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Your search keyword '"Sohn, M. H."' showing total 203 results
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203 results on '"Sohn, M. H."'

2. Single-filament Composite MgB2/SUS Ribbons by Powder-In-Tube Process

Author

Song, K. J., Lee, N. J., Jang, H. M., Ha, H. S., Ha, D. W., OH, S. S., Sohn, M. H., Kwon, Y. K., and Ryu, K. S.

Subjects
Condensed Matter - Superconductivity, Condensed Matter - Materials Science
Abstract

We report the successful fabrication of single-filament composite MgB2/SUS ribbons, as an ultra-robust conductor type, employing the powder-in-tube (PIT) process, by swaging and cold rolling only. The remarkable transport critical current (Ic) of the non-sintered MgB2/SUS ribbon has observed, as an unexpected result. Transport critical currents Ic ~ 316 A at T = 4.2 K and Ic ~ 82 A at T = 20 K were observed at self-field, for the non-sintered composite MgB2/SUS ribbon. In addition, the persistent current density Jp values, that were estimated by Bean formula, were more than ~ 7  105 A/cm2 at T = 5 K, and ~ 1.2  105 A/cm2 at T = 30 K, for the sintered composite MgB2/SUS ribbon, at H = 0 G., Comment: 10 pages, 4 figures

Published
2001
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25. Retrocaval ureter

Author

Lee, S, Kim, W, Jeong, H J, Sohn, M H, Kim, Y G, and Park, S K

Published
2006

34. Chitotriosidase inhibits allergic asthmatic airways via regulation of TGF‐β expression and Foxp3+ Treg cells.

Author

Hong, J. Y., Kim, M., Sol, I. S., Kim, K. W., Lee, C.‐M., Elias, J. A., Sohn, M. H., and Lee, C. G.

Subjects
T cells, ALLERGIES, IMMUNOTHERAPY, GENE expression, LABORATORY mice
Abstract

Abstract: Background: Chitotriosidase (chitinase 1, Chit1), a major true chitinase in humans, is induced in childhood asthma and has been implicated in the pathogenesis of a variety of inflammatory and tissue remodeling responses. However, the role and the mechanisms that underlie these contributions to the diseases have not been defined. We hypothesized that Chit1 plays a significant role in the pathogenesis of allergic asthma. Methods: Wild‐type and Chit1‐deficient mice and cells in culture were used to define the roles of Chit1 in models of allergic adaptive Th2 inflammation. In addition, the levels of sputum Chit1 were evaluated in pediatric asthma patients and compared to control. Results: The levels of sputum Chit1 were significantly increased in the patients with childhood asthma. Mice with Chit1 null mutation demonstrated enhanced allergic Th2 inflammatory and cytokine and IgE responses to OVA or house dust mite allergen sensitization and challenge. However, the expression levels of TGF‐β1 were significantly decreased with a diminished number of Foxp3+ regulatory T cells (Treg) in the lungs of Chit1−/− mice compared to WT controls. In vitro, the absence of Chit1 significantly reduced TGF‐β‐stimulated conversion of CD4+CD25− naïve T cells to CD4+Foxp3+ Treg cells, suggesting Chit1 is required for optimal effect of TGF‐β1 in Treg cell differentiation. Conclusion: Chit1 plays a protective role in the pathogenesis of allergic inflammation and asthmatic airway responses via regulation of TGF‐β expression and Foxp3+ Treg cells. [ABSTRACT FROM AUTHOR]

Published
2018
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