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      Proteoglycan 4 is a diagnostic biomarker for COPD

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          Abstract

          Introduction

          The measurement of C-reactive protein (CRP) to confirm the stability of COPD has been reported. However, CRP is a systemic inflammatory biomarker that is related to many other diseases.

          Objective

          The objective of this study is to discover a diagnostic biomarker for COPD.

          Methods

          Sixty-one subjects with COPD and 15 healthy controls (10 healthy non-smokers and 5 smokers) were recruited for a 1-year follow-up study. Data regarding the 1-year acute exacerbation frequency and changes in lung function were collected. CRP and the identified biomarkers were assessed in the validation COPD cohort patients and healthy subjects. Receiver operating characteristic values of CRP and the identified biomarkers were determined. A validation COPD cohort was used to reexamine the identified biomarker. Correlation of the biomarker with 1-year lung function decline was determined.

          Results

          Proteoglycan 4 (PRG4) was identified as a biomarker in COPD. The serum concentrations of PRG4 in COPD Global initiative for chronic Obstructive Lung Disease (GOLD) stages 1+2 and 3+4 were 10.29 ng/mL and 13.20 ng/mL, respectively; 4.99 ng/mL for healthy controls ( P<0.05); and 4.49 ng/mL for healthy smokers ( P<0.05). PRG4 was more sensitive and specific than CRP for confirming COPD severity and acute exacerbation frequency. There was no correlation between CRP and PRG4 levels, and PRG4 was negatively correlated with the 1-year change in predicted forced vital capacity percent ( R 2=0.91, P=0.013).

          Conclusion

          PRG4 may be a biomarker for identification of severity in COPD. It was related to the 1-year forced vital capacity decline in COPD patients.

          Related collections

          Most cited references 19

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          New consensus nomenclature for mammalian keratins

          Keratins are intermediate filament–forming proteins that provide mechanical support and fulfill a variety of additional functions in epithelial cells. In 1982, a nomenclature was devised to name the keratin proteins that were known at that point. The systematic sequencing of the human genome in recent years uncovered the existence of several novel keratin genes and their encoded proteins. Their naming could not be adequately handled in the context of the original system. We propose a new consensus nomenclature for keratin genes and proteins that relies upon and extends the 1982 system and adheres to the guidelines issued by the Human and Mouse Genome Nomenclature Committees. This revised nomenclature accommodates functional genes and pseudogenes, and although designed specifically for the full complement of human keratins, it offers the flexibility needed to incorporate additional keratins from other mammalian species.
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            The consequences of sample pooling in proteomics: an empirical study.

            Pooling of samples in proteomics experiments might help overcome resource constraints when many individuals are analysed. The measured biological variation should be reduced giving increased power to detect treatment differences. Pooling has been advocated in microarray work but there are few tests of its potential in proteomics. In this study, we examine three issues on which the success of the pooling approach might hinge and provide evidence that: (i) the protein expression in a pool matches the mean expression of the individuals making up the pool for the majority of proteins, although for some proteins the pool expression is different; (ii) the biological variance between pools is reduced compared with that between individuals, as predicted in theory, but this reduction is not as large as expected. A practical consequence of this is that power could be reduced; (iii) proteins detectable in individual samples are usually but not always visible when samples are pooled. We conclude that pooling of samples in proteomics work is a valid and potentially valuable procedure but consideration should be given to these issues in experimental design.
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              C-reactive protein and lung diseases.

              C-reactive protein (CRP), a member of the pentraxin family of plasma proteins, is one of the most distinctive acute phase reactants. In response to inflammation, cell damage or tissue injury, plasma level of CRP rapidly and dramatically increases up to 1000-fold, a phenomenon that has been used for years to monitor infections and many destructive/inflammatory conditions. The magnitude of CRP increase usually correlates with the severity of injury or inflammation and reflects an important physiological role of this interesting but still under-investigated protein. It is now generally accepted that CRP is involved in host defense and inflammation. However, the exact function of this protein in health and disease remains unclear. Many studies have demonstrated that in different pathophysiological conditions CRP might be involved in the regulation of lung function and may participate in the pathogenesis of various pulmonary disorders. The fluctuation of CRP concentrations in both alveolar fluid and serum associated with different pulmonary diseases suggests its important role in lung biology. Discussion of the still controversial functions of CRP in lung physiology and diseases is the main focus of this review. Copyright © 2014 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                18 September 2015
                : 10
                : 1999-2007
                Affiliations
                [1 ]Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan
                [2 ]Department of Internal Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan
                [3 ]School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
                [4 ]Division of Pulmonary Medicine, Department of Internal Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan
                Author notes
                Correspondence: Shu-Chuan Ho, School of Respiratory Therapy, College of Medicine, Taipei Medical University, 250 Wuxing Street, Taipei 110, Taiwan, Tel +886 2 2736 1661 ext 3512, Fax +886 2 2739 1143, Email shu-chuan@ 123456tmu.edu.tw
                Article
                copd-10-1999
                10.2147/COPD.S90926
                4583110
                © 2015 Lee et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Respiratory medicine

                c-reactive protein, exacerbation, inflammation, lung function decline

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