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Tesi sul tema "Emphysema"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 25 luglio 2025

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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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Abstract (sommario):
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.<br>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.<br>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 potent
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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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3

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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4

Haruna, Akane. "CT emphysema predicts mortality in COPD." Kyoto University, 2010. http://hdl.handle.net/2433/123335.

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5

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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6

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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Abstract (sommario):
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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7

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
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8

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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9

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
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10

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
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11

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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Abstract (sommario):
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. Ch
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12

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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Abstract (sommario):
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 mechani
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13

Grimsley, Christina, and 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 subcutan
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14

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.<br>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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15

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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Abstract (sommario):
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
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16

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.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (pages 45-47).<br>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 ne
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17

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
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18

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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Abstract (sommario):
Thesis (Ph.D.)--Boston University<br>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.<br>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
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19

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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Abstract (sommario):
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 so
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20

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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Abstract (sommario):
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)
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21

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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Abstract (sommario):
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 whic
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22

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 fir
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23

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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24

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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25

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/S0954611115300172<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(医学)<br>甲第19577号<br>医博第4084号<br>新制||医||1013(附属図書館)<br>32613<br>京都大学大学院医学研究科医学専攻<br>(主査)教授 伊達 洋至, 教授 平家 俊男, 教授 松田 秀一<br>学位規則第4条第1項該当
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26

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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27

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 a
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28

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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29

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 F
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30

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
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31

Skrońska-Wąsek, Wioletta [Verfasser], and 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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32

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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33

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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34

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 an
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35

Кравченко, Е. А., та 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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36

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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37

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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38

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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Abstract (sommario):
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, rifiu
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39

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 - MSc<br>The 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 c
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40

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 co
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41

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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Abstract (sommario):
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 wi
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42

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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Abstract (sommario):
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.<br>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 wil
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43

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.<br>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)<br>Approved for entry into archive by Edvander Pires(edvanderpires@gmail.com) on 2015-10-23T19:38:27Z (GMT) No. of bitstreams: 1 2013_dis_caalv
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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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45

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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<p><font face="TimesNewRomanPSMT"> <p align="left">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
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46

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 wi
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47

Sarker, Rim Sabrina Jahan [Verfasser], and 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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48

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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49

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
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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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