• Tuberculosis and Respiratory Diseases
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• v.53 no.1
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• pp.36-45
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• 2002

Background : In mammals, the activity of antioxidant enzymes is increased in adult lung to adapt to hyperoxia. The increase of these activities is augmented in neonates and is known as an important mechanism of tolerance to high oxygen levels. Peroxiredoxin(Prx) is an abundant and ubiquitous intracellular antioxidant enzyme. Prx I and II are major cytosolic subtypes. The aim of this study was to examine th Prx I and II mRNA and protein expression levels in adult rat lungs and to compare then with those of neonatal rat lungs exposed to hyperoxia. Materials and Methods : Adult Sprague-Dawley rats and neonates that were delivered from timed pregnant Sprague-Dawley rat were randomly exposed to normoxia or hyperoxia. After exposure to high oxygen level for a set time, the bronchoalveolar lavage fluid and lung tissue were obtained. The Prx I and II protein expression levels were measured by western blot analysis using polyclonal rabbit anti-Prx I or anti-Prx II antibodies and the relative expression of the Prx I and Prx II per Actin protein were obtained as an internal standard. The Prx I and II mRNA expression levels were measured by northernblot analysis using Prx I and Prx II-specific cDNA prepared from pCRPrx I and pCRPrx II, and the relative Prx I and Prx II expression levels per Actin mRNA were obtained as an internal standard. Results : Hyperoxia induced some peak increase in the Prx I mRNA levels after 24 hour in adult rats. Interestingly, hyperoxia induced a marked increase of Prx I mRNA 24 hour in neonatal rats. However, hyperoxia did not induce an alteration in the expression of Prx II mRNA in both the adult and neonatal rat lungs. Hyperoxia did not induce an alteration in the expression of the Prx I and Prx II protein in both the adult and neonatal rat lungs. Hyperoxia did not induce an alteration in the amount of Prx I and Prx II protein all the times in the bronchoalveolar fluid of adult rats. Conclusion : Prx I and II is differently regulated by hyperoxia in adult and neonatal rat lung at the transcriptional level. The prominent upregulation of Prx I mRNA in neonates compared to those in adults by hyperoxia may be another mechanism of resistance to high oxygen levels in neonate.

• Journal of the Korean Vacuum Society
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• v.14 no.2
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• pp.78-83
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• 2005

Nanometric crystalline silicon (no-Si) embedded in dielectric medium has been paid attention as an efficient light emitting center for more than a decade. In nc-Si, excitonic electron-hole pairs are considered to attribute to radiative recombination. However the surface defects surrounding no-Si is one of non-radiative decay paths competing with the radiative band edge transition, ultimately which makes the emission efficiency of no-Si very poor. In order to passivate those defects - dangling bonds in the $Si:SiO_2$ interface, hydrogen is usually utilized. The luminescence yield from no-Si is dramatically enhanced by defect termination. However due to relatively high mobility of hydrogen in a matrix, hydrogen-terminated no-Si may no longer sustain the enhancement effect on subsequent thermal processes. Therefore instead of easily reversible hydrogen, phosphorus was introduced by ion implantation, expecting to have the same enhancement effect and to be more resistive against succeeding thermal treatments. Samples were Prepared by 400 keV Si implantation with doses of $1\times10^{17}\;Si/cm^2$ and by multi-energy Phosphorus implantation to make relatively uniform phosphorus concentration in the region where implanted Si ions are distributed. Crystalline silicon was precipitated by annealing at $1,100^{\circ}C$ for 2 hours in Ar environment and subsequent annealing were performed for an hour in Ar at a few temperature stages up to $1,000^{\circ}C$ to show improved thermal resistance. Experimental data such as enhancement effect of PL yield, decay time, peak shift for the phosphorus implanted nc-Si are shown, and the possible mechanisms are discussed as well.