15,292 research outputs found

    Bridge Design between AXI Lite and AHB Bus Protocol

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    Architecture of bridge model between AXI Lite and AHB for this paper were simulated using Synopsys VCS and DC in Verilog HDL. Bridge structure mainly comprises of arbitration techniques, control signals, multiplexing techniques for writing data signals and Decoder for reading data section. In this work, bridge model between AHB and AXI lite was simulated and characterized. The proposed model of bridge design provides efficient communication between on chip bus protocols like AXI and AHB on chip in the era of deep sub-micron technology where channel side is reduced as much as 5 nm

    Comment on Reparametrization Invariance of Quark-Lepton Complementarity

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    We study the complementarity between quark and lepton mixing angles (QLC), the sum of an angle in quark mixing and the corresponding angle in lepton mixing is π/4\pi/4. Experimentally in the standard PDG parametrization, two such relations exist approximately. These QLC relations are accidental which only manifest themselves in the PDG parametrization. We propose reparametrization invariant expressions for the complementarity relations in terms of the magnitude of the elements in the quark and lepton mixing matrices. In the exact QLC limit, it is found that ∣Vus/Vud∣+∣Ve2/Ve1∣+∣Vus/Vud∣∣Ve2/Ve1∣=1|V_{us}/V_{ud}| + |V_{e2}/V_{e1}| + |V_{us}/V_{ud}| |V_{e2}/V_{e1}| =1 and ∣Vcb/Vtb∣+∣Vμ3/Vτ3∣+∣Vcb/Vtb∣∣Vμ3/Vτ3∣=1|V_{cb}/V_{tb}| + |V_{\mu 3}/V_{\tau 3}| +|V_{cb}/V_{tb}|| {V_{\mu 3}}/V_{\tau 3}| =1. Expressions with deviations from exact complementarity are obtained. Implications of these relations are also discussed.Comment: 5 pages and 1 figure. Implications for recent Daya-Bay neutrino data on theta_{13} discusse

    Emerging nanotechnology for treatment of Alzheimer\u27s and Parkinson\u27s disease

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    The prevalence of the two most common neurodegenerative diseases, Parkinson\u27s disease (PD) and Alzheimer\u27s Disease (AD), are expected to rise alongside the progressive aging of society. Both PD and AD are classified as proteinopathies with misfolded proteins α-synuclein, amyloid-β, and tau. Emerging evidence suggests that these misfolded aggregates are prion-like proteins that induce pathological cell-to-cell spreading, which is a major driver in pathogenesis. Additional factors that can further affect pathology spreading include oxidative stress, mitochondrial damage, inflammation, and cell death. Nanomaterials present advantages over traditional chemical or biological therapeutic approaches at targeting these specific mechanisms. They can have intrinsic properties that lead to a decrease in oxidative stress or an ability to bind and disaggregate fibrils. Additionally, nanomaterials enhance transportation across the blood-brain barrier, are easily functionalized, increase drug half-lives, protect cargo from immune detection, and provide a physical structure that can support cell growth. This review highlights emergent nanomaterials with these advantages that target oxidative stress, the fibrillization process, inflammation, and aid in regenerative medicine for both PD and AD
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