Bibliografie tematiche / Emphysema, Pulmonary Pathophysiology

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Letteratura scientifica selezionata sul tema "Emphysema, Pulmonary Pathophysiology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 febbraio 2022

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Articoli di riviste sul tema "Emphysema, Pulmonary Pathophysiology"

Jonathan, Steven, Triya Damayanti, and Budhi Antariksa. "Pathophysiology of Emphysema." Jurnal Respirologi Indonesia 39, no. 1 (January 2, 2019): 60–69. http://dx.doi.org/10.36497/jri.v39i1.43.

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Abstract (sommario):

Pulmonary emphysema is part of pathological condition in chronic obstructive pulmonary disease (COPD) which is characterized by lung parenchymal destruction. Morphology classification of emphysema had been made according to histologic structure in pathology. There were some causes known to be the culprit of emphysema; one that caught most attention is protease-antiprotease activity from cigarette smoke exposure. Destructive effect of emphysema gives disturbance of lung function in expiration (obstruction). The primary mechanism is elastic recoil reduction which causes air trapping, lung volume

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Amariei, Diana E., Neal Dodia, Janaki Deepak, Stella E. Hines, Jeffrey R. Galvin, Sergei P. Atamas, and Nevins W. Todd. "Combined Pulmonary Fibrosis and Emphysema: Pulmonary Function Testing and a Pathophysiology Perspective." Medicina 55, no. 9 (September 10, 2019): 580. http://dx.doi.org/10.3390/medicina55090580.

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Combined pulmonary fibrosis and emphysema (CPFE) has been increasingly recognized over the past 10–15 years as a clinical entity characterized by rather severe imaging and gas exchange abnormalities, but often only mild impairment in spirometric and lung volume indices. In this review, we explore the gas exchange and mechanical pathophysiologic abnormalities of pulmonary emphysema, pulmonary fibrosis, and combined emphysema and fibrosis with the goal of understanding how individual pathophysiologic observations in emphysema and fibrosis alone may impact clinical observations on pulmonary funct

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Keller, Cesar A. "Pathophysiology and classification of emphysema." Chest Surgery Clinics of North America 13, no. 4 (November 2003): 589–613. http://dx.doi.org/10.1016/s1052-3359(03)00092-9.

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Gronbach, Judith, Harald Ehrhardt, Klaus-Peter Zimmer, and Markus Waitz. "Early Pulmonary Interstitial Emphysema in Preterm Neonates—Respiratory Management and Case Report in Nonventilated Very Low Birth Weight Twins." American Journal of Perinatology Reports 08, no. 02 (April 2018): e99-e105. http://dx.doi.org/10.1055/s-0038-1648253.

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AbstractEarly pulmonary interstitial emphysema in extreme preterm neonates is closely linked with respiratory distress syndrome and exposure to mechanical ventilation. In severe cases, maintaining adequate gas exchange aiming to avoid further lung damage and other neonatal morbidities associated with systemic/pulmonary hypoperfusion, prolonged hypoxia, and respiratory acidosis can be challenging and requires in-depth knowledge into the pathophysiology of the disease. Herein, we report on very low birth weight twins who developed early pulmonary interstitial emphysema during noninvasive respira

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Portillo, Karina, and Josep Morera. "Combined Pulmonary Fibrosis and Emphysema Syndrome: A New Phenotype within the Spectrum of Smoking-Related Interstitial Lung Disease." Pulmonary Medicine 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/867870.

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Abstract (sommario):

Combined pulmonary fibrosis and emphysema (CPFE) is a recently defined syndrome, in which centrilobular and/or paraseptal emphysemas in upper lung zones coexist with pulmonary fibrosis in lower lobes in individuals. These patients have a characteristic lung function profile, with unexpected subnormal dynamic and static lung volumes, contrasting with a significant reduction of carbon monoxide transfer (DLco) and exercise hypoxemia. Pulmonary hypertension is highly prevalent in CPFE and is the leading determinant of death. Tobacco smoking has been proposed as the main factor in its etiology, tho

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Lilburn, David M. L., Clémentine Lesbats, Joseph S. Six, Eric Dubuis, Liang Yew-Booth, Dominick E. Shaw, Maria G. Belvisi, Mark A. Birrell, Galina E. Pavlovskaya, and Thomas Meersmann. "Hyperpolarized 83 Kr magnetic resonance imaging of alveolar degradation in a rat model of emphysema." Journal of The Royal Society Interface 12, no. 107 (June 2015): 20150192. http://dx.doi.org/10.1098/rsif.2015.0192.

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Hyperpolarized 83 Kr surface quadrupolar relaxation (SQUARE) generates MRI contrast that was previously shown to correlate with surface-to-volume ratios in porous model surface systems. The underlying physics of SQUARE contrast is conceptually different from any other current MRI methodology as the method uses the nuclear electric properties of the spin I = 9/2 isotope 83 Kr. To explore the usage of this non-radioactive isotope for pulmonary pathophysiology, MRI SQUARE contrast was acquired in excised rat lungs obtained from an elastase-induced model of emphysema. A significant 83 Kr T 1 relax

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Kozma, Rodrigo de las Heras, Edson Marcelino Alves, Valter Abraao Barbosa-de-Oliveira, Fernanda Degobbi Tenorio Quirino dos Santos Lopes, Renan Cenize Guardia, Henrique Vivi Buzo, Carolina Arruda de Faria, et al. "A new experimental model of cigarette smoke-induced emphysema in Wistar rats." Jornal Brasileiro de Pneumologia 40, no. 1 (January 2014): 46–54. http://dx.doi.org/10.1590/s1806-37132014000100007.

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Abstract (sommario):

OBJECTIVE: To describe a new murine model of cigarette smoke-induced emphysema. METHODS: Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day) every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm). RESULTS: The mean weigh

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Cappetta, Donato, Antonella De Angelis, Giuseppe Spaziano, Gioia Tartaglione, Elena Piegari, Grazia Esposito, Loreta Pia Ciuffreda, et al. "Lung Mesenchymal Stem Cells Ameliorate Elastase-Induced Damage in an Animal Model of Emphysema." Stem Cells International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/9492038.

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Abstract (sommario):

Pulmonary emphysema is a respiratory condition characterized by alveolar destruction that leads to airflow limitation and reduced lung function. Although with extensive research, the pathophysiology of emphysema is poorly understood and effective treatments are still missing. Evidence suggests that mesenchymal stem cells (MSCs) possess the ability to engraft the injured tissues and induce repair via a paracrine effect. Thus, the aim of this study was to test the effects of the intratracheal administration of lung-derived mouse MSCs in a model of elastase-induced emphysema. Pulmonary function (

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Ingenito, Edward P., Larry W. Tsai, Arnab Majumdar, and Bela Suki. "On the Role of Surface Tension in the Pathophysiology of Emphysema." American Journal of Respiratory and Critical Care Medicine 171, no. 4 (February 15, 2005): 300–304. http://dx.doi.org/10.1164/rccm.200406-770pp.

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Sasaki, Mamoru, Shotaro Chubachi, Naofumi Kameyama, Minako Sato, Mizuha Haraguchi, Masaki Miyazaki, Saeko Takahashi, and Tomoko Betsuyaku. "Evaluation of cigarette smoke-induced emphysema in mice using quantitative micro-computed tomography." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 10 (May 15, 2015): L1039—L1045. http://dx.doi.org/10.1152/ajplung.00366.2014.

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Abstract (sommario):

Chronic cigarette smoke (CS) exposure provokes variable changes in the lungs, and emphysema is an important feature of chronic obstructive pulmonary disease. The usefulness of micro-computed tomography (CT) to assess emphysema in different mouse models has been investigated, but few studies evaluated the dynamic structural changes in a CS-induced emphysema mouse model. A novel micro-CT technique with respiratory and cardiac gating has resulted in high-quality images that enable processing for further quantitative and qualitative analyses. Adult female C57BL/6J mice were repeatedly exposed to m

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Più fonti

Tesi sul tema "Emphysema, Pulmonary Pathophysiology"

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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Libri sul tema "Emphysema, Pulmonary Pathophysiology"

1926-, Grassi Carlo, and Workshop "Update in Biochemistry of Pulmonary Emphysema" (1990 : Pavia, Italy), eds. Biochemistry of pulmonary emphysema. London: Springer-Verlag, 1992.

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Weinbaum, George, Ralph E. Giles, and Robert D. Krell. Pulmonary emphysema : The rationale for therapeutic intervention. New York Academy of Sciences, 1991.

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George, Weinbaum, Giles Ralph E, Krell Robert D, New York Academy of Sciences., and American Thoracic Society, eds. Pulmonary emphysema: The rationale for therapeutic intervention. New York, N.Y: New York Academy of Sciences, 1991.

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(Designer), R. Corsico, and C. Grassi (Editor), eds. Biochemistry Of Pulmonary Emphysema (Current Topics in Rehabilitation)). Springer, 1993.

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Weinbaum, George, and Ralph E. Giles. Pulmonary Emphysema: The Rationale for Therapeutic Intervention (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1991.

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Nutrition and ventilatory function (Current topics in rehabilitation). Bi & Gi Publishers, 1992.

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