Search

Your search keyword '"Nishimatsu, Hiroaki"' showing total 354 results
Start Over Author "Nishimatsu, Hiroaki" Publication Type Academic Journals
354 results on '"Nishimatsu, Hiroaki"'

1. Subclassification of pT3 upper tract urothelial carcinoma: a multicenter retrospective study

Author

Yamada, Yukio, Nakagawa, Tohru, Miyakawa, Jimpei, Kawai, Taketo, Taguchi, Satoru, Tabata, Mariko, Kaneko, Tomoyuki, Ishikawa, Akira, Miyazaki, Hideyo, Kondo, Yasushi, Matsumoto, Akihiko, Naito, Akihiro, Hikatsu, Masahiro, Fujii, Yoichi, Akiyama, Yoshiyuki, Yamada, Yuta, Sato, Yusuke, Nomiya, Akira, Yamada, Daisuke, Murata, Taro, Suzuki, Motofumi, Enomoto, Yutaka, Nishimatsu, Hiroaki, Takeuchi, Takumi, Tanaka, Yoshinori, and Kume, Haruki

Published
2023
Full Text
View/download PDF

2. Efficacy and safety of darolutamide in Japanese patients with nonmetastatic castration-resistant prostate cancer: a sub-group analysis of the phase III ARAMIS trial

Author

Uemura, Hiroji, Matsushima, Hisashi, Kobayashi, Kazuki, Mizusawa, Hiroya, Nishimatsu, Hiroaki, Fizazi, Karim, Smith, Matthew, Shore, Neal, Tammela, Teuvo, Tabata, Ken-ichi, Matsubara, Nobuaki, Iinuma, Masahiro, Uemura, Hirotsugu, Oya, Mototsugu, Momma, Tetsuo, Kawakita, Mutsushi, Fukasawa, Satoshi, Kobayashi, Tadahiro, Kuss, Iris, Le Berre, Marie-Aude, Snapir, Amir, Sarapohja, Toni, and Suzuki, Kazuhiro

Published
2021
Full Text
View/download PDF

4. Prognostic significance of the albumin-to-globulin ratio for advanced urothelial carcinoma treated with pembrolizumab: a multicenter retrospective study

Author

Taguchi, Satoru, Kawai, Taketo, Nakagawa, Tohru, Nakamura, Yu, Kamei, Jun, Obinata, Daisuke, Yamaguchi, Kenya, Kaneko, Tomoyuki, Kakutani, Shigenori, Tokunaga, Mayuko, Uemura, Yukari, Sato, Yusuke, Fujimura, Tetsuya, Fukuhara, Hiroshi, Enomoto, Yutaka, Nishimatsu, Hiroaki, Takahashi, Satoru, and Kume, Haruki

Published
2021
Full Text
View/download PDF

6. Oncologic Outcome of Metastasectomy for Urothelial Carcinoma: Who Is the Best Candidate?

Author

Nakagawa, Tohru, Taguchi, Satoru, Kanatani, Atsushi, Kawai, Taketo, Ikeda, Masaomi, Urakami, Shinji, Matsumoto, Akihiko, Komemushi, Yoshimitsu, Miyakawa, Jimpei, Yamada, Daisuke, Suzuki, Motofumi, Enomoto, Yutaka, Nishimatsu, Hiroaki, Kondo, Yasushi, Nagase, Yasushi, Hirano, Yoshikazu, Okaneya, Toshikazu, Tanaka, Yoshinori, Miyazaki, Hideyo, Fujimura, Tetsuya, Fukuhara, Hiroshi, Kume, Haruki, Igawa, Yasuhiko, and Homma, Yukio

Published
2017
Full Text
View/download PDF

7. Efficacy of post-nephroureterectomy cisplatin-based adjuvant chemotherapy for locally advanced upper tract urothelial carcinoma: a multi-institutional retrospective study

Author

Nakagawa, Tohru, Komemushi, Yoshimitsu, Kawai, Taketo, Otsuka, Masafumi, Miyakawa, Jimpei, Uemura, Yukari, Kanatani, Atsushi, Taguchi, Satoru, Naito, Akihiro, Suzuki, Motofumi, Nishimatsu, Hiroaki, Hirano, Yoshikazu, Tanaka, Yoshinori, Matsumoto, Akihiko, Miyazaki, Hideyo, Fujimura, Tetsuya, Fukuhara, Hiroshi, Kume, Haruki, Igawa, Yasuhiko, and Homma, Yukio

Published
2017
Full Text
View/download PDF

8. Prognostic significance of serum neuron-specific enolase in small cell carcinoma of the urinary bladder

Author

Naito, Akihiro, Taguchi, Satoru, Nakagawa, Tohru, Matsumoto, Akihiko, Nagase, Yasushi, Tabata, Mariko, Miyakawa, Jimpei, Suzuki, Motofumi, Nishimatsu, Hiroaki, Enomoto, Yutaka, Takahashi, Shintaro, Okaneya, Toshikazu, Yamada, Daisuke, Tachikawa, Takamitsu, Minowada, Shigeru, Fujimura, Tetsuya, Fukuhara, Hiroshi, Kume, Haruki, and Homma, Yukio

Published
2017
Full Text
View/download PDF

17. SERUM NEURON-SPECIFIC ENOLASE IS A SIGNIFICANT PROGNOSTIC FACTOR FOR SMALL CELL CARCINOMA OF THE URINARY BLADDER: PD38-08

Author

Naito, Akihiro, Taguchi, Satoru, Nakagawa, Tohru, Matsumoto, Akihiko, Nagase, Yasushi, Miyakawa, Jimpei, Suzuki, Motofumi, Nishimatsu, Hiroaki, Enomoto, Yutaka, Takahashi, Shintaro, Okaneya, Toshikazu, Yamada, Daisuke, Tachikawa, Takamitsu, Minowada, Shigeru, Fujimura, Tetsuya, Fukuhara, Hiroshi, Kume, Haruki, and Homma, Yukio

Published
2016
Full Text
View/download PDF

18. OUTCOME OF METASTASECTOMY FOR UROTHELIAL CARCINOMA: A MULTI-INSTITUTIONAL RETROSPECTIVE STUDY: PD33-01

Author

Nakagawa, Tohru, Taguchi, Satoru, Kanatani, Atsushi, Ikeda, Masaomi, Matsumoto, Akihiko, Kawai, Taketo, Yoshida, Kanae, Yamada, Daisuke, Komemushi, Yoshimitsu, Urakami, Shinji, Suzuki, Motofumi, Enomoto, Yutaka, Kondo, Yasushi, Nagase, Yasushi, Nishimatsu, Hiroaki, Hirano, Yoshikazu, Okaneya, Toshikazu, Tanaka, Yoshinori, Minowada, Shigeru, Miyazaki, Hideyo, Fujimura, Tetsuya, Fukuhara, Hiroshi, Kume, Haruki, and Homma, Yukio

Published
2016
Full Text
View/download PDF

22. Adipose tissue-derived stem cells inhibit neointimal formation in a paracrine fashion in rat femoral artery

Author

Takahashi, Masao, Suzuki, Etsu, Oba, Shigeyoshi, Nishimatsu, Hiroaki, Kimura, Kenjiro, Nagano, Tetsuo, Nagai, Ryozo, and Hirata, Yasunobu

Subjects
Stem cells -- Physiological aspects, Stem cells -- Research, Endothelium -- Physiological aspects, Endothelium -- Research, Adipose tissues -- Physiological aspects, Adipose tissues -- Research, Biological sciences
Abstract

Subcutaneous adipose tissue contains a lot of stem cells [adipose-derived stem cells (ASCs)] that can differentiate into a variety of cell lineages. In this study, we isolated ASCs from Wistar rats and examined whether ASCs would efficiently differentiate into vascular endothelial cells (ECs) in vitro. We also administered ASCs in a wire injury model of rat femoral artery and examined their effects. ASCs expressed CD29 and CD90, but not CD34, suggesting that ASCs resemble bone marrow-derived mesenchymal stem cells. When induced to differentiate into ECs with endothelial growth medium (EGM), ASCs expressed Flt-1, but not Flk-1 or mature EC markers such as CD31 and vascular endothelial cadherin. ASCs produced angiopoietin-1 when they were cultured in EGM. ASCs stimulated the migration of EC, as assessed by chemotaxis assay. When ASCs that were cultured in EGM were injected in the femoral artery, the ASCs potently and significantly inhibited neointimal formation without being integrated in the endothelial layer. EGM-treated ASCs significantly suppressed neointimal formation even when they were administered from the adventitial side. ASC administration significantly promoted endothelial repair. These results suggested that although ASCs appear to have little capacity to differentiate into mature ECs, ASCs have the potential to secrete paracrine factors that stimulate endothelial repair. Our results also suggested that ASCs inhibited neointimal formation via their paracrine effect of stimulation of EC migration in situ rather than the direct integration into the endothelial layer. vascular endothelial cells; endothelial repair doi: 10.1152/ajpheart.00391.2009

Published
2010

33. Angiotensin II and tumor necrosis factor-[alpha] synergistically promote monocyte chemoattractant protein-1 expression: roles of NF-[kappa]B, p38, and reactive oxygen species

Author

Takahashi, Masao, Suzuki, Etsu, Takeda, Ryo, Oba, Shigeyoshi, Nishimatsu, Hiroaki, Kimura, Kenjiro, Nagano, Tetsuo, Nagai, Ryozo, and Hirata, Yasunobu

Subjects
Angiotensin -- Influence, Tumor necrosis factor -- Influence, Monocytes -- Properties, Atherosclerosis -- Physiological aspects, Blood vessels -- Properties, Biological sciences
Abstract

We examined whether ANG II and TNF-[alpha] cooperatively induce vascular inflammation using the expression of monocyte chemoattractant protein (MCP)-1 as a marker of vascular inflammation. ANG II and TNF-[alpha] stimulated MCP-1 expression in a synergistic manner in vascular smooth muscle cells. ANG II-induced MCP-1 expression was potently inhibited to a nonstimulated basal level by blockade of the p38-dependent pathway but only partially inhibited by blockade of the NF-[kappa]B-dependent pathway. In contrast, TNF-[alpha]-induced MCP-1 expression was potently suppressed by blockade of NF-[kappa]B activation but only modestly suppressed by blockade of p38 activation. ANG II-and TNF-[alpha]-induced activation of NF-[kappa]B- and p38-dependent pathways was partially inhibited by pharmacological inhibitors of ROS production. Furthermore, ANG II- and TNF-[alpha]-stimulated MCP-1 expression was partially suppressed by ROS inhibitors. We also examined whether endogenous ANG II and TNF-[alpha] cooperatively promote vascular inflammation in vivo using a wire injury model of the rat femoral artery. Blockade of both ANG II and TNF-[alpha] further suppressed neointimal formation, macrophage infiltration, and MCP-1 expression in an additive manner compared with blockade of ANG II or TNF-[alpha] alone. These results suggested that ANG II and TNF-[alpha] synergistically stimulate MCP-1 expression via the utilization of distinct intracellular signaling pathways (p38- and NF[kapp]B-dependent pathways) and that these pathways are activated in ROS-dependent and -independent manners. These results also suggest that ANG II and TNF-[alpha] cooperatively stimulate vascular inflammation in vivo as well as in vitro. blood vessels; signaling pathway; atherosclerosis

Published
2008

34. Calcineurin is critical for sodium-induced neointimal formation in normotensive and hypertensive rats

Author

Takeda, Ryo, Suzuki, Etsu, Takahashi, Masao, Oba, Shigeyoshi, Nishimatsu, Hiroaki, Kimura, Kenjiro, Nagano, Tetsuo, Nagai, Ryozo, and Hirata, Yasunobu

Subjects
Calcineurin -- Influence, Cellular signal transduction -- Evaluation, Inflammation -- Observations, Hypertension -- Physiological aspects, Biological sciences
Abstract

It is well known that excessive intake of sodium chloride (sodium) is a risk factor for cardiovascular disease because it raises blood pressure. However, sodium loading reportedly promotes cardiovascular disease independently of its effect on blood pressure. To examine the mechanisms by which sodium loading promotes vascular inflammation independently of its effect on blood pressure, we examined the role of calcineurin in sodium loadinginduced vascular inflammation using a wire injury model of the rat femoral artery. Calcineurin mRNA expression in the wire-injured femoral artery was significantly higher in sodium-loaded normotensive rats, such as Wistar-Kyoto (WKY) rats, than that in control WKY rats. Neointimal formation was also significantly enhanced in sodium-loaded WKY rats compared with control WKY rats. Gene transfer of an adenovirus expressing a dominant negative mutant of calcineurin (AdCalAAC92Q) significantly suppressed neointimal formation in sodium-loaded WKY rats to a level similar to that observed in control WKY rats. Calcineurin expression and neointimal formation were more significantly enhanced in hypertensive rats, such as spontaneously hypertensive rats (SHRs), than those in control WKY rats. AdCalAAC92Q infection significantly suppressed neointimal formation in SHRs to a level similar to that observed in control WKY rats. These results suggest that sodium loading promotes neointimal formation, even in normotensive rats, and that hypertension further stimulates neointimal formation. These results also suggest that calcineurin plays a pivotal role in this process. signal transduction; vasculature; inflammation; hypertension

Published
2008

35. Endothelial dysfunction and hypercontractility of vascular myocytes are ameliorated by fluvastatin in obese Zucker rats

Author

Nishimatsu, Hiroaki, Suzuki, Etsu, Satonaka, Hiroshi, Takeda, Ryo, Omata, Masao, Fujita, Toshiro, Nagai, Ryozo, Kitamura, Tadaichi, and Hirata, Yasunobu

Subjects
Diabetes -- Research, Diabetes -- Physiological aspects, Fluvastatin -- Research, Fluvastatin -- Physiological aspects, Biological sciences
Abstract

To study the mechanisms of vascular dysfunction in diabetes mellitus, we examined the responses of the aorta to adrenomedullin (AM) and ANG II in obese Zucker (OZ), lean Zucker (LZ), and OZ rats administered fluvastatin (OZ + Flu). AM-induced endothelium-dependent vasorelaxation was impaired in OZ rats compared with LZ rats, and fluvastatin restored AM-induced, endothelium-dependent vasorelaxation (%[DELTA]tension at [10.sup.-7] mol/l AM; LZ, -85.1 [+ or -] 3.1%; OZ, -50.7 [+ or -] 2.5%; OZ + Flu, -75.6 [+ or -] 2.7%). Expression of endothelial nitric oxide synthase (eNOS) and Akt phosphorylation in response to AM ([10.sup.-7] mol/l) were also diminished in OZ rats. Fluvastatin restored the eNOS expression and Akt phosphorylation [eNOS expression (relative intensity): LZ, 2.3 [+ or -] 0.4; OZ, 1.0 [+ or -] 0.2; OZ + Flu, 1.8 [+ or -] 0.3; Akt phosphorylation (relative intensity): LZ, 2.3 [+ or -] 0.2; OZ, 1.0 [+ or -] 0.3; OZ + Flu, 1.9 [+ or -] 0.2]. ANG II-induced vasoconstriction was enhanced in the aortic rings of OZ rats compared with LZ rats, and this enhanced vasoconstriction was partially normalized by fluvastatin and was abolished when the aorta of OZ rats was preincubated with the Rho kinase inhibitor Y-27632. GTP[gamma]S-induced contraction of permeabilized aortic smooth muscle cells, which is an indicator of the Rho-dependent [Ca.sup.2+] sensitization of contraction, was enhanced in OZ rats compared with LZ rats, and this enhanced contraction was suppressed in OZ + Flu rats. These results suggested that endothelium-dependent vasorelaxation was impaired, [Ca.sup.2+] sensitization of contraction was augmented in blood vessels of OZ rats and that fluvastatin restored vascular function by activating the Akt-dependent pathway and inhibiting the Rho-dependent pathway. nitric oxide; Akt; Rho

Published
2005

Catalog

Books, media, physical & digital resources
See catalog results