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1
Turcotte, Antony. "Description of emphysema in mice with different susceptibilities to cigarette smoke-induced emphysema". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82444.
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The inflammatory response due to chronic smoking in COPD patients has been well characterized with increases in CD3+ T lymphocytes. A murine model was chosen in our laboratory as a good model of human emphysema.The first part of my project was to characterize the lung inflammatory response via immunocytochemistry in each mouse strain exposed to chronic smoke inhalation for a six-month period.
Several T lymphocyte subsets (i.e. naive, central memory and effector memory) have been characterized in the immune system both in humans and mice. These subsets have different homing potentials and effector functions, and can be identified with cell surface markers. The second part of my project was to determine these T-cell subset ratios in the lungs of each strain after chronic smoke exposure.
The third part of my project was to assess apoptosis in each strain after smoke exposure.
2
Jörgensen, Kirsten. "Lung emphysema and cardiac function /". Göteborg : Dept. of Anaesthesiology and Intensive Care Medicine. Institute of Clinical Sciences, The Sahlgrenska Academy at Göteborg University, 2008. http://hdl.handle.net/2077/9635.
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Jones, Jennifer Grace. "A mathematical model of emphysema". Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269229.
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Haruna, Akane. "CT emphysema predicts mortality in COPD". Kyoto University, 2010. http://hdl.handle.net/2433/123335.
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Kariisa, Mbabazi M. "Measuring the Effects of Air Pollution among Persons with Severe Emphysema: The National Emphysema Treatment Trial (NETT)". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1357157519.
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Walsh, Robert Leo. "Leukocyte elastase and anti-elastases in pulmonary emphysema". Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phw2261.pdf.
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Includes bibliographical references (leaves 218-249) The preferred theory to explain the aetiology of emphysema points to an imbalance in the protease-antiprotease systems within the lung with human leukocyte elastase and [alpha]1-protease inhibiter being the main candidates. Examines some aspects of this theory.
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Chrusciel, Sandra. "Rôle de P53 dans les macrophages alvéolaires en réponse à diverses agressions environnementales". Thesis, Paris Est, 2014. http://www.theses.fr/2014PEST1187.
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Il existe plusieurs types d’agressions environnementales : biologiques (virus, bactéries…), chimiques (gaz, fumées, métaux…), physiques (bruits, rayonnements…), et d’autres telles que le stress par exemple. L’appareil respiratoire, qui représente une interface majeure avec l’environnement, est particulièrement vulnérable vis-à-vis de ces agressions, qui ont souvent des conséquences pulmonaires, pouvant parfois conduire au décès. Le tabac notamment est la cause de près de 100 millions de décès au cours du XXème siècle d’après l’Organisation Mondiale de la Santé (OMS), et sera la cause d’environ un milliard de décès au prochain siècle. L’exposition à la fumée de cigarette engendre une inflammation chronique et est souvent corrélée au développement de cancers (1), mais induit aussi de nombreuses autres pathologies pulmonaires telles que la broncho-pneumopathie chronique obstructive (BPCO)There are several types of environmental attacks: biological (viruses, bacteria …), chemical (gases, smokes, metals …), physical appearances (rumours, brilliances …), and others such as the stress for example. The respiratory system, which represents a major interface with the environment, is particularly vulnerable towards these attacks, which often have lung consequences, being able to sometimes lead to the death. The tobacco in particular is the cause of about 100 million deaths during the XXth century according to the World Health Organization (WHO), and will be the cause about a billion deaths in the next century. The exhibition in the smoke of cigarette engenders a chronic inflammation and is often correlated in the development of cancers (1), but also leads of numerous
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Macnee, W. "Right ventricular function in chronic bronchitis and emphysema". Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383973.
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Carter, Richard Ian. "Biomarkers of disease activity in COPD and emphysema". Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4071/.
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The flaws of current methods of assessing disease severity in patients with COPD and emphysema are increasingly recognised, and new methods of assessing disease activity are urgently required. Although many potential biomarkers have been suggested to fulfil this role, few have been effectively validated, and furthermore any biomarker should be based on our current understanding of the pathophysiology the disease process. This is poorly understood, however it is apparent that neutrophil proteases (particularly neutrophil elastase (NE) and proteinase 3 (Pr3)) may represent a final common pathway leading to tissue destruction. The current thesis describes the development and validation of a new marker of NE activity (Aα-Val360), and the identification of a marker of Pr3 activity, as potential biomarkers of COPD and emphysema disease activity. Methods Following in vitro validation, the performance of Aα-Val360 was assessed in a series of patient populations. Mass spectrometry was used to identify a specific marker of Pr3 activity. Results and Conclusion Aα-Val360 demonstrated acceptable in vitro and in vivo variability; related to physiological, radiological and patient reported outcomes in subjects with (or at risk of developing) COPD and emphysema (both with and without A1AT deficiency); increased during acute exacerbations; decreased in response to treatment; and partly related to disease progression in some populations. Also, a Pr3 specific cleavage product was identified which could be used to develop a new specific assay of Pr3 activity. These potential biomarkers of disease activity may be important in the assessment of patients with COPD and emphysema (or who are at risk of developing these conditions), particularly in early phase clinical trials.
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Gagliolo, Jean-Marie. "Rôle de la sénescence des fibroblastes dans la physiopathologie de la bronchopneumopathie chronique obstructive". Thesis, Paris Est, 2013. http://www.theses.fr/2013PEST1065.
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La sénescence, perte irréversible des capacités réplicatives des cellules associée à la sécrétion de médiateurs inflammatoires, pourrait participer au développement de l'atteinte pulmonaire dans la bronchopneumopathie chronique obstructive (BPCO) en initiant, maintenant et propageant un état inflammatoire. L'objectif de ce travail était d'évaluer les mécanismes de la sénescence impliqués dans l'induction et le maintien de l'inflammation au cours de la BPCO. Ainsi, des fibroblastes pulmonaires de témoins et de patients atteints de BPCO ont été mis en culture à long terme. Un phénotype sénescent majoré associée à un sécrétome pro-inflammatoire était détectée dans les fibroblastes de patients avec BPCO par rapport aux témoins. Par ailleurs, ces fibroblastes présentaient une expression accrue des récepteurs à la PGE2 (EP2 /4)au stade non sénescent et une production accrue de PGE2, un médiateur lipidique pro-inflammatoire, au stade sénescent. Dans cette optique, une partie du travail a consisté à déterminer si la PGE2 pouvait induire la sénescence et l'inflammation des fibroblastes pulmonaires de sujets atteints ou non de BPCO. Nous avons pu démontrer que la PGE2 synthétisée par les fibroblastes sénescents induisait, maintenait (effet autocrine) et propageait (effet paracrine) la sénescence et l'inflammation associée via une voie EP2/4 / COX-2 / oxydants / p53. L'implication des oxydants dans l'induction de la sénescence nous a conduit à étudier les effets de l'hème oxygénase (HO)-1, un système anti-oxydant et anti-inflammatoire sur la prévention de la sénescence des fibroblastes pulmonaires. Ainsi, des fibroblastes pulmonaires ont été traités chroniquement avec des substances pharmacologiques modulant l'activité d'HO-1. Des résultats préliminaires nous ont permis d'observer que l'activation de HO-1 prévenait l'induction de la sénescence chez des fibroblastes pulmonaires de témoins et de BPCO. Au total, la modulation des voies de la PGE2 et de l'HO-1 pourrait contribuer à limiter la sénescence des fibroblastes pulmonaires dans la BPCOCellular senescence, a state of irreversible loss of replicative capacity associated with the secretion of inflammatory mediators, could participate in the development of chronic obstructive pulmonary disease (COPD) by initiating, maintaining and propagating an inflammatory state. The aim of this PhD project was to evaluate the mechanisms involved in senescence induction in COPD lung fibroblasts. COPD fibroblasts exhibited an increased senescent phenotype as compared to control cells. In addition, COPD fibroblasts showed an increased PGE2 receptors (EP2 /4) expression at non senescent stage and PGE2 production, apro-inflammatory lipid mediator at senescent stage. In this context, one part of the study was devoted to determine whether PGE2 could induce senescence of lung fibroblasts of subjects with and without COPD. We have shown that PGE2 synthesized by senescent fibroblasts induced, maintained (autocrine effect) and propagated (paracrine effect) senescence and associated inflammation via EP2 /4 / COX-2 / oxidants / p53 pathway. The essential role of oxidants production in the induction of senescence in COPD led us to study the effects of heme oxygenase (HO)-1, an antioxidant and anti-inflammatory system on the prevention of senescence in COPD fibroblasts. Pharmacological activation of HO-1 by hemin prevented the induction of senescence in lung fibroblasts from COPD patients probably in relation with an anti -oxidant effect. The modulation of PGE2 and HO-1 pathways may contribute to attenuate fibroblasts senescence in COPD
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McNulty, William. "Physiological mechanisms of lung volume reduction coils in emphysema". Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/50161.
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Emphysema is characterised by airflow limitation that is a result of both loss of elastic recoil and small airways disease. It is poorly responsive to medical therapy. Lung volume reduction coils improve symptoms and lung function in the short term. However their mechanism of action and medium term effectiveness is not fully understood. Methods A randomised controlled study consisting of thirty patients with severe chronic obstructive pulmonary disease was performed. Control patients crossed over to the treatment arm at 12 months. The primary outcome was 6 minute walk distance at 12 months. Changes in spirometry, lung volumes, computed tomography measured lung volumes and gas trapping were also assessed. In a small subgroup of patients detailed physiological characterization was performed to assess changes in airways resistance, ventilation heterogeneity and lung elastic recoil. Results In the randomised study at 12 months, there was no significant difference in 6 minute walk distance between treatment and controls (between group difference 25m, 95% CI -40 to 59, p = 0.7028). There was a trend to improvement in symptoms measured by SGRQ score (-6.53 points, 96% CI -17 to 0.2, p = 0.0589) and significant improvements in FRC (-0.41L, 95% CI -0.86 to -0.1, p = 0.0077). Including the crossovers there were 4 patient deaths (13.3%). Target lobe volume at both inspiration and expiration was reduced with no overall change in gas trapping. Airways resistance by plethysmography did not change significantly. There was no significant change in elastic recoil. Conclusions Treatment with lung volume reduction coils is effective at reducing lung volume and may achieve its effect through volume loss. There could also be an effect through elastic recoil as there was a non-significant trend towards an increase after the intervention. There appears to be no effect on airways resistance. Careful patient selection is required as there is a risk of death following treatment.
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Dallak, Mohammad A. M. "Respiratory drive in a rabbit model of pulmonary emphysema". Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/21183.
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This thesis describes an investigation of the respiratory drive to breathe in a rabbit model of pulmonary emphysema. I propose that an altered respiratory drive in emphysematous rabbits may model the origin of the sensation of dyspnoea experienced by many human patients with emphysema. Pulmonary emphysema was induced in Dutch rabbits by endotracheal administration of type IV porcine pancreatic elastase. In rats it was induced by endotracheal administration of papain. Respiratory drive was measured as phrenic activity (phrenic slope, G and phrenic height, H). since emphysema changes the mechanical properties of the lungs and ventilation will be changed for a given respiratory drive. Rats' and rabbits' conscious pattern of breathing (expiratory time, tE; inspiratory time, tl and tital volume. VT) was measured barometrically to investigate the role of sensation in changed conscious pattern of breathing. To elucidate the role of pulmonary receptors in changing the pattern of breathing and respiratory drive, the respiratory variables were measured during 3 stages: 1) preSO2: when all pulmonary receptors were intact 2) post SO2: when pulmonary stretch receptors (SARs) were blocked by inhaled sulphur dioxide 3) postvagotomy: when all pulmonary receptors input was removed by bilateral vagotomy. Emphysema increased static lung compliance in rabbits (normal (N): 4.12± .49 ml/cmH2O, n=25 vs. emphysematous (E): 4.61±0.31. n=35) and rats (N: 0.61±0.02 ml/cmH2O, n=10 vs. E: 0.82±0.03, n=10). It also increased mean linear intercept in rabbits (N: 79.71±8.42μm, n=25 vs. E: 99.62±2.32n, n=35) and rats (N: 80.5±2.9, n=10 vs. 108.4±3.2, n=10). Breathing accelerated by 6% CO2 inhalation in all three stages (calculated as Δ %) showed that emphysematous rabbits have a stronger respiratory drive indicating the relative importance of vagal and extravagal inputs (preSO2, G (N): 30.9±3 vs. E: 37.6±1.8; postSO2, G(N): 24.4±2.3 vs. E: 33.92±1.5; postvagotomy, GN(N): 27.95±3.2 vs. E: 45.61±2.08). It is concluded from this study that it is this stronger respiratory drive in eupnoea and in response to CO2, that patients with pulmonary emphysema perceive as dyspnoea.
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Grimsley, Christina y Stephen B. MD FAAEM Blankenship. "Case Report: Tension Pneumothorax Complicated by Massive Subcutaneous Emphysema". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/113.
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Background: Tension pneumothorax is a condition with frequent fatal complications. This condition is caused by a disruption in the lung - that creates a one-way valve allowing air to accumulate in the pleural space. The fatal complication is the prevention of blood returning to the right side of the heart - due intrathoracic pressure compressing the right atrium. The patient can exhibit symptoms of dyspnea, tachypnea, tracheal deviation, jugular venous distention, subcutaneous emphysema, and shock that can lead to rapid deterioration and death.
Case Report: We report a case of massive subcutaneous emphysema complicating tension pneumothorax management. The patient is a 20-year-old male who presented to the emergency department with chest trauma and was in extremis with diffuse severe subcutaneous emphysema. Due to the distorted anatomy, airway management and chest decompression were performed with nonstandard techniques/equipment resulting in rapid patient stabilization. After 4 days in the hospital, he was discharged home with no deficits.
Discussion: Many providers do not have the proper equipment or training to treat patients in this extreme condition. CT images demonstrate the anatomical distortions in this case and the increase in size required for invasive life-saving devices. Images demonstrate where many commercial 14 gauge angiocaths and cricothyrotomy kits will not suffice (due to distortion in the anatomy), and these should not be relied on solely.
Conclusions: While trauma carts frequently maintain (1.75 - 2 inch) 14 gauge angiocaths, they should also have military grade angiocaths that are 3.25” in length, which will work in most cases. Some, but not all, military-grade cricothyrotomy kits, or individually assembled kits, have 6.0 endotracheal tubes and come with a bougie and cricothyrotomy hook which would have been sufficient in this patient. Prehospital and hospital healthcare personnel should be prepared for similar patient encounters.
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Swisher, Anne K. "The effect of emphysema on adaptation of peripheral skeletal muscle to different loading conditions in the Syrian golden hamster". Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3008.
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Thesis (Ph. D.)--West Virginia University, 2003.Title from document title page. Document formatted into pages; contains vii, 141 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Cornejo, Perales Salomon Martin. "Genetic and phenotypic dissection of smoke induced emphysema in mouse". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=99332.
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Chronic obstructive pulmonary disease (COPD) is a composite of conditions that include an abnormal inflammatory response and emphysema. Cigarette smoking is the main risk factor for developing COPD and mouse models are widely used in the study of smoking induced emphysema. The C57BL/6 mouse strain develops airspace enlargement after chronic smoke exposure, with no change in lung mechanics. The broad objective of this thesis is to try to identify in mice, candidate genes that cause a difference in susceptibility to the development of the disease and to better understand the inflammatory process that occurs in response to smoke exposure.A detailed introduction to COPD and proposed mechanisms of its pathophysiology are presented in Chapter I.
Chapter II consists of a manuscript containing data comparing the genetic expression profiles and inflammation in lung tissue of mice (C57BL/6) chronically exposed to cigarette smoke, with age-paired controls. The findings presented in Chapter II are discussed in greater detailed in Chapter III.
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Binder, Polina. "Unsupervised discovery of emphysema subtypes in a large clinical cohort". Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105678.
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Thesis: S.M., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2016.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 45-47).
Emphysema is one of the hallmarks of Chronic Obstructive Pulmonary Disease (COPD), a devastating lung disease often caused by smoking. Emphysema appears on Computed Tomography (CT) scans as a variety of textures that correlate with the disease subtypes. It has been shown that the disease subtypes and the lung texture are linked to physiological indicators and prognosis, although neither is well characterized clinically. Most previous computational approaches to modeling emphysema imaging data have focused on supervised classification of lung textures in patches of CT scans. In this work, we describe a generative model that jointly captures heterogeneity of disease subtypes and of the patient population. We also derive a corresponding inference algorithm that simultaneously discovers disease subtypes and population structure in an unsupervised manner. This approach enables us to create image-based descriptors of emphysema beyond those that can be identified through manual labeling of currently defined phenotypes. By applying the resulting algorithm to a large data set, we identify groups of patients and disease subtypes that correlate with distinct physiological indicators.
by Polina Binder.
S.M.
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Dhapare, Sneha. "SALVIANOLIC ACID B FOR PULMONARY DELIVERY TOWARDS REVERSAL OF EMPHYSEMA". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4812.
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A new pathobiologic hypothesis has recently emerged that the alveolar structural destruction and loss in emphysema are caused by the deficiency of vascular endothelial growth factor (VEGF). Therefore, this project hypothesized that such pathobiologic VEGF deficiency of emphysematous lungs can be recovered with a natural caffeic acid tetramer, salvianolic acid B (SalB), through activation of signal transducer and activator of transcription 3 (STAT3), so that emphysema can be reversed as a result of inhibition of induced cell death, stimulation of cell proliferation and migration, and promotion of stem cell recruitment to the lungs.
SalB was first shown to be potently anti-oxidative (IC50 = 3.7 μM), but devoid of anti-elastase activity. SalB was then administered to the lungs of healthy rats at 0.2 mg/kg for two weeks, verifying ~1.7-fold increased lung tissue expressions of phosphorylated STAT3 (pSTAT3; an activated form of STAT3) and VEGF. Subsequently, SalB was examined in the anti-cell death assay, cell proliferation and migration assays, and trans-
endothelial stem cell recruitment assay in the in vitro lung epithelial (A549) and endothelial (HMVEC-L) cell systems. SalB at 25 μM exerted significant 48-88 % inhibitory activities against cell death induced with oxidative stress and VEGF receptor blockade (with SU5416) in both cell systems, measured by the trypan blue exclusion and propidium iodide-based flow cytometry assays. SalB at 25 μM also stimulated A549 and HMVEC-L cell proliferation by ~1.4-fold and promoted cell migration by ~1.6-fold, while recovering stem cell recruitment impaired with SU5416 by 60 %. The anti-cell death, and proliferation and migration stimulatory activities of SalB were significantly opposed by pharmacological inhibitors of JAK2 (Janus kinase 2; an upper signal of STAT3), STAT3 and VEGF.
SalB was then examined for its in vivo reversal activities in emphysema induced with porcine pancreatic elastase (PPE) and cigarette smoke extract (CSE) in rats. Upon establishment of emphysema on day 21, SalB was administered to the lungs three times weekly over three weeks. SalB at 0.2 mg/kg significantly recovered ~85 %-impaired treadmill exercise endurance by 57-82 %; and reduced abnormal airspace enlargement by 59-75 %. In the PPE-induced emphysematous rats, SalB also reduced the 4-fold greater alveolar destruction index by 61 %. The lung tissue protein expression by Western blot analysis found that cleaved caspase 3 (cell apoptotic marker) was induced by 13-fold, and VEGF was reduced by 60 % in the PPE -induced emphysematous rats. However, pulmonary treatment with SalB at 0.2 mg/kg normalized these proteins, and also significantly increased the expression of a cell proliferation marker, proliferative cell nuclear antigen (PCNA) by 2.6-fold. Note however that SalB treatment did not reduce the neutrophilic myeloperoxidase activity in the lungs induced in the PPE-induced rats. Taken all together, this study has demonstrated that SalB potently inhibited lung cell death, stimulates lung cell proliferation and migration, and restores stem cell migration with its mechanism of STAT3 activation and VEGF elevation and reversed established emphysema in rat models.
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Liu, Jianghuai. "Regulation of lung elastin gene expression and fibroblast migration by elastase-released growth factors". Thesis, Boston University, 2005. https://hdl.handle.net/2144/37163.
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Thesis (Ph.D.)--Boston UniversityPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Degradation of elastin within alveolar walls is an important event in the development of pulmonary emphysema. Elastases release growth factors from extracellular matrices and interstitial cell surfaces, which can regulate the repair process. Brief treatment of matrix-laden rat pulmonary fibroblast cultures with porcine pancreatic elastase results in the release of soluble heparin-binding epidermal growth factor-like growth factor (HB-EGF) together with previously identified fibroblast growth factor-2 (FGF-2). In matrix-laden pulmonary fibroblasts, HB-EGF and two other EGF family ligands, i.e. EGF and transforming growth factor a, significantly down-regulate elastin mRNA via activation of the EGF receptor. HB-EGF treatment initiates a signaling pathway involving extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation and subsequent nuclear accumulation of Fra-1, which leads to inhibition of elastin gene transcription. Co-addition of HB-EGF and FGF-2 results in an additive inhibitory effect on elastin mRNA levels. The increased effect of HB-EGF and FGF-2 on elastin mRNA is associated with their additive actions on ERK1/2 activation, c-fos mRNA induction and Fra-1 nuclear accumulation. Further, HB-EGF induces FGF-2 mRNA and protein, suggesting a potential role of endogenous FGF-2 in mediating HB-EGF-dependent responses. Cell migration represents an important component of injury/repair. A chemotactic activity for pulmonary fibroblasts was identified within the elastase-released products. Characterization of this activity indicates that elastase-released FGF-2 is a major chemotactic component of the elastase digest. Furthermore, our data strongly suggest that the elastase digest contains another component(s) that potentiates the chemotactic activity of FGF-2. Collectively, the present study supports a model in which elastase-released growth factors and other components act in concert to regulate elastin gene expression and cell migration in injury/repair situations.
2031-01-01
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Madani, Afarine. "Quantification de l'emphysème pulmonaire en tomodensitométrie hélicoïdale multi-coupes". Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209993.
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L’emphysème pulmonaire est, avec la bronchite chronique à laquelle il est généralement associé, une bronchopathie chronique obstructive (BPCO). Ce groupe de maladie a été la sixième cause de mortalité au monde en 1990 et pourrait devenir la troisième en 2020.L’emphysème pulmonaire est défini par un élargissement anormal et permanent des espaces aériens en amont des bronchioles terminales avec destruction des parois alvéolaires sans fibrose évidente. Compte tenu de cette définition, son diagnostic devrait idéalement être basé sur l’histopathologie. Cependant, en pratique clinique, si les EFR sont à la base de la définition de la BPCO, elles ne suffisent pas au diagnostic de l’emphysème pulmonaire.La tomodensitométrie (TDM) est une méthode diagnostique d’obtention in vivo de coupes anatomiques qui, formées de milliers de pixels, en font la méthode morphologique la plus précise pour investiguer la structure pulmonaire. Si la juxtaposition de ces pixels – dont la tonalité de gris est fonction de l’atténuation – est à la base de l’image TDM, la même information peut être représentée par la distribution de fréquence de ces atténuations. En présence d’emphysème, la destruction du tissu pulmonaire (et la plus grande proportion d’air) déterminent le déplacement de cette distribution vers les atténuations plus négatives. Plusieurs index TDM dérivés de cette distribution – notamment l’atténuation moyenne, la surface pulmonaire occupée par des valeurs d’atténuation inférieures à un seuil, un percentile particulier de la distribution – sont de possibles mesures de l’étendue de l’emphysème pulmonaire. L’émergence de la technique hélicoïdale, permettant notamment d’explorer tout le parenchyme pulmonaire en une seule apnée, justifie de déterminer les seuils et percentiles adéquats par comparaison à une mesure histologique de référence.
Au cours de nos études, nous avons montré que les index TDM dérivés de la distribution de fréquence d’atténuation tels que les surfaces relatives de poumon occupées par les coefficients d’atténuation inférieures à -960 UH (RA960) ou -970 UH (RA970) et le premier percentile (p1) sont les index les plus appropriés. En revanche, toujours sur base de comparaisons histo-morphométriques, d’autre index qui reflètent la géométrie des espaces emphysémateux – tels que la distribution de la taille des groupes de pixels adjacents occupés par des coefficients d’atténuation inférieurs à un seuil ou à un percentile – ne sont pas des index valables.
La dose d’irradiation peut être abaissée à 20 mAs effectifs. Cette réduction est particulièrement appropriée dans une pathologie susceptible de concerner des patients jeunes et l’objet d’examens répétés. Cependant, la dose d’irradiation influençant ces index, elle doit être maintenue constante au cours de suivis longitudinaux.
En TDM multi-coupes, ces index sont les plus appropriés quelque soit l’épaisseur des coupes. Cependant, cette épaisseur influençant ces index, elle doit aussi être maintenue constante au cours de suivis longitudinaux.
L’inspiration incomplète induit une sous-estimation statistiquement significative mais cliniquement insignifiante de l’étendue de l’emphysème pulmonaire. La destruction du tissu pulmonaire et l’hyperinflation ont des influences séparées sur les index TDM, faisant recommander leur ajustement aux valeurs prédites de la CPT.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
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Wickenden, Julie Anne. "Pathogenesis of emphysema : molecular mechanisms underlying cigarette smoke-induced cell death". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/27662.
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Emphysema is characterised by enlargement of the distal airspaces in the lungs due to destruction of alveolar walls, and was initially thought to be the result of matrix destruction from a protease-antiprotease and oxidant-antioxidant imbalance, leading to detachment of alveolar cells. however, recently apoptosis has been implicated in alveolar cell loss; increased numbers of apoptotic epithelial and endothelial cells have been observed in the lungs of emphysema patients. Thus the effect of cigarette smoke on apoptotic cell death was investigated. Unexpectedly, cigarette smoke condensate (CSC) did not induce apoptosis in either an alveolar epithelial type II cell line (A549) or primary human umbilical vein endothelial cells (HUVECs), but instead it induced necrosis and inhibited staurosporine-induced apoptosis. The anti-apoptotic, pro-necrotic, effect of CSC was reproduced in a model system using Jurkat T cells, when either staurosporine or Fas ligation was used as an apoptotic stimulus. Additional studies indicated that these effects might be oxidant-mediated as the antioxidant compounds glutathione and dithiothreitol presented CSC-mediated apoptosis inhibition, and necrosis. Time course experiments revealed that CSC inhibited an early step in the caspase cascade, whereby caspase-3 was not activated. Moreover, reconstitution of the apoptosome in cytoplasmic extracts from CSC-treated cells, by addition of cytochrome-c and dATP, did not result in activation of caspases-3 or -9. Thus, smoke treatment may alter the levels of pro-and anti-apoptogenic factors downstream of the mitochondria to inhibit active apoptosome formation. Therefore these data demonstrate that CSC treatment did not induce apoptosis as previously reported. More interestingly, CSC inhibited apoptosis by preventing activation of caspases, resulting in necrotic cell death. Thus, cell death in response to cigarette smoke by necrosis, and not apoptosis, may be responsible for the loss of alveolar walls observed in emphysema.
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Mackay, Laura Sutherland. "The role of microvascular endothelial cells in the pathogenesis of emphysema". Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/3079.
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COPD comprising small airways disease and emphysema is a chronic, debilitating often fatal lung condition that approximately 20% of smokers develop. Current therapies mostly target inflammation and airflow obstruction caused by small airways disease however there are no current therapies which treat emphysema, the pathogenesis of which remains poorly understood. The microvascular hypothesis of COPD is a credible alternative to the classical hypothesis of inflammation and protease driven lung destruction, whereby an initial insult to the microvasculature leads to loss of alveolar structure which typifies emphysema. I planned to investigate the role of the microvasculature in the pathogenesis of COPD by isolating susceptible lung microvascular endothelial cells (LMVECs) from individuals with emphysema in an attempt to mimic in vivo conditions more closely. LMVECs were isolated from explanted emphysematous lungs removed at transplantation. Following successful isolation (71%) and characterisation of emphysema LMVECs, I sought to study cellular responses to cigarette smoke injury, namely apoptosis and endothelial to mesenchymal transition. Apoptosis was investigated on tissue blocks via caspase 3 immunohistochemistry and by ex vivo methods including flow cytometry (annexin V), TUNEL and live cell imaging for activated caspase 3. Unfortunately cigarette smoke extract caused autofluorescence of cells and as all of these techniques employed the use of fluorescence for detection, any conclusions that can be made as to whether cells underwent apoptosis are limited. Endothelial to mesenchymal transition was investigated in response to TGFβ1 and cigarette smoke extract. While there was evidence of down regulation of endothelial markers in response to cigarette smoke on confocal imaging there was no convincing evidence of upregulation of mesenchymal markers with no corresponding change in protein expression via western blotting. One explanation may be that such changes in cell structure and endothelial cell expression may be more in keeping with endothelial activation rather than a true phenotypic switch. In summary, this study presents a new model of emphysema, with attempts to gain insight into endothelial injury in the pathogenesis of COPD, highlighting the challenges and limitations of working with primary diseased cells in response to cigarette smoke injury.
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Zoumot, Zaid. "Novel techniques for lung volume reduction and its assessment in emphysema". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24955.
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Many patients with emphysema remain breathless despite optimal medical therapy. Non-pharmacological approaches to reduce the volume of hyperinflated lungs include lung volume reduction surgery (LVRS) which is effective in selected patients with upper lobe predominant emphysema and low exercise capacity. Bronchoscopic techniques to reduce lung volume are also being developed. Studies of two bronchoscopic techniques to achieve lung volume reduction (LVR) are presented in this thesis; LVR coils (LVRCs) and endobronchial autologous blood instillation. In a trial of LVRCs we demonstrate for the first time in a randomised controlled setting, that treatment with LVRCs results in statistically and clinically meaningful improvements in quality of life, lung function and exercise capacity compared with controls, and that benefits are maintained up to 12 months following treatment compared to baseline. In two pilot studies, we used autologous blood instilled endobronchially aiming to achieve lung volume reduction by inducing parenchymal scarring and fibrosis. Instilling 180-240 mls of autologous blood withdrawn from patients during the bronchoscopic procedure directly into a giant bullae resulted in significant reduction in bulla size over subsequent months in three of five patients, with associated improvements in lung function, exercise capacity and quality of life. However a randomised controlled trial of instilling 60 mls of autologous blood into three segments of one lobe in patients with heterogeneous emphysema was ineffective. In addition, I investigated the use of a novel 3-dimentional measurement system, optoelectronic plethysmography (OEP), to track abdominal and chest wall movements during respiration. This showed that successful lung volume reduction approaches were associated with significant improvements in lower rib cage paradoxical inspiratory movements after lung volume reduction. Improvements in chest wall asynchrony were larger the worse the asynchrony was at baseline, and those with larger improvements in asynchrony derived greater benefits in lung function and other clinical outcomes following LVR.
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Sato, Atsuyasu. "Morphological mechanism of the development of pulmonary emphysema in klotho mice". Kyoto University, 2007. http://hdl.handle.net/2433/135746.
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Tanabe, Naoya. "Impact of Exacerbations on Emphysema Progression in Chronic Obstructive Pulmonary Disease". Kyoto University, 2012. http://hdl.handle.net/2433/157447.
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Ikezoe, Kouhei. "Bone mineral density in patients with idiopathic pulmonary fibrosis". Kyoto University, 2016. http://hdl.handle.net/2433/215403.
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Final publication is avilable at http://www.sciencedirect.com/science/article/pii/S0954611115300172Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第19577号
医博第4084号
新制||医||1013(附属図書館)
32613
京都大学大学院医学研究科医学専攻
(主査)教授 伊達 洋至, 教授 平家 俊男, 教授 松田 秀一
学位規則第4条第1項該当
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Dhami, Rajwinder Kaur. "The role of alpha-1-antitrypsin in the development of pulmonary emphysema". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0015/NQ48627.pdf.
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Smith, Benjamin. "Which lung cancer histologies are associated with emphysema on chest computed tomography?" Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106284.
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BACKGROUND: Multiple studies have demonstrated increased risk of lung cancer in the presence of emphysema, independent of smoking history and airflow obstruction, but the relationship of emphysema to specific histologic subtypes remains uncertain. OBJECTIVE: To determine the extent to which emphysema on chest computed tomography (CT) is associated with lung cancer histology. METHODS: Cross-sectional analysis of consecutive lung cancer patients referred to the Jewish General Hospital was performed (2001-2009). All those with demographic data, smoking history (pack-years), documented histology and chest CT were included. Emphysema was graded on CT by three readers, using a standardized rubric. Odds of each lung cancer subtype were compared between patients with and without emphysema, and adjusted for age, sex and smoking history by multiple logistic regression. RESULTS: Complete data were available for 498 lung cancer patients (mean age 68 years; 221 [44%] female; 78 [16%] never smokers; 263 [53%] without emphysema on CT). The most common histologies were adenocarcinoma (242 [49%]), squamous (71 [14%]), undifferentiated (48 [10%]) and small cell carcinoma (42 [8%]). The remaining 19% included bronchioloalveolar, large cell, pleomorphic and basaloid carcinomas. Presence of emphysema was associated with increased odds of squamous (OR 3.1 95%CI 1.8-5.3) and small cell (OR 2.1 95%CI 1.1-4.1) carcinoma. After adjustment for age, sex and smoking history, emphysema was associated with squamous (OR 2.7 95%CI 1.5-4.9) but not small cell (OR 1.5 95%CI 0.8-3.1) carcinoma. CONCLUSIONS: Relative to other histologic subtypes, the odds of squamous carcinoma were significantly increased among lung cancer patients with emphysema after adjustment for smoking history. This was not true of small cell carcinoma, although confidence intervals were wide so an association cannot be entirely excluded. Other common subtypes were not independently associated with emphysema.CONTEXTE: Plusieurs études ont démontré un risque accru de cancer du poumon en présence d'emphysème, indépendamment des antécédents de tabagisme et d'obstruction, mais la relation entre l'emphysème et les types histologiques spécifiques demeure incertaine. OBJECTIF: Déterminer la mesure dans laquelle l'emphysème sur la tomodensitométrie thoracique (TDM) est associé à l'histologie du cancer du poumon. MÉTHODES: L'analyse transversale de patients consécutifs de cancer du poumon référés à l'Hôpital général juif a été réalisée de 2001 à 2009. Tous ceux avec des données démographiques, des antécédents de tabagisme (paquets-années), une histologie documentée et un TDM thoracique ont été inclus. L'emphysème a été évalué sur TDM par trois lecteurs, en utilisant une méthode standardisée. Les proportions de chaque sous-type de cancer du poumon ont été comparées entre les patients avec et sans emphysème, et ajustées selon l'âge, le sexe et les antécédents de tabagisme par régression logistique multiple. RÉSULTATS: Des données complètes étaient disponibles pour 498 patients atteints de cancer du poumon (moyenne d'âge 68 ans; 221 [44%] des femmes; 78 [16%] qui n'ont jamais fumé; 263 [53%] sans emphysème sur TDM). Les histologies les plus fréquentes étaient l'adénocarcinome (242 [49%]), l'épidermoïde (71 [14%]), les indifférenciées (48 [10%]) et le carcinome à petites cellules (42 [8%]). La présence de l'emphysème était associée à une probabilité accrue de carcinomes épidermoïdes (OR 3,1 IC 95%: 1,8-5,3) et de carcinomes à petites cellules (OR 2,1 IC 95% 1,1-4,1). Après ajustement selon l'âge, le sexe et les antécédents de tabagisme, l'emphysème était associé au cancer de type épidermoïde (OR 2,7 IC 95%: 1,5-4,9), mais pas au cancer à petites cellules (OR 1,5 IC 95%: 0,8-3,1). CONCLUSIONS: Comparativement à d'autres sous-types histologiques, la probabilité de carcinome épidermoïde est significativement augmentée chez les patients atteints de cancer du poumon avec emphysème, après ajustement selon les antécédents de tabagisme. Ce n'est pas le cas pour le carcinome à petites cellules, bien que les intervalles de confiance étaient larges, donc une association ne peut pas être entièrement exclue. D'autres sous-types de cancer pulmonaire n'ont pas été indépendamment associés à l'emphysème.
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Kneidinger, Nikolaus [Verfasser]. "Activation of the WNT/beta-catenin pathway attenuates experimental emphysema / Nikolaus Kneidinger". Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1063955424/34.
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Truong, Tien M. "SULFATED DEHYDROPOLYMER OF CAFFEIC ACID FOR REPAIR OF LUNG DAMAGE AND EMPHYSEMA". VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4229.
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The complex pathobiologic mechanisms of emphysema are not fully understood, leaving this deadly disease without effective pharmacotherapy for a cure. This project hypothesized that the sulfated dehydropolymer of caffeic acid (CDSO3) exhibits Fe2+ chelation-based hypoxia inducible factor-1a (HIF-1a) up-regulatory protective activities against in vitro emphysematous cell death and for in vivo reversal of emphysema induced with SU5416, a vascular endothelial growth factor blocker.
Using in vitro chromogenic competitive inhibition assays, CDSO3 was shown to chelate Fe2+ (IC50 of 23 µM), but not Fe3+ ions. The trypan blue exclusion and lactate
dehydrogenase assays were then employed to examine the cytoprotective activities of CDSO3 against inflammatory, oxidative, elastolytic, and apoptotic cell death using alveolar macrophages, epithelial and endothelial cells. CDSO3 at 10 µM produced significant protective activities against these emphysematous cell deaths by 50-154 %. These protective effects were opposed by the addition of the HIF-1a inhibitors, CAY10585 and echinomycin, and excess Fe2+, but not Fe3+, ions.
Emphysema was then induced in rats following a subcutaneous injection of SU5416 at 20 mg/kg, after which CDSO3 at 60 µg/kg was administered to the lungs 3 times/week for two weeks. Treadmill exercise endurance (EE) was measured to assess the functional impairment, while lung tissues were removed for morphological assessments of alveolar airspace enlargement (MLI) and destruction (DI), as well as to measure protein levels using Western blot. SU5416 significantly impaired EE, MLI, and DI by 81 %, 47 %, and 5-fold, compared to the healthy animals, and these were significantly reversed by CDSO3 by 66, 74, and 87 %. CDSO3 treatment did not change the lung cytoplasmic expression of histone deacetylase 2 (HDAC2), HIF-1a, or a pro-apoptotic marker, BAX. However, induction with SU5416 significantly reduced VEGF expression by 52 % and increased cleaved caspase-3 expression by 1.5-fold, compared to the healthy animals, while CDSO3 normalized the expressions of both proteins in these emphysematous animals. However, when CDSO3 was pre-mixed with excess Fe2+, the reversal activities of CDSO3 were diminished. In conclusion, this study has demonstrated the Fe2+ chelation-based HIF-1a up-regulatory dependent in vitro and in vivo lung repairing efficacies for CDSO3 in emphysema.
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Lowman, John D. Jr. "Effects of emphysema and chronic hypoxemia on skeletal muscle oxygen supply and demand". VCU Scholars Compass, 2004. http://scholarscompass.vcu.edu/etd/907.
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Skeletal muscle dysfunction in chronic obstructive pulmonary disease (COPD) is a condition in which peripheral skeletal muscle undergoes myopathic changes which impair muscle function, limit physical performance, and can lead to significant disability. While the etiology of the dysfunction is unknown, this study was conducted to test the hypothesis that chronic hypoxemia leads to alterations in oxygen transport and muscle function. A primary objective was to validate elastase-induced emphysema in rats as an animal model of skeletal muscle dysfunction in COPD.Arterial blood gases were used to determine the severity of hypoxemia and sodium dodecyl sulfate- polyacrylamide gel electrophoresis was used to determine the proportions of myosin heavy chain isoforms I, IIa, IIx, and IIb. Measures of microvascular oxygenation and blood flow in the spinotrapezius muscle allowed for determination of both convective and diffusive oxygen supply to the muscle, as well as calculation of muscle oxygen consumption at rest and during electrically stimulated three-minute muscle contractions. Muscle performance measures included peak force, force-time integral, and fatigue index. Due to a presumed rat respiratory virus, which likely resulted in the control group being nearly as hypoxemic as the elastase-induced emphysema group, this study was not able to definitively test the hypothesis that chronic hypoxemia leads to both a diminished supply and demand of oxygen in skeletal muscle. Although many of the results of the present study were not statistically significant, they exhibited consistent trends over time and are likely of physiological significance. All measures of muscle performance were lower in the emphysema group. In addition, spinotrapezius muscle oxygen consumption and blood flow were lower in the emphysema group. The addition of supplemental oxygen during isolated, small-muscle mass exercise did increase the force-time integral by ~18% in both groups, suggesting that muscle work in these hypoxemic animals may be limited by oxygen supply. Thus, the data on muscle fiber type, oxygen consumption and muscle performance suggest that elastase-induced emphysema in rats leads to a similar skeletal muscle dysfunction that is observed in humans with COPD, and indicates that it is a valid animal model of skeletal muscle dysfunction in COPD.
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Skrońska-Wąsek, Wioletta [Verfasser] y Melanie [Akademischer Betreuer] Königshoff. "WNT/Frizzled signaling in COPD and emphysema / Wioletta Skrońska-Wąsek ; Betreuer: Melanie Königshoff". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1155097548/34.
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Cederlund, Kerstin. "Radiological imaging of pulmonary emphysema : preoperative evaluation of candidates for lung volume reduction surgery /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-195-0.
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Uemasu, Kiyoshi. "Serine Protease Imbalance in the Small Airways and Development of Centrilobular Emphysema in COPD". Kyoto University, 2020. http://hdl.handle.net/2433/258996.
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Pirie, Lindsay Jane Learmonth. "Pattern of breathing and lung receptor activity in an animal model of pulmonary emphysema". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/22560.
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This thesis investigates the pattern of breathing, lung reflex responses and activity of vagal lung receptors in an animal model of emphysema. The specific aim was to investigate if changes in pulmonary receptor activity are produced in an animal model of emphysema, and if these can be related to any changes in breathing pattern and lung reflex responses occurring in the diseased model. Emphysema was induced in rats by an endotracheal instillation of the proteolytic enzyme papain (120 mg/kg body weight). In control and emphysematous anaesthetised rats the pattern of breathing during eupnoea and during administration of 4% and 6% CO2 was measured. The reflex responses to lung inflation and deflation pressures of 5 and 10cm were also recorded. Activity was recorded from either slowly adapting (SARs) or rapidly adapting receptors, (RARs) in single fibres of the left vagus nerve during the above conditions. After bilateral vagotomy the pattern of breathing was measured in both groups of rats. The alveolar walls of the papain treated rats had a significantly increased mean linear intercept value of 109.3+/-2.7 μm compared to 81.5+/- 3.1 μm in the control rats, (P<0.01), indicating that emphysema had been induced. Breathing frequency in the diseased rats with the vagi intact was slightly slower than the controls. Tidal volume was similar in both groups of rats 2.85+/-0.2 ml in the emphysematous and 2.83+/-0.2 ml in the controls. Breathing 4% and 6% CO2 increased tidal volume in both groups of rats although this response was more vigorous in the controls, breathing frequency was not significantly altered in either group. Without the influence of the vagi the diseased rats breathed slightly faster than the controls. The Hering-Breuer inflation reflex response to both 5 and 10cm. H2O pressure was significantly longer in the emphysematous rats.
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Кравченко, Е. А. y В. В. Гуринович. "Основные проявления синдрома врожденной недифференцированной дисплазии соединительной ткани у пациентов с буллезной эмфиземой, осложненной спонтанным пневмотораксом". Thesis, Сумский государственный университет, 2016. http://essuir.sumdu.edu.ua/handle/123456789/47739.
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Fysikopoulos, Athanasios [Verfasser]. "The role of the antioxidant protein sestrin 2 in emphysema development in mice / Athanasios Fysikopoulos". Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1071801090/34.
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Marumo, Satoshi. "p38 mitogen-activated protein kinase determines the susceptibility to cigarette smoke-induced emphysema in mice". Kyoto University, 2015. http://hdl.handle.net/2433/202777.
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MINEO, DAVIDE. "Variations of inflammatory mediators and α1-antitrypsin levels after lung-volume-reduction surgery for emphysema". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/208592.
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Razionale. L’infiammazione cronica, con squilibrio della proteasi-antiproteasi, è responsabile nell’enfisema del declino della funzione polmonare e della progressiva cachessia.
Obiettivo. Valutare le variazioni dei livelli di vari mediatori infiammatori e di α1-antitripsina dopo chirurgia di riduzione di volume polmonare rispetto alla riabilitazione respiratoria.
Metodi. Ventotto pazienti con enfisema di grado moderato-severo, sottoposti a chirurgia di riduzione di volume polmonare con tecnica video-toracoscopica, sono stati confrontati con 26 pazienti dalle caratteristiche simili che, rifiutato l’intervento, hanno seguito un programma standard di riabilitazione respiratoria, e con un gruppo di soggetti sani di pari età e sesso. La funzione respiratoria, la composizione corporea, i mediatori infiammatori circolanti ed i livelli di α1-antitripsina sono stati valutati prima e 12 mesi dopo i rispettivi trattamenti. I livelli di espressione genica dei mediatori infiammatori e delle proteasi-antiproteasi sono stati valutati in campioni di tessuto enfisematoso prelevati da 17 pazienti sottoposti ad intervento e confrontati con il tessuto normale presente nei margini di resezione dei medesimi campioni.
Misurazioni e risultati principali. Solo dopo l’intervento sono stati osservati miglioramenti significativi nella funzione respiratoria (volume espiratorio forzato in 1 secondo +25.2%, p<0.0001; volume residuo -19.5%, p<0.0001; capacità polmonare di diffusione del monossido di carbonio +3.3%, p<0.05) e composizione corporea (massa magra +6.5%, p<0.01; massa grassa +11.9%, p<0.01), con riduzione dei mediatori infiammatori circolanti (tumor-necrosis-factor-α -22.2%, p<0.001; interleuchina-6 -24.5%, p<0.001; interleuchina-8 -20.0%, p<0.001) ed aumento dei livelli delle antiproteasi (α1-antitripsina +27.0%, p<0.001). L’analisi dell’espressione genica ha mostrato attiva infiammazione e iperattività delle proteasi nel tessuto enfisematoso asportato. La riduzione di tumor-necrosis-factor-α e di interleuchina-6 e l’aumento dei livelli di α1-antitripsina sono risultati significativamente correlati con la riduzione di volume residuo (rispettivamente p=0.03, p=0.009 e p=0.001), ed in parte con l’aumento della massa magra (rispettivamente p=0.03, p=0.02 e p=0.09).
Conclusioni. La chirurgia di riduzione di volume polmonare riduce significativamente i mediatori infiammatori circolanti ed aumenta i livelli di antiproteasi rispetto alla riabilitazione respiratoria, migliorando anche la funzione respiratoria e lo stato nutrizionale. Le correlazioni dei mediatori infiammatori e dei livelli di proteasi con il volume residuo ed, in parte, con la composizione corporea, suggerisce che l’eliminazione del tessuto infiammatorio enfisematoso possa spiegare i miglioramenti clinici dopo l’intervento chirurgico.Rationale. In emphysema, chronic inflammation, including protease-antiprotease imbalance, is responsible for declining pulmonary function and progressive cachexia. Objective. To evaluate variations of inflammatory mediators and α1-antitrypsin levels after lung-volume-reduction surgery compared to respiratory rehabilitation. Methods. Twenty-eight patients with moderate-to-severe emphysema, who underwent video-assisted thoracoscopic lung-volume-reduction surgery, were compared to 26 similar patients, who refused operation and followed a standardized rehabilitation program, and to a matched healthy group. Respiratory function, body composition, circulating inflammatory mediators and α1-antitrypsin levels were evaluated pre- and 12-month post-treatment. Gene expression levels of inflammatory mediators and protease-antiprotease were assessed in emphysematous specimens from 17 operated patients by matching to normal tissue from resection margins. Measurements and main results. Significant improvements were only obtained after surgery in respiratory function (one-second forced expiratory volume +25.2%, p<0.0001; residual volume -19.5%, p<0.0001; diffusion lung-capacity for carbon-monoxide +3.3%, p<0.05) and body composition (fat-free mass +6.5%, p<0.01; fat mass +11.9%, p<0.01), with decrement of circulating inflammatory mediators (tumor-necrosis-factor-α -22.2%, p<0.001; interleukin-6 -24.5%, p<0.001; interleukin-8 -20.0%, p<0.001) and increment of antiprotease levels (α1-antitrypsin +27.0%, p<0.001). Supportive gene expression analysis demonstrated active inflammation and protease hyperactivity in the resected emphysematous tissue. Reduction of tumor-necrosis-factor-α and interleukin-6 and increment of α1-antitrypsin levels significantly correlated with reduction of residual volume (p=0.03, p=0.009, p=0.001, respectively), and partially with increment of fat-free mass (p=0.03, p=0.02, p=0.09, respectively). Conclusions. Lung-volume-reduction surgery significantly reduced circulating inflammatory mediators and increased antiprotease levels over respiratory rehabilitation, also improving respiratory function and nutritional status. Correlations of inflammatory mediators and antiprotease levels with residual volume and partly with body composition suggests that elimination of inflammatory emphysematous tissue may explain clinical improvements after surgery.
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Dolley, Larry. "The effect of maternal nicotine exposure on the quantity and quality of neonatal rat lung connective tissue". University of the Western Cape, 1994. http://hdl.handle.net/11394/8386.
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>Magister Scientiae - MScThe infants of smoking mothers (compared to non-smoking mothers) have been shown to have a lower birth mass, a lower brain mass, an increased perinatal mortality rate as well as a predisposition to respiratory abnormalities in later life. Evidence suggests that one of the reasons for the latter is abnormal lung structure due to changes in the connective tissue skeleton. This study evaluated the in vivo effects of maternal nicotine exposure (lmg/kg/day subcutaneously - designated the experimental group), which is equivalent to smoking 32 cigarettes per day, on the connective tissue status of the neonatal (7, 14 and 21 day old) wistar rat lung. The control group received sterile saline as a placebo. The specific aspects investigated were: (1) the morphological changes in lung structure and connective tissue (collagen, elastic tissue and reticulin) distribution by means of light microscopy. (2) the quantities of collagen and Emphysema-like morphological changes are present at all ages. The histochemical appearance of collagen is not affected while reticular fibres appear to be abnormal in structure. On day 7 there appears to be no elastic tissue in the nicotine-exposed lung compared to the control lung. This difference is notelastic tissue in the lung. (3) the ultrastructure of the lung connective tissue skeleton by means of scanning electron microscopy. noticeable on days 14 and 21. Biochemical quantitation indicated that, for the three age groups studied, there was no significant difference in collagen content between experimental and control animals. Elastic tissue was significantly higher in 7 day old experimental lungs than in the control group, contradictory to the results of the histochemical studies. This difference was not significant for 14 and 21 day old lungs Ultrastructural studies of the lung connective tissue skeletons hoed abnormal fibres in the experimental group. Changes included fibre breaks, a beaded appearance of certain fibres and a deficiency in normal fibre arrangement due to the direct or indirect effects of nicotine The effects of nicotine on neonatal rat lung after maternal nicotine exposure is described. The direct mechanisms for these events are still not known but speculation as to this are presented here. Further studies which could explain these mechanisms are also suggested.
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Makinson, Alain. "Prévention, diagnostic précoce et traitement du cancer broncho-pulmonaire chez les personnes vivant avec le VIH : apport de la tomodensitométrie thoracique sans injection de produit de contraste". Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT021/document.
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Cette thèse présente nos travaux sur la prévention, le dépistage, le diagnostic précoce, et traitement du cancer broncho-pulmonaire (CBP) chez les personnes vivant avec le VIH (PVVIH). La finalité de cette synthèse est d’améliorer la prise en charge des PVVIH atteint de ce cancer, mais aussi de développer des axes de recherche après une évaluation rigoureuse de la bibliographie. Nos recherches soulignent tout d’abord que la prise en charge thérapeutique des PVVIH atteintes d’un CBP doit être identique à celle de la population générale, l’infection par le VIH ne constituant finalement qu’une comorbidité supplémentaire. Toutefois, une spécificité de la prise en charge de ce cancer chez les PVVIH est la survenue de complications potentiellement létales secondaires aux interactions et effets toxiques additifs entre les antirétroviraux et les médicaments cytotoxiques. Ce danger nécessite une bonne coordination des équipes oncologiques et infectiologiques, probablement par le biais de réunions de concertation pluridisciplinaires spécifiques, ainsi qu’une bonne connaissance des pharmacocinétiques et pharmacodynamies des produits administrés.Notre étude ANRS EP48 HIV CHEST, qui était une étude transversale multicentrique, a inclus 442 PVVIH à risque de développer un CBP, en raison (principalement) d’un tabagisme > 20 paquets-années, un âge > 40 ans, ainsi qu’un nadir en lymphocytes TCD4 < 350 cellules/ µl. Cette étude a rempli son objectif principal, qui était de démontrer la faisabilité du dépistage du CBP chez les PVVIH en France par TDM thoracique. Le diagnostic d’un nombre important de CBP de stades localisés, et donc guérissables, apporte probablement un bénéfice essentiel aux patients inclus. Le fait qu’aucune complication grave n’ait été engendrée par les explorations diagnostiques, et que la prévalence de nodules significatifs soit dans l’intervalle des résultats d’études en population générale, sont des éléments rassurants. Nos travaux, ainsi que d’autres données de la littérature de prévalence de ce cancer en fonction des âges, font apparaître que l’âge limite de dépistage par TDM faible dose pourrait être de 45 ans chez les PVVIH. Comme en population générale, l’apport du TDM thoracique ne se limite pas au diagnostic de CBP. Il permet d’augmenter l’efficacité du diagnostic précoce de comorbidités ayant un impact sur la qualité de vie et/ou la survie par : 1) le diagnostic des tassements vertébraux, pour la majorité asymptomatique, en rapport avec une prévalence élevée de l’ostéoporose fracturaire dans cette population, 2) l’évaluation de l’emphysème et de la bronchiolite du fumeur, 3) une estimation des calcifications coronaires, qui est associée aux événements cardio-vasculaires. Ce travail a également pour intérêt d’illustrer l’épidémiologie des complications actuelles des PVVIH sous traitement antirétroviral efficace et exposées à une intoxication tabagique. La BPCO, l’emphysème, le CBP, l’athérosclérose coronaire ont une prévalence élevée dans cette population et sont des enjeux importants de santé. Cette épidémiologie rapproche la population des PVVIH de la population générale mais avec des particularités liées, aux antécédents de déficit immunitaire et de traitements antirétroviraux toxiques, et à la prévalence plus élevée des comportements à risque. Pour certaines complications cependant (emphysème, bronchiolite, score calcique), l’absence d’association avec les variables immuno-virologiques souligne la primauté des facteurs comportementaux dans la survenue de ces complications. Ainsi, l’ensemble de ces travaux qui s’articulent principalement autour de l’étude ANRS EP48 HIV CHEST souligne que la réduction des risques liée aux facteurs d’exposition (tabagisme surtout, et probablement cannabis) est une priorité chez les PVVIH à l’ère des combinaisons antirétroviralesThis thesis is an analysis of our on-going or published works on the theme of prevention, early diagnosis, screening, and treatment of subjects living with HIV with lung cancer. The ultimate objective of this work is to improve care and prevention of lung cancer in people living with HIV (PLWHIV), and to promote research in lung cancer in this population. Our work underscores that lung cancer treatment in PLWHIV should be identical to treatments administered for lung cancer in the general population. HIV is an additional comorbidity to be taken into account, but never a contraindication for optimal therapy. However, there exist specificities in management of PLWHIV with lung cancer, including the propensity for drug-to-drug interactions and additive toxicity between cytotoxic compounds for chemotherapy and antiretroviral therapy, with potentially lethal effects. Managing these toxicities implies optimal cooperation between oncologists and specialists in HIV, as well as good knowledge of pharmacokinetics and pharmacodynamics of these different compounds.The ANRS EP48 HIV CHEST Study in a cross-sectional, multicentre study, which included 442 subjects at lung cancer risk, primarily due to their age (> 40 years), smoking hazard (> 20 pack-years), as well as a CD4 cell nadir count < 350 cells/µl. This study showed feasibility of lung cancer screening with chest Computed Tomography (CT) in PLWHIV. The early diagnosis of localized lung cancers, potentially curable, suggests clinical benefits for most participants with cancer. Also, the facts that no serious adverse events occurred with invasive diagnostic procedures and that the prevalence of positive nodules was in the range of those found in lung cancer screening studies in the general population are reassuring. Also, our work, combined with data from previous epidemiological studies, support a lower age limit for screening lung cancer with chest CT in PLWHIV at risk than in the general population, starting as early as 45 years. As in the general population, the impact of lung cancer screening with chest CT is not limited to the diagnosis of early stage lung cancers. The diagnosis of other morbidities, such as vertebral fractures, generally asymptomatic, emphysema, bronchiolitis, and coronary calcifications, have a probable positive impact on quality of life and a benefit in survival if managed adequately. Our works also illustrate the epidemiology of complications in PLWHIV under antiretroviral therapy and exposed to smoking hazards. Chronic obstructive pulmonary diseases, emphysema, lung cancer, coronary atherosclerosis have high prevalence in this subpopulation of PLWHIV. The epidemiology of these emerging morbidities is close to the epidemiology in the smoking general population, but specificities exist, due to the presence of chronic immunodeficiency, antiretroviral toxicities, and an increased prevalence of behavioural risks in PLWHIV in comparison with the general population. However, some complications are not associated with HIV-related and immunological factors, such as prevalence of emphysema, coronary calcifications, and bronchiolitis, underscoring the major impact of behavioural hazards in the occurrence of these complications.Taken together, our work highlights the importance of reducing health hazards in PLWHIV, primarily smoking and probably cannabis, to reduce the emergence of these new life-threatening morbidities in the era of highly active antiretroviral therapy
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Saluja, Bhawana. "NOVEL CINNAMIC ACID-BASED DEHYDROPOLYMERS FOR EMPHYSEMA: IN VITRO AND IN VIVO ASSESSMENT OF THEIR ACTIVITIES". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/130.
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Pulmonary emphysema is a serious worldwide illness, causing progressive and irreversible alveolar wall loss and difficulty in breathing. It is caused mostly by cigarette smoking. However, its unresolved complex and multiple pathogenic mechanisms have left this disease without effective pharmacotherapy. This project hypothesized that cinnamic acid-based dehydropolymers (DHPs), originally discovered as novel anti-coagulants, protect against emphysema through their potent triple inhibitory actions against oxidative stress, inflammation and elastase, some of the pathogenic mechanisms associated with this disease. Three in vitro inhibitory activity assays for oxidative stress, lung inflammation and neutrophil elastase (NE) were developed and used to identify the most potent triple inhibitor DHP. These activities were determined by chromogenic free radical generation in chemical oxidation, lung epithelial (Calu-3) repression of pro-inflammatory nuclear factor κB (NFκB) upon its plasmid transfection and chromogenic substrate NE hydrolysis, respectively. The sulfated caffeic acid DHP, CDS was shown to be the most potent in all three assessments, yielding the half-maximal inhibitory concentrations of 3.52, ~10 and 0.43 µM, respectively. CDS was tested with pulmonary delivery in an in vivo rat model of emphysema induced by elastase and cigarette smoke extract (HSE/CSE). CDS at 5 and 30 μg/kg was instilled into the lung at 2 h prior to HSE/CSE instillation. The lung tissues and bronchoalveolar lavage fluids (BALFs) were taken 1 or 48 h post-HSE/CSE instillation to determine the tissue reduced glutathione (rGSH), airway infiltration of inflammatory neutrophils and airway luminal elastase alongside lung hemorrhage. The HSE/CSE instillation significantly caused 43.0 % decrease in rGSH, 104.8-fold greater neutrophil infiltration, 2.8-fold higher elastase activity and 9.3-fold increased lung hemorrhage, compared to the saline (negative) control. However, all these inductions were significantly protected by CDS at 30 μg/kg, exhibiting 92.9, 76.6, 59.7 and 70.4 % inhibition, respectively; reduced effects were seen at 5 μg/kg, showing its dose-related responses. As a result, the HSE/CSE-induced airspace enlargement assessed on 28th day was also prevented by CDS at 30 μg/kg, yet not at 5 μg/kg. In conclusion, this study has demonstrated the in vitro and in vivo effectiveness of CDS for its possible use in the protection against emphysema development, specifically via inhalation.
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Gil, Julie Zeskind. "Gene expression alterations associated with progression of emphysema and small airway disease in smokers with COPD". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12395.
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Thesis (Ph.D.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.Chronic Obstructive Pulmonary Disease (COPD) is a disease of reduced lung function. It is the fourth leading cause of death in the US. In the US it is primarily caused by smoking, yet only 10-20% of smokers will develop COPD. The exact molecular and genetic mechanisms contributing to the disease are unknown. Current therapies reduce symptoms but cannot halt the lung function decline. COPD is comprised of two subphenotypes - emphysema (alveolar destruction) and small airway disease (airway-wall thickening). The relative combination of airway disease and emphysema is heterogeneous between patients. The degree of disease is heterogeneous within each patient. This study takes two unique approaches to gain insights into the molecular processes that contribute to airway thickening and alveolar destruction. First, it utilizes the regional heterogeneity in each patient as a surrogate for disease progression. Second, it examines the airway disease and emphysematous components separately. [TRUNCATED]
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Alves, Calebe de Andrade. "Dinâmica de degradação e reparação de fibras elásticas sob tensão". reponame:Repositório Institucional da UFC, 2013. http://www.repositorio.ufc.br/handle/riufc/13737.
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ALVES, Calebe de Andrade. Dinâmica de degradação e reparação de fibras elásticas sob tensão. 2013. 71 f. Dissertação (Mestrado em Física) - Programa de Pós-Graduação em Física, Departamento de Física, Centro de Ciências, Universidade Federal do Ceará, Fortaleza, 2013.Submitted by Edvander Pires (edvanderpires@gmail.com) on 2015-10-23T18:48:28Z No. of bitstreams: 1 2013_dis_caalves.pdf: 1922274 bytes, checksum: beae2409f015f4b21f8f423815937fa0 (MD5)
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Extracelular matrix, the biological structure that supports cells in animal tissue, is composed of elastic fibers such as collagen and elastin. It is known that enzymes activity plays an important role in maintenance of these elastic fibers. The imbalance between destruction and repair of the elastic fibers can lead to diseases such as fibrosis and emphysema. In this study, we present a simple model to simulate enzymatic digestion and repair of elastic fibers under tension. The fiber is represented by a chain of linearly elastic springs in series surrounded by two layers of sites along which particles representing enzymes and fragments can diffuse. These particles can biding-unbinding in the fiber simulating the reaction process by changing the local stiffness by a multiplicative factor. We study the distribution of the number of visits of particles to the springs as function of time and the consequent change of the fiber stiffness, under different initial conditions (model parameters). We show that, due to no linearity of the model, the degradation effect prevails even when the concentrations of the two type of agents are the same. There is no relation between the number of degradative and rigidifying particles that garantee that the fiber stiffness remains constant. When an anisotropy factor is included on the model and the system behaviour becomes dependent on the tension applied to the fiber, we show that the increase of tension in general contributes to the increase on enzymatic activity. We believe this study can help better understand progression of diseases such as emphysema and fibrosis.
A Matriz Extracelular, a estrutura biológica que sustenta as células em tecidos animais, é composta de fibras elásticas como colágeno e elastina. Sabe-se que a atividade enzimática desempenha papel fundamental na manutenção dessas fibras elásticas. O desequilíbrio entre destruição e reparo das fibras elásticas pode levar a doenças como fibrose e enfizema. Neste estudo, nós apresentamos um modelo simples para simular digestão enzimática e reparo de fibras sob tensão. A fibra é representada por uma cadeia de molas linearmente elásticas em série. A fibra é cercada por duas camadas de sítios ao longo dos quais partículas representantes de enzimas e fragmentos podem se difundir. Estas partículas podem se ligar e se desligar da fibra, simulando o processo de reação ao alterar a constante elástica local por um fator multiplicativo. Estuda-se a distribuição do número de visitas de partículas degradadoras e enrijecedoras às molas em função do tempo de difusão e a consequente variação da rigidez da fibra, sob diversas condições iniciais (parâmetros do modelo). Mostra-se que, devido a características matemáticas intrínsecas ao modelo, o efeito de degradação prevalece sobre o de enrijecimento ainda quando a concentração de agentes de ambos os tipos é a mesma. Não há relação entre o número de partículas degradadoras e enrijecedoras que garanta a estabilidade da constante elástica da fibra. Quanto um fator de anisotropia é incluído no modelo e o comportamento do sistema passa a depender da tensão aplicada à fibra, mostra-se que o aumento da tensão em geral contribui para o aumento da atividade enzimática. Este estudo poderá ajudar a entender a progressão da degradação de tecidos em doenças como enfisema e fibrose.
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Carroll, Nadine. "The use of protriptyline or nocturnal mechanical ventilatory support for respiratory failure in chronic bronchitis and emphysema". Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235493.
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Abdulkarim, Kayigire Xavier. "Does maternal nicotine exposure during gestation and lactation change the oxidant-antioxidant status of the lungs of the offsprings and is tomato juice protecting the lungs of the offsprings?" Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_1431_1277678988.
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Nicotine exposure to the fetus through tobacco smoking or nicotine replacement therapy during the whole period of gestation and lactation causes diverse effects on fetal and neonatal lung development, integrity and maturation which compromise the gas exchange function of the lungs and renders this vital organ susceptible to gradual damage and different diseases in latter life. Maternal nicotine exposure during gestation and lactation results in gradual destruction of the lung parenchyma, and this leads to the combination of many small air sacs in one bigger alveoli which is a sign of emphysema. Many researchers speculated that the way in which, nicotine causes emphysema and other damage, is by inducing the formation of many reactive oxygen species (ROS), and creating an imbalance between the oxidants and the antioxidants of the body, which is termed oxidative stress. The aim of this study was to assess the effects of nicotine exposure on the lung of the fetal and neonate rat during gestation and lactation as gas exchanger, and also to see whether the supplementation of tomato juice containing lycopene, a powerful carotenoid antioxidant could protect the lungs against these effects of maternal nicotine exposure.
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Cantlay, Ann M. "Polymorphism of the glutathione S-transferase M1 and cytochrome P4501A1 genes and susceptibility to emphysema and lung cancer". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21127.
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Deletion of GSTM1 was associated with emphysema in the presence of concomitant lung cancer, but not with lung cancer alone. No association between the GSTM1 polymorphism and either centriacinar or panacinar patterns of emphysema could be demonstrated, but a small association was found in cases with both centriacinar and panacinar emphysema. The glutathione S-transferase M1 deletion was not associated with chronic obstructive pulmonary disease, the clinical manifestation of emphysema, nor with the severe emphysema found in autopsy specimens. The cytochrome P4501A1 polymorphism was associated with emphysema concomitant with lung cancer, but no association could be demonstrated with a specific pattern of disease. Furthermore, the CYP1A1 polymorphism was found to be associated with very early emphysema, detectable only by microscope. No association was found between cytochrome P4501A1 and lung cancer, nor with chronic obstructive pulmonary disease. This study demonstrates that the GSTM1 and CYP1A1 polymorphisms have a small, but significant, association with emphysema, which cannot be explained by concomitant lung cancer, since lung cancer alone was not associated with either polymorphism. The association of the polymorphisms with mild emphysema, in particular that seen between CYP1A1 and microscopic emphysema, and not with the severe emphysema represented by chronic obstructive pulmonary disease, and in the case of GSTM1 with autopsy emphysema's, indicates that these enzymes have a general role in the early protection of the lung against damage caused by xenobiotics such as cigarette smoke. Sequencing of the CYP1A1 gene identified a novel polymorphism, a C to A substitution, which results in an amino acid change from threonine to asparagine at position 461 of the gene. Of 26 Scottish individuals previously genotyped as heterozygotes for the Ile-Val462 polymorphism, 14 were subsequently shown to actually have the Thr-Asn461 polymorphism.
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Sarker, Rim Sabrina Jahan [Verfasser] y Oliver [Akademischer Betreuer] Eickelberg. "Role of CARM1 in regulation of alveolar epithelial senescence and emphysema susceptibility / Rim Sabrina Jahan Sarker. Betreuer: Oliver Eickelberg". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1078851867/34.
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Rozengurt, Nora. "Studies on inherited pulmonary emphysema and Sendai virus induced bronchiolitis in experimental animal models : alterations in regulatory peptide expression". Thesis, Royal Veterinary College (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307505.
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Fiaux, Gerald W. "A study of the collagen and elastin content of human lung parenchyma in relation to airspace size and emphysema". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/19740.
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A quantitative study of collagen and elastin content in human lung tissue has been made in relation to a morphometric measure of airspace size. The subjects included non-smokers, smokers with and without macroscopic emphysema and three subjects with alpha 1-protease inhibitor (α1-Pi) deficiency. Airspace size was determined morphometrically as Alveolar Wall surface area per Unit Volume of lung (AWUV). The results were as follows: 1. There were no significant differences in AWUV, collagen content or elastin content between the upper and lower lobes with a single lung from both a non-smoker and a smoker without macroscopic emphysema. 2. Analysis of 102 samples from 9 smokers' lungs with no signs of macroscopic emphysema showed significant negative correlations between AWUV and collagen content and between AWUV and elastin content such that as the surface area of alveolar wall per unit volume decreased there was an increase in both the collagen and elastin content of the remaining alveolar tissue. 3. In tissue samples from 14 non-smokers there was no significant correlation between age and collagen content or between AWUV and collagen content. 4. Samples taken from smokers' lungs where either macroscopic centriacinar emphysema or panacinar emphysema or a mixture of centriacinar and panacinar emphysema were present were found to have a significantly higher collagen content than samples from non-smokers. 5. Tissue samples from the lungs of three α1-Pi deficient subjects had a significantly higher collagen content than samples from a non-smoker. In view of these findings the definition of emphysema, which states that no obvious fibrosis is present, may have to be revised.
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Dinger, Katharina [Verfasser]. "Structural and functional analysis of LTBP 4 as a factor of pathogenesis in the development of pulmonary emphysema / Katharina Dinger". Berlin : Freie Universität Berlin, 2017. http://d-nb.info/1129685616/34.
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