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CMOS-compatible batch processing of monolayer MoS<sub>2</sub> MOSFETs
Xiong, Kuanchen,Kim, Hyun,Marstell, Roderick J,Gö,ritz, Alexander,Wipf, Christian,Li, Lei,Park, Ji-Hoon,Luo, Xi,Wietstruck, Matthias,Madjar, Asher,Strandwitz, Nicholas C,Kaynak, Mehmet,Lee, Young IOP 2018 Journal of Physics. D, Applied Physics Vol.51 No.15
<P>Thousands of high-performance 2D metal-oxide-semiconductor field effect transistors (MOSFETs) were fabricated on wafer-scale chemical vapor deposited MoS<SUB>2</SUB> with fully-CMOS-compatible processes such as photolithography and aluminum metallurgy. The yield was greater than 50% in terms of effective gate control with less-than-10 V threshold voltage, even for MOSFETs having deep-submicron gate length. The large number of fabricated MOSFETs allowed statistics to be gathered and the main yield limiter to be attributed to the weak adhesion between the transferred MoS<SUB>2</SUB> and the substrate. With cut-off frequencies approaching the gigahertz range, the performances of the MOSFETs were comparable to that of state-of-the-art MoS<SUB>2</SUB> MOSFETs, whether the MoS<SUB>2</SUB> was grown by a thin-film process or exfoliated from a bulk crystal.</P>
Ihle, Nathan T,Lemos, Robert,Schwartz, David,Oh, Junghwan,Halter, Robert J,Wipf, Peter,Kirkpatrick, Lynn,Powis, Garth American Association for Cancer Research, Inc 2009 Molecular Cancer Therapeutics Vol.8 No.1
<P>The phosphatidylinositol 3-kinase (PI3K)/Akt signaling cascade is an important component of the insulin signaling in normal tissues leading to glucose uptake and homeostasis and for cell survival signaling in cancer cells. Hyperglycemia is an on-target side effect of many inhibitors of PI3K/Akt signaling including the specific PI3K inhibitor PX-866. The peroxisome proliferator-activated receptor gamma agonist pioglitazone, used to treat type 2 diabetes, prevents a decrease in glucose tolerance caused by acute administration of PX-866. Our studies have shown that pioglitazone does not inhibit the antitumor activity of PX-866 in A-549 non-small cell lung cancer and HT-29 colon cancer xenografts. In vitro studies also showed that pioglitazone increases 2-[1-(14)C]deoxy-D-glucose uptake in L-6 muscle cells and prevents inhibition of 2-deoxyglucose uptake by PX-866. Neither pioglitazone nor PX-866 had an effect on 2-deoxyglucose uptake in A-549 lung cancer cells. In vivo imaging studies using [18F]2-deoxyglucose (FDG) positron emission tomography showed that pioglitazone increases FDG accumulation by normal tissue but does not significantly alter FDG uptake by A-549 xenografts. Thus, peroxisome proliferator-activated receptor gamma agonists may be useful in overcoming the increase in blood glucose caused by inhibitors of PI3K signaling by preventing the inhibition of normal tissue insulin-mediated glucose uptake without affecting antitumor activity.</P>