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Journal articles on the topic 'Lung function'

To see the other types of publications on this topic, follow the link: Lung function.

Author: Grafiati

Published: 4 June 2021

Last updated: 14 March 2023

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1

Meenakshi, Dr S. "Determination of Unilateral Lung Function by Spirometry." Journal of Medical Science And clinical Research 05, no. 03 (March 8, 2017): 18578–5582. http://dx.doi.org/10.18535/jmscr/v5i3.52.

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2

Turner, C. J., S. M. Kennedy, S. F. Buechte, P. Morfeld, H. J. Bicker, H. Lenaerts, B. Kalkowsky, et al. "Lung function." Occupational and Environmental Medicine 64, no. 12 (November 16, 2007): e23-e23. http://dx.doi.org/10.1136/oem.64.12.e23.

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3

Becker, Ellen A., and Mary Kay Bossard. "Lung Function." Journal of Asthma & Allergy Educators 4, no. 6 (November 18, 2013): 327–28. http://dx.doi.org/10.1177/2150129713510864.

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4

Young, R., and R. Hopkins. "Lung function predicts lung cancer." European Respiratory Journal 35, no. 6 (May 31, 2010): 1421–22. http://dx.doi.org/10.1183/09031936.00009410.

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5

Harris, R. Scott, and Daniel P. Schuster. "Visualizing lung function with positron emission tomography." Journal of Applied Physiology 102, no. 1 (January 2007): 448–58. http://dx.doi.org/10.1152/japplphysiol.00763.2006.

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Positron emission tomography (PET) provides three-dimensional images of the distributions of radionuclides that have been inhaled or injected into the lungs. By using radionuclides with short half-lives, the radiation exposure of the subject can be kept small. By following the evolution of the distributions of radionuclides in gases or compounds that participate in lung function, information about such diverse lung functions as regional ventilation, perfusion, shunt, gas fraction, capillary permeability, inflammation, and gene expression can be inferred. Thus PET has the potential to provide information about the links between cellular function and whole lung function in vivo. In this paper, recent advancements in PET methodology and techniques and information about lung function that have been obtained with these techniques are reviewed.

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6

Dinwiddie, R. "Lung function in paediatrics. Lung function testing in children." Allergologia et Immunopathologia 38, no. 2 (March 2010): 88–91. http://dx.doi.org/10.1016/j.aller.2009.11.003.

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7

Abratt, RP, PA Willcox, and JA Smith. "Lung function after irradiation in patients with lung cancer and borderline lung functions." Lung Cancer 7 (January 1991): 87. http://dx.doi.org/10.1016/0169-5002(91)91668-2.

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8

Abratt, RP, PA Willcox, and JA Smith. "Lung function after irradiation in patients with lung cancer and borderline lung functions." Lung Cancer 7 (January 1991): 88. http://dx.doi.org/10.1016/0169-5002(91)91670-7.

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9

Helms, P. "Lung function testing." Current Paediatrics 3, no. 2 (June 1993): 92–95. http://dx.doi.org/10.1016/s0957-5839(05)80051-x.

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10

Connolly, C. K. "Lung function testing." Respiratory Medicine 88, no. 10 (November 1994): 795–96. http://dx.doi.org/10.1016/s0954-6111(05)80207-0.

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11

Kodal, Jakob B., Camilla J. Kobylecki, Signe Vedel-Krogh, Børge G. Nordestgaard, and Stig E. Bojesen. "AHRR hypomethylation, lung function, lung function decline and respiratory symptoms." European Respiratory Journal 51, no. 3 (January 18, 2018): 1701512. http://dx.doi.org/10.1183/13993003.01512-2017.

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Epigenome-wide association studies have shown a consistent association between smoking exposure and hypomethylation in the aryl hydrocarbon receptor repressor (AHRR) gene (cg05575921). We tested the hypothesis that AHRR hypomethylation is associated with low lung function, steeper lung function decline, and respiratory symptoms in the general population.AHRR methylation extent was measured in 9113 individuals from the 1991–1994 examination of the Copenhagen City Heart Study, using bisulfite-treated leukocyte DNA. Spirometry at the time of blood sampling was available for all individuals. Lung function was measured again for 4532 of these individuals in 2001–2003.Cross-sectionally, a 10% lower methylation extent was associated with a 0.2 z-score (95% CI 0.1–0.2) lower forced expiratory volume in 1 s (FEV1) after multivariable adjustment including smoking. Hypomethylation was also associated with a lower z-score for both forced vital capacity (FVC) and FEV1/FVC. In prospective analyses, individuals in the lowest versus highest tertile of methylation extent had a steeper decline in FEV1/height3 (p for examination×methylation interaction=0.003) and FVC/height3 (p=0.01), but not FEV1/FVC (p=0.08). Multivariable-adjusted odds ratios per 10% lower methylation extent were 1.31 (95% CI 1.18–1.45) for chronic bronchitis and 1.21 (95% CI 1.13–1.30) for any respiratory symptoms.AHRR hypomethylation was associated with low lung function, steeper lung function decline, and respiratory symptoms.

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12

Stanojevic, Sanja. "Standardisation of lung function test interpretation: Global Lung Function Initiative." Lancet Respiratory Medicine 6, no. 1 (January 2018): 10–12. http://dx.doi.org/10.1016/s2213-2600(17)30472-1.

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13

Koul, Parvaiz A. "Smoking and Lung Function: Taxing the lungs." JMS SKIMS 12, no. 2 (December 13, 2009): 34–36. http://dx.doi.org/10.33883/jms.v12i2.12.

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The cigarette / bidi smoke is a heterogeneous aerosol produced by the incomplete combustion of the tobacco leaf. Smoking is the primary causal factor for at least 30% of all cancer deaths, nearly 80% of deaths from chronic obstructive pulmonary disease (COPD), and for early cardiovascular disease and deaths.6 COPD is an important cause of morbidity and mortality being listed currently as the fourth leading cause of death worldwide, and estimated to register an even further increase by 2020. India is one of the countries identified to have a significant increase in the burden of tobacco related mortality. J Med Sci.2009;12(2):34-36

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14

Massaro, Donald, and Gloria DeCarlo Massaro. "Lung Development, Lung Function, and Retinoids." New England Journal of Medicine 362, no. 19 (May 13, 2010): 1829–31. http://dx.doi.org/10.1056/nejme1002366.

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15

Hachida, Mitsuhiro, and Donald L. Morton. "Lung function after prolonged lung preservation." Journal of Thoracic and Cardiovascular Surgery 97, no. 6 (June 1989): 911–19. http://dx.doi.org/10.1016/s0022-5223(19)34495-2.

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16

Singh, Suchita, Manish Bodas, Naveen K. Bhatraju, Bijay Pattnaik, Atish Gheware, Praveen Kolumam Parameswaran, Michael Thompson, et al. "Hyperinsulinemia adversely affects lung structure and function." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 9 (May 1, 2016): L837—L845. http://dx.doi.org/10.1152/ajplung.00091.2015.

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There is limited knowledge regarding the consequences of hyperinsulinemia on the lung. Given the increasing prevalence of obesity, insulin resistance, and epidemiological associations with asthma, this is a critical lacuna, more so with inhaled insulin on the horizon. Here, we demonstrate that insulin can adversely affect respiratory health. Insulin treatment (1 μg/ml) significantly ( P < 0.05) increased the proliferation of primary human airway smooth muscle (ASM) cells and induced collagen release. Additionally, ASM cells showed a significant increase in calcium response and mitochondrial respiration upon insulin exposure. Mice administered intranasal insulin showed increased collagen deposition in the lungs as well as a significant increase in airway hyperresponsiveness. PI3K/Akt mediated activation of β-catenin, a positive regulator of epithelial-mesenchymal transition and fibrosis, was observed in the lungs of insulin-treated mice and lung cells. Our data suggests that hyperinsulinemia may have adverse effects on airway structure and function. Insulin-induced activation of β-catenin in lung tissue and the contractile effects on ASM cells may be causally related to the development of asthma-like phenotype.

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17

Sharma, Pawan, Javad Alizadeh, Maya Juarez, Afshin Samali, Andrew J. Halayko, Nicholas J. Kenyon, Saeid Ghavami, and Amir A. Zeki. "Autophagy, Apoptosis, the Unfolded Protein Response, and Lung Function in Idiopathic Pulmonary Fibrosis." Cells 10, no. 7 (June 30, 2021): 1642. http://dx.doi.org/10.3390/cells10071642.

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Autophagy, apoptosis, and the unfolded protein response (UPR) are fundamental biological processes essential for manifold cellular functions in health and disease. Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal pulmonary disorder associated with aging that has limited therapies, reflecting our incomplete understanding. We conducted an observational study linking molecular markers of cell stress response pathways (UPR: BiP, XBP1; apoptosis: cleaved caspase-3; autophagy: LC3β) in lung tissues from IPF patients and correlated the expression of these protein markers to each subject’s lung function measures. We hypothesized that changes in lung tissue expression of apoptosis, autophagy, and UPR markers correlate with lung function deficits in IPF. The cell stress markers BiP, XBP1, LC3β puncta, and cleaved caspase-3 were found to be elevated in IPF lungs compared to non-IPF lungs, and, further, BiP and cleaved caspase-3 co-localized in IPF lungs. Considering lung function independently, we observed that increased XBP1, BiP, and cleaved caspase-3 were each associated with reduced lung function (FEV1, FVC, TLC, RV). However, increased lung tissue expression of LC3β puncta was significantly associated with increased diffusion capacity (DLCO), an indicator of alveolar–capillary membrane function. Similarly, the co-localization of UPR (XBP1, BiP) and autophagy (LC3β puncta) markers was positively correlated with increased lung function (FEV1, FVC, TLC, DLCO). However, the presence of LC3β puncta can indicate either autophagy flux inhibition or activation. While the nature of our observational cross-sectional study design does not allow conclusions regarding causal links between increased expression of these cell stress markers, lung fibrosis, and lung function decline, it does provide some insights that are hypothesis-generating and suggests that within the milieu of active UPR, changes in autophagy flux may play an important role in determining lung function. Further research is necessary to investigate the mechanisms linking UPR and autophagy in IPF and how an imbalance in these cell stress pathways can lead to progressive fibrosis and loss of lung function. We conclude by presenting five testable hypotheses that build on the research presented here. Such an understanding could eventually lead to the development of much-needed therapies for IPF.

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18

Wilson, Douglas MC. "Number 3: Chronic Obstructive Pulmonary Disease -- Stopping Smoking: It is Never Too Late." Canadian Respiratory Journal 7, no. 3 (2000): 227–28. http://dx.doi.org/10.1155/2000/279216.

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Smoking is the main cause of chronic obstructive pulmonary disease, and the function of the lungs in smokers deteriorates with time at a much faster rate than in nonsmokers or ex-smokers. Smokers with chronic lung disease can often function better, breathe more easily and cough less, just by stopping smoking. They require less medication (puffers, etc) and the deterioration of lung function is slowed. Within 24 h, the amount of carbon monoxide in the lungs and blood returns to normal, allowing more oxygen to supply body functions.

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19

Kaur, Ankit, Rohit Subhedar, Pallavi Dave, Priyanka Mishra, and Dirgha Sharma. "PHYSIOTHERAPEUTIC STUDY ANALYZING THE RELATIONSHIP BETWEEN BODY COMPOSITION AND LUNG FUNCTION." International Journal of Physiotherapy and Research 3, no. 5 (October 11, 2015): 1233–38. http://dx.doi.org/10.16965/ijpr.2015.182.

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20

Savita, D., and V. Raji Sugumar. "Correlation of Outdoor Games and Lung Function of School Going Children." International Journal of Trend in Scientific Research and Development Volume-1, Issue-5 (August 31, 2017): 950–54. http://dx.doi.org/10.31142/ijtsrd2391.

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21

Isogami, Katsuhiko, Kaoru Koike, Tatsuo Tanita, Genichi Nasu, Masayuki Chida, Satoshi Suzuki, Yugo Ashino, Hiroshi Kubo, Tasuku Nakada, and Shigefumi Fujimura. "Lung function in operated lung after lobectomy." Journal of the Japanese Association for Chest Surgery 5, no. 6 (1991): 619–22. http://dx.doi.org/10.2995/jacsurg1987.5.619.

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22

Portas, Laura, Miguel Pereira, Seif O. Shaheen, Annah B. Wyss, Stephanie J. London, Peter G. J. Burney, Matthew Hind, Charlotte H. Dean, and Cosetta Minelli. "Lung Development Genes and Adult Lung Function." American Journal of Respiratory and Critical Care Medicine 202, no. 6 (September 15, 2020): 853–65. http://dx.doi.org/10.1164/rccm.201912-2338oc.

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23

Diaz-Guzman, Enrique, Daniel L. Davenport, Joseph B. Zwischenberger, and Charles W. Hoopes. "Lung Function and ECMO After Lung Transplantation." Annals of Thoracic Surgery 94, no. 2 (August 2012): 686–87. http://dx.doi.org/10.1016/j.athoracsur.2011.12.014.

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24

Anis, Mursalin M., Scott A. Fulton, Scott M. Reba, Yi Liu, Clifford V. Harding, and W. Henry Boom. "Modulation of Pulmonary Dendritic Cell Function during Mycobacterial Infection." Infection and Immunity 76, no. 2 (November 26, 2007): 671–77. http://dx.doi.org/10.1128/iai.01079-07.

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ABSTRACT We have previously reported that during mycobacterial infection, naïve CD4+ T-cell activation is enhanced in the lungs. We investigated the role of chemokine receptor CCR7 and its ligands in the ability of CD11c+ lung dendritic cells (DCs) to activate naïve CD4+ T cells during pulmonary infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG). BCG infection resulted in the accumulation and maturation in the lungs of DCs that persisted as the mycobacterial burden declined. Lung DCs from infected mice expressed more major histocompatibility complex class II (MHC-II) than those from uninfected mice. CCR7 expression levels on lung DCs were comparable among uninfected and infected mice. The gene expression of the CCR7 ligand CCL19 progressively increased throughout BCG infection, and its expression was MyD88 dependent. CD11c+ lung cells from BCG-infected mice activated ovalbumin (OVA)-specific naïve CD4+ T cells more than CD11c+ lung cells from uninfected mice. Interestingly, during peak mycobacterial infection, CD11chi MHChi lung DCs had slightly decreased chemotaxis toward the CCR7 ligand CCL21 and less efficiency in activating naive CD4+ T cells than DCs from mice during late-stage infection, when few bacilli are found in the lung. These findings suggest that during BCG infection, the inflammation and sustained expression of CCL19 result in the recruitment, activation, and retention in the lung of DCs that can activate naïve CD4+ T cells in situ.

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25

Miller, MR, and OF Pedersen. "Respiratory function in an ageing population." Reviews in Clinical Gerontology 19, no. 3 (August 2009): 149–58. http://dx.doi.org/10.1017/s0959259809990293.

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SummaryWith more elderly people in the population there are more people surviving with lung diseases that need assessing so that the best treatment options can be chosen and delivered. Lung function is known to deteriorate with age and this is largely due to a reduction in muscle strength, an increased alveolar size leading to reduced elastic recoil, and a reduction in chest wall compliance. The processes involved are outlined together with the effects this has on normal lung function. Tests of lung function are commonly used to determine whether an individual patient's lungs are working abnormally, and using a lower limit of normal is the best method to use. The problems and solutions for defining the lower limit of normal for older subjects are discussed. If a subject's lung function is deemed abnormal from comparing their tests against a predicted value, then assessing how severe this abnormality is can be determined by using the results as per cent of predicted, or better still by relating the value to a minimum survivable limit.

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26

Bates, Jason H. T. "CORP: Measurement of lung function in small animals." Journal of Applied Physiology 123, no. 5 (November 1, 2017): 1039–46. http://dx.doi.org/10.1152/japplphysiol.00243.2017.

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The measurement of lung function in mice and rats is crucial for understanding how well small animal models of pulmonary disease recapitulate human clinical pathology but brings with it the challenge of making accurate measurements in animals as small as a mouse. Overcoming these challenges can be achieved in a number of ways, each based on a model idealization of how the lung works as a mechanical system. Accordingly, it is important to understand the theoretical basis on which an assessment of lung function rests to interpret experimental measurements appropriately. It is also crucial to attend to a number of practical issues that determine the quality of the measurements. The most accurate measurements of lung function in small animals are provided by the forced oscillation technique that provides lung resistance and elastance and its multifrequency generalization known as impedance. Measurement quality is maximized when the greatest possible degree of control is exerted over the amplitude and frequency with which air is oscillated in and out of the lungs, the mean or end-expiratory transpulmonary pressure pertaining to when the oscillations are applied, and the immediate past volume history of the lungs. It is also crucial that no spontaneous breathing efforts occur during the measurement period. Finally, there is no substitute for the skill in animal handling and surgical preparation that comes with practice; such a skill should be in place before embarking on any important series of experiments.

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27

K.L, Shobha, Subbramaniam Venkatachalam, Ashriina Nair, Buwanesswaran Elangu, Periyaiyadever Samuganathan,, Barathi Subramanian, Amita Shobha Rao, and Ramachandra L. "Study of lung function on construction workers." International Journal of Health 5, no. 1 (May 30, 2017): 97. http://dx.doi.org/10.14419/ijh.v5i1.7655.

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Lungs are one of the most vital organs which are responsible for gas exchange during respiration .Lung functions can be compromised in working environment especially at building construction work. The aim of the study was to assess the lung functions of the construction workers.Material and Methods: Adult volunteers who had given consent with a field work experience of minimum 2 years were involved in the study. Validated questionnaire was given to them and the responses were collected .Peak flow meter measurement were also analysed.Results: (65.30%) smokers had a peak flow meter reading of less than 400L and plumbers were the group affected by decreased pulmonary function test followed by mason-helpers.Conclusion: Morbidity among the construction workers varied with type of work at the construction site and comorbid factors such as smoking.

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28

AHMAD, D., and W. K. C. MORGAN. "Obesity and lung function." Thorax 56, no. 9 (September 1, 2001): 740.4–741. http://dx.doi.org/10.1136/thx.56.9.740-c.

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29

&NA;. "Lung Function After Lobectomy." Survey of Anesthesiology 53, no. 1 (February 2009): 38–39. http://dx.doi.org/10.1097/sa.0000318700.80604.41.

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30

MURTY, G. E., P. J. KELLY, and D. VEALE. "Tussometry and lung function." Clinical Otolaryngology 19, no. 2 (April 1994): 117–19. http://dx.doi.org/10.1111/j.1365-2273.1994.tb01193.x.

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31

Behr, Jürgen. "Optimizing preoperative lung function." Current Opinion in Anaesthesiology 14, no. 1 (February 2001): 65–69. http://dx.doi.org/10.1097/00001503-200102000-00011.

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32

Neukirch, Françoise, Renata Liard, and René Chansin. "Lung Function in Polynesians." American Review of Respiratory Disease 137, no. 6 (June 1988): 1511. http://dx.doi.org/10.1164/ajrccm/137.6.1511.

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33

Levin-Epstein, Michael. "Replacing the Lung Function." Journal of Clinical Engineering 42, no. 3 (2017): 100. http://dx.doi.org/10.1097/jce.0000000000000221.

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34

HUGHES, D. M., H. NEWTON-JOHN, O. M. CHAY, and L. I. LANDAU. "Lung function after pertussis." Journal of Paediatrics and Child Health 23, no. 5 (October 1987): 277–82. http://dx.doi.org/10.1111/j.1440-1754.1987.tb00271.x.

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35

Wheatley, Courtney M., Caitlin C. Fermoyle, Glenn M. Stewart, Bryan J. Taylor, Loic Chabridon, Alice Gavet, Briana L. Ziegler, Jesse C. Schwartz, Paul Robach, and Bruce D. Johnson. "Lung Function - Ultraendurance Marathon." Medicine & Science in Sports & Exercise 51, Supplement (June 2019): 628–29. http://dx.doi.org/10.1249/01.mss.0000562381.31349.f8.

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36

Booker, Rachel. "CLINIC Lung function testing." Practice Nursing 14, no. 3 (March 2003): 127–30. http://dx.doi.org/10.12968/pnur.2003.14.3.11137.

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37

Booker, Rachel. "CLINIC Lung Function Testing." Practice Nursing 14, no. 4 (April 2003): 175–77. http://dx.doi.org/10.12968/pnur.2003.14.4.13284.

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38

Booker, Rachel. "CLINIC Lung function testing." Practice Nursing 14, no. 5 (May 2003): 215–20. http://dx.doi.org/10.12968/pnur.2003.14.5.11371.

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39

FOWLER, R. W. "AGEING AND LUNG FUNCTION." Age and Ageing 14, no. 4 (1985): 209–15. http://dx.doi.org/10.1093/ageing/14.4.209.

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40

Koegelenberg, Coenraad F. N., and Chris T. Bolliger. "Assessing Regional Lung Function." Thoracic Surgery Clinics 18, no. 1 (February 2008): 19–29. http://dx.doi.org/10.1016/j.thorsurg.2007.10.001.

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41

Williams, A. J. "Standardised lung function testing." Thorax 40, no. 6 (June 1, 1985): 479–80. http://dx.doi.org/10.1136/thx.40.6.479-b.

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42

Ahmad, Nawaid, Koottalai Srinivasan, and Harmesh Moudgil. "Diabetes and Lung Function." Chest 139, no. 1 (January 2011): 235–36. http://dx.doi.org/10.1378/chest.10-2095.

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43

Milner, A. D. "Series: Lung Function Testing." Paediatric Respiratory Reviews 1, no. 2 (June 2000): 135–40. http://dx.doi.org/10.1053/prrv.2000.0039.

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44

Rosenthal, M. "Lung function in adolescence." Current Paediatrics 6, no. 2 (June 1996): 84–87. http://dx.doi.org/10.1016/s0957-5839(96)80067-4.

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45

Sánchez-Solís, M., and L. García Marcos. "Lung function in infants." Paediatric Respiratory Reviews 14 (July 2013): S45—S49. http://dx.doi.org/10.1016/s1526-0542(13)70042-3.

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46

Miller, Martin R. "Lung Function Data Interpretation." Chest 141, no. 3 (March 2012): 832–33. http://dx.doi.org/10.1378/chest.11-2718.

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47

AHMAD, D. "Obesity and lung function." Thorax 56, no. 9 (September 1, 2001): 740c—741. http://dx.doi.org/10.1136/thorax.56.9.740c.

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48

Voelker, R. "Oxidants Impair Lung Function." JAMA: The Journal of the American Medical Association 279, no. 4 (January 28, 1998): 262—d—262. http://dx.doi.org/10.1001/jama.279.4.262-d.

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49

Voelker, Rebecca. "Oxidants Impair Lung Function." JAMA 279, no. 4 (January 28, 1998): 262. http://dx.doi.org/10.1001/jama.279.4.262-jqu71030-5-1.

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50

Wiles, F. J., E. Baskind, P. A. Hessel, B. Bezuidenhout, and E. Hnizdo. "Lung function in silicosis." International Archives of Occupational and Environmental Health 63, no. 6 (February 1992): 387–91. http://dx.doi.org/10.1007/bf00386933.

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