The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

COPD  -  Pulmonary disease, chronic obstructive,...

Homo sapiens

 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of COPD

  • Glucocorticoids are the most effective antiinflammatory agents for the treatment of chronic inflammatory diseases even though some diseases, such as chronic obstructive pulmonary disease (COPD), are relatively glucocorticoid insensitive [1].
  • Nontypeable Haemophilus influenzae (NTHi) is an important human pathogen that causes chronic otitis media with effusion (COME) in children and exacerbation of chronic obstructive pulmonary disease (COPD) in adults [2].
  • Mucin overproduction, a hallmark of both diseases, has been shown to directly cause conductive hearing loss in COME and airway obstruction in COPD [2].
  • CONCLUSION: Activation of the renin-angiotensin system is associated with the development of secondary erythrocytosis in chronically hypoxemic patients with COPD [3].
  • (3) Emphysema involves elastolytic destruction of the alveolar wall; its overall severity, rather than type, appears to be an important determinant of chronic irreversible deterioration of airflow in COPD [4].
 

Psychiatry related information on COPD

  • When subjects were divided according to their current smoking status, levels of sTNF-R55, sTNF-R75, and IL-8 in sputum were significantly elevated in ex-smoking versus currently smoking patients with COPD, suggesting ongoing inflammation in airways and circulation of patients with COPD after smoking cessation [5].
  • Psychometric properties of the RAND-36 among three chronic diseases (multiple sclerosis, rheumatic diseases and COPD) in The Netherlands [6].
  • Besides ineffective antibody-mediated defense mechanisms, it is likely that hiding of the bacteria in tissue contributes to the persistence of these bacteria in patients with COPD [7].
  • These findings do not support an association between regular marijuana smoking and chronic COPD but do not exclude the possibility of other adverse respiratory effects [8].
  • RESULTS: Compared with the controls, COPD affected functional status in most areas, not just those requiring physical activity [9].
 

High impact information on COPD

  • In patients with chronic obstructive pulmonary disease (COPD) and hyperinflation of the lungs, dysfunction of the diaphragm may contribute to respiratory decompensation [10].
  • We evaluated the contractile function of the diaphragm in well-nourished patients with stable COPD, using supramaximal, bilateral phrenic-nerve stimulation, which provides information about the strength and inspiratory action of the diaphragm [10].
  • COPD is associated with a chronic inflammatory response, predominantly in small airways and lung parenchyma, which is characterized by increased numbers of macrophages, neutrophils, and T lymphocytes [11].
  • In conclusion, we show that overexpression of HDAC2 in glucocorticoid-insensitive alveolar macrophages from patients with COPD is able to restore glucocorticoid sensitivity [1].
  • COPD AMs also showed increased basal release of IL-8 and TNF-alpha, which was poorly suppressed by dexamethasone [12].
 

Chemical compound and disease context of COPD

 

Biological context of COPD

 

Anatomical context of COPD

 

Associations of COPD with chemical compounds

 

Physical interactions of COPD

  • Cigarette smoke disrupts VEGF165-VEGFR-2 receptor signaling complex in rat lungs and patients with COPD: morphological impact of VEGFR-2 inhibition [24].
 

Regulatory relationships of COPD

 

Other interactions of COPD

  • METHODS: Two hundred four patients with COPD were studied retrospectively and 10 patients prospectively (8 starting treatment with the drug [group 1] and 2 who suspended its long-term use [group 2]) for the correlation between theophylline therapy and hematocrit and erythropoietin level [13].
  • LBP levels were increased in COPD patients as compared with controls (11.7 +/- 4.5 versus 8.6 +/- 1.0 mg/L, p < 0.05), and showed a positive correlation with REE (r = 0. 49, p = 0.03), a negative correlation with the SumAA in plasma (r = -0.76, p < 0.0001), and no correlation with muscle AA levels [30].
  • In patients with CB or COPD neutrophils were not increased in the mucosa, but neutrophil numbers and myeloperoxidase levels in BALF were significantly increased [18].
  • We have applied immunohistology and in situ hybridization to bronchial biopsies of patients with chronic obstructive pulmonary disease (COPD) to examine neutrophil recruitment and to determine neutrophil chemoattractant and CXC receptor (CXCR) 1 and CXCR2 gene expression associated with acute severe exacerbations [31].
  • Some clinical aspects of COPD occur similarly in cystic fibrosis (CF), particularly in adult patients [32].
 

Analytical, diagnostic and therapeutic context of COPD

References

  1. Histone deacetylase 2-mediated deacetylation of the glucocorticoid receptor enables NF-kappaB suppression. Ito, K., Yamamura, S., Essilfie-Quaye, S., Cosio, B., Ito, M., Barnes, P.J., Adcock, I.M. J. Exp. Med. (2006) [Pubmed]
  2. Novel cytoplasmic proteins of nontypeable Haemophilus influenzae up-regulate human MUC5AC mucin transcription via a positive p38 mitogen-activated protein kinase pathway and a negative phosphoinositide 3-kinase-Akt pathway. Wang, B., Lim, D.J., Han, J., Kim, Y.S., Basbaum, C.B., Li, J.D. J. Biol. Chem. (2002) [Pubmed]
  3. Association between activation of the renin-angiotensin system and secondary erythrocytosis in patients with chronic obstructive pulmonary disease. Vlahakos, D.V., Kosmas, E.N., Dimopoulou, I., Ikonomou, E., Jullien, G., Vassilakos, P., Marathias, K.P. Am. J. Med. (1999) [Pubmed]
  4. Comparative morphology of the airways in asthma and chronic obstructive pulmonary disease. Jeffery, P.K. Am. J. Respir. Crit. Care Med. (1994) [Pubmed]
  5. Local and systemic inflammation in patients with chronic obstructive pulmonary disease: soluble tumor necrosis factor receptors are increased in sputum. Vernooy, J.H., Küçükaycan, M., Jacobs, J.A., Chavannes, N.H., Buurman, W.A., Dentener, M.A., Wouters, E.F. Am. J. Respir. Crit. Care Med. (2002) [Pubmed]
  6. Psychometric properties of the RAND-36 among three chronic diseases (multiple sclerosis, rheumatic diseases and COPD) in The Netherlands. Moorer, P., Suurmeije ThP, n.u.l.l., Foets, M., Molenaar, I.W. Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation. (2001) [Pubmed]
  7. Virulence factors in the colonization and persistence of bacteria in the airways. van Alphen, L., Jansen, H.M., Dankert, J. Am. J. Respir. Crit. Care Med. (1995) [Pubmed]
  8. Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age. Tashkin, D.P., Simmons, M.S., Sherrill, D.L., Coulson, A.H. Am. J. Respir. Crit. Care Med. (1997) [Pubmed]
  9. Functional status and well being in chronic obstructive pulmonary disease with regard to clinical parameters and smoking: a descriptive and comparative study. Engström, C.P., Persson, L.O., Larsson, S., Rydén, A., Sullivan, M. Thorax (1996) [Pubmed]
  10. Contractile properties of the human diaphragm during chronic hyperinflation. Similowski, T., Yan, S., Gauthier, A.P., Macklem, P.T., Bellemare, F. N. Engl. J. Med. (1991) [Pubmed]
  11. Mediators of chronic obstructive pulmonary disease. Barnes, P.J. Pharmacol. Rev. (2004) [Pubmed]
  12. Theophylline restores histone deacetylase activity and steroid responses in COPD macrophages. Cosio, B.G., Tsaprouni, L., Ito, K., Jazrawi, E., Adcock, I.M., Barnes, P.J. J. Exp. Med. (2004) [Pubmed]
  13. Effect of theophylline on erythrocytosis in chronic obstructive pulmonary disease. Oren, R., Beeri, M., Hubert, A., Kramer, M.R., Matzner, Y. Arch. Intern. Med. (1997) [Pubmed]
  14. Effect of adenosine A2A receptor activation in murine models of respiratory disorders. Bonneau, O., Wyss, D., Ferretti, S., Blaydon, C., Stevenson, C.S., Trifilieff, A. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
  15. An increase of soluble Fas, an inhibitor of apoptosis, associated with progression of COPD. Yasuda, N., Gotoh, K., Minatoguchi, S., Asano, K., Nishigaki, K., Nomura, M., Ohno, A., Watanabe, M., Sano, H., Kumada, H., Sawa, T., Fujiwara, H. Respiratory medicine. (1998) [Pubmed]
  16. Serum histidine-rich glycoprotein levels are decreased in acquired immune deficiency syndrome and by steroid therapy. Morgan, W.T. Biochem. Med. Metab. Biol. (1986) [Pubmed]
  17. Determinants of BMI in patients with COPD. Karadag, F., Karul, A.B., Cildag, O., Altun, C., Gurgey, O. Respirology (2004) [Pubmed]
  18. Eosinophilic and neutrophilic inflammation in asthma, chronic bronchitis, and chronic obstructive pulmonary disease. Lacoste, J.Y., Bousquet, J., Chanez, P., Van Vyve, T., Simony-Lafontaine, J., Lequeu, N., Vic, P., Enander, I., Godard, P., Michel, F.B. J. Allergy Clin. Immunol. (1993) [Pubmed]
  19. Glutathione S-transferase P1 (GSTP1) polymorphism in patients with chronic obstructive pulmonary disease. Ishii, T., Matsuse, T., Teramoto, S., Matsui, H., Miyao, M., Hosoi, T., Takahashi, H., Fukuchi, Y., Ouchi, Y. Thorax (1999) [Pubmed]
  20. Systemic and upper and lower airway inflammation at exacerbation of chronic obstructive pulmonary disease. Hurst, J.R., Perera, W.R., Wilkinson, T.M., Donaldson, G.C., Wedzicha, J.A. Am. J. Respir. Crit. Care Med. (2006) [Pubmed]
  21. Transforming growth factor beta1 and recruitment of macrophages and mast cells in airways in chronic obstructive pulmonary disease. de Boer, W.I., van Schadewijk, A., Sont, J.K., Sharma, H.S., Stolk, J., Hiemstra, P.S., van Krieken, J.H. Am. J. Respir. Crit. Care Med. (1998) [Pubmed]
  22. Supplementary oxygen in healthy subjects and those with COPD increases oxidative stress and airway inflammation. Carpagnano, G.E., Kharitonov, S.A., Foschino-Barbaro, M.P., Resta, O., Gramiccioni, E., Barnes, P.J. Thorax (2004) [Pubmed]
  23. Therapy for chronic obstructive pulmonary disease in the 21st century. Donnelly, L.E., Rogers, D.F. Drugs (2003) [Pubmed]
  24. Cigarette smoke disrupts VEGF165-VEGFR-2 receptor signaling complex in rat lungs and patients with COPD: morphological impact of VEGFR-2 inhibition. Marwick, J.A., Stevenson, C.S., Giddings, J., Macnee, W., Butler, K., Rahman, I., Kirkham, P.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
  25. Elevated MMP-12 protein levels in induced sputum from patients with COPD. Demedts, I.K., Morel-Montero, A., Lebecque, S., Pacheco, Y., Cataldo, D., Joos, G.F., Pauwels, R.A., Brusselle, G.G. Thorax (2006) [Pubmed]
  26. Activation of bronchial epithelial cells in smokers without airway obstruction and patients with COPD. Schulz, C., Krätzel, K., Wolf, K., Schroll, S., Köhler, M., Pfeifer, M. Chest (2004) [Pubmed]
  27. Elevated oxidative stress and reciprocal reduction of vascular endothelial growth factor levels with severity of COPD. Kanazawa, H., Yoshikawa, J. Chest (2005) [Pubmed]
  28. Increased activity of matrix metalloproteinase-8 and matrix metalloproteinase-9 in induced sputum from patients with COPD. Vernooy, J.H., Lindeman, J.H., Jacobs, J.A., Hanemaaijer, R., Wouters, E.F. Chest (2004) [Pubmed]
  29. Expression of adhesion molecules in allergic lung diseases. Popper, H.H., Pailer, S., Wurzinger, G., Feldner, H., Hesse, C., Eber, E. Virchows Arch. (2002) [Pubmed]
  30. Plasma and muscle amino acid levels in relation to resting energy expenditure and inflammation in stable chronic obstructive pulmonary disease. Pouw, E.M., Schols, A.M., Deutz, N.E., Wouters, E.F. Am. J. Respir. Crit. Care Med. (1998) [Pubmed]
  31. Biopsy neutrophilia, neutrophil chemokine and receptor gene expression in severe exacerbations of chronic obstructive pulmonary disease. Qiu, Y., Zhu, J., Bandi, V., Atmar, R.L., Hattotuwa, K., Guntupalli, K.K., Jeffery, P.K. Am. J. Respir. Crit. Care Med. (2003) [Pubmed]
  32. The cystic fibrosis gene is not likely to be involved in chronic obstructive pulmonary disease. Gasparini, P., Savoia, A., Luisetti, M., Peona, V., Pignatti, P.F. Am. J. Respir. Cell Mol. Biol. (1990) [Pubmed]
  33. Comprehensive gene expression profiles reveal pathways related to the pathogenesis of chronic obstructive pulmonary disease. Ning, W., Li, C.J., Kaminski, N., Feghali-Bostwick, C.A., Alber, S.M., Di, Y.P., Otterbein, S.L., Song, R., Hayashi, S., Zhou, Z., Pinsky, D.J., Watkins, S.C., Pilewski, J.M., Sciurba, F.C., Peters, D.G., Hogg, J.C., Choi, A.M. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  34. Tumor necrosis factor-alpha levels and weight loss in chronic obstructive pulmonary disease. Di Francia, M., Barbier, D., Mege, J.L., Orehek, J. Am. J. Respir. Crit. Care Med. (1994) [Pubmed]
  35. C-reactive protein in patients with COPD, control smokers and non-smokers. Pinto-Plata, V.M., Müllerova, H., Toso, J.F., Feudjo-Tepie, M., Soriano, J.B., Vessey, R.S., Celli, B.R. Thorax (2006) [Pubmed]
 
WikiGenes - Universities