http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Reduced graphene oxide modified smart conducting paper for cancer biosensor
Kumar, Saurabh,Kumar, Suveen,Srivastava, Saurabh,Yadav, Birendra K.,Lee, Seung H.,Sharma, Jai G.,Doval, Dinesh C.,Malhotra, Bansi D. Elsevier 2015 Biosensors & bioelectronics Vol.73 No.-
<P><B>Abstract</B></P> <P>We report results of the studies relating to the fabrication of a paper based sensor comprising of poly (3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) and reduced graphene oxide (RGO) composite. The effect of various solvents like methanol, ethylene glycol and H<SUB>2</SUB>SO<SUB>4</SUB> on the electrical conductivity of PEDOT:PSS coated Whatman paper has been investigated. The conductivity of this solution processed conducting paper significantly increases from ~1.16×10<SUP>−4</SUP> Scm<SUP>−1</SUP> up to ~3.57×10<SUP>−2</SUP> Scm<SUP>−1</SUP> (~300 times) on treatment with ethylene glycol. The observed significant increase in electrical conductivity is due to conformational rearrangement in the polymer and is due to strong non-covalent cooperative interaction between PEDOT and the cellulose molecules. Further, incorporation of RGO into the conducting paper results in improved electrochemical performance and signal stability. This paper electrode is a promising alternative over the expensive conventional electrodes (ITO, gold and glassy carbon), that are known to have limited application in smart point-of-care (POC) devices. This low cost, flexible and environment friendly conducting paper based biosensor utilized for cancer biomarker (carcinoembryonic antigen, CEA) detection reveals high sensitivity of 25.8µAng<SUP>−1</SUP> mLcm<SUP>−2</SUP> in the physiological range, 1–10ngmL<SUP>−1</SUP>.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Solution processed reduced graphene oxide modified conducting paper sensor is reported for cancer detection. </LI> <LI> This paper sensor is exceptionally low cost, flexible and disposable. </LI> <LI> It exhibits high sensitivity of 25.8µAng<SUP>−1</SUP> mLcm<SUP>−2</SUP> in the detection range of 1–10ngmL<SUP>−1</SUP> for cancer biomarker (carcinoembryonic antigen, CEA) detection. </LI> <LI> This conducting paper electrode is a promising alternative over the expensive conventional electrodes (ITO, gold and glassy carbon) for application to POC devices. </LI> </UL> </P>
( Kyoung Jin Lee ),( Sun Hee Lee ),( Birendra Kumar Yadav ),( Hyun Mi Ju ),( Min Seo Kim ),( Jeong Hyun Park ),( Doo Il Jeoung ),( Han Soo Lee ),( Jang Hee Hahn ) 생화학분자생물학회 2012 BMB Reports Vol.45 No.3
CD99 is known to be involved in the regulation of cell-cell adhesion. However, it remains unclear whether CD99 controls cell-extracellular matrix adhesion. In this study, the effects of CD99 activation on cell-extracellular matrix adhesion were investigated. It was found that engagement of CD99 with the stimulating antibody YG32 downregulated the adhesion of MCF-7 cells to fibronectin, laminin and collagen IV in a dose-dependent manner. The CD99 effect on cell-ECM adhesion was inhibited by overexpression of the dominant negative form of CD99 or CD99 siRNA transfection. Treatment of cells with Mn2+ or by β1 integrin-stimulating antibody restored the inhibitory effect of CD99 on cell-ECM adhesion. Cross-linking CD99 inactivated β1 integrin through conformational change. CD99 activation caused dephosphorylation at Tyr-397 in FAK, which was restored by the β1 stimulating antibody. Taken together, these results provide the first evidence that CD99 inhibits cell-extracellular matrix adhesion by suppressing β1 integrin affinity. [BMB reports 2012; 45(3): 159-164]
Jang-Hee Hahn,이경진,임동영,Yeon Ho Yoo,Eun-Ji Park,Sun-Hee Lee,Birendra Kumar Yadav,Yong-Ki Lee,Jeong Hyun Park,Dae Joong Kim,Kyeong Han Park 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.7
The paired immunoglobulin-like type 2 receptor (PILR) family consists of two functionally opposite members, inhibitory PILR and activating PILR receptors. PILRs are widely expressed in various immune cells and inter-act with their ligands, especially CD99 expressed on activated T cells, to participate in immune responses. Here we investigated whether PILR-derived agonists inhibit 1 integrin activity as ligands for CD99. PILR-derived peptides as well as PILR-Fc fusion proteins prevented cell adhesion to fibronectin through the regu-lation of 1 integrin activity. Especially, PILRpep3, a representative 3-mer peptide covering the conserved motifs of the PILR extracellular domain, prevented the clustering and activation of 1 integrin by dephosphory-lating FAK and vinculin, which are major components of focal adhesion. In addition, PILRpep3 inhibited transen-dothelial migration of monocytes as well as endothelial cell tube formation. Furthermore, upon intraperitoneal injection of PILRpep3 into mice with collagen-induced arthritis, the inflammatory response of rheumatoid arthritis was strongly suppressed. Taken together, these results suggest that PILR-derived agonist ligands may prevent the inflammatory reactions of rheumatoid arthri-tis by activating CD99.
Lee, Kyoung-Jin,Lim, Dongyoung,Yoo, Yeon Ho,Park, Eun-Ji,Lee, Sun-Hee,Yadav, Birendra Kumar,Lee, Yong-Ki,Park, Jeong Hyun,Kim, Daejoong,Park, Kyeong Han,Hahn, Jang-Hee Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.7
The paired immunoglobulin-like type 2 receptor (PILR) family consists of two functionally opposite members, inhibitory $PILR{\alpha}$ and activating $PILR{\beta}$ receptors. PILRs are widely expressed in various immune cells and interact with their ligands, especially CD99 expressed on activated T cells, to participate in immune responses. Here we investigated whether PILR-derived agonists inhibit ${\beta}1$ integrin activity as ligands for CD99. PILR-derived peptides as well as PILR-Fc fusion proteins prevented cell adhesion to fibronectin through the regulation of ${\beta}1$ integrin activity. Especially, PILRpep3, a representative 3-mer peptide covering the conserved motifs of the PILR extracellular domain, prevented the clustering and activation of ${\beta}1$ integrin by dephosphorylating FAK and vinculin, which are major components of focal adhesion. In addition, PILRpep3 inhibited transendothelial migration of monocytes as well as endothelial cell tube formation. Furthermore, upon intraperitoneal injection of PILRpep3 into mice with collagen-induced arthritis, the inflammatory response of rheumatoid arthritis was strongly suppressed. Taken together, these results suggest that PILR-derived agonist ligands may prevent the inflammatory reactions of rheumatoid arthritis by activating CD99.