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Strength Increase of Medium Temperature-carbonized PAN Nano Fibers Made by Mechano-electrospinning
( J H Kim ),( B Bajaj ),( S J Yoon ),( S H Kim ),( J R Lee ) 한국복합재료학회 2013 Composites research Vol.26 No.3
In this study, the effect of phosphoric acid (PA) as a fiber spinning aid on the strength increase of polyacrylonitrile (PAN) nano-fibers by using modified mechano-electrospinning technologies has been analyzed. The medium carbonization temperature of 800℃ has been selected for the future economic production of these new materials. The concentration of PAN in dimethyl sulfoxide (DMSO) was fixed as 5 wt%. The weight fraction of PA was selected as being 2%, 4%, 6%, and 8% in comparison to PAN. These solutions have been used to make the nanofibers. The mechano-electrospinning apparatus installed in KRICT was made by our own design. By using this apparatus the continous and highly aligned precursor nano-fibers have been obtained. The bundle of 50 well aligned nano diameter continuous fibers with the diametr of 10 microns with 6 wt% phosphoric acid for addition showed maximum mechanical properties of 1.6 GPa as tensile strength and 300 GPa as Young`s modulus. The weight of final product can be increased 19%, which can improve the economical benefits for the application of these new materials.
Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia
Kwon, H.,Bajaj, J.,Ito, T.,Blevins, A.,Konuma, T.,Weeks, J.,Lytle, Nikki K.,Koechlein, Claire S.,Rizzieri, D.,Chuah, C.,Oehler, Vivian G.,Sasik, R.,Hardiman, G.,Reya, T. Cell Press 2015 Cell stem cell Vol.17 No.2
Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.