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Gotowe bibliografie tematyczne / Emphysema, Pulmonary Pathophysiology / Artykuły w czasopismach

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Artykuły w czasopismach na temat „Emphysema, Pulmonary Pathophysiology”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 11 lutego 2022

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1

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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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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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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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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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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9

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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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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Kopf, Katrina W., Julie W. Harral, Emily A. Staker, Megan E. Summers, Irina Petrache, Vitaly Kheyfets, David C. Irwin, and Susan M. Majka. "Optimization of combined measures of airway physiology and cardiovascular hemodynamics in mice." Pulmonary Circulation 10, no. 1 (January 2020): 204589402091293. http://dx.doi.org/10.1177/2045894020912937.

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Pulmonary hypertension may arise as a complication of chronic lung disease typically associated with tissue hypoxia, as well as infectious agents or injury eliciting a type 2 immune response. The onset of pulmonary hypertension in this setting (classified as Group 3) often complicates treatment and worsens prognosis of chronic lung disease. Chronic lung diseases such as chronic obstructive lung disease (COPD), emphysema, and interstitial lung fibrosis impair airflow and alter lung elastance in addition to affecting pulmonary vascular hemodynamics that may culminate in right ventricle dysfuncti

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Le Rouzic, Olivier, Muriel Pichavant, Emilie Frealle, Antoine Guillon, Mustapha Si-Tahar, and Philippe Gosset. "Th17 cytokines: novel potential therapeutic targets for COPD pathogenesis and exacerbations." European Respiratory Journal 50, no. 4 (October 2017): 1602434. http://dx.doi.org/10.1183/13993003.02434-2016.

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Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the airways caused mainly by cigarette smoke exposure. COPD progression is marked by exacerbations of the disease, often associated with infections. Recent data show the involvement in COPD pathophysiology of interleukin (IL)-17 and IL-22, two cytokines that are important in the control of lung inflammation and infection. During the initiation and progression of the disease, increased IL-17 secretion causes neutrophil recruitment, leading to chronic inflammation, airways obstruction and emphysema. In the establis

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13

Pierre, Alexandre, Flora Lemaire, Aïda Meghraoui-Kheddar, Sandra Audonnet, Stéphanie Héry-Huynh, and Richard Le Naour. "Impact of aging on inflammatory and immune responses during elastin peptide-induced murine emphysema." American Journal of Physiology-Lung Cellular and Molecular Physiology 316, no. 4 (April 1, 2019): L608—L620. http://dx.doi.org/10.1152/ajplung.00402.2018.

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Deterioration of lung functions and degradation of elastin fibers with age are accelerated during chronic obstructive pulmonary disease (COPD). Excessive genesis of soluble elastin peptides (EP) is a key factor in the pathophysiology of COPD. We have previously demonstrated that 6-wk-old mice exhibited emphysematous structural changes associated with proinflammatory immune response after EP instillation. In this study, we investigated the consequences of aging on inflammatory, immune, and histological criteria associated with murine emphysema progression after EP exposure. Young (6 wk old) and

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14

Triantaphyllopoulos, Kostas, Farhana Hussain, Mariona Pinart, Min Zhang, Feng Li, Ian Adcock, Paul Kirkham, Jie Zhu, and Kian Fan Chung. "A model of chronic inflammation and pulmonary emphysema after multiple ozone exposures in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 5 (May 2011): L691—L700. http://dx.doi.org/10.1152/ajplung.00252.2010.

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Oxidative stress plays a role in the pathophysiology of emphysema through the activation of tissue proteases and apoptosis. We examined the effects of ozone exposure by exposing BALB/c mice to either a single 3-h exposure or multiple exposures over 3 or 6 wk, with two 3-h exposures per week. Compared with air-exposed mice, the increase in neutrophils in bronchoalveolar lavage fluid and lung inflammation index was greatest in mice exposed for 3 and 6 wk. Lung volumes were increased in 3- and 6-wk-exposed mice but not in single-exposed. Alveolar space and mean linear intercept were increased in

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Vlahos, Ross, and Steven Bozinovski. "Recent advances in pre-clinical mouse models of COPD." Clinical Science 126, no. 4 (October 14, 2013): 253–65. http://dx.doi.org/10.1042/cs20130182.

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COPD (chronic obstructive pulmonary disease) is a major incurable global health burden and will become the third largest cause of death in the world by 2020. It is currently believed that an exaggerated inflammatory response to inhaled irritants, in particular cigarette smoke, causes progressive airflow limitation. This inflammation, where macrophages, neutrophils and T-cells are prominent, leads to oxidative stress, emphysema, small airways fibrosis and mucus hypersecretion. The mechanisms and mediators that drive the induction and progression of chronic inflammation, emphysema and altered lu

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Hao, Wendong, Manxiang Li, Yunqing Zhang, Cailian Zhang, and Ping Wang. "Severity of chronic obstructive pulmonary disease with ‘exacerbator with emphysema phenotype’ is associated with potential biomarkers." Postgraduate Medical Journal 96, no. 1131 (August 2, 2019): 28–32. http://dx.doi.org/10.1136/postgradmedj-2019-136599.

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ObjectiveThe present study was designed to investigate the biomarkers levels of fractalkine (FKN), neutrophil elastase (NE) and matrix metalloproteinase-12 (MMP-12) in chronic obstructive pulmonary disease (COPD) with ‘exacerbator with emphysema phenotype’ and to evaluate the associations between the biomarkers levels and the severity of disease by spirometric measurements.MethodsA total of 84 COPD patients and 49 healthy controls were enrolled in our study. ELISA were utilised to detect the FKN, MMP-12 and NE in serum from all subjects.ResultsFKN (p<0.001), NE (p=0.039) and MMP-12 (p<0.

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Shimizu, Kaoruko, Satoshi Konno, Hironi Makita, Hirokazu Kimura, Hiroki Kimura, Masaru Suzuki, and Masaharu Nishimura. "Transfer coefficients better reflect emphysematous changes than carbon monoxide diffusing capacity in obstructive lung diseases." Journal of Applied Physiology 125, no. 1 (July 1, 2018): 183–89. http://dx.doi.org/10.1152/japplphysiol.01062.2017.

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The overlap between asthma and chronic obstructive pulmonary disease (COPD) has attracted the interest of pulmonary physicians; thus, measurement of carbon monoxide diffusion capacity (DLco) and/or transfer coefficients (Kco, DLco/VA) may become valuable in clinical settings. How these parameters behave in chronic obstructive lung diseases is poorly understood. We predicted that Kco might more accurately reflect emphysematous changes in the lungs than DLco. We examined DLco and Kco in nonsmokers and smokers with asthma and investigated their relationships with forced expiratory volume in 1 s (

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Braber, Saskia, Pim J. Koelink, Paul A. J. Henricks, Patricia L. Jackson, Frans P. Nijkamp, Johan Garssen, Aletta D. Kraneveld, J. Edwin Blalock, and Gert Folkerts. "Cigarette smoke-induced lung emphysema in mice is associated with prolyl endopeptidase, an enzyme involved in collagen breakdown." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 2 (February 2011): L255—L265. http://dx.doi.org/10.1152/ajplung.00304.2010.

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There is increasing evidence that the neutrophil chemoattractant proline-glycine-proline (PGP), derived from the breakdown of the extracellular matrix, plays an important role in neutrophil recruitment to the lung. PGP formation is a multistep process involving neutrophils, metalloproteinases (MMPs), and prolyl endopeptidase (PE). This cascade of events is now investigated in the development of lung emphysema. A/J mice were whole body exposed to cigarette smoke for 20 wk. After 20 wk or 8 wk after smoking cessation, animals were killed, and bronchoalveolar lavage fluid and lung tissue were col

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Stadler, Alfred, Leopold Stiebellehner, Peter M. Jakob, Johannes F. T. Arnold, Edith Eisenhuber, Isabella von Katzler, and Alexander A. Bankier. "Quantitative and O2Enhanced MRI of the Pathologic Lung: Findings in Emphysema, Fibrosis, and Cystic Fibrosis." International Journal of Biomedical Imaging 2007 (2007): 1–7. http://dx.doi.org/10.1155/2007/23624.

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Purpose: beyond the pure morphological visual representation, MR imaging offers the possibility to quantify parameters in the healthy, as well as, in pathologic lung parenchyma. Gas exchange is the primary function of the lung and the transport of oxygen plays a key role in pulmonary physiology and pathophysiology. The purpose of this review is to present a short overview of the relaxation mechanisms of the lung and the current technical concepts of T1 mapping and methods of oxygen enhanced MR imaging.Material and Methods: molecular oxygen has weak paramagnetic properties so that an increase i

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Sinden, Nicola J., Michael J. Baker, David J. Smith, Jan-Ulrich Kreft, Timothy R. Dafforn та Robert A. Stockley. "α-1-Antitrypsin variants and the proteinase/antiproteinase imbalance in chronic obstructive pulmonary disease". American Journal of Physiology-Lung Cellular and Molecular Physiology 308, № 2 (15 січня 2015): L179—L190. http://dx.doi.org/10.1152/ajplung.00179.2014.

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The excessive activities of the serine proteinases neutrophil elastase and proteinase 3 are associated with tissue damage in chronic obstructive pulmonary disease. Reduced concentrations and/or inhibitory efficiency of the main circulating serine proteinase inhibitor α-1-antitrypsin result from point mutations in its gene. In addition, α-2-macroglobulin competes with α-1-antitrypsin for proteinases, and the α-2-macroglobulin-sequestered enzyme can retain its catalytic activity. We have studied how serine proteinases partition between these inhibitors and the effects of α-1-antitrypsin mutation

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Kim, Yun-Ho, Min-Kyung Kang, Eun-Jung Lee, Dong Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh, et al. "Astragalin Inhibits Cigarette Smoke-Induced Pulmonary Thrombosis and Alveolar Inflammation and Disrupts PAR Activation and Oxidative Stress-Responsive MAPK-Signaling." International Journal of Molecular Sciences 22, no. 7 (April 1, 2021): 3692. http://dx.doi.org/10.3390/ijms22073692.

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Epidemiological evidence shows that smoking causes a thrombophilic milieu that may play a role in the pathophysiology of chronic obstructive pulmonary disease (COPD) as well as pulmonary thromboembolism. The increased nicotine level induces a prothrombotic status and abnormal blood coagulation in smokers. Since several anticoagulants increase bleeding risk, alternative therapies need to be identified to protect against thrombosis without affecting hemostasis. Astragalin is a flavonoid present in persimmon leaves and green tea seeds and exhibits diverse activities of antioxidant and anti-inflam

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Nichols, Larry, Rachel Saunders, and Friedrich D. Knollmann. "Causes of Death of Patients With Lung Cancer." Archives of Pathology & Laboratory Medicine 136, no. 12 (December 1, 2012): 1552–57. http://dx.doi.org/10.5858/arpa.2011-0521-oa.

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Context.—The causes of death for patients with lung cancer are inadequately described. Objective.—To categorize the immediate and contributing causes of death for patients with lung cancer. Design.—The autopsies from 100 patients who died of lung cancer between 1990 and February 2011 were analyzed. Results.—Tumor burden was judged the immediate cause of death in 30 cases, including 26 cases of extensive metastases and 4 cases with wholly or primarily lung tumor burden (causing respiratory failure). Infection was the immediate cause of death for 20 patients, including 8 with sepsis and 12 with

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Kumar, S., S. K. Sharma, B. Medhi, and K. L. Khanduja. "Therapeutic Potential of Cytosolic PLA2 Isoform–Specific Inhibitor Arachidonyl Trifluromethyl Ketone in Cigarette Smoke Condensate–Induced Pathological Conditions in Alveolar Type I and II Epithelial Cells." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 221s. http://dx.doi.org/10.1200/jgo.18.89300.

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Background: Cigarette smoking is responsible for various lung pathologies including chronic lung inflammation, emphysema, chronic obstructive pulmonary disease (COPD), cancer, and annually causes almost 10 million deaths globally. During smoke exposure, most affected cells are the alveolar epithelial cells where as a repair mechanism, activation of cytosolic phospholipase A2 enzymes takes place. High free radicals and cPLA2 activity due to continuous exposure of smoke exposure leads to elevated levels of secondary metabolites and various pathophysiologic conditions such as chronic inflammation

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Ivovic, Miomira, Biljana Radojkovic, Zorana Penezic, Mirjana Stojkovic, Milina Tancic, Svetlana Vujovic, Andrija Bogdanovic, and Milka Drezgic. "Agranulocytosis and acute coronary syndrom in apathetic hyperthyreoidism." Srpski arhiv za celokupno lekarstvo 131, no. 5-6 (2003): 249–53. http://dx.doi.org/10.2298/sarh0306249i.

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INTRODUCTION Tissue expose to excessive levels of circulating thyroid hormones results in thyrotoxicosis. In most cases, thyrotoxicosis is due to hyper-activity of the thyroid gland. Cardiovascular and myopathic manifestations are predominant clinical features in most hyperthyroid patients, aged 60 years and older. Some of patients have apathetic hyperthyreoidism which presents with weight loss, small goiter, severe depression and without clinical features of increased sympathetic activity [3, 6]. About 50% of patients with cardiovascular manifestations have no evidence of underlying heart dis

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Marsh, Regan H. "Chronic Obstructive Pulmonary Disease." DeckerMed Emergency Medicine, February 1, 2017. http://dx.doi.org/10.2310/em.4208.

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Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow obstruction that is not fully reversible. The airflow obstruction is usually progressive and associated with an inflammatory response of the lungs to noxious particles and gases, often from smoking. COPD is the third leading cause of death in the United States, with both its prevalence and mortality continuing to increase. It has also become one of the leading causes of death and disability worldwide. COPD is estimated to affect more than 5% of the total population in the United States; approximately 5 mil

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Tripathi, Lokesh P., Mari N. Itoh, Yoshito Takeda, Kazuyuki Tsujino, Yasushi Kondo, Atsushi Kumanogoh, and Kenji Mizuguchi. "Integrative Analysis Reveals Common and Unique Roles of Tetraspanins in Fibrosis and Emphysema." Frontiers in Genetics 11 (December 10, 2020). http://dx.doi.org/10.3389/fgene.2020.585998.

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While both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are multifactorial disorders characterized by distinct clinical and pathological features, their commonalities and differences have not been fully elucidated. We sought to investigate the preventive roles of tetraspanins Cd151 and Cd9 -that are involved in diverse cellular processes in lung pathophysiology- in pulmonary fibrosis and emphysema, respectively, and to obtain a deeper understanding of their underlying molecular mechanisms toward facilitating improved therapeutic outcomes. Using an integr

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Kang, Ji Hee, Jiwoong Choi, Kum Ju Chae, Kyung Min Shin, Chang-Hoon Lee, Junfeng Guo, Ching-Long Lin, Eric A. Hoffman, and Changhyun Lee. "CT-derived 3D-diaphragm motion in emphysema and IPF compared to normal subjects." Scientific Reports 11, no. 1 (July 21, 2021). http://dx.doi.org/10.1038/s41598-021-93980-5.

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AbstractImage registration-based local displacement analysis enables evaluation of respiratory motion between two computed tomography-captured lung volumes. The objective of this study was to compare diaphragm movement among emphysema, idiopathic pulmonary fibrosis (IPF) and normal subjects. 29 normal, 50 emphysema, and 51 IPF subjects were included. A mass preserving image registration technique was used to compute displacement vectors of local lung regions at an acinar scale. Movement of the diaphragm was assumed to be equivalent to movement of the basal lung within 5 mm from the diaphragm.

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Khiroya, Heena, and Alice M. Turner. "The role of iron in pulmonary pathology." Multidisciplinary Respiratory Medicine 10 (December 20, 2019). http://dx.doi.org/10.4081/mrm.2015.337.

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Respiratory disease accounts for a large proportion of emergency admissions to hospital and diseaseassociated mortality. Genetic association studies demonstrate a link between iron metabolism and pulmonary disease phenotypes. IREB2 is a gene that produces iron regulatory protein 2 (IRP2), which has a key role in iron homeostasis. This review addresses pathways involved in iron metabolism, particularly focusing on the role of IREB2 . In addition to this, environmental factors also influence phenotypic variation in respiratory disease, for example inhaled iron from cigarette smoke is deposited i

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Dunican, Eleanor M., Brett M. Elicker, Travis Henry, David S. Gierada, Mark L. Schiebler, Wayne Anderson, Igor Barjaktarevic, et al. "Mucus Plugs and Emphysema in the Pathophysiology of Airflow Obstruction and Hypoxemia in Smokers." American Journal of Respiratory and Critical Care Medicine, November 12, 2020. http://dx.doi.org/10.1164/rccm.202006-2248oc.

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Cárdenes, Nayra, John Sembrat, Kentaro Noda, Tyler Lovelace, Diana Álvarez, Humberto E. Trejo Bittar, Brian J. Philips, et al. "Human ex vivo lung perfusion: a novel model to study human lung diseases." Scientific Reports 11, no. 1 (January 12, 2021). http://dx.doi.org/10.1038/s41598-020-79434-4.

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AbstractExperimental animal models to predict physiological responses to injury and stress in humans have inherent limitations. Therefore, the development of preclinical human models is of paramount importance. Ex vivo lung perfusion (EVLP) has typically been used to recondition donor lungs before transplantation. However, this technique has recently advanced into a model to emulate lung mechanics and physiology during injury. In the present study, we propose that the EVLP of diseased human lungs is a well-suited preclinical model for translational research on chronic lung diseases. Throughout

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Stewart, Neil J., Laurie J. Smith, Ho-Fung Chan, James A. Eaden, Smitha Rajaram, Andrew J. Swift, Nicholas D. Weatherley, et al. "Lung MRI with hyperpolarised gases: current & future clinical perspectives." British Journal of Radiology, June 9, 2021, 20210207. http://dx.doi.org/10.1259/bjr.20210207.

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The use of pulmonary MRI in a clinical setting has historically been limited. Whilst CT remains the gold-standard for structural lung imaging in many clinical indications, technical developments in ultrashort and zero echo time MRI techniques are beginning to help realise non-ionising structural imaging in certain lung disorders. In this invited review, we discuss a complementary technique – hyperpolarised (HP) gas MRI with inhaled 3He and 129Xe – a method for functional and microstructural imaging of the lung that has great potential as a clinical tool for early detection and improved underst

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Pouwels, Simon D., Laura Hesse, Xinhui Wu, Venkata Sita Rama Raju Allam, Daan van Oldeniel, Linsey J. Bhiekharie, Simon Phipps, et al. "LL-37 and HMGB1 induce alveolar damage and reduce lung tissue regeneration via RAGE." American Journal of Physiology-Lung Cellular and Molecular Physiology, August 18, 2021. http://dx.doi.org/10.1152/ajplung.00138.2021.

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The receptor for advanced glycation end-products (RAGE) has been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). However, it is still unknown whether RAGE directly contributes to alveolar epithelial damage and abnormal repair responses. We hypothesize that RAGE activation not only induces lung tissue damage but also hampers alveolar epithelial repair responses. The effects of the RAGE ligands LL-37 and HMGB1 were examined on airway inflammation and alveolar tissue damage in wild-type and RAGE deficient mice and on lung damage and repair responses using murine

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Esteve-Codina, Anna, Thomas P. Hofer, Dorothe Burggraf, Marion S. Heiss-Neumann, Wolfgang Gesierich, Anne Boland, Robert Olaso, et al. "Gender specific airway gene expression in COPD sub-phenotypes supports a role of mitochondria and of different types of leukocytes." Scientific Reports 11, no. 1 (June 18, 2021). http://dx.doi.org/10.1038/s41598-021-91742-x.

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AbstractChronic obstructive pulmonary disease (COPD) is a destructive inflammatory disease and the genes expressed within the lung are crucial to its pathophysiology. We have determined the RNAseq transcriptome of bronchial brush cells from 312 stringently defined ex-smoker patients. Compared to healthy controls there were for males 40 differentially expressed genes (DEGs) and 73 DEGs for females with only 26 genes shared. The gene ontology (GO) term “response to bacterium” was shared, with several different DEGs contributing in males and females. Strongly upregulated genes TCN1 and CYP1B1 wer

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Dirjayanto, Valerie Josephine. "Evidence on the Efficacy of Omega-3 Polyunsaturated Fatty Acids as an Adjunct Therapy for Chronic Obstructive Pulmonary Disease." Journal of Asian Medical Students' Association 9, no. 1 (September 4, 2021). http://dx.doi.org/10.52629/jamsa.v9i1.238.

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Background: As the fourth leading cause of death worldwide, Chronic Obstructive Pulmonary Disease (COPD) places a significant burden on healthcare-related costs. COPD is characterized by airflow impairment, including chronic bronchitis, small airways obstruction, and emphysema. COPD pathophysiology involves inflammation correlated with lung decline, body composition alteration, and decreased quality of life. Since preceding studies have shown its roles in inflammatory processes, omega-3 is proposed as a potential adjunct treatment in slowing down COPD progression.Aim: To analyse the efficacy o

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Crowley, George, Sophia Kwon, Erin J. Caraher, Syed Hissam Haider, Rachel Lam, Prag Batra, Daniel Melles, Mengling Liu, and Anna Nolan. "Quantitative lung morphology: semi-automated measurement of mean linear intercept." BMC Pulmonary Medicine 19, no. 1 (November 9, 2019). http://dx.doi.org/10.1186/s12890-019-0915-6.

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Abstract Background Quantifying morphologic changes is critical to our understanding of the pathophysiology of the lung. Mean linear intercept (MLI) measures are important in the assessment of clinically relevant pathology, such as emphysema. However, qualitative measures are prone to error and bias, while quantitative methods such as mean linear intercept (MLI) are manually time consuming. Furthermore, a fully automated, reliable method of assessment is nontrivial and resource-intensive. Methods We propose a semi-automated method to quantify MLI that does not require specialized computer know

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