Journal articles on the topic 'Lungs Diseases, Obstructive Australia'
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1
Chan, Yik Lung, Baoming Wang, Hui Chen, Kin Fai Ho, Junji Cao, Guo Hai, Bin Jalaludin, et al. "Pulmonary inflammation induced by low-dose particulate matter exposure in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 3 (September 1, 2019): L424—L430. http://dx.doi.org/10.1152/ajplung.00232.2019.
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Air pollution is a ubiquitous problem and comprises gaseous and particulate matter (PM). Epidemiological studies have clearly shown that exposure to PM is associated with impaired lung function and the development of lung diseases, such as chronic obstructive pulmonary disease and asthma. To understand the mechanisms involved, animal models are often used. However, the majority of such models represent high levels of exposure and are not representative of the exposure levels in less polluted countries, such as Australia. Therefore, in this study, we aimed to determine whether low dose PM10 exposure has any detrimental effect on the lungs. Mice were intranasally exposed to saline or traffic-related PM10 (1μg or 5μg/day) for 3 wk. Bronchoalveolar lavage (BAL) and lung tissue were analyzed. PM10 at 1 μg did not significantly affect inflammatory and mitochondrial markers. At 5 μg, PM10 exposure increased lymphocytes and macrophages in BAL fluid. Increased NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and IL-1β production occurred following PM10 exposure. PM10 (5 μg) exposure reduced mitochondrial antioxidant manganese superoxide (antioxidant defense system) and mitochondrial fusion marker (OPA-1), while it increased fission marker (Drp-1). Autophagy marker light-chain 3 microtubule-associated protein (LC3)-II and phosphorylated-AMPK were reduced, and apoptosis marker (caspase 3) was increased. No significant change of remodeling markers was observed. In conclusion, a subchronic low-level exposure to PM can have an adverse effect on lung health, which should be taken into consideration for the planning of roads and residential buildings.
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Ivey, Marsha A., Graeme P. Maguire, Brett G. Toelle, Guy B. Marks, Michael J. Abramson, and Richard Wood-Baker. "Characteristics in Stages of Change and Decisional Balance among Smokers: The Burden of Obstructive Lung Diseases (BOLD)-Australia Study." International Journal of Environmental Research and Public Health 16, no. 18 (September 12, 2019): 3372. http://dx.doi.org/10.3390/ijerph16183372.
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Smoking cessation remains a health promotion target. Applying the Transtheoretical Model to Australian Burden of Obstructive Lung Diseases (BOLD) data, we examined differences in stages of change (SoC) and readiness to quit decisional behaviours. Factors were identified likely to influence readiness of smokers, ≥40 years old, to quit. Analysis was restricted to current smokers classified to one of three stages: pre-contemplation (PC), contemplation (C) or preparation (P) to quit. Their ability to balance positive and negative consequences was measured using decisional balance. Among 314 smokers, 43.0% females and 60.8% overweight/obese, the distribution of SoC was: 38.1% PC, 38.3% C and 23.5% P. Overweight/obesity was associated with readiness to quit in stages C and P and there were more negative than positive attitudes towards smoking in those stages. Males were significantly heavier smokers in PC and C stages. Females used smoking cessation medication more frequently in PC stage, were more embarrassed about smoking and had greater negative reinforcements from smoking. Age started smoking and factors related to smoking history were associated with readiness to quit and increased the odds of being in stage C or P. An overweight/obese smoker was likely to be contemplating or preparing to quit. In these stages, smokers have more negative attitudes toward smoking. Starting smoking later, taking advice on cessation from health providers and using quit medications indicate increased readiness to quit. Evaluating these factors in smokers and developing cessation gain-framed messages may prove useful to healthcare providers.
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Peter, Lavanya S. "Spirometric surveillance of obstructive lung diseases." Panacea Journal of Medical Sciences 12, no. 2 (August 15, 2022): 249–55. http://dx.doi.org/10.18231/j.pjms.2022.048.
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Obstructive Lung Disease (OLD) becomes global health issues that influencing the physical health and economic conditions of people. Chronic Respiratory Disease (CRD) is the disease of airways characterized by obstruction and influencing the structure of the lungs. It includes chronic bronchitis, COPD, emphysema and asthma. The most common disease is Chronic Obstructive Pulmonary Disease (COPD). The major causes of COPD involve exposure to an irritant that damage the lungs and airways that can cause such disease.1):Assess the prevalence of OLD among the patients admitted to general medical wards using spirometry; 2): Use a symptom questionnaire for screening patients with OLD and compare it with Spirometry; 3): Association of various medical co-morbidities with the diagnosis of OLD.The screening for OLDs and factors that are influencing it along with co morbidities were analyzed. This is a descriptive study conducted on patients admitted to general medical wards in hospital of South India for a period of 2 years. The study has involved the patients who are admitted in general wards and aged > 40 years.The physician diagnosis of OLD at admission was in 21 out of 144 patients. It was by symptom alone in 11% (16 of 144 patients) and based on spirometry in 3.48% (5 of 144) only. During the hospitalization the diagnosis of OLD increased by 2.08% (3 of 144) on the basis of symptom alone and 1.4% (2 of 144) by spirometry, cumulatively by 3.48% (5 of 144). Therefore, at admission about 14.48% were diagnosed to have OLD. An ROC curve was plotted and the area under the curve was 0.77 95% CI (0.688 — 0.865). By ROC coordinates a cut off of 15.5 for detecting OLDs showed a sensitivity and specificity of 71% and 78% respectively with a positive predictive value of 56% and negative predictive value of 87%.With the additional yield of Spirometry and association of medical comorbidities can help identify the conditions of patients earlier and pave way for offering appropriate holistic treatment.
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Aghali, Arbi, Maunick Lefin Koloko Ngassie, Christina M. Pabelick, and Y. S. Prakash. "Cellular Senescence in Aging Lungs and Diseases." Cells 11, no. 11 (May 29, 2022): 1781. http://dx.doi.org/10.3390/cells11111781.
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Cellular senescence represents a state of irreversible cell cycle arrest occurring naturally or in response to exogenous stressors. Following the initial arrest, progressive phenotypic changes define conditions of cellular senescence. Understanding molecular mechanisms that drive senescence can help to recognize the importance of such pathways in lung health and disease. There is increasing interest in the role of cellular senescence in conditions such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) in the context of understanding pathophysiology and identification of novel therapies. Herein, we discuss the current knowledge of molecular mechanisms and mitochondrial dysfunction regulating different aspects of cellular senescence-related to chronic lung diseases to develop rational strategies for modulating the senescent cell phenotype in the lung for therapeutic benefit.
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Kouanda, Bakey, Zeeshan Sattar, and Patrick Geraghty. "Periodontal Diseases: Major Exacerbators of Pulmonary Diseases?" Pulmonary Medicine 2021 (November 2, 2021): 1–10. http://dx.doi.org/10.1155/2021/4712406.
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Periodontal diseases are a range of polymicrobial infectious disorders, such as gingivitis and periodontitis, which affect tooth-supporting tissues and are linked to playing a role in the exacerbation of several pulmonary diseases. Pulmonary diseases, such as pneumonia, chronic obstructive pulmonary disease (COPD), asthma, tuberculosis, COVID-19, and bronchiectasis, significantly contribute to poor quality of life and mortality. The association between periodontal disease and pulmonary outcomes is an important topic and requires further attention. Numerous resident microorganisms coexist in the oral cavity and lungs. However, changes in the normal microflora due to oral disease, old age, lifestyle habits, or dental intervention may contribute to altered aspiration of oral periodontopathic bacteria into the lungs and changing inflammatory responses. Equally, periodontal diseases are associated with the longitudinal decline in spirometry lung volume. Several studies suggest a possible beneficial effect of periodontal therapy in improving lung function with a decreased frequency of exacerbations and reduced risk of adverse respiratory events and morbidity. Here, we review the current literature outlining the link between the oral cavity and pulmonary outcomes and focus on the microflora of the oral cavity, environmental and genetic factors, and preexisting conditions that can impact oral and pulmonary outcomes.
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Mohammad, Yousser, Loai Nahass, Ismael Zakaria, and Bisher Sawaf. "Waterpipe Tobacco Smoking and the Lungs – Short Notice." US Respiratory & Pulmonary Diseases 13, no. 1 (2018): 25. http://dx.doi.org/10.17925/usrpd.2018.13.1.25.
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Waterpipe tobacco smoking (WTS) is increasingly popular among young people. Although perceived to be safer than cigarettes as smoke is filtered through water, narghile smoke is rich in carbon monoxide, as well as containing numerous toxins and carcinogens. Detrimental effects of WTS may include nicotine addiction, bronchitis, chronic obstructive pulmonary diseases and enhancing asthma susceptibility and exacerbations.
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Karzilov, A. I. "The respiratory system biomechanical homeostasis and its maintenance mechanisms in normal conditions and at obstructive pulmonary diseases." Bulletin of Siberian Medicine 6, no. 1 (March 30, 2007): 13–38. http://dx.doi.org/10.20538/1682-0363-2007-1-13-38.
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Parameters of breathing biomechanics in healthy persons (n = 20), patients with bronchial asthma (n = 30) and chronic obstruc-tive pulmonary disease (n = 30) are analyzed during electrical stimulation of the diaphragm. Methodology of homeostatic parame-ters searching and their classification is offered. Descriptive and comparative analyses are performed. Homeostatic parameters of biomechanics describing the condition of elastic and non -elastic properties of respiratory system, of respiratory muscles, of general pulmonary hysteresis, breathing regulation are differentiated. Basic homeostatic parameter is the ratio of inspiratory capacity to the lungs elastic recoil. The model of lungs with the biomechanical buffer and retractive-elastic- surfactant complex of lungs is offered. Biomechanical homeostasis idea of respiratory system as ability of an organism to support in dynamics balance normal and patho-logical conditions essentially important for preservation of respiratory system biomechanical parameters in admissible limits is for-mulated.
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Shamsutdinov, A. S., N. Sh Akhmedova, and U. K. Abdullaeva. "Peculiarities Of The Current Of Acute Bronchopulmonary Diseases In Children With Adverse Premorbid Condition." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 02 (February 28, 2021): 155–60. http://dx.doi.org/10.37547/tajmspr/volume03issue02-23.
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The article also examines the consequences of family relations, the health and age of the mother, the course of pregnancy, premorbid background in the form of childhood rickets, anemia, the state of the immune status in acute pneumonia, bronchiolitis, obstructive bronchitis in children. Sociopathic families and children with dangerous factors are more likely to suffer from acute respiratory infections, fever, shortness of breath, prolonged coughing and pathological changes in the lungs. Compared to 2014, the incidence of pneumonia decreased by 22.7%, and the number of children with obstructive syndrome increased from 33.4% to 47.5%.
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Zani, Marie-Louise, Annabelle Tanga, Ahlame Saidi, Hélène Serrano, Sandrine Dallet-Choisy, Kévin Baranger, and Thierry Moreau. "SLPI and trappin-2 as therapeutic agents to target airway serine proteases in inflammatory lung diseases: current and future directions." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1441–46. http://dx.doi.org/10.1042/bst0391441.
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It is now clear that NSPs (neutrophil serine proteases), including elastase, Pr3 (proteinase 3) and CatG (cathepsin G) are major pathogenic determinants in chronic inflammatory disorders of the lungs. Two unglycosylated natural protease inhibitors, SLPI (secretory leucocyte protease inhibitor) and elafin, and its precursor trappin-2 that are found in the lungs, have therapeutic potential for reducing the protease-induced inflammatory response. This review examines the multifaceted roles of SLPI and elafin/trappin-2 in the context of their possible use as inhaled drugs for treating chronic lung diseases such as CF (cystic fibrosis) and COPD (chronic obstructive pulmonary disease).
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Neves, Joana, Thomas Haider, Max Gassmann, and Martina U. Muckenthaler. "Iron Homeostasis in the Lungs—A Balance between Health and Disease." Pharmaceuticals 12, no. 1 (January 1, 2019): 5. http://dx.doi.org/10.3390/ph12010005.
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A strong mechanistic link between the regulation of iron homeostasis and oxygen sensing is evident in the lung, where both systems must be properly controlled to maintain lung function. Imbalances in pulmonary iron homeostasis are frequently associated with respiratory diseases, such as chronic obstructive pulmonary disease and with lung cancer. However, the underlying mechanisms causing alterations in iron levels and the involvement of iron in the development of lung disorders are incompletely understood. Here, we review current knowledge about the regulation of pulmonary iron homeostasis, its functional importance, and the link between dysregulated iron levels and lung diseases. Gaining greater knowledge on how iron contributes to the pathogenesis of these diseases holds promise for future iron-related therapeutic strategies.
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MacNee, William. "Accelerated lung aging: a novel pathogenic mechanism of chronic obstructive pulmonary disease (COPD)." Biochemical Society Transactions 37, no. 4 (July 22, 2009): 819–23. http://dx.doi.org/10.1042/bst0370819.
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An enhanced or abnormal inflammatory response to the lungs to inhaled particles and gases, usually from cigarette smoke, is considered to be a general pathogenic mechanism in COPD (chronic obstructive pulmonary disease). Activation of leucocytes and the development of oxidant–antioxidant and protease–anti-protease imbalances are thought to be important aspects of this enhanced inflammatory response to cigarette smoke. The mechanisms involved in the perpetuation of the inflammatory response in the lungs in patients who develop COPD, even after smoking cessation, are not fully established and are key to our understanding of the pathogenic mechanisms in COPD and may be important for the development of new therapies. There is a relationship between chronic inflammatory diseases and aging, and the processes involved in aging may provide a novel mechanism in the pathogenesis of COPD. There is good evidence linking aging and COPD. During normal aging, pulmonary function deteriorates progressively and pulmonary inflammation increases, accompanied in the lungs by the features of emphysema. These features are accelerated in COPD. Emphysema is associated with markers of accelerated aging in the lungs, and COPD is also associated with features of accelerated aging in other organs, such as the cardiovascular and musculoskeletal systems. Cigarette smoke and other oxidative stresses result in cellular senescence and accelerate lung aging. There is also evidence that anti-aging molecules such as histone deacetylases and sirtuins are decreased in the lungs of COPD patients, compared with smokers without COPD, resulting in enhanced inflammation and further progression of COPD. The processes involved in accelerated aging may provide novel targets for therapy in COPD. The present article reviews the evidence for accelerated aging as a mechanism in the pathogenesis of COPD.
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Wu, Yifan, Evan Li, Morgan Knight, Grace Adeniyi-Ipadeola, Li-zhen Song, Alan R. Burns, Ana Clara Gazzinelli-Guimaraes, Ricardo Fujiwara, Maria Elena Bottazzi, and Jill E. Weatherhead. "Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice." PLOS Neglected Tropical Diseases 15, no. 12 (December 16, 2021): e0010050. http://dx.doi.org/10.1371/journal.pntd.0010050.
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Ascariasis is one of the most common infections in the world and associated with significant global morbidity. Ascaris larval migration through the host’s lungs is essential for larval development but leads to an exaggerated type-2 host immune response manifesting clinically as acute allergic airway disease. However, whether Ascaris larval migration can subsequently lead to chronic lung diseases remains unknown. Here, we demonstrate that a single episode of Ascaris larval migration through the host lungs induces a chronic pulmonary syndrome of type-2 inflammatory pathology and emphysema accompanied by pulmonary hemorrhage and chronic anemia in a mouse model. Our results reveal that a single episode of Ascaris larval migration through the host lungs leads to permanent lung damage with systemic effects. Remote episodes of ascariasis may drive non-communicable lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), and chronic anemia in parasite endemic regions.
13
Panachevа, L. A., and L. A. Shpagina. "Chronic obstructive pulmonary disease among workers exposed to in-dustrial aerosols: literature review." Perm Medical Journal 37, no. 6 (January 28, 2021): 61–70. http://dx.doi.org/10.17816/pmj37661-70.
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The article presents a literature review regarding the formation of chronic obstructive pulmonary disease in conditions of the exposure of industrial aerosols. It shows a high frequency of occupational respiratory hazards, characterizes the diseases caused by air pollution with industrial and indoor pollutants, allergens and toxins in different occupational groups as well as basic conditions for development of dust pathology of the lungs.
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Ortiz-Zapater, Elena, Jaime Signes-Costa, Paula Montero, and Inés Roger. "Lung Fibrosis and Fibrosis in the Lungs: Is It All about Myofibroblasts?" Biomedicines 10, no. 6 (June 15, 2022): 1423. http://dx.doi.org/10.3390/biomedicines10061423.
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In the lungs, fibrosis is a growing clinical problem that results in shortness of breath and can end up in respiratory failure. Even though the main fibrotic disease affecting the lung is idiopathic pulmonary fibrosis (IPF), which affects the interstitial space, there are many fibrotic events that have high and dangerous consequences for the lungs. Asthma, chronic obstructive pulmonary disease (COPD), excessive allergies, clearance of infection or COVID-19, all are frequent diseases that show lung fibrosis. In this review, we describe the different kinds of fibrosis and analyse the main types of cells involved—myofibroblasts and other cells, like macrophages—and review the main fibrotic mechanisms. Finally, we analyse present treatments for fibrosis in the lungs and highlight potential targets for anti-fibrotic therapies.
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Zhang, Yan, Jin Zhang, and Zhiling Fu. "Role of autophagy in lung diseases and ageing." European Respiratory Review 31, no. 166 (December 21, 2022): 220134. http://dx.doi.org/10.1183/16000617.0134-2022.
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The lungs face ongoing chemical, mechanical, biological, immunological and xenobiotic stresses over a lifetime. Advancing age progressively impairs lung function. Autophagy is a “housekeeping” survival strategy involved in numerous physiological and pathological processes in all eukaryotic cells. Autophagic activity decreases with age in several species, whereas its basic activity extends throughout the lifespan of most animals. Dysregulation of autophagy has been proven to be closely related to the pathogenesis of several ageing-related pulmonary diseases. This review summarises the role of autophagy in the pathogenesis of pulmonary diseases associated with or occurring in the context of ageing, including acute lung injury, chronic obstructive pulmonary disease, asthma and pulmonary fibrosis, and describes its potential as a therapeutic target.
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Calendine, Jacob, Sesha Batra, Jade Cherfils, Omar Said, and Vanloan Nguyen. "Gene Therapy Avenues for Chronic Obstructive Pulmonary Disease." Berkeley Pharma Tech Journal of Medicine 1, no. 2 (July 19, 2022): 58–80. http://dx.doi.org/10.52243/bptjm.v1i2.23.
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Gene therapy is a growing field in research and development that may offer a long-lasting solution to several complex diseases, including chronic obstructive pulmonary disease (COPD). COPD is characterized by chronic inflammation in the lungs and the airways, leading to respiratory problems. COPD includes chronic bronchitis and emphysema. Optimizing treatments for gene therapy in COPD is of paramount importance given COPD's prominence as the fourth leading cause of disease-related death in the United States. We reviewed delivery methods in the current research, including liposomes, nanoparticles, electroporation, adeno-viruses, and adenoassociated viruses (AAV). The broad customizability in the diagnostic and treatment methods is evident in the recent studies. In this paper we explore each method and/or biomarker and evaluate several gene therapy avenues for COPD.
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Shpagin, I. S., A. V. Shabalin, L. A. Shpagina, O. N. Gerasimenko, and N. V. Shlyakhtina. "Features of clinical-functional parameters of the heart, vessels and microcirculation in patients with arterial hypertension in the combination to chronic obstructive pulmonary diseases." Bulletin of Siberian Medicine 9, no. 6 (December 28, 2010): 80–86. http://dx.doi.org/10.20538/1682-0363-2010-6-80-86.
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The clinical and functional status of the heart, peripheral vessels and microcirculation. The features of structural-functional state of the heart and peripheral vessels. Showing violations cardiohemodynamic and peripheral blood flow. Identified various pathological hemodynamic types. The worst-case remodeling and blood flow disturbances were detected in patients with arterial hypertension in combination to chronic obstructive diseases of lungs against pulmonary hypertensia.
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Si, Xiuhua April, and Jinxiang Xi. "Deciphering Exhaled Aerosol Fingerprints for Early Diagnosis and Personalized Therapeutics of Obstructive Respiratory Diseases in Small Airways." Journal of Nanotheranostics 2, no. 3 (June 22, 2021): 94–117. http://dx.doi.org/10.3390/jnt2030007.
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Respiratory diseases often show no apparent symptoms at their early stages and are usually diagnosed when permanent damages have been made to the lungs. A major site of lung pathogenesis is the small airways, which make it highly challenging to detect using current techniques due to the diseases’ location (inaccessibility to biopsy) and size (below normal CT/MRI resolution). In this review, we present a new method for lung disease detection and treatment in small airways based on exhaled aerosols, whose patterns are uniquely related to the health of the lungs. Proof-of-concept studies are first presented in idealized lung geometries. We subsequently describe the recent developments in feature extraction and classification of the exhaled aerosol images to establish the relationship between the images and the underlying airway remodeling. Different feature extraction algorithms (aerosol density, fractal dimension, principal mode analysis, and dynamic mode decomposition) and machine learning approaches (support vector machine, random forest, and convolutional neural network) are elaborated upon. Finally, future studies and frequent questions related to clinical applications of the proposed aerosol breath testing are discussed from the authors’ perspective. The proposed breath testing has clinical advantages over conventional approaches, such as easy-to-perform, non-invasive, providing real-time feedback, and is promising in detecting symptomless lung diseases at early stages.
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Iftikhar, Shagufta, Iqra Naz, Anmol Zahra, and Syeda zainab Yousuf Zaidi. "Report Generation of Lungs Diseases From Chest X-ray using NLP." Vol 3 Issue 5 3, no. 5 (February 26, 2022): 223–33. http://dx.doi.org/10.33411/ijist/2021030518.
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Pulmonary diseases are very severe health complications in the world that impose a massive worldwide health burden. These diseases comprise of pneumonia, asthma, tuberculosis, Covid-19, cancer, etc. The evidences show that around 65 million people undergo the chronic obstructive pulmonary disease and nearly 3 million people pass away from it each year that make it the third prominent reason of death worldwide. To decrease the burden of lungs diseases timely diagnosis is very essential. Computer-aided diagnostic, are systems that support doctors in the analysis of medical images. This study showcases that Report Generation System has automated the Chest X-Ray interpretation procedure and lessen human effort, consequently helped the people for timely diagnoses of chronic lungs diseases to decrease the death rate. This system provides great relief for people in rural areas where the doctor-to-patient ratio is only 1 doctor per 1300 people. As a result, after utilizing this application, the affected individual can seek further therapy for the ailment they have been diagnosed with. The proposed system is supposed to be used in the distinct architecture of deep learning (Deep Convolution Neural Network), this is fine tuned to CNN-RNN trainable end-to-end architecture. By using the patient-wise official split of the OpenI dataset we have trained a CNN-RNN model with attention. Our model achieved an accuracy of 94%, which is the highest performance.
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Tikendra, Sahu, and S. Choubey Aakanksha. "A review on lungs disease detection using image processing." i-manager's Journal on Information Technology 11, no. 1 (2022): 48. http://dx.doi.org/10.26634/jit.11.1.18536.
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The global fitness company estimates that by 2030, Chronic Obstructive Pulmonary Disease (COPD) will be the third leading cause of death in the world. Computerized Tomography (CT) of the lungs includes a number of structures that may be important in the prognosis and evaluation of lung disease. CT images of the lungs show a section of the chest that constitutes a large number of systems, including blood vessels, arteries, respiratory vessels, pulmonary pleura, and parenchyma, each with its own information. For this reason, the phasing of the lung systems is very important for the analysis and diagnosis of lung diseases. Segmentation is an important step in the photographic structure for the correct diagnosis of lung disease, as it delimits lung systems on CT images. Of course, imaging strategies can aid in computer analysis if the lung area is properly obtained. After the segmentation procedure, an automatic technique is used to identify possible diseases on CT scans of the lungs so the radiologist can focus on the prognosis of the patient. Several studies have shown promising results in detecting violations.
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Teboul, J. L., P. Andrivet, M. Ansquer, M. Besbes, N. Rekik, F. Lemaire, and C. Brun-Buisson. "Bedside evaluation of the resistance of large and medium pulmonary veins in various lung diseases." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 998–1003. http://dx.doi.org/10.1152/jappl.1992.72.3.998.
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To evaluate the contribution of large and medium pulmonary veins to the total pulmonary vascular resistance in various human lung diseases, we compared in 64 patients the pulmonary arterial proximal wedge pressure (Ppw), obtained when the balloon of a 7F pulmonary artery catheter was inflated with 1.5 ml air, with the distal wedge pressure (Pdw), obtained after the tip of the catheter was advanced until wedged in a small artery without balloon inflation. Ppw, reflecting the pressure in a large pulmonary vein, approximates the left atrial pressure, whereas Pdw reflects the pressure in a smaller pulmonary vein. Pdw was greater than Ppw in all 64 patients. The Pdw-Ppw gradient was 1.1 +/- 0.5 mmHg in nine patients with normal lungs and was significantly higher in 13 patients with chronic congestive heart failure (3.8 +/- 0.8 mmHg, P less than 0.01) and in 22 patients with adult respiratory distress syndrome (3.8 +/- 0.8 mmHg; P less than 0.01), but not in 20 patients with chronic obstructive pulmonary disease (1.8 +/- 0.7 mmHg). The distribution of the pulmonary vascular resistance was clearly different among the four groups. The fraction of the total pulmonary vascular resistance attributable to large and medium pulmonary veins was significantly increased (P less than 0.01) in adult respiratory distress syndrome (27.5 +/- 12%) and cardiac patients (27.5 +/- 9%) compared with patients with chronic obstructive pulmonary disease (13 +/- 5%) and normal lungs (13.5 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)
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Eedara, Basanth Babu, Rakesh Bastola, and Shyamal C. Das. "Dissolution and Absorption of Inhaled Drug Particles in the Lungs." Pharmaceutics 14, no. 12 (November 30, 2022): 2667. http://dx.doi.org/10.3390/pharmaceutics14122667.
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Dry powder inhalation therapy has been effective in treating localized lung diseases such asthma, chronic obstructive pulmonary diseases (COPD), cystic fibrosis and lung infections. In vitro characterization of dry powder formulations includes the determination of physicochemical nature and aerosol performance of powder particles. The relationship between particle properties (size, shape, surface morphology, porosity, solid state nature, and surface hydrophobicity) and aerosol performance of an inhalable dry powder formulation has been well established. However, unlike oral formulations, there is no standard dissolution method for evaluating the dissolution behavior of the inhalable dry powder particles in the lungs. This review focuses on various dissolution systems and absorption models, which have been developed to evaluate dry powder formulations. It covers a summary of airway epithelium, hurdles to developing an in vitro dissolution method for the inhaled dry powder particles, fine particle dose collection methods, various in vitro dissolution testing methods developed for dry powder particles, and models commonly used to study absorption of inhaled drug.
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Mao, Yun, Ishita Choudhary, Sonika Patial, and Yogesh Saini. "Epithelial cell-specific role of HMGB1 in murine lungs with muco-obstructive lung disease." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 105.24. http://dx.doi.org/10.4049/jimmunol.208.supp.105.24.
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Abstract Introduction Mucoobstructive lung diseases are characterized by defective mucociliary clearance, mucin hypersecretion, and mucoobstruction. High mobility group box 1 protein (HMGB1) plays a key role as an inflammatory mediator. However, the role of HMGB1 in mucoobstructive lung diseases remains unclear. Using Scnn1b-Tg+ mice, a mouse model of cystic fibrosis, we hypothesized that the airway epithelial cell-specific HMGB1 acts as an anti-inflammatory mediator in the Scnn1b-Tg+ lungs. Methods Airway epithelial cell-specific HMGB1-deficient (CCSP-iCre+/Hmgb1flox/flox) and control (CCSP-iCre− /Hmgb1flox/flox) mice were generated. The bronchoalveolar lavage fluid (BALF) and lung tissue were collected for endpoints analyses. Results Compared with wild-type (WT) mice, HMGB1 expression was significantly increased in BALF and airway epithelial cells of Scnn1b-Tg+ mice. Unlike HMGB1-sufficient Scnn1b-Tg+ mice, HMGB1-deficient Scnn1b-Tg+ mice exhibited enhanced lung inflammation evident from the elevated total protein and dsDNA contents in the BALF. HMGB1 deletion in airway epithelial cells in Scnn1b-Tg+ mice also exaggerated immune cell recruitment, which was accompanied by increased levels of chemokines and cytokines, including KC, G-CSF, MCP-1, MIP-2, MIP-1α, MIP-1β, and IP-10. Furthermore, HMGB1 deletion in airway epithelial cells in Scnn1b-Tg+ mice enhanced the type 2 inflammation manifested by increased levels of Th2 cytokines such as IL-4 and IL-5. Additionally, HMGB1-deficient Scnn1b-Tg+ mice showed increased airway mucus plugging and impaired bacterial clearance. Conclusion Epithelial cell-derived HMGB1 may play an anti-inflammatory role in murine lungs with mucoobstructive lung disease. Supported by NIEHS (RO1, ES030125)
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Despois, Olivier, Sharon C.-A. Chen, Nicole Gilroy, Michael Jones, Peter Wu, and Justin Beardsley. "Chronic Pulmonary Aspergillosis: Burden, Clinical Characteristics and Treatment Outcomes at a Large Australian Tertiary Hospital." Journal of Fungi 8, no. 2 (January 25, 2022): 110. http://dx.doi.org/10.3390/jof8020110.
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Chronic pulmonary aspergillosis (CPA) is a fungal lung infection associated with high morbidity and mortality. Yet, it remains under-recognized worldwide, with few Australian clinical data available. This retrospective study aimed to investigate CPA at a major tertiary referral hospital in Sydney. We identified patients having International Classification of Diseases (ICD-10) codes for “aspergillosis” and/or positive respiratory microbiology samples for Aspergillus species from January 2012–December 2018 at Westmead Hospital. Eligible cases were classified using European Respiratory Society 2016 CPA guidelines. We diagnosed 28 CPA patients: median age 60 years (IQR: 57–66), with 17 (60.7%) being males. Most had chronic cavitary pulmonary aspergillosis phenotype (n = 17, 60.7%). Twenty-three patients had outcomes data returned. Nineteen (82.6%) received antifungal therapy (median duration: 10.5 months (IQR: 6.5–20.7)). Eight (34.7%) patients received <6 months of antifungals, including three (38%) deaths. Two (13%) patients receiving ≥6 months of antifungals died. Chronic obstructive pulmonary disease (COPD) (n = 9, 32.1%) was the leading predisposing factor for CPA in our cohort. This contrasts with the global picture, where prior tuberculosis generally predominates, but is similar to findings from other high-income countries. Nevertheless, further larger-scale studies are required to determine whether these results are generalizable to the wider Australian population.
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Liu, Piaoyang, Shun Li, and Liling Tang. "Nerve Growth Factor: A Potential Therapeutic Target for Lung Diseases." International Journal of Molecular Sciences 22, no. 17 (August 24, 2021): 9112. http://dx.doi.org/10.3390/ijms22179112.
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The lungs play a very important role in the human respiratory system. However, many factors can destroy the structure of the lung, causing several lung diseases and, often, serious damage to people’s health. Nerve growth factor (NGF) is a polypeptide which is widely expressed in lung tissues. Under different microenvironments, NGF participates in the occurrence and development of lung diseases by changing protein expression levels and mediating cell function. In this review, we summarize the functions of NGF as well as some potential underlying mechanisms in pulmonary fibrosis (PF), coronavirus disease 2019 (COVID-19), pulmonary hypertension (PH), asthma, chronic obstructive pulmonary disease (COPD), and lung cancer. Furthermore, we highlight that anti-NGF may be used in future therapeutic strategies.
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Agraval, Hina, and Hong Wei Chu. "Lung Organoids in Smoking Research: Current Advances and Future Promises." Biomolecules 12, no. 10 (October 12, 2022): 1463. http://dx.doi.org/10.3390/biom12101463.
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Tobacco smoking has been established to contribute to the pathogenesis of various respiratory diseases including chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. However, major hurdles in mechanistic studies on the role of smoking in human lungs remain in part due to the lack of ex vivo experimental models and ambiguous data from animal models that can best recapitulate the architecture and pathophysiology of the human lung. Recent development of the lung organoid culture system has opened new avenues for respiratory disease research as organoids are proving to be a sophisticated ex vivo model that functionally and structurally mimics the human lungs better than other traditionally used models. This review will discuss how recent advances in lung organoid systems may help us better determine the injurious and immunological effect of smoking on human lungs and will provide some suggestions for future research directions.
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Salsabila, Sharifa Audi, Alfian Nur Rosyid, Maulana Antiyan Empitu, Ika Nindya Kadariswantiningsih, Satriyo Dwi Suryantoro, Mutiara Rizki Haryati, Mochammad Thaha, and Yusuke Suzuki. "Kidney-Pulmonary Crosstalk from Pathophysiological Perspective." Jurnal Respirasi 8, no. 1 (January 30, 2022): 44. http://dx.doi.org/10.20473/jr.v8-i.1.2022.44-51.
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Lungs and kidneys are distant organs which are functionally related in physiological and pathological contexts. Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are common complications in acute kidney injury (AKI) or acute-on-chronic kidney disease. On the other hand, there is a considerable risk of AKI in respiratory diseases such as ARDS and chronic obstructive pulmonary disease (COPD). From a pathophysiological point of view, the kidney-lung crosstalk involves interdependency in the regulation of fluid hemodynamic, acid-base and electrolyte balance, and carbon dioxide partial pressure. Aside from the closely related function, the crosstalk may also occur by non-classical mechanisms such as through activation of systemic inflammation, excessive cytokine release, and the formation of auto-antibody which targets both kidneys and lungs. This review discussed several disease mechanisms by which kidney and lungs affect each other or are simultaneously affected by pathological processes. Particularly, this review discussed some specific mechanisms in lungs and kidneys, such as how hypoxemia and hypercapnia induced by ARDS may reduce kidney function and how distance injury on kidney may affect the development of non-cardiogenic edema lungs.
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Ito, Juliana T., Juliana D. Lourenço, Renato F. Righetti, Iolanda F. L. C. Tibério, Carla M. Prado, and Fernanda D. T. Q. S. Lopes. "Extracellular Matrix Component Remodeling in Respiratory Diseases: What Has Been Found in Clinical and Experimental Studies?" Cells 8, no. 4 (April 11, 2019): 342. http://dx.doi.org/10.3390/cells8040342.
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Changes in extracellular matrix (ECM) components in the lungs are associated with the progression of respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS). Experimental and clinical studies have revealed that structural changes in ECM components occur under chronic inflammatory conditions, and these changes are associated with impaired lung function. In bronchial asthma, elastic and collagen fiber remodeling, mostly in the airway walls, is associated with an increase in mucus secretion, leading to airway hyperreactivity. In COPD, changes in collagen subtypes I and III and elastin, interfere with the mechanical properties of the lungs, and are believed to play a pivotal role in decreased lung elasticity, during emphysema progression. In ARDS, interstitial edema is often accompanied by excessive deposition of fibronectin and collagen subtypes I and III, which can lead to respiratory failure in the intensive care unit. This review uses experimental models and human studies to describe how inflammatory conditions and ECM remodeling contribute to the loss of lung function in these respiratory diseases.
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Zheng, David Jiao, Maria Abou Taka, and Bryan Heit. "Role of Apoptotic Cell Clearance in Pneumonia and Inflammatory Lung Disease." Pathogens 10, no. 2 (January 29, 2021): 134. http://dx.doi.org/10.3390/pathogens10020134.
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Pneumonia and inflammatory diseases of the pulmonary system such as chronic obstructive pulmonary disease and asthma continue to cause significant morbidity and mortality globally. While the etiology of these diseases is highly different, they share a number of similarities in the underlying inflammatory processes driving disease pathology. Multiple recent studies have identified failures in efferocytosis—the phagocytic clearance of apoptotic cells—as a common driver of inflammation and tissue destruction in these diseases. Effective efferocytosis has been shown to be important for resolving inflammatory diseases of the lung and the subsequent restoration of normal lung function, while many pneumonia-causing pathogens manipulate the efferocytic system to enhance their growth and avoid immunity. Moreover, some treatments used to manage these patients, such as inhaled corticosteroids for chronic obstructive pulmonary disease and the prevalent use of statins for cardiovascular disease, have been found to beneficially alter efferocytic activity in these patients. In this review, we provide an overview of the efferocytic process and its role in the pathophysiology and resolution of pneumonia and other inflammatory diseases of the lungs, and discuss the utility of existing and emerging therapies for modulating efferocytosis as potential treatments for these diseases.
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Figat, Magdalena, Grzegorz Kardas, Piotr Kuna, and Michał G. Panek. "Beneficial Influence of Exendin-4 on Specific Organs and Mechanisms Favourable for the Elderly with Concomitant Obstructive Lung Diseases." Brain Sciences 12, no. 8 (August 17, 2022): 1090. http://dx.doi.org/10.3390/brainsci12081090.
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Exendin-4 (Ex-4), better known in its synthetic form and used clinically as exenatide, currently applied in the treatment of diabetes, induces a beneficial impact on nerve cells, and shows promising effects in obstructive lung diseases. At an advanced age, the development of the neurodegenerative process of brain tissue is masked by numerous concomitant diseases. The initial latent phase of neurodegenerative disease results in occurrence of manifestations at an advanced stage. To protect the brain and to simultaneously ensure proper treatment of common coexisting conditions in late life, such as diabetes, chronic obstructive pulmonary disease, or asthma, a pleiotropic medication should be chosen. Molecular mechanisms of Ex-4 exert neuroprotective effects or lead to secondary neurogenesis. Additionally, Ex-4 plays an important role in anti-inflammatory actions which are necessary both in the case of asthma and Parkinson’s disease. Specific receptors in the lungs also reduce the secretion of surfactants, which decreases the risk of exacerbation in chronic obstructive lung disease. In a great number of patients suffering from diabetes, asthma, or chronic lung disease, there is a great potential for both treatment of the main condition and protection against brain neurodegeneration.
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Aisanov, Z. R., A. G. Chuchalin, and E. N. Kalmanova. "Chronic obstructive pulmonary disease and cardiovascular comorbidity." Kardiologiia 59, no. 8S (September 16, 2019): 24–36. http://dx.doi.org/10.18087/cardio.2572.
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In recent years, a greater understanding of the heterogeneity and complexity of chronic obstructive pulmonary disease (COPD) has come from the point of view of an integrated clinical assessment of severity, pathophysiology, and the relationship with other pathologies. A typical COPD patient suffers on average 4 or more concomitant diseases and every day about a third of patients take from 5 to 10 different drugs. The mechanisms of the interaction of COPD and cardiovascular disease (CVD) include the effects of systemic inflammation, hyperinflation (hyperinflation) of the lungs and bronchial obstruction. The risk of developing CVD in patients with COPD is on average 2–3 times higher than in people of a comparable age in the general population, even taking into account the risk of smoking. The prevalence of coronary heart disease, heart failure, and rhythm disturbances among COPD patients is significantly higher than in the general population. The article discusses in detail the safety of prescribing various groups of drugs for the treatment of CVD in patients with COPD. Achieving success in understanding and managing patients with COPD and CVD is possible using an integrated multidisciplinary approach.
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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 (%FEV1) by group. We then selected nonsmokers (As-NS) and smokers with asthma (As-Sm) in both groups and those with COPD while controlling for the degree of airflow limitation across groups. Emphysema volumes [%lung attenuation volume (%LAV)] and percentage of cross-sectional area of small pulmonary vessels <5 mm2 (%CSA<5) were measured by computed tomography. In As-NS, %Kco was significantly higher when FEV1% was reduced, but such a correlation was not seen in As-Sm. %Kco successfully differentiated among the three groups when airflow limitation levels were matched. However, %DLc, was significantly reduced only in patients with COPD. Both %LAV and %CSA<5 were better correlated with %Kco than with %DLco. There was discordance between %DLCO and %Kco in As-Sm, which was not seen in As-NS. Overall, %Kco better reflects emphysematous changes in obstructive lung diseases than %DLco. NEW & NOTEWORTHY Despite differing behaviors of %Kco and %DLco in several diseases, the characteristics of these parameters have not been fully examined in smokers with asthma. Here, we demonstrated that %Kco is a more sensitive parameter of pathophysiology, better reflecting emphysematous changes in chronic obstructive lung diseases overall, compared with %DLco. Thus, more precise interpretations of %DLco and %Kco may provide clues for understanding the pathophysiology of obstructive lung diseases.
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Kasai, Akiko, Naomi Yamashita, and Naoko Utsunomiya-Tate. "Collagen Racemization and Deposition in the Lungs of Aged Rats." Biochemistry Insights 3 (January 2010): BCI.S4210. http://dx.doi.org/10.4137/bci.s4210.
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Isomerization of amino acids in proteins has recently been identified as a part of the aging process. Increases in D-amino acids as a consequence of isomerization influence the function and structure of proteins. Senescence-related pulmonary diseases, such as chronic obstructive pulmonary disease, are thought to be caused by reductions of lung function with age. We hypothesized that changes of protein structure in lung tissue induced by the isomerization of amino acids could result in decreased lung function. Therefore, we examined whether isomerization of amino acids takes place in the lungs of rats as they age. We measured the content of L- and D-amino acids in collagen 1 by HPLC using a chiral column. We found that collagen 1 was increasingly racemized with age, so that significantly higher proportions of D-Ser were present in 12- and 24-month-old rats than in 8-week-old rats. D-Asp increased slightly but not significantly. We also investigated the localization of collagen 1 in lung tissue. Stacks of collagen 1 were observed in the parenchyma and airway wall, and age-dependent changes were especially prominent in the airway wall. Racemization of collagen 1 could therefore influence lung function and contribute to pulmonary diseases.
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Wu, Jin-nan, Jian-rong Chen, and Jin-liang Chen. "Role of Farnesoid X Receptor in the Pathogenesis of Respiratory Diseases." Canadian Respiratory Journal 2020 (November 26, 2020): 1–8. http://dx.doi.org/10.1155/2020/9137251.
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Farnesoid X receptor (FXR) is a bile acid receptor encoded by the Nr1h4 gene. FXR plays an important role in maintaining the stability of the internal environment and the integrity of many organs, including the liver and intestines. The expression of FXR in nondigestible tissues other than in the liver and small intestine is known as the expression of “nonclassical” bile acid target organs, such as blood vessels and lungs. In recent years, several studies have shown that FXR is widely involved in the pathogenesis of various respiratory diseases, such as chronic obstructive pulmonary disease, bronchial asthma, and idiopathic pulmonary fibrosis. Moreover, a number of works have confirmed that FXR can regulate the bile acid metabolism in the body and exert its anti-inflammatory and antifibrotic effects in the airways and lungs. In addition, FXR may be used as a potential therapeutic target for some respiratory diseases. For example, FXR can regulate the tumor microenvironment by regulating the balance of inflammatory and immune responses in the body to promote the occurrence and development of non-small-cell lung cancer (NSCLC), thereby being considered a potential target for immunotherapy of NSCLC. In this article, we provide an overview of the internal relationship between FXR and respiratory diseases to track the progress that has been achieved thus far in this direction and suggest potential therapeutic prospects of FXR in respiratory diseases.
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Schullcke, Benjamin, Bo Gong, Sabine Krueger-Ziolek, and Knut Moeller. "Reconstruction of conductivity change in lung lobes utilizing electrical impedance tomography." Current Directions in Biomedical Engineering 3, no. 2 (September 7, 2017): 513–16. http://dx.doi.org/10.1515/cdbme-2017-0108.
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AbstractElectrical Impedance Tomography (EIT) is a novel medical imaging technology which is expected to give valuable information for the treatment of mechanically ventilated patients as well as for patients with obstructive lung diseases. In lung-EIT electrodes are attached around the thorax to inject small alternating currents and to measure resulting voltages. These voltages depend on the internal conductivity distribution and thus on the amount of air in the lungs. Based on the measured voltages, image reconstruction algorithms are employed to generate tomographic images reflecting the regional ventilation of the lungs. However, the ill-posedness of the reconstruction problem leads to reconstructed images that are severely blurred compared to morphological imaging technologies, such as X-ray computed tomography or Magnetic Resonance Imaging. Thus, a correct identification of the particular ventilation in anatomically assignable units, e.g. lung-lobes, is often hindered. In this study a 3D-FEM model of a human thorax has been used to simulate electrode voltages at different lung conditions. Two electrode planes with 16 electrodes at each layer have been used and different amount of emphysema and mucus plugging was simulated with different severity in the lung lobes. Patient specific morphological information about the lung lobes is used in the image reconstruction process. It is shown that this kind of prior information leads to better reconstructions of the conductivity change in particular lung lobes than in classical image reconstruction approaches, where the anatomy of the patients’ lungs is not considered. Thus, the described approach has the potential to open new and promising applications for EIT. It might be used for diagnosis and disease monitoring for patients with obstructive lung diseases but also in other applications, e.g. during the placement of endobronchial valves in patients with severe emphysema.
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Salaeva, Muborak, Nargiza Salimova, Nargiza Aripova, Naila Khuday berganova, and Otabek Yangibaev. "Evaluation of Clinical and Functional Disorders in Patients with Chronic Obstructive Diseases of the Lungs and Bronchial Asthma." International Journal of Psychosocial Rehabilitation 24, Special Issue 1 (February 28, 2020): 468–79. http://dx.doi.org/10.37200/ijpr/v24sp1/pr201179.
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Guerrina, Necola, Hussein Traboulsi, David Eidelman, and Carolyn Baglole. "The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health." International Journal of Molecular Sciences 19, no. 12 (December 5, 2018): 3882. http://dx.doi.org/10.3390/ijms19123882.
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Much of what is known about the Aryl Hydrocarbon Receptor (AhR) centers on its ability to mediate the deleterious effects of the environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin). However, the AhR is both ubiquitously-expressed and evolutionarily-conserved, suggesting that it evolved for purposes beyond strictly mediating responses to man-made environmental toxicants. There is growing evidence that the AhR is required for the maintenance of health, as it is implicated in physiological processes such as xenobiotic metabolism, organ development and immunity. Dysregulation of AhR expression and activity is also associated with a variety of disease states, particularly those at barrier organs such as the skin, gut and lungs. The lungs are particularly vulnerable to inhaled toxicants such as cigarette smoke. However, the role of the AhR in diseases such as chronic obstructive pulmonary disease (COPD)—a respiratory illness caused predominately by cigarette smoking—and lung cancer remains largely unexplored. This review will discuss the growing body of literature that provides evidence that the AhR protects the lungs against the damaging effects of cigarette smoke.
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Tseymakh, I. Ya, and Y. N. Shoykhet. "Factors of vascular endothelial dysfunction and thrombogenic risk in patients with chronic obstructive pulmonary disease in combination with obstructive sleep apnea after an exacerbation." PULMONOLOGIYA 31, no. 3 (June 10, 2021): 329–37. http://dx.doi.org/10.18093/0869-0189-2021-31-3-329-337.
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Obstructive sleep apnea (OSA) is a common disease. The incidence is higher in patients with chronic obstructive pulmonary disease with moderate to severe bronchial obstruction or hypoxemia. OSA is associated with increased risks of fatal outcomes of acute cardiovascular diseases in such patients. Objective. To assess the effect of long-term non-invasive ventilation of the lungs in the spontaneous breathing mode with positive airway pressure (CPAP) on the indicators of systemic inflammation, insulin resistance, and thrombogenic risk together with clinical outcomes during the rehabilitation period after an exacerbation in patients with concomitant chronic obstructive pulmonary disease and obstructive sleep apnea who do not need long-term oxygen therapy. Methods. The effects of long-term CPAP therapy as a part of complex treatment were analyzed in an openlabel, prospective, comparative six-week study that enrolled 65 patients with concomitant chronic obstructive pulmonary disease and obstructive sleep apnea. The main group included 26 people who received CPAP therapy as a part of complex treatment. The comparison group included 39 people who did not use non-invasive ventilation of the lungs. The patients’ age was 55.5 ± 2.1 years in the main group and 57.1 ± 1.5 years in the comparison group (p > 0.1). Men prevailed in both groups – 92.3% in the main group and 100.0% in the comparison group (p > 0.1). Results. The clinical efficacy of CPAP therapy was confirmed by an improvement in the quality of life of patients on the SF-36 questionnaire, a decrease in the degree of daytime sleepiness on the Epworth scale (Johns, 1991). CPAP-therapy was associated with a drop in the serum levels of tumor necrosis factor α and the blood level of endothelin 1, a more pronounced decrease in the levels of C-reactive protein, interleukin 8, C-peptide, vascular endothelial growth factor, homocysteine versus the comparison group. Conclusion. The use of CPAP-therapy in patients with concomitant chronic obstructive pulmonary disease and obstructive sleep apnea who do not need long-term oxygen therapy during the rehabilitation period after an exacerbation is associated with a decrease in systemic inflammation, vascular endothelial dysfunction, and hyperhomocysteinemia.
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Ikhsan, Mukhtar. "Air Pollution and Respiratory Diseases During The Hajj Season in The Holy City of Makkah." Respiratory Science 2, no. 2 (February 28, 2022): 124–31. http://dx.doi.org/10.36497/respirsci.v2i2.37.
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The holy city of Makkah is one of the big cities in Saudi Arabia that is densely populated, especially during the Hajj season. In recent years, air pollution in Makkah has been a growing problem due to construction activities, motor vehicle fumes, rising temperatures, rainfall and humidity. The higher the level of air pollution exposure, the more it has an impact on human health, especially the lungs and airways. The health impacts associated with air pollution include an increase in the incidence of respiratory infections, asthma, chronic obstructive pulmonary disease and other lung diseases. Better knowledge of the correlation between air pollution and lung and airway diseases will contribute to developing more strategies to reduce air pollution in the holy city of Makkah.
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Shivanna, Binoy, Chun Chu, and Bhagavatula Moorthy. "The Aryl Hydrocarbon Receptor (AHR): A Novel Therapeutic Target for Pulmonary Diseases?" International Journal of Molecular Sciences 23, no. 3 (January 28, 2022): 1516. http://dx.doi.org/10.3390/ijms23031516.
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The aryl hydrocarbon receptor (AHR) is a cytoplasmic transcription factor that is well-known for regulating xenobiotic metabolism. Studies in knockout and transgenic mice indicate that the AHR plays a vital role in the development of liver and regulation of reproductive, cardiovascular, hematopoietic, and immune homeostasis. In this focused review on lung diseases associated with acute injury and alveolar development, we reviewed and summarized the current literature on the mechanistic role(s) and therapeutic potential of the AHR in acute lung injury, chronic obstructive pulmonary disease, and bronchopulmonary dysplasia (BPD). Pre-clinical studies indicate that endogenous AHR activation is necessary to protect neonatal and adult lungs against hyperoxia- and cigarette smoke-induced injury. Our goal is to provide insight into the high translational potential of the AHR in the meaningful management of infants and adults with these lung disorders that lack curative therapies.
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Grunig, Gabriele, Aram Baghdassarian, Sung-Hyun Park, Serhiy Pylawka, Bertram Bleck, Joan Reibman, Erika Berman-Rosenzweig, and Nedim Durmus. "Challenges and Current Efforts in the Development of Biomarkers for Chronic Inflammatory and Remodeling Conditions of the Lungs." Biomarker Insights 10s4 (January 2015): BMI.S29514. http://dx.doi.org/10.4137/bmi.s29514.
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This review discusses biomarkers that are being researched for their usefulness to phenotype chronic inflammatory lung diseases that cause remodeling of the lung's architecture. The review focuses on asthma, chronic obstructive pulmonary disease (COPD), and pulmonary hypertension. Biomarkers of environmental exposure and specific classes of biomarkers (noncoding RNA, metabolism, vitamin, coagulation, and microbiome related) are also discussed. Examples of biomarkers that are in clinical use, biomarkers that are under development, and biomarkers that are still in the research phase are discussed. We chose to present examples of the research in biomarker development by diseases, because asthma, COPD, and pulmonary hypertension are distinct entities, although they clearly share processes of inflammation and remodeling.
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Yao, H., S. R. Yang, A. Kode, S. Rajendrasozhan, S. Caito, D. Adenuga, R. Henry, I. Edirisinghe, and I. Rahman. "Redox regulation of lung inflammation: role of NADPH oxidase and NF-κB signalling." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1151–55. http://dx.doi.org/10.1042/bst0351151.
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Regulation of reduction/oxidation (redox) state is critical for cell viability, activation, proliferation and organ function, and imbalance of oxidant/antioxidant balance is implicated in various chronic respiratory inflammatory diseases, such as asthma, pulmonary fibrosis and chronic obstructive pulmonary disease. CS (cigarette smoke) is a complex mixture of various noxious gases and condensed tar particles. These components elicit oxidative stress in lungs by continuous generation of ROS (reactive oxygen species) and various inflammatory mediators. In the present review, we have discussed the role of oxidative stress in triggering the inflammatory response in the lungs in response to CS by demonstrating the role of NADPH oxidase, redox-sensitive transcription factors, such as pro-inflammatory NF-κB (nuclear factor κB) and antioxidant Nrf2 (nuclear factor-erythroid 2 p45 subunit-related factor 2), as well as HDAC (histone deacetylase) in pro-inflammatory cytokine release by disruption of HDAC–RelA/p65 NF-κB complex.
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Shi, Canxia, Sanne de Wit, Emina Učambarlić, George Markousis-Mavrogenis, Elles M. Screever, Wouter C. Meijers, Rudolf A. de Boer, and Joseph Pierre Aboumsallem. "Multifactorial Diseases of the Heart, Kidneys, Lungs, and Liver and Incident Cancer: Epidemiology and Shared Mechanisms." Cancers 15, no. 3 (January 25, 2023): 729. http://dx.doi.org/10.3390/cancers15030729.
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Within the aging population, the frequency of cancer is increasing dramatically. In addition, multiple genetic and environmental factors lead to common multifactorial diseases, including cardiovascular disease, chronic kidney disease, chronic obstructive pulmonary disease, and metabolic-associated fatty liver disease. In recent years, there has been a growing awareness of the connection between cancer and multifactorial diseases, as well as how one can affect the other, resulting in a vicious cycle. Although the exact mechanistic explanations behind this remain to be fully explored, some progress has been made in uncovering the common pathologic mechanisms. In this review, we focus on the nature of the link between cancer and common multifactorial conditions, as well as specific shared mechanisms, some of which may represent either preventive or therapeutic targets. Rather than organ-specific interactions, we herein focus on the shared mechanisms among the multifactorial diseases, which may explain the increased cancer risk. More research on this subject will highlight the significance of developing new drugs that target multiple systems rather than just one disease.
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Lucas, Rudolf, Yalda Hadizamani, Joyce Gonzales, Boris Gorshkov, Thomas Bodmer, Yves Berthiaume, Ueli Moehrlen, et al. "Impact of Bacterial Toxins in the Lungs." Toxins 12, no. 4 (April 2, 2020): 223. http://dx.doi.org/10.3390/toxins12040223.
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Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate lung barrier function and to impair host defense in order to promote infection. Although in general, these toxins target common cellular signaling pathways and host compartments, toxin- and cell-specific effects have also been reported. Toxins can affect resident pulmonary cells involved in alveolar fluid clearance (AFC) and barrier function through impairing vectorial Na+ transport and through cytoskeletal collapse, as such, destroying cell-cell adhesions. The resulting loss of alveolar-capillary barrier integrity and fluid clearance capacity will induce capillary leak and foster edema formation, which will in turn impair gas exchange and endanger the survival of the host. Toxins modulate or neutralize protective host cell mechanisms of both the innate and adaptive immunity response during chronic infection. In particular, toxins can either recruit or kill central players of the lung’s innate immune responses to pathogenic attacks, i.e., alveolar macrophages (AMs) and neutrophils. Pulmonary disorders resulting from these toxin actions include, e.g., acute lung injury (ALI), the acute respiratory syndrome (ARDS), and severe pneumonia. When acute infection converts to persistence, i.e., colonization and chronic infection, lung diseases, such as bronchitis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) can arise. The aim of this review is to discuss the impact of bacterial toxins in the lungs and the resulting outcomes for pathogenesis, their roles in promoting bacterial dissemination, and bacterial survival in disease progression.
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Benam, Kambez Hajipouran. "Organ-on-Chip Meets Immunology: Let’s Start with the Lungs." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 159.14. http://dx.doi.org/10.4049/jimmunol.204.supp.159.14.
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Abstract Organs-on-chips are biomimetic, microfluidic, cell culture devices created with microchip manufacturing methods that contain continuously perfused hollow microchannels inhabited by living tissue cells arranged to simulate organ-level physiology. By recapitulating the multicellular architectures, tissue-tissue interfaces, chemical gradients, mechanical cues, and vascular perfusion of the body, these devices produce levels of tissue and organ functionality not possible with conventional 2D or 3D culture systems. They also enable high-resolution, real-time imaging and in vitro analysis of biochemical, genetic and metabolic activities of living human cells in a functional human tissue and organ context. Here, we discuss development of ‘Human Lung Small Airway-on-a-Chip’ – an engineered cell-by-cell reconstituted microfluidic device with living human tissues to model airway inflammation in the context of debilitating lung diseases, including asthma and chronic obstructive pulmonary disease (COPD). In addition, we will present our preliminary data on recreating a hematopoietically active bone marrow niche in vitro (‘BM-on-a-Chip’) for microphysiological integration with the Small Airway-on-a-Chip to emulate innate immune cell egress into circulation (from the BM) and their recruitment to the lung airway.
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Davidovskaya, Е. I., A. S. Dubrovski, and О. В. Zelmanski. "Respiratory failure: technical means for diagnosis and respiratory support." Doklady BGUIR 18, no. 8 (December 27, 2020): 29–36. http://dx.doi.org/10.35596/1729-7648-2020-18-8-29-36.
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The necessity of early diagnosis of respiratory diseases, especially in the context of the COVID-19 pandemic, by means of pulse oximetric screening and monitoring has been substantiated. The expediency of using portable pulse oximeters by therapists and general practitioners has been shown. The main respiratory diseases accompanied by respiratory failure, which can be detected in time by pulse oximetry, are the chronic obstructive pulmonary disease and the obstructive sleep apnea-hypopnea syndrome. Early detection of these diseases is an important task because of the mild symptoms of these diseases in the early stages, and as a result, the prevalence of late diagnosis. Special attention is given to the pulse oximetry for COVID-19 detection, as this infection is also accompanied by respiratory failure. The use of oxygen concentrators and auto CPAP devices for the treatment of respiratory failure as well as rehabilitation has been argued. The effectiveness of the appointment of long-term oxygen therapy using oxygen concentrators for patients with chronic obstructive pulmonary disease, CPAP therapy using automatic CPAP devices for patients with obstructive sleep apnea-hypopnea syndrome with mandatory pulse oximetry monitoring has been confirmed. The analysis of 120 cases of treatment of moderate and severe COVID-19 cases complicated by the pneumonia has been carried out. The efficiency of the use of oxygen concentrators for supplying oxygen to patients at a flow rate not more than 5 l/min has been proven. It has been found that no more than 10 % of patients needed an oxygen flow rate more than 5 l/min. At the same time, the possibility of using CPAP devices for non-invasive ventilation of lungs using full-face masks has been shown. The expediency of using oxygen concentrators and CPAP devices for the rehabilitation of patients after COVID-19 has been noted.
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Patel, Princal Shaileshkumar. "A MINI-REVIEW ON RESPIRATORY DISEASES- CHRONIC OBSTRUCTIVE PULMONARY DISEASE, TUBERCULOSIS, AND PNEUMONIA- A GLOBAL HEALTH ISSUE." International Journal of Medical Laboratory Research 07, no. 03 (2022): 18–28. http://dx.doi.org/10.35503/ijmlr.2022.7303.
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The lungs are the crucial organ that can be infected or injured by airborne particles. Respiratory disorders are the main cause of mortality and morbidity worldwide. COPD affects around 65 million people globally and kills three million people annually, the world's third greatest reason for mortality. Pneumonia kills millions of citizens each year and is the top cause of mortality in kids under the age of five. Every year, about Ten million people contract tuberculosis (TB), and more than one million people die from it, ranking it as the most prevalent fatal infectious illness. "Prevention, control, and cure" of these disorders, as well as improvement of lung diseases, must be primary concerns in global health judgment. The current article will, without hesitation, raise global understanding about the major respiratory illnesses and spur actions among all stakeholders. This article presents a comprehensive study and highlights the recent changes in respiratory diseases such as Chronic Obstructive Pulmonary Disease, Tuberculosis, and Pneumonia considering the extent of a global problem, Epidemiology, Pathology and pathogenesis, preventive strategies, and treatment.
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Pinto, Bruna G. G., Antonio E. R. Oliveira, Youvika Singh, Leandro Jimenez, Andre N. A. Gonçalves, Rodrigo L. T. Ogava, Rachel Creighton, Jean Pierre Schatzmann Peron, and Helder I. Nakaya. "ACE2 Expression Is Increased in the Lungs of Patients With Comorbidities Associated With Severe COVID-19." Journal of Infectious Diseases 222, no. 4 (June 11, 2020): 556–63. http://dx.doi.org/10.1093/infdis/jiaa332.
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Abstract Patients who died from COVID-19 often had comorbidities, such as hypertension, diabetes, and chronic obstructive lung disease. Although angiotensin-converting enzyme 2 (ACE2) is crucial for SARS-CoV-2 to bind and enter host cells, no study has systematically assessed the ACE2 expression in the lungs of patients with these diseases. Here, we analyzed over 700 lung transcriptome samples from patients with comorbidities associated with severe COVID-19 and found that ACE2 was highly expressed in these patients compared to control individuals. This finding suggests that patients with such comorbidities may have higher chances of developing severe COVID-19. Correlation and network analyses revealed many potential regulators of ACE2 in the human lung, including genes related to histone modifications, such as HAT1, HDAC2, and KDM5B. Our systems biology approach offers a possible explanation for increased COVID-19 severity in patients with certain comorbidities.
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Beaulieu, Delphine, Aya Attwe, Marielle Breau, Larissa Lipskaia, Elisabeth Marcos, Emmanuelle Born, Jin Huang, et al. "Phospholipase A2 receptor 1 promotes lung cell senescence and emphysema in obstructive lung disease." European Respiratory Journal 58, no. 2 (January 28, 2021): 2000752. http://dx.doi.org/10.1183/13993003.00752-2020.
Full textAbstract:
BackgroundCell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence acting via Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling. Its role in pathology, however, remains unknown. Here, we assessed PLA2R1-induced senescence in COPD and lung emphysema pathogenesis.MethodsWe assessed cell senescence in lungs and cultured lung cells from patients with COPD and controls subjected to PLA2R1 knockdown, PLA2R1 gene transduction and treatment with the JAK1/2 inhibitor ruxolitinib. To assess whether PLA2R1 upregulation caused lung lesions, we developed transgenic mice overexpressing PLA2R1 (PLA2R1-TG) and intratracheally injected wild-type mice with a lentiviral vector carrying the Pla2r1 gene (LV-PLA2R1 mice).ResultsWe found that PLA2R1 was overexpressed in various cell types exhibiting senescence characteristics in COPD lungs. PLA2R1 knockdown extended the population doubling capacity of these cells and inhibited their pro-inflammatory senescence-associated secretory phenotype (SASP). PLA2R1-mediated cell senescence in COPD was largely reversed by treatment with the potent JAK1/2 inhibitor ruxolitinib. Five-month-old PLA2R1-TG mice exhibited lung cell senescence, and developed lung emphysema and lung fibrosis together with pulmonary hypertension. Treatment with ruxolitinib induced reversal of lung emphysema and fibrosis. LV-PLA2R1-treated mice developed lung emphysema within 4 weeks and this was markedly attenuated by concomitant ruxolitinib treatment.ConclusionsOur data support a major role for PLA2R1 activation in driving lung cell senescence and lung alterations in COPD. Targeting JAK1/2 may represent a promising therapeutic approach for COPD.
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Sattar, Zeeshan, Alnardo Lora, Bakr Jundi, Christopher Railwah, and Patrick Geraghty. "The S100 Protein Family as Players and Therapeutic Targets in Pulmonary Diseases." Pulmonary Medicine 2021 (June 18, 2021): 1–20. http://dx.doi.org/10.1155/2021/5488591.
Full textAbstract:
The S100 protein family consists of over 20 members in humans that are involved in many intracellular and extracellular processes, including proliferation, differentiation, apoptosis, Ca2+ homeostasis, energy metabolism, inflammation, tissue repair, and migration/invasion. Although there are structural similarities between each member, they are not functionally interchangeable. The S100 proteins function both as intracellular Ca2+ sensors and as extracellular factors. Dysregulated responses of multiple members of the S100 family are observed in several diseases, including the lungs (asthma, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, cystic fibrosis, pulmonary hypertension, and lung cancer). To this degree, extensive research was undertaken to identify their roles in pulmonary disease pathogenesis and the identification of inhibitors for several S100 family members that have progressed to clinical trials in patients for nonpulmonary conditions. This review outlines the potential role of each S100 protein in pulmonary diseases, details the possible mechanisms observed in diseases, and outlines potential therapeutic strategies for treatment.