1.
[Using biocomplexes in therapeutic-and-prophylactic and palliative measures in chronic obstructive lung disease].
Lushchaev, AIu, Vishniakov, AA, Kozlov, BI, Frolov, NA
Advances in gerontology = Uspekhi gerontologii. 2009;(3):512-5
Abstract
The paper presents the results of a clinical study of the use of biocomplexes in therapy for chronic obstructive lung disease and shows possibility to use them in therapeutic-and-prophylactic and palliative measures.
2.
Inhaled NO and markers of oxidant injury in infants with respiratory failure.
Van Meurs, KP, Cohen, TL, Yang, G, Somaschini, M, Kuruma, P, Dennery, PA
Journal of perinatology : official journal of the California Perinatal Association. 2005;(7):463-9
Abstract
BACKGROUND Inhaled nitric oxide (iNO) is an effective adjunct in the treatment of infants with respiratory failure. Although there are clear benefits to this therapy, potential toxicity could result from reactive nitrosylated species. OBJECTIVE To evaluate whether iNO therapy is associated with increased serum markers of oxidative stress. DESIGN/METHOD Multiple markers were prospectively evaluated in the serum of term infants with severe respiratory failure treated with iNO for 1 to 72 hours. These were compared to those of patients exposed to greater than 80% oxygen for more than 6 hours and room air controls. RESULTS After 24 hours of exposure, the iNO-treated infants had increased serum lipid hydroperoxides (LPO), protein carbonyls and nitrotyrosine residues as well as increased serum total glutathione (GSH) content. The increase in LPO peaked at 24 hours and correlated with the cumulative dose of iNO whereas other markers did not. The presence of chronic lung disease (CLD) did not correlate with serum markers of oxidative injury. CONCLUSIONS In term infants with respiratory failure, prolonged iNO exposure is associated with a transient increase in markers of oxidative stress, but this finding does not appear to predict the development of CLD.
3.
Fluticasone induces T cell apoptosis in the bronchial wall of mild to moderate asthmatics.
O'Sullivan, S, Cormican, L, Burke, CM, Poulter, LW
Thorax. 2004;(8):657-61
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Abstract
BACKGROUND Cytokines which signal via the gamma chain of the interleukin (IL)-2 receptor and the interferons (IFNs) have been shown to enhance T cell survival in vitro by rescuing cells from apoptosis. METHODS A study was undertaken to determine whether treatment with inhaled fluticasone propionate (FP; 250 microg twice daily) for 2 weeks could modulate production of IL-15 or IFN-beta and thereby affect T cell survival in bronchial tissue of 10 patients with mild/moderate asthma. Bronchial biopsy specimens were taken before and on completion of treatment. RESULTS The mean (95% CI) number of T cells per unit area decreased in the asthmatic group following 2 weeks of treatment with FP (from 7.0 (5.6 to 8.4) to 4.5 (4.0 to 5.1); p = 0.001). There was an increase in the percentage of T cells undergoing apoptosis following FP treatment as assessed by T cell/TUNEL staining (from 4.5 (2.6 to 6.4) to 8.7 (6.6 to 10.8); p = 0.0001). The percentage of cells staining for IL-15 and IFN-beta in the lamina propria, determined by an alkaline phosphatase biotin streptavidin technique, decreased significantly from baseline values of 31.6 (23.4 to 39.7) to 19.6 (12.5 to 26.7), p = 0.039 for IL-15 and from 18.9 (13.5 to 24.4) to 9.5 (5.9 to 13.1), p = 0.007 for IFN-beta following 2 weeks of treatment with FP. However, only the decrease in the percentage of cells staining for IL-15 was significantly correlated with an increased number of apoptotic T cells following treatment (p = 0.008). CONCLUSION These findings support a novel mechanism for the ability of inhaled corticosteroids to decrease T cell numbers, possibly by downregulation of the cytokine IL-15.