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RISS 인기검색어
- 검색키워드
- 저자 : Toshio MORIKAWA (검색결과 3 건)
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A New Approach for RTL Power Macro-Modeling
Hirofumi KAWAUCHI,Toshio MORIKAWA,Ryohei MURASHIMA,Ittetsu TANIGUCHI,Masahiro FUKUI 대한전자공학회 2009 ITC-CSCC :International Technical Conference on Ci Vol.2009 No.7
This paper presents a new power macro-modeling technique for resister transfer level (RTL). RTL power macro-modeling technique is well known as promising technique for fast power estimation. Our method is based on a table look-up constructed by statistical information extracted from the primary inputs to the circuit. In this paper, we propose a novel power estimation method with a new parameter SD. This parameter characterizes switching activity of an internal circuit. The switching activities of each gate are strongly related with the power consumption. Experimental results show that the proposed method improves RMS error about 10% in average with the ISCAS-85 combinational circuits. The average RMS error of our model was 4.5%.
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Masakazu Kobayashi,Junji Akaki,Kiyofumi Ninomiya,Masayuki Yoshikawa,Osamu Muraoka,Toshio Morikawa,Masato Odawara 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.1
The number of diabetes mellitus and borderline diabetes cases is increasing and poses a serious problem worldwide. Plants of the genus Salacia are known to have α-glucosidase inhibitory activity and to lower postprandial hyperglycemia. Two randomized, double-blind, placebo-controlled clinical trials were conducted to evaluate the efficacy of Salacia chinensis extract. Study 1 was a single-dose crossover study of 150, 300, or 600 mg of Salacia extract or placebo to determine the dose dependency of the effect on postprandial hyperglycemia. The duration of the washout period between each experimental day was a minimum of 6 days. Study 2 was a 12-week, multiple-dose, parallel-group study to evaluate the effects of 600 mg/day of Salacia extract on blood glucose parameters. In Study 1, Salacia induced significant dose-dependent suppression of postprandial blood glucose, insulin, and their incremental area under the curve values. The dose of 600 mg appeared to have the most significant effect. In Study 2, Salacia significantly improved several blood glucose-related parameters, such as hemoglobin A1c, and glucose tolerance after glucose challenge. These results suggest that S. chinensis extract may have beneficial effects in patients with diabetes.
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Park, Eun-Ji,Lee, Yoon-Mi,Oh, Taek-In,Kim, Byeong Mo,Lim, Beong-Ou,Lim, Ji-Hong,Morikawa, Toshio MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.3
<P>Recent studies have shown that vanillin has anti-cancer, anti-mutagenic, and anti-metastatic activity; however, the precise molecular mechanism whereby vanillin inhibits metastasis and cancer progression is not fully elucidated. In this study, we examined whether vanillin has anti-cancer and anti-metastatic activities via inhibition of hypoxia-inducible factor-1α (HIF-1α) in A2058 and A375 human malignant melanoma cells. Immunoblotting and quantitative real time (RT)-PCR analysis revealed that vanillin down-regulates HIF-1α protein accumulation and the transcripts of HIF-1α target genes related to cancer metastasis including fibronectin 1 (<I>FN1</I>), lysyl oxidase-like 2 (<I>LOXL2</I>), and urokinase plasminogen activator receptor (<I>uPAR</I>). It was also found that vanillin significantly suppresses HIF-1α mRNA expression and de novo HIF-1α protein synthesis. To understand the suppressive mechanism of vanillin on HIF-1α expression, chromatin immunoprecipitation was performed. Consequently, it was found that vanillin causes inhibition of promoter occupancy by signal transducer and activator of transcription 3 (STAT3), but not nuclear factor-κB (NF-κB), on <I>HIF1A</I>. Furthermore, an in vitro migration assay revealed that the motility of melanoma cells stimulated by hypoxia was attenuated by vanillin treatment. In conclusion, we demonstrate that vanillin might be a potential anti-metastatic agent that suppresses metastatic gene expression and migration activity under hypoxia via the STAT3-HIF-1α signaling pathway.</P>
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