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Institution

Mitsubishi

CompanyTokyo, Japan
About: Mitsubishi is a company organization based out in Tokyo, Japan. It is known for research contribution in the topics: Layer (electronics) & Signal. The organization has 53115 authors who have published 54821 publications receiving 870150 citations. The organization is also known as: Mitsubishi Group of Companies & Mitsubishi Companies.


Papers
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Journal ArticleDOI
TL;DR: Presepsin is useful for the diagnosis of sepsis, and it is superior to conventional markers and blood culture.

243 citations

Journal ArticleDOI
TL;DR: To visualize and isolate live dopamine (DA)-producing neurons in the embryonic ventral mesencephalon and isolate an enriched population of DA neurons from brain tissue, transgenic mice expressing green fluorescent protein (GFP) are generated under the control of the rat tyrosine hydroxylase gene promoter.
Abstract: To visualize and isolate live dopamine (DA)-producing neurons in the embryonic ventral mesencephalon, we generated transgenic mice expressing green fluorescent protein (GFP) under the control of the rat tyrosine hydroxylase gene promoter. In the transgenic mice, GFP expression was observed in the developing DA neurons containing tyrosine hydroxylase. The outgrowth and cue-dependent guidance of GFP-labeled axons was monitored in vitro with brain culture systems. To isolate DA neurons expressing GFP from brain tissue, cells with GFP fluorescence were sorted by fluorescence-activated cell sorting. More than 60% of the sorted GFP+ cells were positive for tyrosine hydroxylase, confirming that the population had been successfully enriched with DA neurons. The sorted GFP+ cells were transplanted into a rat model of Parkinson's disease. Some of these cells survived and innervated the host striatum, resulting in a recovery from Parkinsonian behavioral defects. This strategy for isolating an enriched population of DA neurons should be useful for cellular and molecular studies of these neurons and for clinical applications in the treatment of Parkinson's disease.

241 citations

Journal Article
TL;DR: Double staining for either TPKI or TPKII and NFT in the brain of Down's syndrome patients clearly demonstrated that TPKI and TPK II are both associated with NFTIn vivo, suggesting that the level of TPKI/TPKII is elevated in AD brain by some mechanism.
Abstract: Alzheimer's disease (AD) is characterized by neuronal cell death and two kinds of deposits, neurofibrillary tangles (NFT) and senile plaques. The main component of NFT is paired helical filaments (PHF), which mainly consist of hyperphosphorylated tau protein. Tau protein kinases I and II were found as candidate enzymes responsible for hyperphosphorylation of tau to induce the formation of PHF. Since prior phosphorylation of tau by TPKII strongly enhanced the action of TPKI, it was thought that TPKII was involved in the formation of PHF-tau in concert with TPKI. After cloning, TPKI was found to be identical with glycogen synthase kinase 3 beta (GSK3 beta), while TPKII consists of a novel 23 kDa protein activator and a catalytic subunit that is identical with cyclin-dependent kinase 5 (CDK5). The phosphorylation sites on tau by TPKI and TPKII could account for the most, but not all, of the major phosphorylation sites of fetal tau and PHF-tau. An antibody for a site specifically phosphorylated by TPKI (Ser413) could identify all three neurofibrillary lesions in the AD brain, and double staining for either TPKI or TPKII and NFT in the brain of Down's syndrome patients clearly demonstrated that TPKI and TPKII are both associated with NFT in vivo, suggesting that the level of TPKI or TPKII is elevated in AD brain by some mechanism. On the other hand, the levels of both TPKs change developmentally, being high in the neonatal period when the phosphorylation of fetal tau proceeds actively, suggesting that the TPKI/TPKII cooperative system has an important physiological role in the formation of neural networks. In AD brain, aberrant accumulation of amyloid-beta protein (A beta) occurs ahead of the accumulation of PHF in NFT. When a primary culture of embryonic rat hippocampus was treated with 20 microM A beta, induction of TPKI, extensive phosphorylation of tau and then programmed cell death were observed, indicating that TPKI induced by A beta phosphorylates tau, followed by disruption of axonal transportation and finally cell death. By using a yeast two hybrid system, TPKI was found to interact with pyruvate dehydrogenase (PDH), which is a key enzyme in the glycolytic pathway. PDH was phosphorylated in vitro by TPKI to reduce the activity converting pyruvate into acetyl-CoA, which is required for acetylcholine synthesis. In a primary culture of rat hippocampal cells treated with A beta, PDH was inactivated in inverse relation to the activation of TPKI, resulting in accumulation of pyruvate or lactate, energy failure induced by the disturbance of glucose metabolism, and a shortage of acetylcholine owing to deficiency of acetyl-CoA, all of which are characteristic of AD brain. In cholinergic neurons such as those of the septum, non-aggregated A beta, specifically A beta (1-42), not A beta (1-40), caused a shortage of acetylcholine by activation of TPKI and inactivation of PDH without cell death.

240 citations

Patent
08 Mar 1999
TL;DR: In this article, the authors present an easy-to-use mobile information terminal equipment which also functions as an electronic note, word processor, personal computer, and so on, which enables the user to obtain the desired screen with fewer number of operations and with less waiting time.
Abstract: The objective of the present invention is to have a desired screen displayed with shortened waiting time in using functions for the electronic note, etc., while engaging in telephone talk. Another prime objective of the present invention is to achieve an easy-to-use mobile information terminal equipment which also functions as an electronic note, word processor, personal computer, and so on. In transitting from telephone mode (cover closed status) to information terminal mode (cover opened status), the screen to be displayed is determined to be either a historical information, talk log information, or user setting screen. This enables the user to obtain the desired screen with fewer number of operations and with less waiting time.

240 citations

Patent
02 Nov 1989
TL;DR: In this article, a method of manufacturing a stacked-type semiconductor device is presented. But the method is limited to a single semiconductor substrate and is not suitable for the case of multiple semiconductor substrates.
Abstract: In a method of manufacturing a stacked-type semiconductor device, firstly, a first semiconductor substrate having a first device formed thereon is covered with an interlayer insulating layer and a planarized polycrystalline silicon layer is formed on the interlayer insulating layer. The first semiconductor substrate and a second semiconductor substrate are joined together by putting the surface of the polycrystalline silicon layer in close contact with the surface of a refractory metal layer formed on the second semiconductor substrate, applying thermal treatment at 700° C. or below and changing the refractory metal layer to silicide.

240 citations


Authors

Showing all 53117 results

NameH-indexPapersCitations
Thomas S. Huang1461299101564
Kazunari Domen13090877964
Kozo Kaibuchi12949360461
Yoshimi Takai12268061478
William T. Freeman11343269007
Tadayuki Takahashi11293257501
Takashi Saito112104152937
H. Vincent Poor109211667723
Qi Tian96103041010
Andreas F. Molisch9677747530
Takeshi Sakurai9549243221
Akira Kikuchi9341228893
Markus Gross9158832881
Eiichi Nakamura9084531632
Michael Wooldridge8754350675
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20231
20222
2021199
2020310
2019389
2018422