritten digits or other object recognition datasets, implying the need of redesigning the network or enriching the system to learn meaningful textural features from input data. This work addresses an automated quantitative assessment of different disorders based on lung texture classification. The proposed approach exploits a cascade of CNNs (specially redesigned for texture categorization) for a hierarchical classification and a specific preprocessing of input data based on locally connected filtering (applied to the lung images to attenuate the vessel densities while preserving high opacities related to pathologies). The classification targeting the whole lung parenchyma achieves an average of 84% accuracy (75.8% for normal, 90% for emphysema and fibrosis, 81.5% for ground glass)
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"Spectrum of diffuse parenchymal lung disease with special reference to idiopathic pulmonary fibrosis: experience at Charlotte Maxeke Johannesburg Academic Hospital." Thesis, 2017. https://hdl.handle.net/10539/25322.

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A research report submitted to the University of the Witwatersrand, Johannesburg, in fulfilment for the requirements of the degree of Master of Medicine in Internal Medicine 2017
Background Diffuse parenchymal lung diseases (DPLD) encompass a group of diseases with a wide range of causes with varied presentations and prognosis. The known causes include occupational or environmental exposure, drug induced lung diseases, hypersensitivity pneumonitis and connective tissue disease (CTD). Among the DPLD with unknown cause, idiopathic pulmonary fibrosis (IPF) is the commonest and has the worst outcome. The earlier publications from this country described cryptogenic fibrosing alveolitis. With subsequent characterisation of idiopathic interstitial pneumonia (IIP), and an increase in the burden of IPF reported worldwide, we evaluated the clinical features of patients with IPF in the South African context. Objectives To evaluate the clinical spectrum of DPLD encountered in Johannesburg, South Africa, and to describe the clinical profile of patients with IPF. Methods A retrospective record review of patient files was conducted who attended the Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) Respiratory Clinic in the past 5 years from January 2011 to December 2015. Patients with DPLD were identified and the diagnoses were noted. The records of patients with IPF were further analysed. v Results We identified 132 patients with DPLD. Sarcoidosis (37.8%), IPF (21.2%), connective tissue associated diffuse parenchymal lung disease (CTD-DPLD) (14.3%), and hypersensitivity pneumonitis (HP) (9.8%) were the four most common subtypes. IPF was seen in all racial groups. Of the 28 patients with IPF in our cohort, there was a slight female predominance (1.3:1). The mean age of the patients in our study was 63.8 years and the majority were Whites. Cough (96.4%), dyspnoea (92.8%) and bilateral crackles (96.4%) were the commonest clinical features. The majority of patients (78.5%) were diagnosed by high resolution computerised tomography (HRCT) scan. Conclusion IPF is the second most common DPLD disease encountered after sarcoidosis at the CMJAH. IPF is seen in all racial groups in Johannesburg, South Africa, and the characteristics of patients with IPF are similar to those seen in other parts of the world.
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Κορφιάτης, Παναγιώτης. "Image analysis methods for diagnosis of diffuse lung disease in multi-detector computed tomography." Thesis, 2010. http://nemertes.lis.upatras.gr/jspui/handle/10889/4778.

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Image analysis techniques have been broadly used in computer aided diagnosis tasks in recent years. Computer-aided image analysis is a popular tool in medical imaging research and practice, especially due to the development of different imag- ing modalities and due to the increased volume of image data. Image segmenta- tion, a process that aims at identifying and separating regions of an image, is crucial in many medical applications, such as in identification (delineation) of anatomical structures and pathological regions, providing objective quantitative assessment and monitoring of the onset and progression of the disease. Multidetector CT (MDCT) allows acquisition of volumetric datasets with almost isotropic voxels, enabling visualization, characterization and quantification of the entire extent of lung anatomy, thus lending itself to characterization of Interstitial Lung Diseases (ILDs), often characterized by non uniform (diffuse) distribution in the lung volume. Interpretation of ILDs is characterized by high inter and intra- observer variability, due to lack of standardized criteria in assessing its complex and variable morphological appearance, further complicated by the increased vol- ume of image data being reviewed. Computer-Aided Diagnosis (CAD) schemes that automatically identify and char- acterize radiologic patterns of ILDs in CT images have been proposed to improve diagnosis and follow-up management decisions. These systems typically consist of two stages. The first stage is the segmentation of left and right Lung Parenchyma (LP) region, resulting from lung field segmentation and vessel tree removal, while the second stage performs classification of LP into normal and abnormal tissue types. The segmentation of Lung Field (LF) and vessel tree structures are crucial preprocessing steps for the subsequent characterization and quantification of ILD patterns. Systems proposed for identification and quantification of ILDpatterns havemainly exploited 2D texture extraction techniques, while only a few have investigated 3D texture features. Specifically, texture feature extraction methods that have been exploited towards lung parenchyma analysis are: first order statistics, grey level co-occurrence matrices, gray level run length matrices, histogram signatures and fractals. The identification and quantification of lung parenchyma into normal and abnormal tissue type has been achieved by means of supervised classification tech- niques (e.g. Artificial Neural Networks, ANN, Bayesian classifier, linear discrimi- nant analysis (LDA) and k-Nearest Neighboor (k-NN). However, the previously proposed identification and quantification schemes in- corporate preprocessing segmentation algorithms, effective on normal patient data. In addition the effect of the preprocessing stages (i.e. segmentation of LF and ves- sel tree structures) on the performance of ILD characterization and quantification schemes has not been investigated. Finally, the complex interaction of such automated schemes with the radiologists remains an open issue. The current thesis deals with identification and quantification of ILD in lung CT. The thesis aims at optimizing all major steps encountered in a computer aided ILD quantification scheme, by exploiting 3D texture feature extraction techniques and supervised and unsupervised pattern classification schemes to derive 3D disease segments. The specific objectives of the current thesis are focused on: • Development of LF segmentation algorithms adapted to pathology. • Development of vessel tree segmentation adapted to presence of pathology. • Development of ILD identification and quantification algorithms. • Investigation of the interaction of an ILD identification and quantification scheme with the radiologist, by an interactive image editing tool.
Η Διάμεση Νόσος (ΔΝ) του πνεύμονα αποτελεί το 15% των παθήσεων του πνεύμονα που εμφανίζονται στην κλινική πρακτική. Η ΔΝ επηρεάζει κυρίως το πνευμονικό παρέγχυμα και εμφανίζεται στις εικόνες Υπολογιστικής Τομογραφίας (ΥΤ) του πνεύμονα με την μορφή διάχυτων περιοχών χαρακτηριστικών προτύπων υφής που παρεκκλίνουν από αυτό του φυσιολογικού παρεγχύματος. Η Πολυτομική Υπολογιστική Τομογραφία (ΠΥΤ) επιτρέπει την απόκτηση τρισδιάστατων απεικονίσεων με σημαντική μείωση του χρόνου λήψης και αποτελεί την απεικονιστική τεχνική επιλογής για την ποσοτικοποίηση και τη διάγνωση της ΔΝ. Η διάγνωση της ΔΝ χαρακτηρίζεται από μειωμένη διαγνωστική ακρίβεια χαρακτηρισμού και ακρίβεια ποσοτικοποίησης έκτασης ακόμα και για τον έμπειρο ακτινολόγο, αλλά και από χαμηλή επαναληψιμότητα. Η δυσκολία διάγνωσης οφείλεται στη μειωμένη ικανότητα του ανθρώπινου παράγοντα ως προς το καθορισμό έκτασης των προτύπων υφής λόγω ομοιότητας ακτινολογικής εμφάνισης τους σε συνδυασμό με το φόρτο εργασίας του ακτινολόγου και τον αυξημένο όγκο δεδομένων της ΠΥΤ. Αυτοματοποιημένα συστήματα ανάλυσης εικόνας μπορούν να αντιμετωπίσουν τα παραπάνω προβλήματα παρέχοντας σημαντική υποβοήθηση στο έργο της διάγνωσης και παρακολούθησης της νόσου. Η ανάπτυξη αυτοματοποιημένων συστημάτων ανάλυσης εικόνας για υποβοήθηση διάγνωσης στην ΥΤ του πνεύμονα έχει αποτελέσει θέμα εκτεταμένης έρευνας την τελευταία δεκαετία με ένα μικρό τμήμα της να επικεντρώνεται στο χαρακτηρισμό και ποσοτικοποίηση της έκτασης της ΔΝ. Σημαντικά στάδια προεπεξεργασίας των συστημάτων αυτών αποτελούν οι τμηματοποίησεις των Πνευμονικών Πεδίων (ΠΠ) και του αγγειακού δένδρου για τον καθορισμό του προς ανάλυση όγκου του πνευμονικού παρεγχύματος. Τα έως σήμερα προταθέντα συστήματα αυτόματης ανίχνευσης και ποσοτικοποίησης της έκτασης της ΔΝ αξιοποιούν κυρίως μεθόδους ανάλυσης δισδιάστατης (2Δ) υφής εικόνας, ενώ μόνο δύο μελέτες έως σήμερα έχουν αξιοποιήσει ανάλυση 3Δ υφής. Συγκεκριμένα, μέθοδοι ανάλυσης υφής εικόνας που έχουν αξιοποιηθεί είναι: στατιστική 1ης τάξης (ιστόγραμμα), μήτρες συνεμφάνισης αποχρώσεων του γκρι (Grey level Co-occurrence Matrices), μήτρες μήκους διαδρομής απόχρωσης του γκρι (Gray Level Run Length Matrices), υπογραφές ιστογράμματος και Fractals. Ο χαρακτηρισμός και η ποσοτικοποίηση περιοχών του πνευμονικού παρεγχύματος που αντιστοιχούν σε φυσιολογικό παρέγχυμα και υποκατηγορίες παθολογίας υλοποιείται με μεθόδους επιβλεπόμενης ταξινόμησης προτύπων όπως: τεχνητά νευρωνικά δίκτυα (Artificial Neural Networks, ΑΝΝ), Bayesian ταξινομητής, ανάλυση γραμμικού διαχωρισμού ( Linear Discriminant Analysis, LDΑ) και ταξινομητής πλησιέστερου γείτονα (k-Nearest Neighboor, k-NN). Στα έως σήμερα προταθέντα συστήματα, η τμηματοποίηση των ΠΠ υλοποιείται με συμβατικές μεθόδους τμηματοποίησης με βάση τις αποχρώσεις του γκρί (τιμές έντασης) εικονοστοιχείων. Ανοικτό ζήτημα παραμένει και η αξιολόγηση της επίδρασης των σταδίων προ-επεξεργασίας (τμηματοποίηση ΠΠ και αγγειακού δένδρου) στην ακρίβεια συστημάτων χαρακτηρισμού και ποσοτικοποίησης της έκτασης της ΔΝ. Τέλος, η αξιολόγηση της αλληλεπίδρασης αυτόματων συστημάτων ποσοτικοποίησης και ακτινολόγου στη λήψη αποφάσεων χαρακτηρισμού και ποσοτικοποίησης της έκτασης που αφορούν την ΔΝ δεν έχει διερευνηθεί. Η παρούσα διδακτορική διατριβή επικεντρώνεται στην ανάπτυξη ολοκληρωμένου συστήματος ανάλυσης εικόνας το οποίο χαρακτηρίζει και ποσοτικοποιεί την έκταση περιοχών με ΔΝ σε απεικονίσεις ΠΥΤ θώρακος, στοχεύοντας στη βελτιστοποίηση όλων των σταδίων του, καθώς και στην αξιολόγηση της συμβολής του συστήματος στην λήψη διαγνωστικών αποφάσεων. Για το σκοπό αυτό διερευνώνται τεχνικές 3Δ ενίσχυσης εικόνας, 3Δ τμηματοποίησης εικόνας καθώς και 3Δ χαρακτηριστικά υφής εικόνας σε συνδυασμό με επιβλεπόμενα και μη επιβλεπόμενα συστήματα ταξινόμησης. Συγκεκριμένα η συμβολή της παρούσας διατριβής επικεντρώνεται στα ακόλουθα: • Ανάπτυξη μεθόδων τμηματοποίησης των ΠΠ και του αγγειακού δένδρου παρουσία παθολογίας. • Διερεύνηση της συμβολής αλγορίθμων εξαγωγής 3Δ υφής εικόνας στην ακρίβεια μεθόδων ταξινόμησης προτύπων ΔΝ. • Βελτιστοποίηση μεθόδων χαρακτηρισμού και ποσοτικοποίησης έκτασης με χρήση τεχνικών επιβλεπόμενης και μη επιβλεπόμενης ταξινόμησης. • Αξιολόγηση της επίδρασης των σταδίων προεπεξεργασίας στην ακρίβεια συστημάτων ποσοτικοποίησης. • Αξιολόγηση της συμβολής συστημάτων ποσοτικοποίησης στη διάγνωση της ΔΝ.
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Books on the topic "Diffuse parenchymal lung diseases"

1

Poletti, Venerino, ed. Transbronchial cryobiopsy in diffuse parenchymal lung disease. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14891-1.

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MD) Hales Lung Conference (1st 2009 Baltimore. Proceedings of 2009 Hales Lung Conference: Clinical and pathophysiolgic aspects of diffuse parenchymal disease, April 27, 2009, Baltimore, MD : clinical and pathophysiologic aspects of diffuse parenchymal lung disease. Ellicott City, MD: BoBitField, 2011.

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Cancellieri, Alessandra, Giorgia Dalpiaz, Mario Maffessanti, Alberto Pesci, Roberta Polverosi, and Maurizio Zompatori. Diffuse Lung Diseases. Edited by Mario Maffessanti and Giorgia Dalpiaz. Milano: Springer Milan, 2006. http://dx.doi.org/10.1007/88-470-0430-6.

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Gupta, Nishant, Kathryn A. Wikenheiser-Brokamp, and Francis X. McCormack, eds. Diffuse Cystic Lung Diseases. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63365-3.

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Dalpiaz, Giorgia, and Alessandra Cancellieri, eds. Atlas of Diffuse Lung Diseases. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-42752-2.

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Diffuse lung disease: A practical approach. 2nd ed. New York: Springer, 2012.

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V, Colby Thomas, ed. Surgical pathology of diffuse infiltrative lung disease. Orlando: Grune & Stratton, 1987.

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Bush, Andrew, and Jane C. Davies. Paediatric respiratory disease: Parenchymal diseases : an atlas of investigation and management. Oxford, UK: Clinical Pub., 2011.

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Diffuse parenchymal lung disease. Basel: Karger, 2007.

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Costabel, U., R. M. du Bois, and J. J. Egan, eds. Diffuse Parenchymal Lung Disease. S. Karger AG, 2007. http://dx.doi.org/10.1159/isbn.978-3-318-01377-1.

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Book chapters on the topic "Diffuse parenchymal lung diseases"

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Bratis, Livia, and Thomas F. Morley. "Diffuse Parenchymal Lung Diseases." In Challenging Cases in Pulmonology, 233–49. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7098-5_14.

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Clement, Annick, and Brigitte Fauroux. "Interstitial Lung Diseases in Children." In Diffuse Parenchymal Lung Disease, 323–31. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102701.

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Chilosi, Marco, Bruno Murer, and Venerino Poletti. "Diffuse Parenchymal Lung Diseases – Histopathologic Patterns." In Diffuse Parenchymal Lung Disease, 44–57. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102625.

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Behr, Jürgen. "Novel Aspects of Treatment for Interstitial Lung Diseases." In Diffuse Parenchymal Lung Disease, 117–26. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102632.

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Collard, Harold R. "Diseases: Other Entities of the Idiopathic Interstitial Pneumonias." In Diffuse Parenchymal Lung Disease, 175–84. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102689.

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Irani, Sarosh, and Annette Boehler. "Lung Transplantation for Diffuse Parenchymal Lung Disease." In Diffuse Parenchymal Lung Disease, 332–40. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102702.

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Poletti, Venerino, Pier Luigi Zinzani, Sara Tomassetti, and Marco Chilosi. "Lymphoproliferative Lung Disorders." In Diffuse Parenchymal Lung Disease, 307–22. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102700.

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Olson, Amy L., and Marvin I. Schwarz. "Diffuse Alveolar Hemorrhage." In Diffuse Parenchymal Lung Disease, 250–63. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102695.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Diffuse Parenchymal Lung Disease." In Encyclopedia of Molecular Mechanisms of Disease, 533. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7710.

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Gomez, Antonio D., and Talmadge E. King Jr. "Classification of Diffuse Parenchymal Lung Disease." In Diffuse Parenchymal Lung Disease, 1–10. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102577.

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Conference papers on the topic "Diffuse parenchymal lung diseases"

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Ashiq, J., FM Daroowalla, and PS Richman. "Making a Decision on Lung Biopsy in Diffuse Parenchymal Lung Diseases." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4047.

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Strumiliene, Edita, and Vygantas Gruslys. "Complications - based learning curve of transbronchial lung cryobiopsy in diffuse parenchymal lung diseases." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1191.

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Okumus, Gulfer, Berker Ozkan, Zuleyha Bingol, Melike Ulker, Berivan Karatekin, Esen Kiyan, Zeki Kilicaslan, Murat Kara, Dilek Yılmazbayhan, and Alper Toker. "Surgical biopsy results of our patients with diffuse parenchymal lung diseases." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2990.

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Behera, Digambar, Sahajal Dhooria, Ritesh Agarwal, Inderpaul Singh Sehgal, Mandeep Garg, Amanjit Bal, and Ashutosh Nath Aggarwal. "Spectrum of diffuse parenchymal lung diseases at a tertiary care center in India." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa875.

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Cunha Machado, Daniela Patrícia, Gisela Lage, Catarina Marques, Filipa Lima, Inês Marques, Carla Nogueira, Ana Oliveira, et al. "Transbronchial cryobiopsy from two different lobes versus one lobe in diffuse parenchymal lung diseases." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa2164.

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Koslow, M., E. S. Edell, T. Moua, A. C. Roden, E. S. Yi, P. Decker, and J. H. Ryu. "Bronchoscopic Lung Biopsy for Diffuse Parenchymal Lung Disease: Comparison of Forceps with Cryobiopsy." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4317.

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Hanta, Ismail, Efraim Güzel, Oya Baydar, Emine Kiliçbagir, and Alper Avci. "A case of Non-Hodgkin lyphoma mimicking diffuse parenchymal lung disease." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3719.

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Fedyna, S., W. Bulman, C. Shu, A. Saqi, J. Sonett, and P. Stanifer. "A Clinocopathological Study of Lung Cancer in Patients with Non-Idiopathic Pulmonary Fibrosis (IPF) Diffuse Parenchymal Lung Diseases." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3367.

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Massoptier, Laurent, Avishkar Misra, and Arcot Sowmya. "Automatic lung segmentation in HRCT images with diffuse parenchymal lung disease using graph-cut." In 2009 24th International Conference Image and Vision Computing New Zealand (IVCNZ). IEEE, 2009. http://dx.doi.org/10.1109/ivcnz.2009.5378398.

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Ravaglia, Claudia, Sara Tomassetti, Alessandra Dubini, Sara Piciucchi, and Venerino Poletti. "Cryobiopsy in the diagnosis of diffuse parenchymal lung diseases: diagnostic strategy and complications in 699 patients." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2206.

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