14 research outputs found

    Automated Generation of Integrated Digital and Spiking Neuromorphic Machine Learning Accelerators

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    The growing numbers of application areas for artificial intelligence (AI) methods have led to an explosion in availability of domain-specific accelerators, which struggle to support every new machine learning (ML) algorithm advancement, clearly highlighting the need for a tool to quickly and automatically transition from algorithm definition to hardware implementation and explore the design space along a variety of SWaP (size, weight and Power) metrics. The software defined architectures (SODA) synthesizer implements a modular compiler-based infrastructure for the end-to-end generation of machine learning accelerators, from high-level frameworks to hardware description language. Neuromorphic computing, mimicking how the brain operates, promises to perform artificial intelligence tasks at efficiencies orders-of-magnitude higher than the current conventional tensor-processing based accelerators, as demonstrated by a variety of specialized designs leveraging Spiking Neural Networks (SNNs). Nevertheless, the mapping of an artificial neural network (ANN) to solutions supporting SNNs is still a non-trivial and very device-specific task, and completely lacks the possibility to design hybrid systems that integrate conventional and spiking neural models. In this paper, we discuss the design of such an integrated generator, leveraging the SODA Synthesizer framework and its modular structure. In particular, we present a new MLIR dialect in the SODA frontend that allows expressing spiking neural network concepts (e.g., spiking sequences, transformation, and manipulation) and we discuss how to enable the mapping of spiking neurons to the related specialized hardware (which could be generated through middle-end and backend layers of the SODA Synthesizer). We then discuss the opportunities for further integration offered by the hardware compilation infrastructure, providing a path towards the generation of complex hybrid artificial intelligence systems

    SO(DA)^2: End-to-end Generation of Specialized Reconfigurable Architectures (Invited Talk)

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    Potentiation of carbon tetrachloride hepatotoxicity and lethality in type 2 diabetic rats

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    ABSTRACT There is a need for well characterized and economical type 2 diabetic model that mimics the human disease. We have developed a type 2 diabetes rat model that closely resembles the diabetic patients and takes only 24 days to develop robust diabetes. Nonlethal doses of allyl alcohol (35 mg/kg i.p.), CCl 4 (2 ml/kg i.p.), or thioacetamide (300 mg/kg i.p.) yielded 80 to 100% mortality in diabetic rats. The objective of the present study was to investigate two hypotheses: higher CCl 4 bioactivation and/or inhibited compensatory tissue repair were the underlying mechanisms for increased CCl 4 hepatotoxicity in diabetic rats. Diabetes was induced by feeding high fat diet followed by a single dose of streptozotocin on day 14 (45 mg/kg i.p.) and was confirmed on day 24 by hyperglycemia, normoinsulinemia, and oral glucose intolerance. Time course studies (0 -96 h) of CCl 4 (2 ml/kg i.p.) indicated that although initial liver injury was the same in nondiabetic and diabetic rats, it progressed only in the latter, culminating in hepatic failure, and death. Hepatomicrosomal CYP2E1 protein and activity, lipid peroxidation, glutathione, and 14 CCl 4 covalent binding to liver tissue were the same in both groups, suggesting that higher bioactivation-based injury is not the mechanism. Inhibited tissue repair resulted in progression of injury and death in diabetic rats, whereas in the nondiabetic rats robust tissue repair resulted in regression of injury and survival after CCl 4 administration. These studies show high sensitivity of type 2 diabetes to model hepatotoxicants and suggest that CCl 4 hepatotoxicity is potentiated due to inhibited tissue repair. Several animal models resembling type 2 diabetes either occur spontaneously or can be induced experimentally. Most of the commonly used models of type 2 diabetes are genetic and have the disadvantage of prohibitive costs, unavailability, and failure to represent etiology of human disease. Consumption of high fat diet leads to insulin resistance and is considered to be a major predisposing factor for type 2 diabetes To address this need, we have refined and characterized an existing model based on high fat diet and a single dose of streptozotocin (STZ, 45 mg/kg i.p.). The principle behind the development of type 2 diabetes is simple. High fat diet elicits insulin resistance, and the rats maintain normoglycemia due to compensatory hyperinsulinemia. Administration of STZ (45 mg/kg i.p.) decreases insulin levels, destroying a population of pancreatic ␤-cells such that the insulin-resistant rats are now unable to maintain normal glucose levels and develop hyperglycemia, even though insulin levels in these rats are comparable with normal diet-fed normoglycemic rats. This is exactly what is seen in human diabetes where insulin resistance precedes hyperglycemia, thereby making this model a good representative of human type 2 diabetic (DB) condition. Article, publication date, and citation information can be found at http://jpet.aspetjournals.org. DOI: 10.1124/jpet.103.058834. ABBREVIATIONS: STZ, streptozotocin; DB, diabetic; NDB, nondiabetic; ND ϩ STZ, normal diet-fed rats injected streptozotocin; TA, thioacetamide; AA, allyl alcohol; SD, Sprague-Dawley; 3 H-T, tritiated thymidine; HFD, high fat diet-fed rats injected citrate buffer; HFD ϩ STZ, high fat diet-fed rats injected streptozotocin; ND, normal diet fed rats injected citrate buffer; ALT, alanine aminotransferase; AST, aspartate aminotransferase; PCNA, proliferating cell nuclear antigen; MES, 2-(N-morpholino)ethanesulfonic acid
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