Home About us Contact
|
Home About us Contact | ||
|
|
||
Level Lead (level + lead)
Selected AbstractsA binary-based on-chip CNN solution for pixel-level snakesINTERNATIONAL JOURNAL OF CIRCUIT THEORY AND APPLICATIONS, Issue 4 2006V. M. Brea Abstract This paper introduces a binary-based on-chip cellular neural network (CNN) solution for pixel-level snakes. Every cell in the array comprises circuitry for B/W and grey-scale processing. The B/W processing is performed with a positive range high-gain discrete-time (DT)CNN model with 1-bit of programmability. The grey-scale processing is executed on a dedicated sub-cell. The design efforts are mainly focused on area consumption and processing speed. The result is a chip with a resolution of 9 × 9 cells in a 0.18 µm CMOS technology process and a density of more than 700cells/mm2. Simulations at schematic level lead to a time of less than 100ns for every DTCNN step. The peak power dissipation is kept at a few watts in a hypothetical chip of 128 × 128 cells. Copyright © 2006 John Wiley & Sons, Ltd. [source] Synthesis and properties of new dialkoxyphenylene quinoxaline-based donor-acceptor conjugated polymers and their applications on thin film transistors and solar cellsJOURNAL OF POLYMER SCIENCE (IN TWO SECTIONS), Issue 3 2009Mei-Hsiu Lai Abstract Synthesis, properties, and optoelectronic device applications of four new bis-[4-(2-ethyl-hexyloxy)-phenyl]quinoxaline(Qx(EHP))-based donor-acceptor conjugated copolymers are reported, in which the donors are thiophene(T), dithiophene(DT), dioctylfluorene(FO), and didecyloxyphenylene(OC10). The optical band gaps (Eg) of PThQx(EHP), PDTQ(EHP), POC10DTQ(EHP), and PFODTQ(EHP) estimated from the onset absorption are 1.57, 1.65, 1.77, and 1.92 eV, respectively. The smallest Eg of PThQx(EHP) among the four copolymers is attributed to the balanced donor/acceptor ratio and backbone coplanarity, leading to a strong intramolecular charge transfer. The hole mobilities obtained from the thin film transistor (TFT) devices of PThQx(EHP), PDTQ(EHP), POC10DTQ(EHP), and PFODTQ(EHP) are 2.52 × 10,4, 4.50 × 10,3, 4.72 × 10,5, and 9.31 × 10,4 cm2 V,1 s,1, respectively, with the on-off ratios of 2.00 × 104, 1.89 × 103, 4.07 × 103, and 2.30 × 104. Polymer solar cell based on the polymer blends of PFODTQ(EHP), PThQx(EHP), POC10DTQ(EHP), and PDTQ(EHP) with [6, 6]-phenyl C61-butyric acid methyl ester (PCBM) under illumination of AM1.5 (100 mW cm,2) solar simulator exhibit power conversion efficiencies of 1.75, 0.92, 0.79, and 0.43%, respectively. The donor/acceptor strength, molecular weight, miscibility, and energy level lead to the difference on the TFT or solar cell characteristics. The present study suggests that the prepared bis[4-(2-ethyl-hexyloxy)-phenyl]quinoxaline donor-acceptor conjugated copolymers would have promising applications on electronic device applications. © 2008 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 47: 973,985, 2009 [source] Myth and Reality in the Attitude toward Valence-Bond (VB) Theory: Are Its ,Failures' Real?HELVETICA CHIMICA ACTA, Issue 4 2003Sason Shaik According to common wisdom propagated in textbooks and papers, valence-bond (VB) theory fails and makes predictions in contradiction with experiment. Four iconic ,failures' are: a) the wrong prediction of the ground state of the O2 molecule, b) the failure to predict the properties of cyclobutadiene (CBD) viz. those of benzene, c) the failure to predict the aromaticity/anti-aromaticity of molecular ions like C5H and C5H, C3H and C3H, C7H and C7H, etc; and d) the failure to predict that, e.g., CH4 has two different ionization potentials. This paper analyzes the origins of these ,failures' and shows that two of them (stated in a and d) are myths of unclear origins, while the other two originate in misuse of an oversimplified version of VB theory, i.e., simple resonance theory that merely enumerate resonance structures. It is demonstrated that, in each case, a properly used VB theory at a simple and portable level leads to correct predictions, as successful as those made by use of molecular-orbital (MO) theory. This notion of VB ,failure', which is traced back to the VB-MO rivalry, in the early days of quantum chemistry, should now be considered obsolete, unwarranted, and counterproductive. A modern chemist should know that there are two ways of describing electronic structure, which are not two contrasting theories, but rather two representations or two guises of the same reality. Their capabilities and insights into chemical problems are complementary, and the exclusion of any one of them undermines the intellectual heritage of chemistry. [source] Adrenergic regulation of cardiac myocyte apoptosisJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2001Krishna Singh The direct effects of catecholamines on cardiac myocytes may contribute to both normal physiologic adaptation and pathologic remodeling, and may be associated with cellular hypertrophy, apoptosis, and alterations in contractile function. Norepinephrine (NE) signals via ,- and ,-adrenergic receptors (AR) that are coupled to G-proteins. Pharmacologic studies of cardiac myocytes in vitro demonstrate that stimulation of ,1 -AR induces apoptosis which is cAMP-dependent and involves the voltage-dependent calcium influx channel. In contrast, stimulation of ,2 -AR exerts an anti-apoptotic effect which appears to be mediated by a pertussis toxin-sensitive G protein. Stimulation of ,1 -AR causes myocyte hypertrophy and may exert an anti-apoptotic action. In transgenic mice, myocardial overexpression of either ,1 -AR or G,s is associated with myocyte apoptosis and the development of dilated cardiomyopathy. Myocardial overexpression of ,2 -AR at low levels results in improved cardiac function, whereas expression at high levels leads to dilated cardiomyopathy. Overexpression of wildtype ,1B -AR does not result in apoptosis, whereas overexpression of G,q results in myocyte hypertrophy and/or apoptosis depending on the level of expression. Differential activation of the members of the mitogen-activated protein kinase (MAPK) superfamily and production of reactive oxygen species appear to play a key role in mediating the actions of adrenergic pathways on myocyte apoptosis and hypertrophy. This review summarizes current knowledge about the molecular and cellular mechanisms involved in the regulation of cardiac myocyte apoptosis via stimulation of adrenergic receptors and their coupled effector pathways. © 2001 Wiley-Liss, Inc. [source] The radical scavenger CR-6 protects SH-SY5Y neuroblastoma cells from oxidative stress-induced apoptosis: effect on survival pathwaysJOURNAL OF NEUROCHEMISTRY, Issue 3 2006Nuria Sanvicens Abstract Reactive oxygen species (ROS) and oxidative stress have long been linked to cell death of neurons in many neurodegenerative conditions. However, the exact molecular mechanisms triggered by oxidative stress in neurodegeneration are at present unclear. In the current work we have used the human neuroblastoma SH-SY5Y cell line as a model for studying the molecular events occurring after inducing apoptosis with H2O2. We show that treatment of SH-SY5Y cells with H2O2 up-regulates survival pathways during early stages of apoptosis. Subsequently, the decline of anti-apoptotic protein levels leads to the activation of the calcium-dependent proteases calpains and the cysteine proteases caspases. Additionally, we demonstrate that CR-6 (3,4-dihydro-6-hydroxy-7-methoxy-2,2-dimethyl-1(2H)-benzopyran) acts as a scavenger of ROS and prevents apoptosis by enhancing and prolonging up-regulation of survival pathways. Furthermore, we show that pre-treatment of SH-SY5Y cells with a cocktail containing CR-6, the pan-caspase inhibitor zVAD-fmk (zVal-Ala-Asp-fluoro-methylketone) and the calpain inhibitor SJA6017 confers almost total protection against apoptosis. In summary, the present work characterizes the molecular mechanisms involved in oxidative stress-induced apoptosis in SH-SY5Y cells. Our findings highlight the relevance of CR-6, alone or in combination with other drugs, as potential therapeutic strategy for the treatment of neurodegenerative diseases. [source] | ||||||||||