Disease relevance of Pulmonary Emphysema

• Patients with diabetes mellitus were identified by prescriptions for insulin, pulmonary emphysema by prescriptions for ipratropium bromide, and psychotic syndromes by prescriptions for haloperidol [1].
• alpha 1-antitrypsin (alpha 1AT) of the Pi type Z is associated with two diseases: pulmonary emphysema and cirrhosis of the liver [2].
• Moreover, abnormal expression of HME may contribute to destructive processes such as pulmonary emphysema and vascular aneurysm formation [3].
• We investigated the relationship between the extent of pulmonary emphysema, assessed by quantitative high-resolution computed tomography (HRCT), and lung mechanics in 24 patients with chronic obstructive pulmonary disease (COPD) [4].
• To clarify the changes in bronchial cartilage in diseased airways, we performed morphometric analysis of airways in autopsied lungs of 16 patients with chronic bronchitis (Group CB), pulmonary emphysema (Group PE), and bronchial asthma (Group BA), and in control patients without respiratory diseases (Group CN) [5].

Psychiatry related information on Pulmonary Emphysema

• METHODS: The relation of elastin peptide concentration to some factors closely related to pulmonary emphysema (age, smoking habits, FEV1 alpha protease inhibitor (PI) phenotype) and to alcohol consumption was examined in an epidemiological study of 310 working men [6].

High impact information on Pulmonary Emphysema

• Collagenase expression in the lungs of transgenic mice causes pulmonary emphysema [7].
• We have uncovered a pathway in which the loss of integrin-mediated activation of latent TGF-beta causes age-dependent pulmonary emphysema through alterations of macrophage Mmp12 expression [8].
• Retinoic acid treatment abrogates elastase-induced pulmonary emphysema in rats [9].
• Elastin fragments attract macrophage precursors to diseased sites in pulmonary emphysema [10].
• Interferon gamma induction of pulmonary emphysema in the adult murine lung [11].

Chemical compound and disease context of Pulmonary Emphysema

• Impaired angiotensin conversion and bradykinin clearance in experimental canine pulmonary emphysema [12].
• Cadmium and pulmonary emphysema [13].
• To assess Stat3 physiological function, overexpression of a dominant negative Stat3 in respiratory epithelial cells in a doxycycline-controlled double transgenic mouse line caused pulmonary emphysema and increase of animal death during hyperoxia [14].
• The severity of pulmonary emphysema investigated with fractal analysis: regional dependence [15].
• Antioxidant and other actions of vitamin C may protect against pulmonary emphysema, or reduce bronchoconstrictor responses to environmental pollutants [16].

Biological context of Pulmonary Emphysema

• Homozygotes of Pi type Z have only 10 to 20 percent of the normal serum A1PI concentration and have a high risk of developing pulmonary emphysema [17].
• Interactions of regional respiratory mechanics and pulmonary ventilatory impairment in pulmonary emphysema: assessment with dynamic MRI and xenon-133 single-photon emission CT [18].
• The klotho gene, originally identified by insertional mutagenesis in mice, suppresses multiple aging phenotypes (e.g., arteriosclerosis, pulmonary emphysema, osteoporosis, infertility, and short life span) [19].
• In conclusion, there is compensatory upregulation of secretory leukocyte protease inhibitor in peripheral airways in subclinical pulmonary emphysema, which is in sharp contrast to the decreased level of secretory leukocyte protease inhibitor reported in some chronic airway diseases [20].
• Inhalation administration of all-trans-retinoic acid for treatment of elastase-induced pulmonary emphysema in Fischer 344 rats [21].

Anatomical context of Pulmonary Emphysema

• This study suggests one mechanism by which alveolar macrophages accumulate in the lung in pulmonary emphysema: elastin fragments generated at the diseased sites are potent chemoattractants for monocytes, the precursors of the macrophages [10].
• Quantum proteolysis by neutrophils: implications for pulmonary emphysema in alpha 1-antitrypsin deficiency [22].
• Targeted ablation of the surfactant protein D (SP-D) gene caused progressive pulmonary emphysema associated with pulmonary infiltration by foamy alveolar macrophages (AMs), increased hydrogen peroxide production, and matrix metalloproteinase (MMP)-2, -9, and -12 expression [23].
• A decreased secretion of HGF by pulmonary fibroblasts could contribute to the insufficient alveolar repair in pulmonary emphysema [24].
• The enzymatic breakdown of human lung elastin by leukocyte elastase precedes the development of pulmonary emphysema, and releases elastin-derived peptides (EDPs) into the circulation [25].

Gene context of Pulmonary Emphysema

• Extracellular regulated kinase/mitogen activated protein kinase is up-regulated in pulmonary emphysema and mediates matrix metalloproteinase-1 induction by cigarette smoke [26].
• CONCLUSION: An accelerated response of IL-8 to chronic smoking is a factor that characterises those smokers who are susceptible to pulmonary emphysema, although the cellular source of IL-8 remains to be determined [27].
• In this study, the role of SLPI in subclinical pulmonary emphysema was examined [20].
• These findings suggest that imbalance of MMP-9 and TIMP-1 is associated with the development of pulmonary emphysema in Klotho mice [28].
• To address the role of neutrophil elastase in pulmonary emphysema, neutrophil elastase-deficient mice and wild-type littermate controls were exposed to long-term cigarette smoke [29].

Analytical, diagnostic and therapeutic context of Pulmonary Emphysema

• Polymorphism in the HO-1 gene promoter was shown to be associated with susceptibility to pulmonary emphysema and restenosis after angioplasty [30].
• Preliminary application of dynamic pulmonary xenon-133 single-photon emission tomography in the evaluation of patients with pulmonary emphysema for thoracoscopic lung volume reduction surgery [31].
• These MR images revealed that the pulmonary arterial blood flow in the affected areas of COPD was relatively preserved as compared with pulmonary artery-occlusive diseases, and also showed significant decrease in blood flow, even in the areas with homogeneous perfusion on SPECT images in patients with focal pulmonary emphysema [32].
• Alpha 1-antitrypsin alleles in patients with pulmonary emphysema, detected by DNA amplification (PCR) and oligonucleotide probes [33].
• The effects of inhaling 400 micrograms of salbutamol were compared with identical placebo inhaler in a double blind cross-over study of 20 patients with radiological evidence of pulmonary emphysema [34].

References