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Design of Low-Power and Low-Latency 256-Radix Crossbar Switch Using Hyper-X Network Topology
Baek, Seung-Heon,Jung, Sung-Youb,Kim, Jaeha The Institute of Electronics and Information Engin 2015 Journal of semiconductor technology and science Vol.15 No.1
This paper presents the design of a low-power, low area 256-radix 16-bit crossbar switch employing a 2D Hyper-X network topology. The Hyper-X crossbar switch realizes the high radix of 256 by hierarchically combining a set of 4-radix sub-switches and applies three modifications to the basic Hyper-X topology in order to mitigate the adverse scaling of power consumption and propagation delay with the increasing radix. For instance, by restricting the directions in which signals can be routed, by restricting the ports to which signals can be connected, and by replacing the column-wise routes with diagonal routes, the fanout of each circuit node can be substantially reduced from 256 to 4~8. The proposed 256-radix, 16-bit crossbar switch is designed in a 65 nm CMOS and occupies the total area of $0.93{\times}1.25mm^2$. The simulated worst-case delay and power dissipation are 641 ps and 13.01 W when operating at a 1.2 V supply and 1 GHz frequency. In comparison with the state-of-the-art designs, the proposed crossbar switch design achieves the best energy-delay efficiency of $2.203cycle/ns{\cdot}fJ{\cdot}{\lambda}2$.
Design of Low-Power and Low-Latency 256-Radix Crossbar Switch Using Hyper-X Network Topology
Seung-Heon Baek,Sung-Youb Jung,Jaeha Kim 대한전자공학회 2015 Journal of semiconductor technology and science Vol.15 No.1
This paper presents the design of a low-power, low area 256-radix 16-bit crossbar switch employing a 2D Hyper-X network topology. The Hyper-X crossbar switch realizes the high radix of 256 by hierarchically combining a set of 4-radix sub-switches and applies three modifications to the basic Hyper-X topology in order to mitigate the adverse scaling of power consumption and propagation delay with the increasing radix. For instance, by restricting the directions in which signals can be routed, by restricting the ports to which signals can be connected, and by replacing the column-wise routes with diagonal routes, the fanout of each circuit node can be substantially reduced from 256 to 4~8. The proposed 256-radix, 16-bit crossbar switch is designed in a 65 ㎚ CMOS and occupies the total area of 0.93×1.25 ㎟. The simulated worst-case delay and power dissipation are 641 ps and 13.01 W when operating at a 1.2 V supply and 1 ㎓ frequency. In comparison with the state-of-the-art designs, the proposed crossbar switch design achieves the best energy-delay efficiency of 2.203 cycle/ns?fJ?λ².
Lee, Dong-Youb,Won, Kyung-Jong,Lee, Kang Pa,Jung, Seung Hyo,Baek, Suji,Chung, Hyun Woo,Choi, Wahn Soo,Lee, Hwan Myung,Lee, Byeong Han,Jeon, Byeong Hwa,Kim, Bokyung Elsevier 2018 Toxicology and applied pharmacology Vol.347 No.-
<P><B>Abstract</B></P> <P>Angiotensin II (Ang II) is implicated in the development of cardiovascular disorders including hypertension and atherosclerosis. However, the role of Ang II in the interaction between apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) and sphingosine-1-phosphate (S1P) signals in relation to vascular disorders remains to be clarified. This study aimed to determine whether APE/Ref-1 plays a role in epigenetic regulation of the S1P receptor (S1PR) in response to Ang II in vascular smooth muscle cell (VSMC) migration and vascular neointima formation. Ang II augmented the expression of S1PR1 in aortic smooth muscle cells of Sprague Dawley rats (RASMCs), which was attenuated by Ang II receptor (AT) 1 inhibitors, antioxidants, and APE/Ref-1 knockdown with small interference RNA. Ang II stimulation produced H<SUB>2</SUB>O<SUB>2</SUB>, and exogenous H<SUB>2</SUB>O<SUB>2</SUB> elevated S1PR1 expression in RASMCs. Moreover, Ang II caused translocation of cytoplasmic APE/Ref-1 into the nucleus in RASMCs. H3 histone acetylation and APE/Ref-1 binding at the S1PR1 promoter were increased in RASMCs treated with Ang II. In addition, Ang II induced migration in RASMCs, which was suppressed by AT1 and S1PR1 inhibitors. The expression of S1PR1, and colocalization of APE/Ref-1 and acetylated histone H3 in vascular neointima, were greater in Ang II-infused rats compared with a control group. These findings demonstrate that Ang II stimulates the epigenetic regulation of S1PR1 expression via H<SUB>2</SUB>O<SUB>2</SUB>-mediated APE/Ref-1 translocation, which may consequently be involved in Ang II-induced VSMC migration and vascular neointima formation. Therefore, APE/Ref-1-mediated overexpression of S1PR1 may be implicated in the vascular dysfunction evoked by Ang II.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ang II increased S1PR1 expression and H<SUB>2</SUB>O<SUB>2</SUB> generation in VSMCs. </LI> <LI> H<SUB>2</SUB>O<SUB>2</SUB> elevated S1PR1 expression in VSMCs. </LI> <LI> Ang II epigenetically enhanced S1PR1 expression via APE/Ref-1 translocation by H<SUB>2</SUB>O<SUB>2</SUB>. </LI> <LI> These events may be linked to Ang II-increased VSMC migration and vascular neointima. </LI> </UL> </P>