| 1. |
- Huang, Yue, et al.
(författare)
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Memory Effect of Metal-Oxide-Silicon Capacitors with Self-Assembly Double-Layer Au Nanocrystals Embedded in Atomic-Layer-Deposited HfO2 Dielectric
- 2009
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Ingår i: Chinese Physics Letters. - 0256-307X .- 1741-3540. ; 26:10
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Tidskriftsartikel (refereegranskat)abstract
- We report the chemical self-assembly growth of Au nanocrystals on atomic-layer-deposited HfO2 films aminosilanized by (3-Aminopropyl)-trimethoxysilane aforehand for memory applications. The resulting Au nanocrystals show a density of about 4 x 10(11) cm(-2) and a diameter range of 5-8 nm. The metal-oxide-silicon capacitor with double-layer Au nanocrystals embedded in HfO2 dielectric exhibits a large C - V hysteresis window of 11.9 V for +/- 11 V gate voltage sweeps at 1 MHz, a flat-band voltage shift of 1.5 V after the electrical stress under 7 V for 1 ms, a leakage current density of 2.9 x 10(-8) A/cm(-2) at 9 V and room temperature. Compared to single-layer Au nanocrystals, the double-layer Au nanocrystals increase the hysteresis window significantly, and the underlying mechanism is thus discussed.
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| 2. |
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| 3. |
- Liao, Zhong-Wei, et al.
(författare)
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Robust Low Voltage Program-Erasable Cobalt-Nanocrystal Memory Capacitors with Multistacked Al2O3/HfO2/Al2O3 Tunnel Barrier
- 2009
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Ingår i: Chinese Physics Letters. - 0256-307X .- 1741-3540. ; 26:8, s. 087303-
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Tidskriftsartikel (refereegranskat)abstract
- An atomic-layer-deposited Al2O3/HfO2/Al2O3 (A/H/A) tunnel barrier is investigated for Co nanocrystal memory capacitors. Compared to a single Al2O3 tunnel barrier, the A/H/A barrier can significantly increase the hysteresis window, i. e., an increase by 9V for +/- 12V sweep range. This is attributed to a marked decrease in the energy barriers of charge injections for the A/H/A tunnel barrier. Further, the Co-nanocrystal memory capacitor with the A/H/A tunnel barrier exhibits a memory window as large as 4.1V for 100 mu s program/erase at a low voltage of +/- 7V, which is due to fast charge injection rates, i. e., about 2.4 x 10(16) cm(-2) s(-1) for electrons and 1.9 x 10(16) cm(-2) s(-1) for holes.
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| 4. |
- An, Xiaojin, et al.
(författare)
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Response gene to complement 32, a novel hypoxia-regulated angiogenic inhibitor.
- 2009
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Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 120:7, s. 617-27
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Response gene to complement 32 (RGC-32) is induced by activation of complement and regulates cell proliferation. To determine the mechanism of RGC-32 in angiogenesis, we examined the role of RGC-32 in hypoxia-related endothelial cell function.METHODS AND RESULTS: Hypoxia/ischemia is able to stimulate both angiogenesis and apoptosis. Hypoxia-inducible factor-1/vascular endothelial growth factor is a key transcriptional regulatory pathway for angiogenesis during hypoxia. We demonstrated that the increased RGC-32 expression by hypoxia was via hypoxia-inducible factor-1/vascular endothelial growth factor induction in cultured endothelial cells. However, overexpression of RGC-32 reduced the proliferation and migration and destabilized vascular structure formation in vitro and inhibited angiogenesis in Matrigel assays in vivo. Silencing RGC-32 had an opposing, stimulatory effect. RGC-32 also stimulated apoptosis as shown by the increased apoptotic cells and caspase-3 cleavage. Mechanistic studies revealed that the effect of RGC-32 on the antiangiogenic response was via attenuating fibroblast growth factor 2 expression and further inhibiting expression of cyclin E without affecting vascular endothelial growth factor and fibroblast growth factor 2 signaling in endothelial cells. In the mouse hind-limb ischemia model, RGC-32 inhibited capillary density with a significant attenuation in blood flow. Additionally, treatment with RGC-32 in the xenograft tumor model resulted in reduced growth of blood vessels that is consistent with reduced colon tumor size.CONCLUSIONS: We provide the first direct evidence for RGC-32 as a hypoxia-inducible gene and antiangiogenic factor in endothelial cells. These data suggest that RGC-32 plays an important homeostatic role in that it contributes to differentiating the pathways for vascular endothelial growth factor and fibroblast growth factor 2 in angiogenesis and provides a new target for ischemic disorder and tumor therapies.
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