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408 results on '"Tamura, Yusuke"'

102. Immediate effects of percutaneous transvenous mitral commissurotomy on pulmonary hemodynamics at rest and during exercise in mitral stenosis

Author

Ohshima, Mitsuru, Yamazoe, Masaru, Tamura, Yusuke, Matsubara, Taku, Suzuki, Masataka, Igarashi, Yutaka, Tanabe, Yasuhiko, Yamazaki, Yuko, Koyama, Sen, Yamaguchi, Toshio, Mito, Motoko, Izumi, Tohru, Shibata, Akira, Miida, Tsutomu, Oda, Hirotaka, Toeda, Tetsuro, and Higuma, Norio

Subjects
Mitral valve stenosis -- Care and treatment, Mitral valve, Health
Abstract

Hemodynamics were evaluated during exercise in 33 patients with mitral stenosis who underwent percutaneous transvenous mitral commissurotomy (PTMC). PTMC was performed using an Inoue balloon. Each patient underwent a supine ergometer exercise test before and on the day after PTMC. Ergometer work load was started at 20 W and increased in increments of 20 W at 3-minute intervals until terminated by the patient's fatigue or shortness of breath. Mitral valve area increased by 0.8 [+ or -] 0.4 [cm.sup.2] (1.1 [ or -] 0.3 to 1.9 [ or -] 0.4 [cm.sup.2], p

Published
1992

103. Possible role of coronary artery spasm in unexplained syncope

Author

Igarashi, Yutaka, Yamazoe, Masaru, Suzuki, Kaoru, Tamura, Yusuke, Matsubara, Taku, Tanabe, Yasuhiko, Yamaguchi, Toshio, Watanabe, Kenichi, Aizawa, Yoshifusa, and Shibata, Akira

Subjects
Coronary vasospasm -- Complications, Methylergonovine, Fainting -- Causes of, Health
Abstract

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 [plus or minus] 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of [greater than or equal to] 75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. in 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiologic study. These results suggest that coronary spasm is involved in unexplained syncope. (Am J Cardiol 1990;65:713-717), This study seeks to evaluate the possibility of the existence of coronary spasm among patients with unexplained syncope, or fainting, using the methylergonovine provocation test. After routine arteriography, an X-ray of the blood vessels of the heart, methylergometrine maleate, a naturally occurring chemical that constricts blood vessels, was continuously infused into the patient for a period of up to five minutes. When ischemia, or the loss of blood flow, was evident according to changes on an electrocardiogram, methylergonovine administration was terminated and coronary arteriography was immediately performed. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis (narrowing) in more than 75 percent of the coronary arteries. Six patients had no history of chest pain even when syncope developed. Serious arrhythmia was documented in two patients, cardiac standstill in one, and complete atrioventricular block (a heart block in which electrical impulses are impeded in both the atrium and ventricle) in the other. Coronary spasm was induced in nine patients using the methylergonovine provocation test. Multi-vessel spasms were found in three patients, and induced in the artery supplying the inferior wall in seven of nine patients who had positive results. In four of those nine patients, there was no prior history of chest pain. In one patient, whose electrocardiogram was recorded during syncope, cardiac standstill, (cessation of contractions of the heart) was documented, and cardiac standstill and syncope also occurred during the provocation test. Ventricular tachycardia (rapid beat of the left ventricle, at more than 100 beats per minute, but at a constant rate, usually 150 to 200 beats per minute) was not induced by the electrophysiologic study. These results suggest that coronary vasospasm in involved in unexplained syncope. Accurate diagnosis is important to prevent not only the recurrence of syncope but also sudden death. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

104. Comparative analysis of TTF‐1 binding DNA regions in small‐cell lung cancer and non‐small‐cell lung cancer.

Author

Hokari, Satoshi, Tamura, Yusuke, Kaneda, Atsushi, Katsura, Akihiro, Morikawa, Masato, Murai, Fumihiko, Ehata, Shogo, Tsutsumi, Shuichi, Ishikawa, Yuichi, Aburatani, Hiroyuki, Kikuchi, Toshiaki, Miyazono, Kohei, and Koinuma, Daizo

Abstract

Thyroid transcription factor‐1 (TTF‐1, encoded by the NKX2‐1 gene) is highly expressed in small‐cell lung carcinoma (SCLC) and lung adenocarcinoma (LADC), but how its functional roles differ between SCLC and LADC remains to be elucidated. Here, we compared the genome‐wide distributions of TTF‐1 binding regions and the transcriptional programs regulated by TTF‐1 between NCI‐H209 (H209), a human SCLC cell line, and NCI‐H441 (H441), a human LADC cell line, using chromatin immunoprecipitation‐sequencing (ChIP‐seq) and RNA‐sequencing (RNA‐seq). TTF‐1 binding regions in H209 and H441 cells differed by 75.0% and E‐box motifs were highly enriched exclusively in the TTF‐1 binding regions of H209 cells. Transcriptome profiling revealed that TTF‐1 is involved in neuroendocrine differentiation in H209 cells. We report that TTF‐1 and achaete‐scute homolog 1 (ASCL1, also known as ASH1, an E‐box binding basic helix–loop–helix transcription factor, and a lineage‐survival oncogene of SCLC) are coexpressed and bound to adjacent sites on target genes expressed in SCLC, and cooperatively regulate transcription. Furthermore, TTF‐1 regulated expression of the Bcl‐2 gene family and showed antiapoptotic function in SCLC. Our findings suggest that TTF‐1 promotes SCLC growth and contributes to neuroendocrine and antiapoptotic gene expression by partly coordinating with ASCL1. [ABSTRACT FROM AUTHOR]

Published
2020
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105. Effect of Physical Therapy on Muscle Synergy Structure During Standing-Up Motion of Hemiplegic Patients

Author

Kogami, Hiroki, primary, Itkonen, Matti, additional, Shibata-Alnajjar, Fady, additional, Hattori, Noriaki, additional, Kinomoto, Makoto, additional, Takahashi, Kouji, additional, Fujii, Takanori, additional, Otomune, Hironori, additional, Miyai, Ichiro, additional, An, Qi, additional, Yang, Ningjia, additional, Yamakawa, Hiroshi, additional, Tamura, Yusuke, additional, Yamashita, Atsushi, additional, Asama, Hajime, additional, Shimoda, Shingo, additional, and Yamasaki, Hiroshi, additional

Published
2018
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107. Generation of tumor antigen-specific murine CD8+ T cells with enhanced anti-tumor activity via highly efficient CRISPR/Cas9 genome editing

Author

Ouchi, Yasuo, primary, Patil, Ashwini, additional, Tamura, Yusuke, additional, Nishimasu, Hiroshi, additional, Negishi, Aina, additional, Paul, Sudip Kumar, additional, Takemura, Naoki, additional, Satoh, Takeshi, additional, Kimura, Yasumasa, additional, Kurachi, Makoto, additional, Nureki, Osamu, additional, Nakai, Kenta, additional, Kiyono, Hiroshi, additional, and Uematsu, Satoshi, additional

Published
2018
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118. ZEB 1‐regulated inflammatory phenotype in breast cancer cells

Author

Katsura, Akihiro, primary, Tamura, Yusuke, additional, Hokari, Satoshi, additional, Harada, Mayumi, additional, Morikawa, Masato, additional, Sakurai, Tsubasa, additional, Takahashi, Kei, additional, Mizutani, Anna, additional, Nishida, Jun, additional, Yokoyama, Yuichiro, additional, Morishita, Yasuyuki, additional, Murakami, Takashi, additional, Ehata, Shogo, additional, Miyazono, Kohei, additional, and Koinuma, Daizo, additional

Published
2017
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124. Remote Control Technology and Human Resource Development for Decommissioning of Fukushima Daiichi Nuclear Power Station

Author

TAMURA, Yusuke, primary, OKAMOTO, Koji, additional, SUZUKI, Shunichi, additional, ASAMA, Hajime, additional, OTA, Jun, additional, YAMAMOTO, Akio, additional, YAMASHITA, Atsushi, additional, FUKUI, Rui, additional, KONYO, Masashi, additional, OHNO, Kazunori, additional, MATSUNO, Fumitoshi, additional, TAKAHASHI, Takayuki, additional, NARUSE, Keitaro, additional, SUZUKI, Shigekazu, additional, and YOKOKOHJI, Yasuyoshi, additional

Published
2017
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130. Palbociclib enhances activin‐SMAD‐induced cytostasis in estrogen receptor‐positive breast cancer.

Author

Harada, Mayumi, Morikawa, Masato, Ozawa, Takayuki, Kobayashi, Mai, Tamura, Yusuke, Takahashi, Kei, Tanabe, Masahiko, Tada, Keiichiro, Seto, Yasuyuki, Miyazono, Kohei, and Koinuma, Daizo

Abstract

Cyclin‐dependent kinase (CDK) 4 and CDK6 inhibitors are effective therapeutic options for hormone receptor (HR)‐positive, human epidermal growth factor receptor 2 (HER2)‐negative advanced breast cancer. Although CDK4/6 inhibitors mainly target the cyclin D‐CDK4/6‐retinoblastoma tumor suppressor protein (RB) axis, little is known about the clinical impact of inhibiting phosphorylation of other CDK4/6 target proteins. Here, we focused on other CDK4/6 targets, SMAD proteins. We showed that a CDK4/6 inhibitor palbociclib and activin‐SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal‐type breast cancer cell line T47D. Palbociclib enhanced SMAD2 binding to the genome by inhibiting CDK4/6‐mediated linker phosphorylation of the SMAD2 protein. We also showed that cyclin G2 plays essential roles in SMAD2‐dependent cytostatic response. Moreover, comparison of the SMAD2 ChIP‐seq data of T47D cells with those of Hs578T (triple‐negative breast cancer cells) indicated that palbociclib augmented different SMAD2‐mediated functions based on cell type, and enhanced SMAD2 binding to the target regions on the genome without affecting its binding pattern. In summary, palbociclib enhances the cytostatic effects of the activin‐SMAD2 signaling pathway, whereas it possibly strengthens the tumor‐promoting aspect in aggressive breast cancer. A CDK4/6 inhibitor palbociclib and activin‐SMAD2 signaling cooperatively inhibited cell cycle progression of a luminal‐type breast cancer cell line T47D. Palbociclib enhanced SMAD2 binding to the genome by inhibiting CDK4/6‐mediated linker phosphorylation of the SMAD2 protein. [ABSTRACT FROM AUTHOR]

Published
2019
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131. Direct determination of chemical oxygen demand by anodic decomposition of organic compounds at a diamond electrode

Author

Takeshi Kondo, Tamura Yusuke, Takeshi Watanabe, Yasuaki Einaga, Tatsuo Aikawa, Masaki Hoshino, and Makoto Yuasa

Subjects
Working electrode, Standard hydrogen electrode, Chemistry, mental disorders, Inorganic chemistry, Electrode, Analytical chemistry, Oxygen evolution, Electrolyte, Glassy carbon, Electrochemistry, Analytical Chemistry, Anode
Abstract

Chemical oxygen demand (COD) was measured directly with a simple electrochemical method using a boron-doped diamond (BDD) electrode. By applying a highly positive potential (+2.5 V vs Ag/AgCl) to an aqueous electrolyte containing potassium hydrogen phthalate, glucose, and lactic acid or sodium dodecylbenzenesulfonate using a BDD electrode, an anodic current corresponding to the electrolytic decomposition of these organic compounds was observed. No such current was seen on glassy carbon or platinum electrodes due to a significant background current caused by the oxygen evolution reaction. The electric charge for the anodic current observed at the BDD electrode was found to be consistent with the theoretical charge required for the electrolytic decomposition of the organic compounds to CO2 and was used to calculate COD. This analysis was performed by a simple I-t measurement at constant potential using a BDD electrode, and no calibration was needed. This new simple indicator, "ECOD" (electrochemical oxygen demand), will be useful for continuous monitoring of industrial wastewater with low protein concentrations and on-site instant analysis of natural water with a BDD electrode-based portable ECOD meter.

Published
2014

132. Alterations in the Expression of Intercellular Adhesion Molecule-1(ICAM-1) on Neutrophils and in the Serum in the Coronary Circulationof Patients with Coronary Artery Disease

Author

HIGUCHI, Kotaro, MATSUBARA, Taku, TOBA, Ken, HORI, Tomoyuki, IDA, Toru, TAKEMOTO, Minoru, TAMURA, Yusuke, YAMAZOE, Masaru, OITE, Takashi, and AIZAWA, Yoshifusa

Subjects
ICAM-1, coronary circulation, coronary artery disease
Abstract

The intercellular adhesion molecule-1 (ICAM-1) is expressed on the surface of endothelial cells as well as neutrophils. Because neutrophils in the coronary circulation may play an important role in the progression of coronary artery disease, ICAM-1 and other adhesion molecules expressed on them were studied in the coronary circulation of patients with coronary artery disease. We used flow cytofluorometry to evaluate the amount of ICAM-1,CD18,and L-selectin expressed on neutrophils entering and leaving the coronary circulation in 18 patients who underwent coronary angiography. In addition, the serum level of the circulating form of ICAM-1 (cICAM-1) was measured in the same samples by using an enzyme-linked immunosorbent assay. Expression as the percentage of change between the left coronary artery and coronary sinus showed that neutrophil ICAM-1 (nICAM-1) decreased and serum cICAM-1 increased in patients with severe left coronary artery stenosis, compared with those with angiographically normal coronary arteries or only mild stenosis (nICAM-1,-9.7±2.9% vs 1.0±4.0%, p

Published
2000

133. Gait analysis of patients with knee osteoarthritis by using elevation angle: confirmation of the planar law and analysis of angular difference in the approximate plane

Author

Ishikawa, Yuki, primary, An, Qi, additional, Nakagawa, Junki, additional, Oka, Hiroyuki, additional, Yasui, Tetsuro, additional, Tojima, Michio, additional, Inokuchi, Haruhi, additional, Haga, Nobuhiko, additional, Yamakawa, Hiroshi, additional, Tamura, Yusuke, additional, Yamashita, Atsushi, additional, and Asama, Hajime, additional

Published
2016
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143. Generation of tumor antigen-specific murine CD8+ T cells with enhanced anti-tumor activity via highly efficient CRISPR/Cas9 genome editing.

Author

Ouchi, Yasuo, Patil, Ashwini, Tamura, Yusuke, Nishimasu, Hiroshi, Negishi, Aina, Paul, Sudip Kumar, Takemura, Naoki, Satoh, Takeshi, Kimura, Yasumasa, and Kurachi, Makoto

Subjects
CANCER immunotherapy, TUMOR antigens, CD8 antigen, CRISPRS, GENOME editing, NUCLEOPROTEINS
Abstract

Immunotherapies have led to the successful development of novel therapies for cancer. However, there is increasing concern regarding the adverse effects caused by non-tumor-specific immune responses. Here, we report an effective strategy to generate high-avidity tumor-antigen-specific CTLs, using Cas9/single-guide RNA (sgRNA) ribonucleoprotein (RNP) delivery. As a proof-ofprinciple demonstration, we selected the gp100 melanoma-associated tumor antigen, and cloned the gp100-specific high-avidity TCR from gp100-immunized mice. To enable rapid structural dissection of the TCR, we developed a 3D protein structure modeling system for the TCR/antigenmajor histocompatibility complex (pMHC) interaction. Combining these technologies, we efficiently generated gp100-specific PD-1(-) CD8+ T cells, and demonstrated that the genetically engineered CD8+ T cells have high avidity against melanoma cells both in vitro and in vivo. Our methodology offers computational prediction of the TCR response, and enables efficient generation of tumor antigen-specific CD8+ T cells that can neutralize tumor-induced immune suppression leading to a potentially powerful cancer therapeutic. [ABSTRACT FROM AUTHOR]

Published
2018
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