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- Sjökvist, Niclas, et al.
(author)
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State retention flip flop architectures with different tradeoffs using crystalline indium gallium zinc oxide transistors implemented in a 32-bit normally-off microprocessor
- 2014
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In: Japanese Journal of Applied Physics. - : Japan Society of Applied Physics. - 0021-4922 .- 1347-4065. ; 53:4, s. 04EE10-
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Journal article (peer-reviewed)abstract
- As leakage power continues to increase when transistor sizes are downscaled, it becomes increasingly hard to achieve low power consumption in modern chips. Normally-off processors use state-retention and non-volatile circuits to make power gating more efficient with less static power. In this paper, we propose two novel state-retention flip-flop designs based on a parallel and series retention circuit architectures utilizing crystalline indium gallium zinc oxide transistors, which can achieve state retention with zero static power. To demonstrate the application of these different designs, they are implemented in a 32-bit normally-off microprocessor with an energy break-even time of 1.47 mu s for the parallel type design and 0.93 mu s for the series type design, at a clock frequency of 15 MHz. We show that decreasing the power supply duty cycle to 0.9%, the average current of the processor core can be decreased by over 99% using either type of flip-flop.
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| 2. |
- Tan-No, Koichi, et al.
(author)
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Antinociceptive effect produced by intracerebroventricularly administered dynorphin A is potentiated by p-hydroxymercuribenzoate or phosphoramidon in the mouse formalin test
- 2001
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In: Brain Research. - 0006-8993 .- 1872-6240. ; 891:1-2, s. 274-280
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Journal article (peer-reviewed)abstract
- The antinociceptive effects of intracerebroventricularly (i.c.v.) administered dynorphin A, an endogenous agonist for kappa-opioid receptors, in combination with various protease inhibitors were examined using the mouse formalin test in order to clarify the nature of the proteases involved in the degradation of dynorphin A in the mouse brain. When administered i.c.v. 15 min before the injection of 2% formalin solution into the dorsal surface of a hindpaw, 1-4 nmol dynorphin A produced a dose-dependent reduction of the nociceptive behavioral response consisting of licking and biting of the injected paw during both the first (0-5 min) and second (10-30 min) phases. When co-administered with p-hydroxymercuribenzoate (PHMB), a cysteine protease inhibitor, dynorphin A at the subthreshold dose of 0.5 nmol significantly produced an antinociceptive effect during the second phase. This effect was significantly antagonized by nor-binaltorphimine, a selective kappa-opioid receptor antagonist, but not by naltrindole, a selective delta-opioid receptor antagonist. At the same dose of 0.5 nmol, dynorphin A in combination with phosphoramidon, an endopeptidase 24.11 inhibitor, produced a significant antinociceptive effect during both phases. The antinociceptive effect was significantly antagonized by naltrindole, but not by nor-binaltorphimine. Phenylmethanesulfonyl fluoride (PMSF), a serine protease inhibitor, bestatin, a general aminopeptidase inhibitor, and captopril, an angiotensin-converting enzyme inhibitor, were all inactive. The degradation of dynorphin A by mouse brain extracts in vitro was significantly inhibited only by the cysteine protease inhibitors PHMB and N-ethylmaleimide, but not by PMSF, phosphoramidon, bestatin or captopril. The present results indicate that cysteine proteases as well as endopeptidase 24.11 are involved in two steps in the degradation of dynorphin A in the mouse brain, and that phosphoramidon inhibits the degradation of intermediary delta-opioid receptor active fragments enkephalins which are formed from dynorphin A.
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