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EFFECT OF Na₂O ADDITION ON MAGNETIC PROPERTIES OF SrZn₂-W TYPE HEXAGONAL FERRITE
Hiroshi Yamamoto,Hiroshi Fujii,Takayuki Mitsuoka 한국자기학회 1995 韓國磁氣學會誌 Vol.5 No.5
An experiment was carried out to investigate the effect of Na₂O additive on the magnetic and physical properties of SrZn₂-W type hexagonal ferrite. The specimens were prepared by the conventional manufacturing methods without atmosphere control. It was found that the magnetic properties of SrOㆍ2ZnOㆍ8Fe₂O₃ are considerably improved on adding 1.5wt% Na₂O. The optimum condition of making magnet with suitable properties are as follows : chemical analysis composition: Sr²+_(0.852)Zn²+_(l.721)Na+_(0.301)Fe²+_(0.723)Fe³+_(15.703)O_(27) ; semisintering condition: 1300℃ × 1h in air; sintering condition: 1250℃ × 0.5h in air. The magnetic properties are: Jm= 0.390 T, Jr= 0.348 T, H_(cJ)= 133.7 ㎄/m, H_(cB)= 129.7 ㎄/m, (BH)max = 21.50 kJ/㎥, Tc=371℃, H_A= 1091.5㎄/m, K_A = 2.13 × 10^5J/㎥ and n_B= 31.8 μB.
Yamamoto, Yukio,Lee, Dongwon,Kim, Yoonhee,Lee, Bokyoung,Seo, Changwoo,Kawasaki, Hiroshi,Kuroda, Shinya,Tanaka-Yamamoto, Keiko The Society 2012 The Journal of neuroscience Vol.32 No.41
<P>It was demonstrated previously that a positive feedback loop, including protein kinase C (PKC) and mitogen-activated protein kinase (MAPK), is required for the gradual expression of cerebellar long-term depression (LTD). PKC and MAPK are mutually activated in this loop. MAPK-dependent PKC activation is likely to be mediated by phospholipase A2. On the other hand, it is not clear how PKC activates MAPK. Therefore, the entire picture of this loop was not fully understood. We here test the hypothesis that this loop is completed by the PKC substrate, Raf kinase inhibitory protein (RKIP). To test this hypothesis, we used a mutant form of RKIP that is not phosphorylated by PKC and thus constitutively inhibits Raf-1 and MEK, upstream kinases of MAPK. When this RKIP mutant was introduced into Purkinje cells of mouse cerebellar slices through patch-clamp electrodes, LTD was blocked, while wild-type (WT) RKIP had no effect on LTD. Physiological epistasis experiments demonstrated that RKIP works downstream of PKC and upstream of MAPK during LTD induction. Furthermore, biochemical analyses demonstrated that endogenous RKIP dissociates from Raf-1 and MEK during LTD induction in a PKC-dependent manner, suggesting that RKIP binding-dependent inhibition of Raf-1 and MEK is removed upon LTD induction. We therefore conclude that PKC-dependent regulation of RKIP leads to MAPK activation, with RKIP completing the positive feedback loop that is required for LTD.</P>
Development of Autonomous Excavation Technology for Hydraulic Excavators
Hiroshi Yamamoto,Masaharu Moteki,Hui Shao,Takashi Ootuki 제어로봇시스템학회 2009 제어로봇시스템학회 국제학술대회 논문집 Vol.2009 No.8
Because extensive dangerous and grueling work is still performed at disaster restoration work sites, research and development of unmanned execution technologies for use to enhance safety has been undertaken. This reportpresents an outline of research and development concerning autonomous excavation by hydraulic excavator performed by applying an IT execution system. As a result of the verification of the excavation motion, finishing excavation wasconfirmed that the difference between the planned trajectory and the trajectory of the actual movement of the tip of the bucket can be kept within 0.1m. It also achieved autonomous loading of the crawler dump truck.
The Mechanism of Vascular Injury in Diabetes : Lessons from Cells, Organelles and Transgenic Animals
Yamamoto,Hiroshi 한국생명과학회 2001 한국생명과학회 학술발표회 Vol.33 No.-
Microvessels are composed of endothelial cells and pericytes. They show peculiar changes in diabetes. Pericytes decrease (pericyte loss), while endothelial cells proliferate (angiogenesis) but with dysfunction (thrombogenesis). All of these changes were induced in vitro when each cell type was exposed to advanced glycation endproducts (AGE), non- enzymatically glycosylated protein derivatives which are formed at an accelerated rate during prolonged hyperglycemic exposure. And, those vascular cell responses were dependent on the presence of a cell surface receptor for AGE (RAGE). Coculture experiments revealed that loss of proximal interaction between the two cell types augments the microvascular derangement. To evaluate in vivo the functional role of the AGE-RAGE system in diabetes-induced vascular injury, we then created a double transgenic mouse model in which RAGE is overexpressed in vascular cells and insulin-dependent diabetes develops early after birth. The RAGE-overexpressing animals exhibited advanced diabetic nephropathy exemplified by mesangial expansion and glomerulosclerosis, and this was prevented by the treatment with an inhibitor of AGE formation. Retinopathy indices were also exacerbated in the double transgenic model. Lessons from the endothelial cell nucleus revealed that AGE ligands themselves, TNF-alpha and estradiol activate the transcription of RAGE gene, and that NF-kappa B mediates the induction by the former two, while the and estrogen receptor alpha complex mediates the estradiol induction. Analysis of vascular cell-derived polysomal poly(A)+RNA led to the isolation of novel splice variants of RAGE mRRNA coding for an N-terminally truncated protein and for a C-terminally truncated secretable form. The latter protein had an ability to capture AGE and to neutralize their action on endothelial cells, and was detected in human sera. In conclusion, the AGE-RAGE system would seem to be a promising target for overcoming diabetic vascular complications. Circulating soluble RAGE could contribute to resistance against this life-and QOL-threatening disease.