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Institution

Nagoya Institute of Technology

EducationNagoya, Japan
About: Nagoya Institute of Technology is a education organization based out in Nagoya, Japan. It is known for research contribution in the topics: Thin film & Turbulence. The organization has 10766 authors who have published 19140 publications receiving 255696 citations. The organization is also known as: Nagoya Kōgyō Daigaku & Nitech.


Papers
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Journal ArticleDOI
TL;DR: Apoptosis induced by neurotoxins may be a mechanism underlying the cell death of dopamine neurons in the substantia nigra of Parkinson's disease.
Abstract: Recently, an endogenous neurotoxin, 1(R),2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline [N-methyl-(R)-salsolinol], was found to elicit parkinsonism in rats with selective depletion of dopamine neurons in the substantia nigra without necrotic tissue reaction. The mechanism of the cell death was examined by detection of DNA damage using a single-cell gel electrophoresis (comet) assay in human dopaminergic neuroblastoma SH-SY5Y cells. Only N-methylsalsolinol was found to induce DNA damage, whereas other catechol isoquinolines, such as (R)-salsolinol, (S)-salsolinol, and 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion, did not. The (R)-enantiomer of N-methylsalsolinol damaged DNA much more profoundly than the (S)-enantiomer. Cycloheximide protected the cells from DNA damage, suggesting that an apoptotic process may account for the DNA damage. Morphological changes indicating apoptotic cell death were also confirmed. Antioxidants and deprenyl reduced DNA damage, indicating that the damage was initiated by oxidative stress and that neuroprotection by deprenyl may be partially ascribed to its prevention of DNA damage. Apoptosis induced by neurotoxins may be a mechanism underlying the cell death of dopamine neurons in the substantia nigra of Parkinson's disease.

99 citations

Journal ArticleDOI
TL;DR: A reductive transmetalation of the pi-allylpalladium(II) complexes, generated in situ from a catalytic amount of a palladium(0) complex and a variety of allylic substrates, with indium(I) salts proceeded smoothly in various solvents, providing a new route for allylindium(III) reagents.

99 citations

Journal ArticleDOI
TL;DR: The findings support the use of BCAA supplements for patients with liver cirrhosis, and alpha-Chloroisocaproate, the analogue of leucine and the most potent known inhibitor of the kinase, is more effective than alpha-ketoisocAProate in promoting release of BCKDH kinase from the complex.
Abstract: Branched-chain alpha-keto acid dehydrogenase (BCKDH) complex, the enzyme catalyst for the second step of the BCAA catabolic pathway, plays a central role in the regulation of BCAA catabolism. The activity of the complex is regulated by a covalent modification cycle in which phosphorylation by BCKDH kinase inactivates and dephosphorylation by BCKDH phosphatase activates the complex. Many studies suggest that control of the activity of the kinase is a primary determinant of the activity of the complex. The kinase exists at all times in the mitochondrial matrix space in two forms, with a large amount being free and a smaller amount bound rather tightly to the BCKDH complex. Only the bound form of the kinase appears to be catalytically active and, therefore, responsible for phosphorylation and inactivation of the complex. alpha-Ketoisocaproate, the transamination product of leucine and the most important known physiological inhibitor of BCKDH kinase, promotes release of the kinase from the complex. alpha-Chloroisocaproate, the analogue of leucine and the most potent known inhibitor of the kinase, is more effective than alpha-ketoisocaproate in promoting release of BCKDH kinase from the complex. Exercise and chronic liver disease (liver cirrhosis) likewise decrease the amount of the kinase bound to the complex in rat liver. The resulting activation of the BCKDH complex appears responsible for the increase in BCAA catabolism caused by exercise and liver cirrhosis. Our findings support the use of BCAA supplements for patients with liver cirrhosis.

99 citations

Journal ArticleDOI
TL;DR: In this paper, Nb2C and Ta2C MXenes exhibit a remarkable SERS enhancement, which is synergistically enabled by the charge transfer resonance enhancement and electromagnetic enhancement.
Abstract: The outbreak of coronavirus disease 2019 has seriously threatened human health. Rapidly and sensitively detecting SARS-CoV-2 viruses can help control the spread of viruses. However, it is an arduous challenge to apply semiconductor-based substrates for virus SERS detection due to their poor sensitivity. Therefore, it is worthwhile to search novel semiconductor-based substrates with excellent SERS sensitivity. Herein we report, for the first time, Nb2C and Ta2C MXenes exhibit a remarkable SERS enhancement, which is synergistically enabled by the charge transfer resonance enhancement and electromagnetic enhancement. Their SERS sensitivity is optimized to 3.0 × 106 and 1.4 × 106 under the optimal resonance excitation wavelength of 532 nm. Additionally, remarkable SERS sensitivity endows Ta2C MXenes with capability to sensitively detect and accurately identify the SARS-CoV-2 spike protein. Moreover, its detection limit is as low as 5 × 10−9 M, which is beneficial to achieve real-time monitoring and early warning of novel coronavirus. This research not only provides helpful theoretical guidance for exploring other novel SERS-active semiconductor-based materials but also provides a potential candidate for the practical applications of SERS technology.

99 citations


Authors

Showing all 10804 results

NameH-indexPapersCitations
Luis M. Liz-Marzán13261661684
Hideo Hosono1281549100279
Shunichi Fukuzumi111125652764
Andrzej Cichocki9795241471
Kwok-Hung Chan9140644315
Kimoon Kim9041235394
Alex Martin8840636063
Manijeh Razeghi82104025574
Yuichi Ikuhara7597424224
Richard J. Cogdell7348023866
Masaaki Tanaka7186022443
Kiyotomi Kaneda6537813337
Yulin Deng6464116148
Motoo Shiro6472017786
Norio Shibata6357414469
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202316
202272
2021631
2020718
2019701
2018764