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Bryan L. Jackson

Researcher at IBM

Publications -  53
Citations -  6985

Bryan L. Jackson is an academic researcher from IBM. The author has contributed to research in topics: TrueNorth & Phase-change memory. The author has an hindex of 21, co-authored 53 publications receiving 5502 citations. Previous affiliations of Bryan L. Jackson include Lawrence Berkeley National Laboratory.

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A million spiking-neuron integrated circuit with a scalable communication network and interface

TL;DR: Inspired by the brain’s structure, an efficient, scalable, and flexible non–von Neumann architecture is developed that leverages contemporary silicon technology and is well suited to many applications that use complex neural networks in real time, for example, multiobject detection and classification.
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TrueNorth: Design and Tool Flow of a 65 mW 1 Million Neuron Programmable Neurosynaptic Chip

TL;DR: This work developed TrueNorth, a 65 mW real-time neurosynaptic processor that implements a non-von Neumann, low-power, highly-parallel, scalable, and defect-tolerant architecture, and successfully demonstrated the use of TrueNorth-based systems in multiple applications, including visual object recognition.
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Phase change memory technology

TL;DR: In this article, the authors survey the current state of phase change memory (PCM), a nonvolatile solid-state memory technology built around the large electrical contrast between the highly resistive amorphous and highly conductive crystalline states in so-called phase change materials.
Proceedings ArticleDOI

Cognitive computing building block: A versatile and efficient digital neuron model for neurosynaptic cores

TL;DR: A simple, digital, reconfigurable, versatile spiking neuron model that supports one-to-one equivalence between hardware and simulation and is implementable using only 1272 ASIC gates is developed.
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T-cell triggering thresholds are modulated by the number of antigen within individual T-cell receptor clusters

TL;DR: In this paper, the authors designed an experimental strategy that enables control over the number of activating peptide-major histocompatibility complex (pMHC) ligands per TCR cluster, without altering the total number engaged by the cell.