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Academic literature on the topic 'Lungs Diseases, Obstructive Australia'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Lungs Diseases, Obstructive Australia"

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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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Dissertations / Theses on the topic "Lungs Diseases, Obstructive Australia"

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Roberts, Della Kim. "The family experience with chronic obstructive pulmonary disease." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24422.

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This study was designed to gain an understanding of the family experience when an adult member has chronic obstructive pulmonary disease (COPD). It is recognized that illness within the family affects the well-being of the family unit and the health of all members. To understand the impact of COPD upon the family, however, the literature provides only knowledge of the experience of the individual who has COPD and the spouse, not that of the family unit. Thus, the purpose of this study was to describe and explain the COPD experience from the perspective of the family unit. A qualitative method, phenomenology, was chosen for this investigation. Data were collected through semi-structured interviews with eight families who shared their experiences. From the content analysis of these data, three themes that were common throughout the families' accounts were identified and developed to describe and explain family life with COPD. The first theme, disease-dictated family life, describes four aspects of a common lifestyle that is imposed on the family by the characteristics of COPD. The second theme, isolation, describes the isolation that accompanies the illness experience, for the family group and the individual members within the group. The final theme, family work, describes the four primary challenges the families face and the coping strategies they use to deal with them. These findings revealed that COPD acts as an intense stressor within the family, requiring extensive family work to cope with COPD in a way that maintains the well-being of the family unit. Furthermore, it was found that living with COPD in many ways inhibits the resources within the family and those external sources of support that foster the family's ability to manage the stress associated with living with COPD. The implications for nursing practice and nursing research were delineated in light of the research findings.
Applied Science, Faculty of
Nursing, School of
Graduate
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Lo, Iek-long, and 羅奕龍. "Impacts of cognitive impairment on acute exacerbations of chronic obstructive pulmonary disease among Chinese elderly patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45830770.

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Ubhi, Baljit Kaur. "A metabolomic study of chronic obstructive pulmonary disease (COPD) and its phenotypes." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608237.

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Bayliss, Daniel John. "Evaluation of outcomes of a six-month exercise maintenance pulmonary rehabilitation program in patients with chronic obstructive pulmonary disease." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1137788.

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To date, there is a scant amount of research on the long-term benefits of exercise training for individuals with moderate to severe chronic obstructive pulmonary disease. The purpose of this study was to evaluate standardized outcomes of a six-month maintenance pulmonary rehabilitation program to determine maintenance of functional capacity. Twenty-three subjects (sixteen men, seven women) diagnosed with clinical COPD ages 30-82 (65 + 12 years) participated in the retrospective study. The subjects were referred to an eight-week comprehensive pulmonary rehabilitation program after which upon twelve subjects continued onto a maintenance program. Eleven subjects chose not to participate in the maintenance program and were given a home exercise program and were encouraged to remain active. Hemodynamic, functional, and educational measures were taken prior to entry, upon completion of the hospital program, and again six-months post-program. Outcome tests were standardized using the Indiana Society of Cardiovascular and Pulmonary Rehabilitation Outcomes Manual. Significant differences were found between the maintenance and non-maintenance groups for systolic blood pressure in resting, exercise, and recovery measures at six monthsreevaluation. Differences in oxygen saturation were also found to reach significance between the two groups during recovery from the six-minute walk test. Interestingly, duration of exercise was found to be statistically significant between the two groups as well as emergency room visits and physician visits within the last six months. The maintenance group tended to have fewer emergency room and physician visits in addition to having self-reported higher durations of exercise. In conclusion, maintenance pulmonary rehabilitation programs have been shown to maintain physical activity levels for COPD patients and as a result, fewer quality of life consequences specifically the number of hospital admissions and emergency room visits.
School of Physical Education
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Li, Meng. "Hospitalization cost analysis of COPD patients in Guangdong province." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952154.

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Rycroft, Ashley McLean. "Development of a constant rate step test to assess exertional dyspnea in the primary care setting in patients with chronic obstructive pulmonary disease (COPD)." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112359.

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Rationale. There is a need for the development of a field test to evaluate exertional dyspnea in the primary care setting. This study examined the applicability of a 3-minute constant rate step test in patients with COPD.
Methods. This test involved 4 stepping rates (18, 22, 26, 32 steps.min-1) equivalent to approximately 4.5, 5.3, 6.0, and 7.2 MET with the ultimate goal that in its final development, the assessment will be made a single stepping rate based on disease severity. Stable COPD patients (N = 43; 65 +/- 6.5 years; FEV1 = 49 +/- 16% pred.; SpO2 (%) rest: 95 +/- 2) were equipped with a portable Jaeger Oxycon MobileRTM metabolic system and followed an audio signal for stepping up and down a single 20 cm step for 3 minutes. Borg dyspnea scores were obtained at the end each stepping bout. A 10-min rest was given between each stepping bout.
Results. Of the 43 patients, 80% completed stages 1 and 2, 74 and 37% stages 3 and 4 while no patient of MRC class 4 or 5 (N = 8) completed stage 1. Breathing frequency (breaths.min-1) spanned from 26.5 +/- 4.1 to 39.0 +/- 6.4 but VT (L) remained unchanged (1.4 +/- 0.3 vs. 1.5 +/- 0.4) from stage 1 to 4 while Borg scores were 3 +/- 1, 4 +/- 1, 5 +/- 2, 6 +/- 3 respectively and SpO2 (%) were 92 +/- 5, 91 +/- 4, 91 +/- 4 and 90 +/- 4.
Conclusions. Preliminary findings indicate that a 3-minute constant rate step test may present a feasible alternative to laboratory testing to assess exertional dyspnea in moderately severe COPD. In this population, a stepping rate of 26 steps.min-1 could be sustained by the majority of patients while producing a level of dyspnea potentially amenable to therapy.
This study was supported by an unrestricted grant from Boehringer-Ingelheim/Pfizer.
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Henophy, Sara Catherine 1983. "Test-re-test reproducibility of constant rate step and shuttle walking tests for the assessment of exertional dyspnea in patients with chronic obstructive pulmonary disease (COPD)." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116085.

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Purpose: Exercise testing modalities to assess the effects of a given intervention should prove to be reliable and reproducible. This study reports on test-retest reproducibility of the 3-min shuttle walking and step testing exercise protocols to assess exertional dyspnea and exercise physiology in COPD patients.
Methods: Stable COPD patients (N=43; 65 +/- 6.5 years; FEV1 = 49 +/- 16% pred.) equipped with a portable Jaeger Oxycon MobileRTM metabolic system repeated the walking or stepping tests on two occasions separated by 7 to 14 days. At each visit, participants performed, in a randomized order, four externally paced 3-min bouts of shuttle walking at speeds of 1.5, 2.5, 4.0 and 6.0 km·h-1 or of stepping at a constant rate of 18, 22, 26 and 32 steps·min-1, respectively. Each exercise bout was separated by a 10-min rest period. Ventilation, heart rate, gas exchange parameters and Borg dyspnea score were obtained for each bout during the last 30-seconds of exercise.
Results: The majority of patients completed stepping or walking at the slowest cadence but only 33% completed walking at 6.0 km·h -1 and 40% completed stepping at 32 steps·min-1. Test-retest Pearson correlation coefficients for ventilation, heart rate, gas exchange parameters and dyspnea scores over the four exercise bouts, all exceeded 0.80 with the highest coefficient found for ventilation (r≥.95). Intra-class correlation coefficients were similar to Pearson. Bland & Altman representation showed that a similar proportion of dyspnea data points (92 vs. 96%) lied within 2 SD of the mean difference between test-retest values for dyspnea Borg scores during walking and stepping.
Conclusion: Results show very good reproducibility for both 3-min shuttle walking and stepping exercise protocols in patients with COPD.
This study was supported by an unrestricted grant from Boehringer-Ingelheim/Pfizer.
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Harvey, K. "Ipratropium bromide mediated myocardial injury in in vitro models of myocardial ischaemia/reperfusion." Thesis, Coventry University, 2015. http://curve.coventry.ac.uk/open/items/f03ffc6e-3554-4062-99c2-1c243feb582a/1.

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Ipratropium bromide is a short-acting, non-selective, muscarinic antagonist frequently prescribed for the treatment of Chronic Obstructive Pulmonary Disease (COPD) and as an emergency adjunct therapy for acute asthma. Within the past decade, there has been an accumulating wealth of clinical evidence which indicates that anti-muscarinic drugs, such as ipratropium, are responsible for an increased risk of stroke or, an adverse cardiovascular outcome (including increasing the risk and severity of myocardial infarction (MI)). MI remains the highest risk factor of death for COPD patients due to the systemic co-morbidities associated with COPD, which includes ischaemic heart disease (IHD). Despite the knowledge that approximately 22% of COPD patients also suffer from underlying IHD, the cardiovascular safety of muscarinic antagonists, such as ipratropium, has not been tested in a non-clinical setting of IHD or MI. In order to address this, the current project was designed to investigate, for the first time, the effects of ipratropium on the myocardium in a non-clinical setting. It was identified that under normoxic conditions, ipratropium did not have a significant effect on cardiac myocyte viability or infarction, from 3 month Sprague Dawley rats. In addition to this, following simulated ischaemia, ipratropium also did not appear to exacerbate myocardial injury. However, when ipratropium was administered in the context of simulated ischaemia followed by reperfusion, there was a significant exacerbation in myocardial injury which was characterised by increases in infarction, apoptosis, necrosis and a loss of resilience of oxidative stress. In order to characterise the mechanism by which ipratropium exerts the observed cardio-toxic effects, it was investigated whether acetylcholine (ACh) or cyclosporin A (CsA) were capable of attenuating the ipratropium induced cardiotoxicity. Both agents showed significant limitation of injury when co-administered with ipratropium indicating that ipratropium exerts its cardio-toxic effect through a mechanism which links muscarinic signalling to the mitochondrial permeability transition pore (mPTP). This supports previously published work where the protective signalling of ACh has been shown to promote the phosphorylation of pro-survival kinases, such as Akt and Erk1/2 and that this provides inhibition of the mPTP. Western blotting was employed to identify whether there was an involvement of the pro-survival kinases Akt and Erk1/2, as well as the stress induced kinase JNK. Ipratropium significantly increased levels of phospho-Akt and phospho-Erk1/2. However, JNK levels appeared to be insignificantly altered in comparison with the control groups. Both ACh and CsA were capable of limiting these increases. Further to this, an aged study was carried out, which showed that, within the aged myocardium, ipratropium is capable of eliciting further injury in comparison with the 3 month age groups. The effect of ipratropium on tolerance of oxidative stress was not significant, but, also, ACh and CsA were shown as unable to protect. Significant levels of JNK were also observed in the aged animals in comparison with the 3 month groups. In combination, the results presented here demonstrate, for the first time, that ipratropium is capable of exacerbating ischaemia/reperfusion injury in in vitro models of myocardial ischaemia/reperfusion. In addition, ACh and CsA are capable of limiting this injury, implying a role for pro-survival kinases and the mPTP in ipratropium induced myocardial injury. In the aged study, ipratropium still exacerbated injury, however, ACh and CsA appeared unable to protect, therefore promoting previous work that cellular signalling is altered in the senescent myocardium. In conclusion, further studies must be carried out in order to fully characterise the cardio-vascular safety profile of ipratropium.
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Baril, Jacinthe. "Interaction between circulatory and respiratory exercise adaptation in chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF)." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97901.

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Chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF) patients show a marked reduction in exercise capacity compared to that of healthy age-matched individuals. While inadequate gas exchange and resulting hypoxemia appears as the primary factor in COPD, an impaired cardiac output is the predominant explanation for the reduced oxygen delivery in CHF. However, the extent of the contributions of other systemic factors remains unclear. In light of the potential interactions between cardiac output (Qc) and pulmonary hyperinflation, there is surprisingly little data thus far on ventilatory constraints in CHF and on the role of blood flow delivery in COPD which may further limit the exercise capacity. Thus, the purpose of this study was to compare the slope of the Qc versus oxygen uptake (VO2) response through several submaximal cycling loads in patients with moderately severe COPD and with that of moderate to severe CHF patients as well as age-matched healthy control subjects (CTRL). Also examined was the possibility that ventilatory constraints such as dynamic hyperinflation contribute to an abnormal stroke volume response in both diseases. Cardiac output was measured using the CO 2-rebreathing equilibrium technique during baseline conditions and cycling at 20, 40 and 65% of peak power in 17 COPD (Age: 64 +/- 8 yrs; FEV 1/FVC: 37 +/- 11%; FEV1: 41 +/- 15 % predicted), 10 CHF (Age: 57+/- 10 yrs; FEV1/FVC: 73.8 +/- 5.6%; FEV 1: 93 +/- 13% predicted) and 10 age-matched CTRL subjects. Inspiratory capacity (IC) was also measured for the determination of dynamic hyperinflation during the steady state exercise bouts. The results indicate that while the absolute Qc values are lower in COPD and in CHF than in CTRL during 65% peak power cycling (11.30 +/- 2.38 vs 12.40 +/- 2.08 vs 15.63 +/- 2.15 L•min-1 respectively, p < 0.01), likely due to their lower exercise metabolic demand. The Qc/VO2 response to increasing levels of exercise intensity was lower or normal in CHF patients compared to CTRL, while normal or hyperdynamic in most COPD patients. Indeed, the majority of patients with COPD exhibited Qc/VO2 slopes greater than 7.0, which may be indicative of a peripheral muscle bioenergetic disturbance that may drive the need for greater oxygen delivery, and thus result in an exaggerated central circulatory response.
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De, Klerk Danelle Ria. "An adapted rehabilitation programme for a cross section of South African chronic obstructive pulmonary disease patients." Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/776.

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Books on the topic "Lungs Diseases, Obstructive Australia"

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Gall, Malcolm. Asthma, chronic obstructive pulmonary disease, and other respiratory diseases in Australia. Canberra: Australian Institute of Health and Welfare, 2010.

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Australian Centre for Asthma Monitoring. Asthma and chronic obstructive pulmonary disease among older people in Australia: Deaths and hospitalisations. Canberra, A.C.T: Australian Institute of Health and Welfare, 2006.

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Celli, Bartolome R., and Stephen I. Rennard. Chronic obstructive pulmonary disease. Philadelphia, Pennsylvania: Saunders, an imprint of Elsevier, Inc., 2012.

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Currie, Graeme P. Chronic obstructive pulmonary disease. Oxford: Oxford University Press, 2009.

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A, Stockley Robert, ed. Chronic obstructive pulmonary disease. Malden, Mass: Blackwell Pub., 2005.

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Petty, Thomas L. Enjoying life with chronic obstructive pulmonary disease. 3rd ed. Cedar Grove, NJ: Laennec Pub., Inc., 1995.

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1950-, Bach John R., ed. Pulmonary rehabilitation: The obstructive and paralytic conditions. Philadelphia: Hanley & Belfus, 1996.

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1946-, Barnes Peter J., ed. An atlas of chronic obstructive pulmonary disease, COPD. Boca Raton, [Fla.]: Parthenon Pub. Group, 2004.

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ABC of COPD. 2nd ed. Chichester, West Sussex, UK: Wiley-Blackwell, BMJ Books, 2011.

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P, Currie Graeme, ed. ABC of COPD. Malden, Mass: BMJ Books, Blackwell Pub., 2007.

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Book chapters on the topic "Lungs Diseases, Obstructive Australia"

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Blair, Janis E. "Histoplasma capsulatum." In Mayo Clinic Infectious Diseases Board Review, 157–63. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199827626.003.0015.

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Histoplasmosis is caused by Histoplasma capsulatum, one of the most common opportunistic infections in persons with AIDS. Varieties include Histoplasma capsulatum var capsulatum and Histoplasma capsulatum var duboisii (Histoplasma duboisii). Histoplasma capsulatum var capsulatum causes histoplasmosis in the Americas, parts of Africa, eastern Asia, and Australia rarely, in Europe. Histoplasma capsulatum var duboisii (Histoplasma duboisii) causes African histoplasmosis, which occurs only in Africa between the Tropic of Cancer and the Tropic of Capricorn and on the island of Madagascar. It manifests as a subacute granuloma of the skin or bone but may disseminate to the skin, lymph nodes, bones, joints, lungs, and abdomen.
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Nevzorova, Vera, Tatiana Brodskaya, and Eugeny Gilifanov. "Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms." In Update in Respiratory Diseases. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.85927.

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This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.
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Picchio, Vittorio, Vittoria Cammisotto, Francesca Pagano, Roberto Carnevale, and Isotta Chimenti. "Innovative In Vitro Models for the Study of Lung Diseases." In Cell Interaction - Regulation of Immune Responses, Disease Development and Management Strategies [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.95300.

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Basic and translational research on lung biology and pathology can greatly benefit from the development of 3D in vitro models with physiological relevance. Lung organoids and lungs-on-chip allow the creation of different kinds of in vitro microenvironments, that can be useful for the elucidation of novel pathogenetic pathways, for example concerning tissue fibrosis in chronic diseases. Moreover, they represent important translational models for the identification of novel therapeutic targets, and for preliminary testing of new drugs. In this chapter, we provide a selected overview of recent studies on innovative 3D in vitro models that have enhanced our knowledge on chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), particularly concerning oxidative stress and pro-fibrotic pathogenetic mechanisms. Despite several limitations, these complex models must be considered as complementary in all respects to in vivo studies on animal models and clinical research.
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Gupta, Tanvi, and Supriya P. P. "Smart Prediction of Pulmonary Diseases Using Artificial Intelligence and Deep Learning." In Smart Healthcare for Sustainable Urban Development, 65–79. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-2508-4.ch005.

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As a result of global urbanization and the drive for more sustainable and livable cities, smart cities are becoming increasingly significant. It is widely known that air pollution exists all around us as a result of numerous automobiles on the road, stubble burning, and industrial air pollution, all of which impair our health, particularly our lungs. Chronic diseases are growing more common as our society ages. Chronic respiratory problems such as asthma and chronic obstructive pulmonary disease (COPD) impact millions of people globally, and the number is growing every day. COPD, for example, afflicted roughly 251 million individuals worldwide in 2016, and claimed the lives of 3.17 million people (i.e., 5% of the population). There are many distinct sorts of the pulmonary diseases: COPD, pulmonary fibrosis, asthma, and lung cancer, to name a few. This chapter explains the three machine learning algorithms that helped to diagnose pulmonary diseases based on the dataset.
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Sato, Takashi, and Takeshi Shimosato. "Intratracheally Therapeutic Option for COPD: A Potential Usage of the Therapeutic Microbe for Delivering Specific Protein to the Lungs." In Chronic Obstructive Pulmonary Disease - A Compendium of Medicine and the Humanities [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106491.

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Currently, inhaled therapy using corticosteroids and/or bronchodilators is the major established treatment for chronic obstructive pulmonary disease (COPD). The topic to be covered in this chapter is the recently developed experimental approach using biologically active molecules secreted by the live genetically modified lactic acid bacteria (gmLAB). The strategy to use gmLAB as a therapeutic/delivering tool targeting disease-specific active molecules/cites is proceeding. The role of inflammation and oxidative stress in COPD development is a valid target point. Heme oxygenase (HO)-1 as an anti-inflammatory and antioxidative stress molecule has been examined to attenuate the lung function decline and inflammation in the murine model of COPD. Recently, HO-1-secreting gmLAB as a tool for targeting inflammatory diseases has been developed and examined in several disease models including COPD. When administered intratracheally, the gmLAB showed migration to the peripheral lung and overexpression of anti-inflammatory/oxidative HO-1 in both lung and serum, protecting the lung from COPD development.
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Wray, Jo. "The Impact of Congenital Heart Disease on Cognitive and Behavioral Functioning." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0011.

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Congenital heart disease (CHD) has been defined as “. . . a gross structural abnormality of the heart or intrathoracic great vessels that is actually or potentially of functional significance” (Mitchell, Korones, and Berendes 1971). Congenital heart disease is the most common single group of congenital abnormalities, accounting for about 30% of the total. The incidence is reported as varying between 0.3% and 1% of all live births. Ten to 15% of children with congenital heart defects have more than one cardiac abnormality; up to one-third also have one or more associated noncardiac congenital abnormalities (Wernovsky 2006). Although some forms of CHD are minor and do not require any medical or surgical intervention, others are very complex and may necessitate a series of staged surgical procedures and/or require life-long medications. Significant improvements in medical and surgical techniques have resulted in increasing numbers of children and adults living with CHD, and it is currently anticipated that 80%–85% of children born with CHD today will survive into adulthood (British Cardiac Society 2002). However, although survival rates have improved dramatically over the last 40 years or so, morbidity remains a concern. Congenital heart defects can be broadly subdivided into two groups, based on changes in the circulation. Acyanotic defects may be due to either a left-to-right shunt or to an obstructive lesion; there is no mixing of desaturated blood in the systemic arterial circulation. With cyanotic defects, there may be either increased or diminished pulmonary flow, and desaturated blood enters the systemic arterial circulation, regardless of whether cyanosis is clinically evident. Unsaturated venous blood bypassing the lungs can result in secondary polycythemia, which is a compensatory mechanism to carry more oxygen to the tissues. This causes increased viscosity, which in turn results in sluggish blood circulation and impeded blood flow, particularly in the capillaries. Poor peripheral blood flow and clubbing of the fingers and toes can result, breathlessness and fatigue often result in a reduced exercise tolerance, and growth may be affected.
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Sinharay, Rudy. "Chest Medicine." In Oxford Assess and Progress: Clinical Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198812968.003.0009.

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Respiratory conditions are common, and the burden of morbidity on the general population is high. You only have to take part in a few general medical takes as a junior doctor to realize this. As the on- call bleep goes off again, you are referred another exacerbation of chronic obstructive pulmonary disease (COPD) or asthma, a breathless patient (is it a pul­monary embolism, pneumothorax, or something less common?), or a patient with haemoptysis and weight loss [is it lung cancer or tuberculosis (TB)?] or productive cough (pneumonia or bronchiectasis?). The number of different respiratory conditions can be bewildering, and it is essential for the developing physician to be able to manage ‘common presenta­tions’, as well as potentially life- threatening situations such as an asthma attack or an acute pulmonary embolism. The nuances of history taking is often key to successfully clinching a diagnosis: ● What chronic conditions, respiratory or otherwise, do your patients have? ● What is the onset of symptoms? Sudden breathlessness may indicate a pneumothorax or pulmonary embolus. A chronic productive cough may indicate COPD or bronchiectasis. ● Social history— do they smoke, what are their living conditions, what is their occupation? Luckily, we have other tools to help us. The age- old art of inspec­tion, palpation, percussion, and auscultation during an examination is essential when assessing the patient. Combined with imaging techniques, including chest radiography, CT scanning, and bedside thoracic ultra­sound, the answer is often easily obtained. Keeping an open mind to the less common causes of breathlessness, cough, and haemoptysis is important. Combined with lung function testing, autoimmune blood tests, and bronchoscopy, subtler diagnoses such as interstitial lung dis­ease, fungal lung disease, and autoantibody- induced haemoptysis may be revealed. And a word to the wise— not all breathlessness originates from the lungs! For instance, an increased body mass index will cause a physical restriction on the mechanics of breathing and a compensated metabolic acidosis may cause tachypnoea. As with all chronic diseases, the management of chronic respira­tory disease is becoming increasingly complicated with the advent of biologics, immunotherapy, antifibrotic therapy, and a genuinely confusing array of inhalers.
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Conference papers on the topic "Lungs Diseases, Obstructive Australia"

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Korosec, Peter, Katarina Osolnik, Darja Polak, Mateja Marc Malovrh, and Sabina Skrgat. "Cytokine profiles in the lungs of patients with interstitial and obstructive lung diseases." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa959.

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Garg, Ishita, Ronald A. Karwoski, Jon J. Camp, Brian J. Bartholmai, and Richard A. Robb. "Automated segmentation of the lungs from high resolution CT images for quantitative study of chronic obstructive pulmonary diseases." In Medical Imaging, edited by Robert L. Galloway, Jr. and Kevin R. Cleary. SPIE, 2005. http://dx.doi.org/10.1117/12.595827.

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Bian, Shiyao, Ying Zheng, Shuichi Takayama, and James B. Grotberg. "Micro-PIV Measurements of an Airway Closure Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206831.

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A thin liquid layer coating the airway can be unstable and forms a plug. Airway closure usually happens at the small airways near the end of expiration, often accompanied with hypersecretion or/and surfactant deficiency in the airway in a variety of lung diseases, such as chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS). Modeling work by Halpern and Grotberg [1] has shown that several forces could contribute to airway closure, such as the surface tension instability and the wall compliance. Experiments in a capillary tube were conducted by Cassidy et al. [2] who found that adding surfactant increased the airway closure time and the critical film thickness. In vitro studies [3] [4] illustrated that exposure of primary human airway epithelial cells to plug propagation and rupture led to significant cell injury. Experimental studies [5] [6] on excised lungs or in vivo animal models have shown that severe tissue damage was found in surfactant-deficient lungs due to the repetitive airway reopening. However, mechanical forces induced by airway closure have not been experimentally evaluated.
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Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
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