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The aim of the study was to evaluate the quality of life and its changes in patients with idiopathic pulmonary fibrosis (IPF), waiting for lung transplantation. Sixteen IPF patients, who qualified for lung transplantation, and 14 chronic obstructive pulmonary disease (COPD) patients on long term oxygen therapy, taken as a reference group, were assessed. The quality of life was estimated twice, using an SF-36-questionnaire, at the time of qualification for lung transplantation and 12 months later. The IPF and reference patients had similarly profound disturbances in lung function and arterial blood gas content. The IPF patients had a statistically greater score in their physical functioning (PF; 45 vs. 18), the role of limitations due to physical problems (RP; 43 vs. 11), social functioning (SF; 58 vs. 30), and the role of emotional limitations in everyday life (RE; 65 vs. 12) than the reference ones. After a year's observation, there were no differences in SF-36 questionnaire results, except for the role of limitations due to physical problems (RP). A correlation was noted between spirometry and blood gas results and SF-36 questionnaire results in IPF patients qualified for lung transplantation. There was a positive correlation between the partial pressure of oxygen (PaO2), on one side, and mental and general health, on the other. There also were positive correlations between FEV1 and SF and FEV1 and the level of bodily pain (BP). We conclude that the SF-36 questionnaire is a sensitive tool to assess the quality of life in IPF patients qualified for lung transplantation. The information gained can help assess the severity of the disease, clinical symptoms, and functional impairment in these patients.
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Human cytomegalovirus DNA level in patients with idiopathic pulmonary fibrosis

84%
The objectives of the study were to estimate human cytomegalovirus (HCMV) DNA copy number in broncho-alveolar lavage cells, blood leukocytes, and serum of patients with idiopathic pulmonary fibrosis (IPF). The study groups consisted of 16 patients, newly diagnosed with IPF and never treated, (mean age 40.9 ±11.0 yr; F/M-7/9) and in 16 adult healthy volunteers (mean age 36.8 ±6.4 yr; F/M-4/12) used as controls. The HCMV DNA copy number was calculated by a Q-PCR method using TaqMan ABI PRISMTM7700. We found that the prevalence of the HCMV DNA positive subjects in the patient group (75%) did not differ significantly from that in the control group (69%). We also found that in both patient and control groups the mean HCMV DNA copy number in BAL cells was significantly higher than that in blood leukocytes (log10=2.7 vs. 1.2 for patients and 2.8 vs. 0.9 for controls, respectively). However, a higher HCMV DNA copy number in blood serum was observed in IPF patients than in controls (log10=3.2 vs. 2.0, respectively). We conclude that the lungs play an important role in the human pathobiology of cytomegalovirus sustenance.
The aim of this study was to investigate whether transforming growth factor-β1 (TGF-β1) could induce alveolar epithelial-mesenchymal transition (EMT) in vitro, and whether Smad7 gene transfer could block this transition. We also aimed to elucidate the possible mechanisms of these processes. The Smad7 gene was transfected to the rat type II alveolar epithelial cell line (RLE-6TN). Expression of the EMT-associated markers was assayed by Western Blot and Real-time PCR. Morphological alterations were examined via phase-contrast microscope and fluorescence microscope, while ultrastructural changes were examined via electron microscope. TGF-β1 treatment induced a fibrotic phenotype of RLE-6TN with increased expression of fibronectin (FN), α-smooth muscle actin (α-SMA) and vimentin, and decreased expression of E-cadherin (E-cad) and cytokeratin19 (CK19). After transfecting the RLE-6TN with the Smad7 gene, the expression of the mesenchymal markers was downregulated while that of the epithelial markers was upregulated. TGF-β1 treatment for 48 h resulted in the separation of RLE-6TN from one another and a change into elongated, myofibroblast-like cells. After the RLE-6TN had been transfected with the Smad7 gene, TGF-β1 treatment had no effect on the morphology of the RLE-6TN. TGF-β1 treatment for 48 h resulted in an abundant expression of α-SMA in the RLE-6TN. If the RLE-6TN were transfected with the Smad7 gene, TGF-β1 treatment for 48 h could only induce a low level of α-SMA expression. Furthermore, TGF-β1 treatment for 12 h resulted in the degeneration and swelling of the osmiophilic multilamellar bodies, which were the markers of type II alveolar epithelial cells. TGF-β1 can induce alveolar epithelialmesenchymal transition in vitro, which is dependent on the Smads signaling pathway to a certain extent. Overexpression of the Smad7 gene can partially block this process.
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