Mitsubishi

About: Mitsubishi is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Layer (electronics) & Signal. The organization has 53115 authors who have published 54821 publications receiving 870150 citations. The organization is also known as: Mitsubishi Group of Companies & Mitsubishi Companies.

Leading-zero anticipatory logic for high-speed floating point addition

Abstract: This paper describes a new leading-zero anticipatory (LZA) logic for high-speed floating-point addition (FADD). This logic carries out the pre-decoding for normalization concurrently with addition for the significand. It also performs the shift operation of normalization in parallel with the rounding operation. The use of simple Boolean algebra allows the proposed logic to be constructed from a simple CMOS circuit. Its area penalty is as small as 30% of the conventional LZA method. The FADD core using the proposed logic was fabricated by 0.5 /spl mu/m CMOS technology with triple metal interconnections and runs at 164 MHz under the condition of V/sub DD/=3.3 V.

Using linked volumes to model object collisions, deformation, cutting, carving, and joining

Abstract: In volume graphics, objects are represented by arrays or clusters of sampled 3D data. A volumetric object representation is necessary in computer modeling whenever interior structure affects an object's behavior or appearance. However, existing volumetric representations are not sufficient for modeling the behaviors expected in applications such as surgical simulation, where interactions between both rigid and deformable objects and the cutting, tearing, and repairing of soft tissues must be modeled in real time. Three-dimensional voxel arrays lack the sense of connectivity needed for complex object deformation, while finite element models and mass-spring systems require substantially reduced geometric resolution for interactivity and they can not be easily cut or carved interactively. This paper discusses a linked volume representation that enables physically realistic modeling of object interactions such as: collision detection, collision response, 3D object deformation, and interactive object modification by carving, cutting, tearing, and joining. The paper presents a set of algorithms that allow interactive manipulation of linked volumes that have more than an order of magnitude more elements and considerably more flexibility than existing methods. Implementation details, results from timing tests, and measurements of material behavior are presented.

Method of making multilayer capacitor memory device

Abstract: A semiconductor device comprising a capacitor of a laminated structure and a method of manufacturing thereof, in which first conductive layer and second conductive layer of different materials or different compositions are stacked alternately with dielectric films interposed therebetween and the first conductive layers and the second conductive layers are interconnected respectively at a time by suitably combining a selective etching method and an anisotropic etching method.

Calpain Mediates Calcium-Induced Activation of the Erk1,2 MAPK Pathway and Cytoskeletal Phosphorylation in Neurons: Relevance to Alzheimer's Disease

Abstract: Aberrant phosphorylation of the neuronal cytoskeleton is an early pathological event in Alzheimer's disease (AD), but the underlying mechanisms are unclear. Here, we demonstrate in the brains of AD patients that neurofilament hyperphosphorylation in neocortical pyramidal neurons is accompanied by activation of both Erk1,2 and calpain. Using immunochemistry, Western blot analysis, and kinase activity measurements, we show in primary hippocampal and cerebellar granule (CG) neurons that calcium influx activates calpain and Erk1,2 and increases neurofilament phosphorylation on carboxy terminal polypeptide sites known to be modulated by Erk1,2 and to be altered in AD. Blocking Erk1,2 activity either with antisense oligonucleotides to Erk1,2 mRNA sequences or by specifically inhibiting its upstream activating kinase MEK1,2 markedly reduced neurofilament phosphorylation. Calpeptin, a cell-permeable calpain inhibitor, blocked both Erk1,2 activation and neurofilament hyperphosphorylation at concentrations that inhibit calpain-mediated cleavage of brain spectrin. By contrast, inhibiting Erk1,2 with U-0126, a specific inhibitor of Mek1,2, had no appreciable effect on ionomycin-induced calpain activation. These findings demonstrate that, under conditions of calcium injury in neurons, calpains are upstream activators of Erk1,2 signaling and are likely to mediate in part the hyperphosphorylation of neurofilaments and tau seen at early stages of AD as well as the neuron survival-related functions of the MAP kinase pathway.