Institution
Nagoya Institute of Technology
Education•Nagoya, 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 & Catalysis. The organization has 10766 authors who have published 19140 publications receiving 255696 citations. The organization is also known as: Nagoya Kōgyō Daigaku & Nitech.
Topics: Thin film, Catalysis, Dielectric, Enantioselective synthesis, Turbulence
Papers published on a yearly basis
Papers
More filters
••
TL;DR: The results suggest that GIST is not, in epigenetic terms, a uniform disease and that DNA methylation in a set of genes is associated with aggressive clinical behavior and unfavorable prognosis.
Abstract: Background and aims The majority of gastrointestinal stromal tumors (GISTs) have KIT mutations; however, epigenetic abnormalities that could conceivably potentiate the aggressiveness of GISTs are largely unidentified. Our aim was to establish epigenetic profiles associated with the malignant transformation of GISTs. Methods Methylation of four tumor suppressor genes, RASSF1A, p16, CDH1, and MGMT was analyzed in GISTs. Additionally, genome-wide DNA methylation profiles were compared between small, malignant-prone, and malignant GISTs using methylated GpG island amplification microarrays (MCAM) in a training set (n=40). Relationships between the methylation status of genes identified by MCAM and clinical features of the disease were tested in a validation set (n=75). Results Methylation of RASSF1A progressively increased from small to malignant GISTs. p16 was specifically methylated in malignant-prone and malignant GISTs. MCAM analysis showed that more genes were methylated in advanced than in small GISTs (average of 473 genes vs 360 genes, respectively, P =0.012). Interestingly, the methylation profile of malignant GISTs was prominently affected by their location. Two genes, REC8 and PAX3 , which were newly-identified via MCAM analysis, were differentially methylated in small and malignant GISTs in the training and validation sets. Patients with methylation of at least REC8 , PAX3 , or p16 had a significantly poorer prognosis ( P =0.034). Conclusion Our results suggest that GIST is not, in epigenetic terms, a uniform disease and that DNA methylation in a set of genes is associated with aggressive clinical behavior and unfavorable prognosis. The genes identified may potentially serve as biomarkers for predicting aggressive GISTs with poor survivability.
60 citations
••
TL;DR: In this paper, the formation process of the fuzzy tungsten nanostructure induced by exposure to the helium plasma was studied, and it was proven that the growth of the nanostructures was brought about by bursting of the helium bubbles.
Abstract: For the purposes of long-term use of tungsten divertor walls, the formation process of the fuzzy tungsten nanostructure induced by exposure to the helium plasma was studied. In the present paper, the fuzzy nanostructure's formation has been successfully reproduced by the new hybrid simulation method in which the deformation of the tungsten material due to pressure of the helium bubbles was simulated by the molecular dynamics and the diffusion of the helium atoms was simulated by the random walk based on the Monte Carlo method. By the simulation results, the surface height of the fuzzy nanostructure increased only when helium retention was under the steady state. It was proven that the growth of the fuzzy nanostructure was brought about by bursting of the helium bubbles. Moreover, we suggest the following key formation mechanisms of the fuzzy nanostructure: (1) lifting in which the surface lifted up by the helium bubble changes into a convexity, (2) bursting by which the region of the helium bubble changes into a concavity, and (3) the difference of the probability of helium retention by which the helium bubbles tend to appear under the concavity. Consequently, the convex-concave surface structure was enhanced and grew to create the fuzzy nanostructure.
60 citations
••
TL;DR: It is shown that dynamic induction of chirality on the sulfur by coordination of a chiral Lewis acid to the pyridine nitrogen and one of the prochiral sulfonyl oxygens induces enantioselectivity.
Abstract: Enantioselective C-C bond formation to 2-pyridinesulfonylimines afforded products with good enantioselectivity. Dynamic induction of chirality on the sulfur by coordination of a chiral Lewis acid to the pyridine nitrogen and one of the prochiral sulfonyl oxygens induces enantioselectivity. Since the 2-pyridine-sulfonyl group can easily be removed after the reaction, it acts not only as an activating group but also as an efficient stereocontroller.
59 citations
••
TL;DR: Hydrogen bond of the Schiff base is further strengthened in the L(1) intermediate, whereas the halide dependence revealed that the acceptor is not Cl(-), but presumably a water molecule, so it is concluded that the hydrogen-bonding interaction between the Schiffbase and Cl(-) is not a driving force of the motion of Cl(-.
Abstract: Halorhodopsin is a light-driven chloride ion pump. Chloride ion is bound in the Schiff base region of the retinal chromophore, and unidirectional chloride transport is probably enforced by the specific hydrogen-bonding interaction with the protonated Schiff base and internal water molecules. In this article, we study hydrogen-bonding alterations of the Schiff base and water molecules in halorhodopsin of Natronobacterium pharaonis (pHR) by assigning their N−D and O−D stretching vibrations in D2O, respectively. Highly accurate low-temperature Fourier transform infrared spectroscopy revealed that hydrogen bonds of the Schiff base and water molecules are weak in the unphotolyzed state, whereas they are strengthened upon retinal photoisomerization. Halide dependence of the stretching vibrations enabled us to conclude that the Schiff base forms a direct hydrogen bond with Cl- only in the K intermediate. Hydrogen bond of the Schiff base is further strengthened in the L1 intermediate, whereas the halide dependenc...
59 citations
••
TL;DR: The progressive reduction of the ROM is probably caused by shortening of muscles or connective tissues due to reduced compliance of joint structures and degenerative changes in spinal alignment, as well as by diminished muscle stretching resulting from a decrease in daily physical activities with advancing age.
59 citations
Authors
Showing all 10804 results
Name | H-index | Papers | Citations |
---|---|---|---|
Luis M. Liz-Marzán | 132 | 616 | 61684 |
Hideo Hosono | 128 | 1549 | 100279 |
Shunichi Fukuzumi | 111 | 1256 | 52764 |
Andrzej Cichocki | 97 | 952 | 41471 |
Kwok-Hung Chan | 91 | 406 | 44315 |
Kimoon Kim | 90 | 412 | 35394 |
Alex Martin | 88 | 406 | 36063 |
Manijeh Razeghi | 82 | 1040 | 25574 |
Yuichi Ikuhara | 75 | 974 | 24224 |
Richard J. Cogdell | 73 | 480 | 23866 |
Masaaki Tanaka | 71 | 860 | 22443 |
Kiyotomi Kaneda | 65 | 378 | 13337 |
Yulin Deng | 64 | 641 | 16148 |
Motoo Shiro | 64 | 720 | 17786 |
Norio Shibata | 63 | 574 | 14469 |