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Journal articles on the topic 'Kimitake'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Brzechczyn, Krzysztof. "Comparative Imperiology edited by Kimitaka Matsuzato." Ab Imperio 2013, no. 4 (2013): 314–18. http://dx.doi.org/10.1353/imp.2013.0093.

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Дигол, Сергей. "Emerging Meso-Areas in the Former Socialist Countries: Histories Revived or Improvised? ed. by Kimitaka Matsuzato." Ab Imperio 2008, no. 1 (2008): 327–37. http://dx.doi.org/10.1353/imp.2008.0122.

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Sablin, Ivan. "Russia and Its Northeast Asian Neighbors: China, Japan, and Korea, 1858–1945 ed. by Kimitaka Matsuzato." Ab Imperio 2018, no. 1 (2018): 345–50. http://dx.doi.org/10.1353/imp.2018.0016.

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4

Lukoianov, Igor V. "Russia and Its Northeast Asian Neighbors: China, Japan, and Korea, 1858–1945, edited by Kimitaka Matsuzato (2017)." Asian Review of World Histories 6, no. 2 (July 19, 2018): 307–11. http://dx.doi.org/10.1163/22879811-12340040.

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5

Somov, Boris V. "Patrick H. Diamond, Sanae-I. Itoh, and Kimitaka Itoh: Modern Plasma Physics, Volume I: Physical Kinetics of Turbulent Plasmas." Space Science Reviews 156, no. 1-4 (October 2010): 255–56. http://dx.doi.org/10.1007/s11214-010-9736-x.

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6

Herizona, Bintang Satria, and Indah Yuliana. "Pengaruh Ukuran Dewan Komisaris, Independensi Dewan Komisaris, dan Komite Audit terhadap Corporate Social Responsibility Disclosure dengan Profitabilitas sebagai Variabel Moderasi." Jurnal Manajemen dan Keuangan 10, no. 1 (July 3, 2021): 108–28. http://dx.doi.org/10.33059/jmk.v10i1.2935.

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Tujuan dari penelitian ini untuk menguji pengaruh parsial dan simultan variabel ukuran dewan komisaris, independensi dewan komisaris, dan komite audit terhadap corporate social responsibility disclosure serta pengaruh dari adanya penambahan variabel profitabilitas sebagai variabel moderasi. Sampel penelitian menggunakan sebanyak 38 perusahaan sektor industri dasar dan kimita tahun 2016-2019 yang ditentukan berdasarkan purposive sampling yang sudah ditetapkan dan analisis penelitian mengunakan moderated regression analysis. Hasil penelitian didapatkan bahwa secara parsial variabel ukuran dewan komisaris dan independensi dewan komisaris memiliki pengaruh yang signifikan. Sementara sercara simultan variabel yang digunakan memiliki pengaruh yang signifikan. Pada uji moderasi return on asset didapatkan hasil bawah variabel tersebut tidak mampu memoderasi hubungan antara variabel independen dengan variabel dependen sedangkan pada uji moderasi return on equity didapatkan hasil bahwa variabel tersebut mampu memoderasi hubungan variabel ukuran dewan komisaris dengan corporate social responsibility disclosure.

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7

Hohler, Susanne. "Russia and Its Northeast Asian Neighbors: China, Japan, and Korea, 1858–1945. Ed. Kimitaka Matsuzato. Lanham: Lexington Books, 2017. xxi, 200 pp. Notes. Index. Tables. Maps. $85.00, hard cover." Slavic Review 77, no. 3 (2018): 831–32. http://dx.doi.org/10.1017/slr.2018.253.

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8

Lankina, Tomila. "Fenomen Vladimira Putina i rossiiskie regiony: Pobeda neozhidannaia Hi zakonomernaia? Ed. Kimitaka Matsuzato. Slavic-Eurasian Studies, vol. 1. Moscow: Slavic Research Center, Hokkaido University, 2004. 368 pp. Notes. Tables. Paper." Slavic Review 64, no. 4 (2005): 918–20. http://dx.doi.org/10.2307/3649958.

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9

Mayuzumi, Akitsu. "Kōza Surabu Yūrasia Gaku (Slavic Eurasian Studies), Tokyo: Kōdansha, 2008: Vol. I (ed.) Osamu Ieda, 278 pages; Vol. II (ed.) Tomohiko Uyama, 322 pages; Vol. III (ed.) Kimitaka Matsuzato, 334 pages." Japanese Slavic and East European Studies 29 (2008): 77–82. http://dx.doi.org/10.5823/jsees.29.0_77.

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10

Soranaka, Isao. "Nihon: 1945 nen no shiten [Japan: In the perspective of the year 1945]. By Miwa Kimitada. Tokyo: Tokyo Daigaku Shuppankai, 1986. xii, 237 pp. ¥1,400 (paper)." Journal of Asian Studies 47, no. 1 (February 1988): 151–53. http://dx.doi.org/10.2307/2056402.

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11

Ren, Zuen, Huizhi Liang, Malindrie Dharmaratne, Miriam Morales-Gallego, Atefeh Taherian Fard, Jessica Mar, Kimita Suyama, et al. "Abstract 968: Loss of glutathione peroxidase 2 promotes epithelial to mesenchymal transition and breast cancer metastasis." Cancer Research 82, no. 12_Supplement (June 15, 2022): 968. http://dx.doi.org/10.1158/1538-7445.am2022-968.

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Abstract The processes regulating tumor metastasis are multivariate and complex. Redox regulation of the tumor phenotype by GPx2 knockdown (KD) in breast cancer led us to uncover dramatic effects on spontaneous metastasis. Analysis of single cell RNA sequencing (scRNAseq) data from GPx2 KD tumor and control tumor, revealed that both tumors were comprised of several luminal-like tumor cell clusters and one mesenchymal-like cell cluster (cluster 3). Notably, GPx2 KD promoted a significant increase in the size of mesenchymal cells (cluster 3) relative to control, which might be due to the stimulation of epithelial-to-mesenchymal transition (EMT) in response to GPx2 loss. In support of this view, GPx2 KD stimulated an increase in mRNA expression of basal/mesenchymal (KRT5, KRT14, KRT17, Vimentin, Twist1, Twist2, CDH2) genes and a decrease in mRNA expression of epithelial/luminal (Cldn7 and Epcam) genes, especially in cluster 3. Moreover, GPx2 KD upregulated mRNA expression of basal/mesenchymal (Twist2, CDH2, and KRT14) genes in most luminal-like clusters expressing epithelial/luminal (Epcam, Cldn3/7, CDH1, KRT8/18) genes, implying these clusters may be undergoing EMT transition in a hybrid epithelial/mesenchymal state in response to GPx2 loss. Validation of these data in cell lines and tumors showed that GPx2 KD dramatically enhanced EMT via activation of ROS/HIF1α-mediated signaling. Importantly, these effects were reversed by GPx2 re-expression or HIF1α inhibition, which was capable of suppressing EMT and metastasis. Collectively, these results indicate that GPx2 loss promotes breast cancer metastasis by stimulating EMT due to HIF1α signaling, highlighting the impact of GPx2 and HIF1 on therapeutic intervention in metastasis. Citation Format: Zuen Ren, Huizhi Liang, Malindrie Dharmaratne, Miriam Morales-Gallego, Atefeh Taherian Fard, Jessica Mar, Kimita Suyama, Outhiriaradjou Benard, Michael B. Prystowsky, Larry Norton, Rachel B. Hazan. Loss of glutathione peroxidase 2 promotes epithelial to mesenchymal transition and breast cancer metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 968.

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12

Liang, Huizhi, Outhiriaradjou Benard, Zuen Ren, Kimita Suyama, Larry Norton, and Rachel B. Hazan. "Abstract 961: TCF7 promotes a mammary cancer-stem-like phenotype leading to metastasis via potentiation of a hybrid epithelial/mesenchymal (E/M) phenotype." Cancer Research 82, no. 12_Supplement (June 15, 2022): 961. http://dx.doi.org/10.1158/1538-7445.am2022-961.

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Abstract Cancer stem cells (CSCs) are a minor population of carcinoma cells that can self-renew and give rise to differentiated progenitors that form the bulk of the tumor. CSCs cause tumor recurrence, chemoresistance and metastasis. The epithelial-to-mesenchymal transition (EMT) promotes tumor cell migration, invasion and cancer stem cell properties. The Wnt signaling pathway is a major driver of cancer stemness and is regulated by the TCF/LEF family of transcription factors. Using loss and gain of function of TCF7 (TCF1) in mouse and human breast cancer cells, we were able to demonstrate that TCF7 promotes cancer stemness through striking regulation of the EMT process. TCF7 knockdown in PyMT mammary tumor cells induced luminal epithelial differentiation, resulting in inhibition of oncosphere formation, migration, tumor growth and lung colonization. However, in keeping with a changing view of EMT as a strictly binary process, we found that TCF7 shifts tumor cells towards a hybrid epithelial/mesenchymal state (E/M) rather than a mesenchymal (M) state. This E/M population was shown to carry stemness and metastatic properties and to be interestingly represented by a small “stem-like” subpopulation in triple negative breast cancer (TNBC) cells. Using CD44 and CD104 (integrin β4) flow cytometry to isolate E/M cells from normal MCF10A and basal-like MDA-MB-468 breast cancer cells, we show that TCF7, Snail, and GSK3β phosphorylation were all highly enriched in this population whereas Zeb-1 (a marker of mesenchymal cells), was absent from E/M cells. These data support a model whereby TCF7 potentiates Wnt signaling which in turn activates GSK3β phosphorylation, resulting in Snail upregulation and enrichment of cells in the E/M state that is conducive of stemness and metastasis. Citation Format: Huizhi Liang, Outhiriaradjou Benard, Zuen Ren, Kimita Suyama, Larry Norton, Rachel B. Hazan. TCF7 promotes a mammary cancer-stem-like phenotype leading to metastasis via potentiation of a hybrid epithelial/mesenchymal (E/M) phenotype [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 961.

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13

Comtois, Claude. "EVANS, Paul M. and FROLIC, Michael B. (Eds.) Reluctant Adversaries. Canada and the People's Republic of China, 1949-70. Toronto, University of Toronto Press, 1991, xii + 280 p. SCHULTZ, John and MIWA, Kimitada (Eds.). Canada and Japan in the Twentieth Century. Toronto, Oxford University Press, 1991, xii + 274 p." Études internationales 23, no. 4 (1992): 919. http://dx.doi.org/10.7202/703113ar.

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14

"9731884 Measurement and analysis of exhaust valve motion Kiyoshi Iwade, Kimitaka Saito, Tokio Kohama (Nippon Soken, Inc.), Toru Hamamoto, Soichiro Fujiwara (Toyota Motor Corporation)." JSAE Review 19, no. 1 (January 1998): 95. http://dx.doi.org/10.1016/s0389-4304(98)90274-0.

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15

"9732586 Oil dilution reduction study with direct injection S.I. engine Masanori Sugiyama, Michikatsu Sato, Kenji Isaka (Toyota Motor Corporation), Kimitaka Saito, Nobuo Imatake (Nippon Soken Inc.)." JSAE Review 19, no. 1 (January 1998): 101. http://dx.doi.org/10.1016/s0389-4304(98)90343-5.

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16

"Kimitada Miwa. Nihon: 1945-nen no shiten [Japan: From the Viewpoint of 1945]. Tokyo: Tōkyō Daigaku Shuppankai. 1986. Pp. xi, 237." American Historical Review, October 1989. http://dx.doi.org/10.1086/ahr/94.4.1155.

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