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2. Efficacy and Tolerability of Ivabradine for Cardiomyopathy in Patients with Duchenne Muscular Dystrophy

Author

Wakisaka, Akiko, primary, Kimura, Koichi, additional, Morita, Hiroyuki, additional, Nakanishi, Koki, additional, Daimon, Masao, additional, Nojima, Masanori, additional, Itoh, Hideki, additional, Takeda, Atsuhito, additional, Kitao, Ruriko, additional, Imai, Tomihiro, additional, Ikeda, Tetsuhiko, additional, Nakajima, Takashi, additional, Watanabe, Chigusa, additional, Furukawa, Toshihiro, additional, Ohno, Ichiro, additional, Ishida, Chiho, additional, Takeda, Norihiko, additional, and Komai, Kiyonobu, additional

Published
2024
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4. Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome

Author

Lahrouchi, Najim, Tadros, Rafik, Crotti, Lia, Mizusawa, Yuka, Postema, Pieter G., Beekman, Leander, Walsh, Roddy, Hasegawa, Kanae, Barc, Julien, Ernsting, Marko, Turkowski, Kari L., Mazzanti, Andrea, Beckmann, Britt M., Shimamoto, Keiko, Diamant, Ulla-Britt, Wijeyeratne, Yanushi D., Kucho, Yu, Robyns, Tomas, Ishikawa, Taisuke, Arbelo, Elena, Christiansen, Michael, Winbo, Annika, Jabbari, Reza, Lubitz, Steven A., Steinfurt, Johannes, Rudic, Boris, Loeys, Bart, Shoemaker, M. Ben, Weeke, Peter E., Pfeiffer, Ryan, Davies, Brianna, Andorin, Antoine, Hofman, Nynke, Dagradi, Federica, Pedrazzini, Matteo, Tester, David J., Bos, J. Martijn, Sarquella-Brugada, Georgia, Campuzano, Óscar, Platonov, Pyotr G., Stallmeyer, Birgit, Zumhagen, Sven, Nannenberg, Eline A., Veldink, Jan H., van den Berg, Leonard H., Al-Chalabi, Ammar, Shaw, Christopher E., Shaw, Pamela J., Morrison, Karen E., Andersen, Peter M., Müller-Nurasyid, Martina, Cusi, Daniele, Barlassina, Cristina, Galan, Pilar, Lathrop, Mark, Munter, Markus, Werge, Thomas, Ribasés, Marta, Aung, Tin, Khor, Chiea C., Ozaki, Mineo, Lichtner, Peter, Meitinger, Thomas, van Tintelen, J. Peter, Hoedemaekers, Yvonne, Denjoy, Isabelle, Leenhardt, Antoine, Napolitano, Carlo, Shimizu, Wataru, Schott, Jean-Jacques, Gourraud, Jean-Baptiste, Makiyama, Takeru, Ohno, Seiko, Itoh, Hideki, Krahn, Andrew D., Antzelevitch, Charles, Roden, Dan M., Saenen, Johan, Borggrefe, Martin, Odening, Katja E., Ellinor, Patrick T., Tfelt-Hansen, Jacob, Skinner, Jonathan R., van den Berg, Maarten P., Olesen, Morten Salling, Brugada, Josep, Brugada, Ramón, Makita, Naomasa, Breckpot, Jeroen, Yoshinaga, Masao, Behr, Elijah R., Rydberg, Annika, Aiba, Takeshi, Kääb, Stefan, Priori, Silvia G., Guicheney, Pascale, Tan, Hanno L., Newton-Cheh, Christopher, Ackerman, Michael J., Schwartz, Peter J., Schulze-Bahr, Eric, Probst, Vincent, Horie, Minoru, Wilde, Arthur A., Tanck, Michael W.T., and Bezzina, Connie R.

Published
2020
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9. The genetics underlying acquired long QT syndrome: impact for genetic screening

Author

Itoh, Hideki, Crotti, Lia, Aiba, Takeshi, Spazzolini, Carla, Denjoy, Isabelle, Fressart, Véronique, Hayashi, Kenshi, Nakajima, Tadashi, Ohno, Seiko, Makiyama, Takeru, Wu, Jie, Hasegawa, Kanae, Mastantuono, Elisa, Dagradi, Federica, Pedrazzini, Matteo, Yamagishi, Masakazu, Berthet, Myriam, Murakami, Yoshitaka, Shimizu, Wataru, Guicheney, Pascale, Schwartz, Peter J., and Horie, Minoru

Published
2016
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10. Microscopic heat pulses activate cardiac thin filaments

Author

Ishii, Shuya, Oyama, Kotaro, Arai, Tomomi, Itoh, Hideki, A. Shintani, Seine, Suzuki, Madoka, Fuyu, Kobirumaki-Shimozawa, Terui, Takako, and Fukuda, Norio

Subjects
macromolecular substances
Abstract

During the excitation-contraction coupling of the heart, sarcomeres are activated via thin filament structural changes (i.e., from the "off" state to the "on" state) in response to a release of Ca2+ from the sarcoplasmic reticulum. This process involves chemical reactions that are highly dependent on ambient temperature; for example, catalytic activity of the actomyosin ATPase rises with increasing temperature. Here, we investigate the effects of rapid heating by focused infrared (IR) laser irradiation on the sliding of thin filaments reconstituted with human α-tropomyosin and bovine ventricular troponin in an in vitro motility assay. We perform high-precision analyses measuring temperature by the fluorescence intensity of rhodamine-phalloidin-labeled F-actin coupled with a fluorescent thermosensor sheet containing the temperature-sensitive dye Europium (III) thenoyltrifluoroacetonate trihydrate. This approach enables a shift in temperature from 25°C to ∼46°C within 0.2 s. We find that in the absence of Ca2+ and presence of ATP, IR laser irradiation elicits sliding movements of reconstituted thin filaments with a sliding velocity that increases as a function of temperature. The heating-induced acceleration of thin filament sliding likewise occurs in the presence of Ca2+ and ATP; however, the temperature dependence is more than twofold less pronounced. These findings could indicate that in the mammalian heart, the on-off equilibrium of the cardiac thin filament state is partially shifted toward the on state in diastole at physiological body temperature, enabling rapid and efficient myocardial dynamics in systole.

Published
2019

13. Enhancing rare variant interpretation in inherited arrhythmias through quantitative analysis of consortium disease cohorts and population controls

Author

Walsh, Roddy, Lahrouchi, Najim, Tadros, Rafik, Kyndt, Florence, Glinge, Charlotte, Postema, Pieter G., Amin, Ahmad S., Nannenberg, Eline A., Ware, James S., Whiffin, Nicola, Mazzarotto, Francesco, Skoric-Milosavljevic, Doris, Krijger, Christian, Arbelo, Elena, Babuty, Dominique, Barajas-Martinez, Hector, Beckmann, Britt M., Bezieau, Stephane, Bos, J. Martijn, Breckpot, Jeroen, Campuzano, Oscar, Castelletti, Silvia, Celen, Candan, Clauss, Sebastian, Corveleyn, Anniek, Crotti, Lia, Dagradi, Federica, de Asmundis, Carlo, Denjoy, Isabelle, Dittmann, Sven, Ellinor, Patrick T., Ortuno, Cristina Gil, Giustetto, Carla, Gourraud, Jean-Baptiste, Hazeki, Daisuke, Horie, Minoru, Ishikawa, Taisuke, Itoh, Hideki, Kaneko, Yoshiaki, Kanters, Jorgen K., Kimoto, Hiroki, Kotta, Maria-Christina, Krapels, Ingrid P. C., Kurabayashi, Masahiko, Lazarte, Julieta, Leenhardt, Antoine, Loeys, Bart L., Lundin, Catarina, Makiyama, Takeru, Mansourati, Jacques, Martins, Raphael P., Mazzanti, Andrea, Mörner, Stellan, Napolitano, Carlo, Ohkubo, Kimie, Papadakis, Michael, Rudic, Boris, Molina, Maria Sabater, Sacher, Frederic, Sahin, Hatice, Sarquella-Brugada, Georgia, Sebastiano, Regina, Sharma, Sanjay, Sheppard, Mary N., Shimamoto, Keiko, Shoemaker, M. Benjamin, Stallmeyer, Birgit, Steinfurt, Johannes, Tanaka, Yuji, Tester, David J., Usuda, Keisuke, van der Zwaag, Paul A., Van Dooren, Sonia, Van Laer, Lut, Winbo, Annika, Winkel, Bo G., Yamagata, Kenichiro, Zumhagen, Sven, Volders, Paul G. A., Lubitz, Steven A., Antzelevitch, Charles, Platonov, Pyotr G., Odening, Katja E., Roden, Dan M., Roberts, Jason D., Skinner, Jonathan R., Tfelt-Hansen, Jacob, van den Berg, Maarten P., Olesen, Morten S., Lambiase, Pier D., Borggrefe, Martin, Hayashi, Kenshi, Rydberg, Annika, Nakajima, Tadashi, Yoshinaga, Masao, Saenen, Johan B., Kaeaeb, Stefan, Brugada, Pedro, Robyns, Tomas, Giachino, Daniela F., Ackerman, Michael J., Brugada, Ramon, Brugada, Josep, Gimeno, Juan R., Hasdemir, Can, Guicheney, Pascale, Priori, Silvia G., Schulze-Bahr, Eric, Makita, Naomasa, Schwartz, Peter J., Shimizu, Wataru, Aiba, Takeshi, Schott, Jean-Jacques, Redon, Richard, Ohno, Seiko, Probst, Vincent, Behr, Elijah R., Barc, Julien, Bezzina, Connie R., Walsh, Roddy, Lahrouchi, Najim, Tadros, Rafik, Kyndt, Florence, Glinge, Charlotte, Postema, Pieter G., Amin, Ahmad S., Nannenberg, Eline A., Ware, James S., Whiffin, Nicola, Mazzarotto, Francesco, Skoric-Milosavljevic, Doris, Krijger, Christian, Arbelo, Elena, Babuty, Dominique, Barajas-Martinez, Hector, Beckmann, Britt M., Bezieau, Stephane, Bos, J. Martijn, Breckpot, Jeroen, Campuzano, Oscar, Castelletti, Silvia, Celen, Candan, Clauss, Sebastian, Corveleyn, Anniek, Crotti, Lia, Dagradi, Federica, de Asmundis, Carlo, Denjoy, Isabelle, Dittmann, Sven, Ellinor, Patrick T., Ortuno, Cristina Gil, Giustetto, Carla, Gourraud, Jean-Baptiste, Hazeki, Daisuke, Horie, Minoru, Ishikawa, Taisuke, Itoh, Hideki, Kaneko, Yoshiaki, Kanters, Jorgen K., Kimoto, Hiroki, Kotta, Maria-Christina, Krapels, Ingrid P. C., Kurabayashi, Masahiko, Lazarte, Julieta, Leenhardt, Antoine, Loeys, Bart L., Lundin, Catarina, Makiyama, Takeru, Mansourati, Jacques, Martins, Raphael P., Mazzanti, Andrea, Mörner, Stellan, Napolitano, Carlo, Ohkubo, Kimie, Papadakis, Michael, Rudic, Boris, Molina, Maria Sabater, Sacher, Frederic, Sahin, Hatice, Sarquella-Brugada, Georgia, Sebastiano, Regina, Sharma, Sanjay, Sheppard, Mary N., Shimamoto, Keiko, Shoemaker, M. Benjamin, Stallmeyer, Birgit, Steinfurt, Johannes, Tanaka, Yuji, Tester, David J., Usuda, Keisuke, van der Zwaag, Paul A., Van Dooren, Sonia, Van Laer, Lut, Winbo, Annika, Winkel, Bo G., Yamagata, Kenichiro, Zumhagen, Sven, Volders, Paul G. A., Lubitz, Steven A., Antzelevitch, Charles, Platonov, Pyotr G., Odening, Katja E., Roden, Dan M., Roberts, Jason D., Skinner, Jonathan R., Tfelt-Hansen, Jacob, van den Berg, Maarten P., Olesen, Morten S., Lambiase, Pier D., Borggrefe, Martin, Hayashi, Kenshi, Rydberg, Annika, Nakajima, Tadashi, Yoshinaga, Masao, Saenen, Johan B., Kaeaeb, Stefan, Brugada, Pedro, Robyns, Tomas, Giachino, Daniela F., Ackerman, Michael J., Brugada, Ramon, Brugada, Josep, Gimeno, Juan R., Hasdemir, Can, Guicheney, Pascale, Priori, Silvia G., Schulze-Bahr, Eric, Makita, Naomasa, Schwartz, Peter J., Shimizu, Wataru, Aiba, Takeshi, Schott, Jean-Jacques, Redon, Richard, Ohno, Seiko, Probst, Vincent, Behr, Elijah R., Barc, Julien, and Bezzina, Connie R.

Abstract

Purpose: Stringent variant interpretation guidelines can lead to high rates of variants of uncertain significance (VUS) for genetically heterogeneous disease like long QT syndrome (LQTS) and Brugada syndrome (BrS). Quantitative and disease-specific customization of American College of Medical Genetics and Genomics/Association for Molecular Pathology (ACMG/AMP) guidelines can address this false negative rate. Methods: We compared rare variant frequencies from 1847 LQTS (KCNQ1/KCNH2/SCN5A) and 3335 BrS (SCN5A) cases from the International LQTS/BrS Genetics Consortia to population-specific gnomAD data and developed disease-specific criteria for ACMG/AMP evidence classes-rarity (PM2/BS1 rules) and case enrichment of individual (PS4) and domain-specific (PM1) variants. Results: Rare SCN5A variant prevalence differed between European (20.8%) and Japanese (8.9%) BrS patients (p = 5.7 x 10(-18)) and diagnosis with spontaneous (28.7%) versus induced (15.8%) Brugada type 1 electrocardiogram (ECG) (p = 1.3 x 10(-13)). Ion channel transmembrane regions and specific N-terminus (KCNH2) and C-terminus (KCNQ1/KCNH2) domains were characterized by high enrichment of case variants and >95% probability of pathogenicity. Applying the customized rules, 17.4% of European BrS and 74.8% of European LQTS cases had (likely) pathogenic variants, compared with estimated diagnostic yields (case excess over gnomAD) of 19.2%/82.1%, reducing VUS prevalence to close to background rare variant frequency. Conclusion: Large case-control data sets enable quantitative implementation of ACMG/AMP guidelines and increased sensitivity for inherited arrhythmia genetic testing.

Published
2021
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17. JCS/JHRS2020 Guideline on Pharmacotherapy of Cardiac Arrhythmias

Author

Ono, Katsushige, Iwasaki, Yu‐ki, Akao, Masaharu, Ikeda, Takanori, Ishii, Kuniaki, Inden, Yasuya, Kusano, Kengo, Kobayashi, Yoshinori, Koretsune, Yukihiro, Sasano, Tetsuo, Sumitomo, Naokata, Takahashi, Naohiko, Niwano, Shinichi, Hagiwara, Nobuhisa, Hisatome, Ichiro, Furukawa, Tetsushi, Honjo, Haruo, Maruyama, Toru, Murakawa, Yuji, Yasaka, Masahiro, Watanabe, Eiichi, Aiba, Takeshi, Amino, Mari, Itoh, Hideki, Ogawa, Hisashi, Okumura, Yasuo, Aoki‐Kamiya, Chizuko, Kishihara, Jun, Kodani, Eitaro, Komatsu, Takashi, Sakamoto, Yusuke, Satomi, Kazuhiro, Shiga, Tsuyoshi, Shinohara, Tetsuji, Suzuki, Atsushi, Suzuki, Shinya, Sekiguchi, Yukio, Nagase, Satoshi, Hayami, Noriyuki, Harada, Masahide, Fujino, Tadashi, Makiyama, Takeru, Maruyama, Mitsunori, Miake, Junichiro, Muraji, Shota, Murata, Hiroshige, Morita, Norishige, Yokoshiki, Hisashi, Yoshioka, Koichiro, Yodogawa, Kenji, Inoue, Hiroshi, Okumura, Ken, Kimura, Takeshi, Tsutsui, Hiroyuki, and Shimizu, Wataru

Published
2022
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19. The E1784K mutation in SCN5A is associated with mixed clinical phenotype of type 3 long QT syndrome

Author

Makita, Naomasa, Behr, Elijah, Shimizu, Wataru, Horie, Minoru, Sunami, Akihiko, Crotti, Lia, Schulze-Bahr, Eric, Fukuhara, Shigetomo, Mochizuki, Naoki, Makiyama, Takeru, Itoh, Hideki, Christiansen, Michael, McKeown, Pascal, Miyamoto, Koji, Kamakura, Shiro, Tsutsui, Hiroyuki, Schwartz, Peter J., George, Alfred L., Jr., and Roden, Dan M.

Subjects
Arrhythmia -- Risk factors, Arrhythmia -- Diagnosis, Arrhythmia -- Drug therapy, Arrhythmia -- Research, Gene mutations -- Complications and side effects, Gene mutations -- Research, Long QT syndrome -- Risk factors, Long QT syndrome -- Diagnosis, Long QT syndrome -- Drug therapy, Long QT syndrome -- Complications and side effects, Long QT syndrome -- Research
Abstract

Phenotypic overlap of type 3 long QT syndrome (LQT3) with Brugada syndrome (BrS) is observed in some carriers of mutations in the Na channel SCN5A. While this overlap is important for patient management, the clinical features, prevalence, and mechanisms underlying such overlap have not been fully elucidated. To investigate the basis for this overlap, we genotyped a cohort of 44 LQT3 families of multiple ethnicities from 7 referral centers and found a high prevalence of the E1784K mutation in SCN5A. Of 41 E1784K carriers, 93% had LQT3, 22% had BrS, and 39% had sinus node dysfunction. Heterologously expressed E1784K channels showed a 15.0-mV negative shift in the voltage dependence of Na channel inactivation and a 7.5-fold increase in flecainide affinity for resting-state channels, properties also seen with other LQT3 mutations associated with a mixed clinical phenotype. Furthermore, these properties were absent in Na channels harboring the T1304M mutation, which is associated with LQT3 without a mixed clinical phenotype. These results suggest that a negative shift of steady-state Na channel inactivation and enhanced tonic block by class IC drugs represent common biophysical mechanisms underlying the phenotypic overlap of LQT3 and BrS and further indicate that class IC drugs should be avoided in patients with Na channels displaying these behaviors., Introduction Congenital long QT syndrome (LQTS) is characterized by the prolongation of the QT interval on surface ECGs and an increased risk of potentially fatal ventricular arrhythmias, especially torsade de [...]

Published
2008

20. Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome

Author

ZL Neuromusculaire Ziekten Medisch, Brain, Projectafdeling ALS, Regenerative Medicine and Stem Cells, Circulatory Health, Genetica, UMC Utrecht, Lahrouchi, Najim, Tadros, Rafik, Crotti, Lia, Mizusawa, Yuka, Postema, Pieter G, Beekman, Leander, Walsh, Roddy, Hasegawa, Kanae, Barc, Julien, Ernsting, Marko, Turkowski, Kari L, Mazzanti, Andrea, Beckmann, Britt M, Shimamoto, Keiko, Diamant, Ulla-Britt, Wijeyeratne, Yanushi D, Kucho, Yu, Robyns, Tomas, Ishikawa, Taisuke, Arbelo, Elena, Christiansen, Michael, Winbo, Annika, Jabbari, Reza, Lubitz, Steven A, Steinfurt, Johannes, Rudic, Boris, Loeys, Bart, Shoemaker, M Ben, Weeke, Peter E, Pfeiffer, Ryan, Davies, Brianna, Andorin, Antoine, Hofman, Nynke, Dagradi, Federica, Pedrazzini, Matteo, Tester, David J, Bos, J Martijn, Sarquella-Brugada, Georgia, Campuzano, Óscar, Platonov, Pyotr G, Stallmeyer, Birgit, Zumhagen, Sven, Nannenberg, Eline A, Veldink, Jan H, van den Berg, Leonard H, Al-Chalabi, Ammar, Shaw, Christopher E, Shaw, Pamela J, Morrison, Karen E, Andersen, Peter M, Müller-Nurasyid, Martina, Cusi, Daniele, Barlassina, Cristina, Galan, Pilar, Lathrop, Mark, Munter, Markus, Werge, Thomas, Ribasés, Marta, Aung, Tin, Khor, Chiea C, Ozaki, Mineo, Lichtner, Peter, Meitinger, Thomas, van Tintelen, J Peter, Hoedemaekers, Yvonne, Denjoy, Isabelle, Leenhardt, Antoine, Napolitano, Carlo, Shimizu, Wataru, Schott, Jean-Jacques, Gourraud, Jean-Baptiste, Makiyama, Takeru, Ohno, Seiko, Itoh, Hideki, Krahn, Andrew D, Antzelevitch, Charles, Roden, Dan M, Saenen, Johan, Borggrefe, Martin, Odening, Katja E, Ellinor, Patrick T, Tfelt-Hansen, Jacob, Skinner, Jonathan R, van den Berg, Maarten P, Olesen, Morten Salling, Brugada, Josep, Brugada, Ramón, Makita, Naomasa, Breckpot, Jeroen, Yoshinaga, Masao, Behr, Elijah R, Rydberg, Annika, Aiba, Takeshi, Kääb, Stefan, Priori, Silvia G, Guicheney, Pascale, Tan, Hanno L, Newton-Cheh, Christopher, Ackerman, Michael J, Schwartz, Peter J, Schulze-Bahr, Eric, Probst, Vincent, Horie, Minoru, Wilde, Arthur A, Tanck, Michael W T, Bezzina, Connie R, ZL Neuromusculaire Ziekten Medisch, Brain, Projectafdeling ALS, Regenerative Medicine and Stem Cells, Circulatory Health, Genetica, UMC Utrecht, Lahrouchi, Najim, Tadros, Rafik, Crotti, Lia, Mizusawa, Yuka, Postema, Pieter G, Beekman, Leander, Walsh, Roddy, Hasegawa, Kanae, Barc, Julien, Ernsting, Marko, Turkowski, Kari L, Mazzanti, Andrea, Beckmann, Britt M, Shimamoto, Keiko, Diamant, Ulla-Britt, Wijeyeratne, Yanushi D, Kucho, Yu, Robyns, Tomas, Ishikawa, Taisuke, Arbelo, Elena, Christiansen, Michael, Winbo, Annika, Jabbari, Reza, Lubitz, Steven A, Steinfurt, Johannes, Rudic, Boris, Loeys, Bart, Shoemaker, M Ben, Weeke, Peter E, Pfeiffer, Ryan, Davies, Brianna, Andorin, Antoine, Hofman, Nynke, Dagradi, Federica, Pedrazzini, Matteo, Tester, David J, Bos, J Martijn, Sarquella-Brugada, Georgia, Campuzano, Óscar, Platonov, Pyotr G, Stallmeyer, Birgit, Zumhagen, Sven, Nannenberg, Eline A, Veldink, Jan H, van den Berg, Leonard H, Al-Chalabi, Ammar, Shaw, Christopher E, Shaw, Pamela J, Morrison, Karen E, Andersen, Peter M, Müller-Nurasyid, Martina, Cusi, Daniele, Barlassina, Cristina, Galan, Pilar, Lathrop, Mark, Munter, Markus, Werge, Thomas, Ribasés, Marta, Aung, Tin, Khor, Chiea C, Ozaki, Mineo, Lichtner, Peter, Meitinger, Thomas, van Tintelen, J Peter, Hoedemaekers, Yvonne, Denjoy, Isabelle, Leenhardt, Antoine, Napolitano, Carlo, Shimizu, Wataru, Schott, Jean-Jacques, Gourraud, Jean-Baptiste, Makiyama, Takeru, Ohno, Seiko, Itoh, Hideki, Krahn, Andrew D, Antzelevitch, Charles, Roden, Dan M, Saenen, Johan, Borggrefe, Martin, Odening, Katja E, Ellinor, Patrick T, Tfelt-Hansen, Jacob, Skinner, Jonathan R, van den Berg, Maarten P, Olesen, Morten Salling, Brugada, Josep, Brugada, Ramón, Makita, Naomasa, Breckpot, Jeroen, Yoshinaga, Masao, Behr, Elijah R, Rydberg, Annika, Aiba, Takeshi, Kääb, Stefan, Priori, Silvia G, Guicheney, Pascale, Tan, Hanno L, Newton-Cheh, Christopher, Ackerman, Michael J, Schwartz, Peter J, Schulze-Bahr, Eric, Probst, Vincent, Horie, Minoru, Wilde, Arthur A, Tanck, Michael W T, and Bezzina, Connie R

Published
2020

21. Bradycardia Is a Specific Phenotype of Catecholaminergic Polymorphic Ventricular Tachycardia Induced by RYR2 Mutations

Author

Miyata, Kazuaki, Ohno, Seiko, Itoh, Hideki, and Horie, Minoru

Subjects
Male, RYR2 mutation, catecholaminergic polymorphic ventricular tachycardia, Adolescent, Infant, Newborn, Infant, Ryanodine Receptor Calcium Release Channel, bradycardia, Phenotype, Child, Preschool, Mutation, cardiovascular system, long QT syndrome, Tachycardia, Ventricular, Humans, Original Article, Female, Genetic Predisposition to Disease, cardiovascular diseases, Child
Abstract

Objective Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a lethal inherited disease characterized by ventricular arrhythmias induced by physical exercise or emotional stress. The major cause of CPVT is mutations in RYR2, which encodes the cardiac ryanodine receptor channel. Recent advances in sequencing technology have yielded incidental findings of RYR2 variants in other cardiac diseases. Analyzing the characteristics of RYR2 variants related to CPVT will be useful for differentiation from those related to other cardiac diseases. We examined the phenotypic characteristics of patients with RYR2 variants. Methods Seventy-nine probands carrying RYR2 variants whose diagnoses were either CPVT (n=68) or long QT syndrome (LQTS; n=11) were enrolled. We compared the characteristics of the electrocardiogram (ECG) and the location of the RYR2 mutations-N-terminal (NT), central region (CR) or C-terminal (CT)-between the two patient groups. Results Using the ECGs available from 53 probands before β-blocker therapies, we analyzed the heart rates (HRs). CPVT probands showed bradycardia more frequently (25/44; 57%) than LQTS probands (1/9; 11%; p=0.024). In CPVT patients, 20 mutations were located in NT, 25 in CR and 23 in CT. In LQTS patients, 5 mutations were located in NT, 2 in CR and 4 in CT. There were no significant differences in the locations of the RYR2 mutations between the phenotypes. Conclusion Bradycardia was highly correlated with the phenotype of CPVT. When a clinically-diagnosed LQTS patient with bradycardia carries an RYR2 mutation, we should be careful to avoid making a misdiagnosis, as the patient may actually have CPVT.

Published
2018

22. High incidence of major bleeding with off-label use of edoxaban

Author

Fukui, Rika, primary, Hira, Daiki, additional, Kunitsu, Yuki, additional, Isono, Tetsuichiro, additional, Tabuchi, Yohei, additional, Ikuno, Yoshihiro, additional, Ueshima, Satoshi, additional, Itoh, Hideki, additional, Tanaka, Toshihiro, additional, and Terada, Tomohiro, additional

Published
2021
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23. Enhancing rare variant interpretation in inherited arrhythmias through quantitative analysis of consortium disease cohorts and population controls

Author

Walsh, Roddy, primary, Lahrouchi, Najim, additional, Tadros, Rafik, additional, Kyndt, Florence, additional, Glinge, Charlotte, additional, Postema, Pieter G., additional, Amin, Ahmad S., additional, Nannenberg, Eline A., additional, Ware, James S., additional, Whiffin, Nicola, additional, Mazzarotto, Francesco, additional, Škorić-Milosavljević, Doris, additional, Krijger, Christian, additional, Arbelo, Elena, additional, Babuty, Dominique, additional, Barajas-Martinez, Hector, additional, Beckmann, Britt M., additional, Bézieau, Stéphane, additional, Bos, J. Martijn, additional, Breckpot, Jeroen, additional, Campuzano, Oscar, additional, Castelletti, Silvia, additional, Celen, Candan, additional, Clauss, Sebastian, additional, Corveleyn, Anniek, additional, Crotti, Lia, additional, Dagradi, Federica, additional, de Asmundis, Carlo, additional, Denjoy, Isabelle, additional, Dittmann, Sven, additional, Ellinor, Patrick T., additional, Ortuño, Cristina Gil, additional, Giustetto, Carla, additional, Gourraud, Jean-Baptiste, additional, Hazeki, Daisuke, additional, Horie, Minoru, additional, Ishikawa, Taisuke, additional, Itoh, Hideki, additional, Kaneko, Yoshiaki, additional, Kanters, Jørgen K., additional, Kimoto, Hiroki, additional, Kotta, Maria-Christina, additional, Krapels, Ingrid P.C., additional, Kurabayashi, Masahiko, additional, Lazarte, Julieta, additional, Leenhardt, Antoine, additional, Loeys, Bart L., additional, Lundin, Catarina, additional, Makiyama, Takeru, additional, Mansourati, Jacques, additional, Martins, Raphaël P., additional, Mazzanti, Andrea, additional, Mörner, Stellan, additional, Napolitano, Carlo, additional, Ohkubo, Kimie, additional, Papadakis, Michael, additional, Rudic, Boris, additional, Molina, Maria Sabater, additional, Sacher, Frédéric, additional, Sahin, Hatice, additional, Sarquella-Brugada, Georgia, additional, Sebastiano, Regina, additional, Sharma, Sanjay, additional, Sheppard, Mary N., additional, Shimamoto, Keiko, additional, Shoemaker, M.Benjamin, additional, Stallmeyer, Birgit, additional, Steinfurt, Johannes, additional, Tanaka, Yuji, additional, Tester, David J., additional, Usuda, Keisuke, additional, van der Zwaag, Paul A., additional, Van Dooren, Sonia, additional, Van Laer, Lut, additional, Winbo, Annika, additional, Winkel, Bo G., additional, Yamagata, Kenichiro, additional, Zumhagen, Sven, additional, Volders, Paul G.A., additional, Lubitz, Steven A., additional, Antzelevitch, Charles, additional, Platonov, Pyotr G., additional, Odening, Katja E., additional, Roden, Dan M., additional, Roberts, Jason D., additional, Skinner, Jonathan R., additional, Tfelt-Hansen, Jacob, additional, van den Berg, Maarten P., additional, Olesen, Morten S., additional, Lambiase, Pier D., additional, Borggrefe, Martin, additional, Hayashi, Kenshi, additional, Rydberg, Annika, additional, Nakajima, Tadashi, additional, Yoshinaga, Masao, additional, Saenen, Johan B., additional, Kääb, Stefan, additional, Brugada, Pedro, additional, Robyns, Tomas, additional, Giachino, Daniela F., additional, Ackerman, Michael J., additional, Brugada, Ramon, additional, Brugada, Josep, additional, Gimeno, Juan R., additional, Hasdemir, Can, additional, Guicheney, Pascale, additional, Priori, Silvia G., additional, Schulze-Bahr, Eric, additional, Makita, Naomasa, additional, Schwartz, Peter J., additional, Shimizu, Wataru, additional, Aiba, Takeshi, additional, Schott, Jean-Jacques, additional, Redon, Richard, additional, Ohno, Seiko, additional, Probst, Vincent, additional, Arnaout, Alain Al, additional, Amelot, Mathieu, additional, Anselme, Frédéric, additional, Billon, Olivier, additional, Defaye, Pascal, additional, Dupuis, Jean-Marc, additional, Jesel, Laurence, additional, Laurent, Gabriel, additional, Maury, Philippe, additional, Pasquie, Jean-Luc, additional, Wiart, Francois, additional, Behr, Elijah R., additional, Barc, Julien, additional, and Bezzina, Connie R., additional

Published
2021
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27. Genetic Background of Catecholaminergic Polymorphic Ventricular Tachycardia in Japan

Author

Kawamura, Mihoko, primary, Ohno, Seiko, additional, Naiki, Nobu, additional, Nagaoka, Iori, additional, Dochi, Kenichi, additional, Wang, Qi, additional, Hasegawa, Kanae, additional, Kimura, Hiromi, additional, Miyamoto, Akashi, additional, Mizusawa, Yuka, additional, Itoh, Hideki, additional, Makiyama, Takeru, additional, Sumitomo, Naokata, additional, Ushinohama, Hiroya, additional, Oyama, Kotaro, additional, Murakoshi, Nobuyuki, additional, Aonuma, Kazutaka, additional, Horigome, Hitoshi, additional, Honda, Takafumi, additional, Yoshinaga, Masao, additional, Ito, Makoto, additional, and Horie, Minoru, additional

Published
2020
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29. Systematic Evaluation of KCNQ1 Variant Using ACMG/AMP Guidelines and Risk Stratification in Long QT Syndrome Type 1

Author

Kashiwa, Asami, primary, Aiba, Takeshi, additional, Makimoto, Hisaki, additional, Shimamoto, Keiko, additional, Yamagata, Kenichiro, additional, Kamakura, Tsukasa, additional, Wada, Mitsuru, additional, Miyamoto, Koji, additional, Inoue-Yamada, Yuko, additional, Ishibashi, Kohei, additional, Noda, Takashi, additional, Nagase, Satoshi, additional, Miyazaki, Aya, additional, Sakaguchi, Heima, additional, Shiraishi, Isao, additional, Yagihara, Nobue, additional, Watanabe, Hiroshi, additional, Aizawa, Yoshifusa, additional, Makiyama, Takeru, additional, Itoh, Hideki, additional, Hayashi, Kenshi, additional, Yamagishi, Masakazu, additional, Sumitomo, Naotaka, additional, Yoshinaga, Masao, additional, Morita, Hiroshi, additional, Ohe, Tohru, additional, Miyamoto, Yoshihiro, additional, Makita, Naomasa, additional, Yasuda, Satoshi, additional, Kusano, Kengo, additional, Ohno, Seiko, additional, Horie, Minoru, additional, and Shimizu, Wataru, additional

Published
2020
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30. Cardiac Conduction Disorders as Markers of Cardiac Events in Myotonic Dystrophy Type 1

Author

Itoh, Hideki, primary, Hisamatsu, Takashi, additional, Tamura, Takuhisa, additional, Segawa, Kazuhiko, additional, Takahashi, Toshiaki, additional, Takada, Hiroto, additional, Kuru, Satoshi, additional, Wada, Chizu, additional, Suzuki, Mikiya, additional, Suwazono, Shugo, additional, Sasaki, Shingo, additional, Okumura, Ken, additional, Horie, Minoru, additional, Takahashi, Masanori P., additional, and Matumura, Tsuyoshi, additional

Published
2020
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31. Single-cell temperature mapping with fluorescent thermometer nanosheets

Author

Oyama, Kotaro, primary, Gotoh, Mizuho, primary, Hosaka, Yuji, primary, Oyama, Tomoko G., primary, Kubonoya, Aya, primary, Suzuki, Yuma, primary, Arai, Tomomi, primary, Tsukamoto, Seiichi, primary, Kawamura, Yuki, primary, Itoh, Hideki, primary, Shintani, Seine A., primary, Yamazawa, Toshiko, primary, Taguchi, Mitsumasa, primary, Ishiwata, Shin’ichi, primary, and Fukuda, Norio, primary

Published
2020
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35. Age, gender, insulin and blood glucose control status alter the risk of ischemic heart disease and stroke among elderly diabetic patients

Author

Hattori Yoshiyuki, Sone Hirohito, Yokote Koutaro, Ohrui Takashi, Watanabe Hiroshi, Itoh Hideki, Nomura Hideki, Kawashima Seinosuke, Hayashi Toshio, Yoshizumi Masao, Ina Koichiro, and Kubota Kiyoshi

Subjects
Elderly, Diabetes mellitus, Insulin, Cerebral ischemia, Ischemic heart disease, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background We analyzed the effects of insulin therapy, age and gender on the risk of ischemic heart disease (IHD) and cerebrovascular accident (CVA) according to glycemic control. Methods and Results We performed a prospective cohort study (Japan Cholesterol and Diabetes Mellitus Study) of type 2 diabetes patients (n = 4014) for 2 years. The primary endpoint was the onset of fatal/non-fatal IHD and/or CVA, which occurred at rates of 7.9 and 7.2 per 1000 person-years, respectively. We divided diabetic patients into four groups based on age (≤ 70 and > 70) and hemoglobin A1C levels (≤ 7.0 and > 7.0%). Multiple regression analysis revealed that IHD was associated with high systolic blood pressure and low HDL-C in patients under 70 years of age with fair glycemic control and was associated with low diastolic blood pressure in the older/fair group. Interestingly, insulin use was associated with IHD in the older/poor group (OR = 2.27, 95% CI = 1.11-5.89; p = 0.026) and was associated with CVA in the older/fair group (OR = 2.09, 95% CI = 1.06-4.25; p = 0.028). CVA was associated with lower HDL-C and longer duration of diabetes in younger/poor glycemic control group. Results by stepwise analysis were similar. Next, patients were divided into four groups based on gender and diabetic control(hemoglobinA1C < or > 7.0%). Multiple regression analysis revealed that IHD was associated with high systolic blood pressure in male/fair glycemic control group, age in male/poor control group, and short duration of diabetic history in females in both glycemic control groups. Interestingly, insulin use was associated with IHD in the male/poor group(OR = 4.11, 95% CI = 1.22-8.12; p = 0.018) and with CVA in the female/poor group(OR = 3.26, 95% CI = 1.12-6.24; p = 0.02). CVA was associated with short duration of diabetes in both female groups. Conclusions IHD and CVA risks are affected by specific factors in diabetics, such as treatment, gender and age. Specifically, insulin use has a potential role in preventing IHD but may also be a risk factor for CVA among the diabetic elderly, thus revealing a need to develop improved treatment strategies for diabetes in elderly patients. The Japan Cholesterol and Diabetes Mellitus Study was formulated to evaluate them(Umin Clinical Trials Registry, clinical trial reg. no. UMIN00000516; http://www.umin.ac.jp/ctr/index.htm).

Published
2011
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36. A hERG mutation E1039X produced a synergistic lesion on IKs together with KCNQ1-R174C mutation in a LQTS family with three compound mutations

Author

90823013, 30528302, Wu, Jie, Mizusawa, Yuka, Ohno, Seiko, Ding, Wei-Guang, Higaki, Takashi, Wang, Qi, Kohjitani, Hirohiko, Makiyama, Takeru, Itoh, Hideki, Toyoda, Futoshi, James, Andrew F., Hancox, Jules C., Matsuura, Hiroshi, Horie, Minoru, 90823013, 30528302, Wu, Jie, Mizusawa, Yuka, Ohno, Seiko, Ding, Wei-Guang, Higaki, Takashi, Wang, Qi, Kohjitani, Hirohiko, Makiyama, Takeru, Itoh, Hideki, Toyoda, Futoshi, James, Andrew F., Hancox, Jules C., Matsuura, Hiroshi, and Horie, Minoru

Abstract

Congenital long QT syndrome (LQTS) caused by compound mutations is usually associated with more severe clinical phenotypes. We identified a LQTS family harboring three compound mutations in different genes (KCNQ1-R174C, hERG-E1039X and SCN5A-E428K). KCNQ1-R174C, hERG-E1039X and SCN5A-E428K mutations and/or relevant wild-type (WT) cDNAs were respectively expressed in mammalian cells. IKs-like, IKr-like, INa-like currents and the functional interaction between KCNQ1-R174C and hERG-E1039X channels were studied using patch-clamp and immunocytochemistry techniques. (1) Expression of KCNQ1-R174C alone showed no IKs. Co-expression of KCNQ1-WT + KCNQ1-R174C caused a loss-of-function in IKs and blunted the activation of IKs in response to isoproterenol. (2) Expression of hERG-E1039X alone and co-expression of hERG-WT + hERG-E1039X negatively shifted inactivation curves and decelerated the recovery time from inactivation. (3) Expression of SCN5A-E428K increased peak INa, but had no effect on late INa. (4) IKs and IKr interact, and hERG-E1039X caused a loss-of-function in IKs. (5) Immunocytochemical studies indicated that KCNQ1-R174C is trafficking defective and hERG-E1039X is defective in biosynthesis/degradation, but the abnormities were rescued by co-expression with WT. Thus, KCNQ1-R174C and hERG-E1039X disrupted IKs and IKr functions, respectively. The synergistic lesion, caused by KCNQ1-R174C and hERG-E1039X in IKs, is very likely why patients showed more severe phenotypes in the compound mutation case.

Published
2018

37. Optical visualisation of thermogenesis in stimulated singlecell brown adipocytes

Author

Kriszt, Rókus, Arai, Satoshi, Itoh, Hideki, Lee, Michelle H., Goralczyk, Anna G., Ang, Xiu Min, Cypess, Aaron M., White, Andrew P., Shamsi, Farnaz, Xue, Ruidan, Lee, Jung Yeol, Lee, Sung-Chan, Hou, Yanyan, Kitaguchi, Tetsuya, Sudhaharan, Thankiah, Ishiwata, Shin’ichi, Lane, E. Birgitte, Chang, Young-Tae, Tseng, Yu-Hua, Suzuki, Madoka, Raghunath, Michael, Kriszt, Rókus, Arai, Satoshi, Itoh, Hideki, Lee, Michelle H., Goralczyk, Anna G., Ang, Xiu Min, Cypess, Aaron M., White, Andrew P., Shamsi, Farnaz, Xue, Ruidan, Lee, Jung Yeol, Lee, Sung-Chan, Hou, Yanyan, Kitaguchi, Tetsuya, Sudhaharan, Thankiah, Ishiwata, Shin’ichi, Lane, E. Birgitte, Chang, Young-Tae, Tseng, Yu-Hua, Suzuki, Madoka, and Raghunath, Michael

Abstract

The identification of brown adipose deposits in adults has led to significant interest in targeting this metabolically active tissue for treatment of obesity and diabetes. Improved methods for the direct measurement of heat production as the signature function of brown adipocytes (BAs), particularly at the single cell level, would be of substantial benefit to these ongoing efforts. Here, we report the first application of a small molecule-type thermosensitive fluorescent dye, ERthermAC, to monitor thermogenesis in BAs derived from murine brown fat precursors and in human brown fat cells differentiated from human neck brown preadipocytes. ERthermAC accumulated in the endoplasmic reticulum of BAs and displayed a marked change in fluorescence intensity in response to adrenergic stimulation of cells, which corresponded to temperature change. ERthermAC fluorescence intensity profiles were congruent with mitochondrial depolarisation events visualised by the JC-1 probe. Moreover, the averaged fluorescence intensity changes across a population of cells correlated well with dynamic changes such as thermal power, oxygen consumption, and extracellular acidification rates. These findings suggest ERthermAC as a promising new tool for studying thermogenic function in brown adipocytes of both murine and human origins.

Published
2018

40. Population pharmacokinetics and pharmacogenomics of apixaban in Japanese adult patients with atrial fibrillation

Author

Ueshima, Satoshi, primary, Hira, Daiki, additional, Kimura, Yuuma, additional, Fujii, Ryo, additional, Tomitsuka, Chiho, additional, Yamane, Takuya, additional, Tabuchi, Yohei, additional, Ozawa, Tomoya, additional, Itoh, Hideki, additional, Ohno, Seiko, additional, Horie, Minoru, additional, Terada, Tomohiro, additional, and Katsura, Toshiya, additional

Published
2018
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41. Novel intracellular transport-refractory mutations in KCNH2 identified in patients with symptomatic long QT syndrome

Author

Fukumoto, Daisuke, primary, Ding, Wei-Guang, additional, Wada, Yuko, additional, Fujii, Yusuke, additional, Ichikawa, Mari, additional, Takayama, Koichiro, additional, Fukuyama, Megumi, additional, Kato, Koichi, additional, Itoh, Hideki, additional, Makiyama, Takeru, additional, Omatsu-Kanbe, Mariko, additional, Matsuura, Hiroshi, additional, Horie, Minoru, additional, and Ohno, Seiko, additional

Published
2018
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42. A hERG mutation E1039X produced a synergistic lesion on IKs together with KCNQ1-R174C mutation in a LQTS family with three compound mutations

Author

Wu, Jie, primary, Mizusawa, Yuka, additional, Ohno, Seiko, additional, Ding, Wei-Guang, additional, Higaki, Takashi, additional, Wang, Qi, additional, Kohjitani, Hirohiko, additional, Makiyama, Takeru, additional, Itoh, Hideki, additional, Toyoda, Futoshi, additional, James, Andrew F., additional, Hancox, Jules C., additional, Matsuura, Hiroshi, additional, and Horie, Minoru, additional

Published
2018
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43. Usefulness of Fluorine-18-Fluorodeoxyglucose Positron Emission Tomography in a Patient With Takayasu's Arteritis Associated With Antiphospholipid Syndrome

Author

Kaku, Bunji, Higuchi, Takahiro, Kanaya, Hounin, Horita, Yuki, Yamazaki, Tsukasa, Uno, Yoshihide, Itoh, Hideki, Namura, Masanobu, Shimizu, Masami, Kaku, Bunji, Higuchi, Takahiro, Kanaya, Hounin, Horita, Yuki, Yamazaki, Tsukasa, Uno, Yoshihide, Itoh, Hideki, Namura, Masanobu, and Shimizu, Masami

Abstract

A 36-year-old woman was admitted for recurring chest pain and hemoptysis. Blood pressure in the right and left arms was equal, and no murmurs or bruits were heard. Body temperature was normal on admission and remained within the normal range during the hospital stay. C-reactive protein was slightly elevated (2.3 mg/dL) and lupus anticoagulant was positive. Angiography showed no abnormality of the aorta or its branches, but the left pulmonary artery showed occlusion at the proximal portion. Computed tomography (CT) revealed segmental wall thickening of the thoracic aorta. Fluorine-18-fluorodeoxyglucose positron emission tomography (18FDG PET) showed high uptake in the proximal portion of the left pulmonary artery and in the thoracic aorta with wall thickening on CT. Based on these findings, a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome was made and high-dose steroid therapy (prednisolone 30 mg/day) was started. Two months later, the C-reactive protein level had decreased from 2.3 mg/dL to 1.1 mg/dL, and both the focal wall thickening and 18FDG uptake of the thoracic aorta were decreased. 18FDG PET was useful for evaluating the efficacy of the steroid therapy in addition to making a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome.

Published
2017

45. Contribution of a KCNH2 variant in genotyped long QT syndrome: Romano–Ward syndrome under double mutations and acquired long QT syndrome under heterozygote

Author

Fujii, Yusuke, primary, Matsumoto, Yuichi, additional, Hayashi, Kenshi, additional, Ding, Wei-Guang, additional, Tomita, Yukinori, additional, Fukumoto, Daisuke, additional, Wada, Yuko, additional, Ichikawa, Mari, additional, Sonoda, Keiko, additional, Ozawa, Junichi, additional, Makiyama, Takeru, additional, Ohno, Seiko, additional, Yamagishi, Masakazu, additional, Matsuura, Hiroshi, additional, Horie, Minoru, additional, and Itoh, Hideki, additional

Published
2017
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46. Optical visualisation of thermogenesis in stimulated single-cell brown adipocytes

Author

Kriszt, Rókus, primary, Arai, Satoshi, additional, Itoh, Hideki, additional, Lee, Michelle H., additional, Goralczyk, Anna G., additional, Ang, Xiu Min, additional, Cypess, Aaron M., additional, White, Andrew P., additional, Shamsi, Farnaz, additional, Xue, Ruidan, additional, Lee, Jung Yeol, additional, Lee, Sung-Chan, additional, Hou, Yanyan, additional, Kitaguchi, Tetsuya, additional, Sudhaharan, Thankiah, additional, Ishiwata, Shin’ichi, additional, Lane, E. Birgitte, additional, Chang, Young-Tae, additional, Tseng, Yu-Hua, additional, Suzuki, Madoka, additional, and Raghunath, Michael, additional

Published
2017
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48. Patient-specific human induced pluripotent stem cell model assessed with electrical pacing validates S107 as a potential therapeutic agent for catecholaminergic polymorphic ventricular tachycardia

Author

30528302, 20447965, 90823013, 10295694, 80359786, Sasaki, Kenichi, Makiyama, Takeru, Yoshida, Yoshinori, Wuriyanghai, Yimin, Kamakura, Tsukasa, Nishiuchi, Suguru, Hayano, Mamoru, Harita, Takeshi, Yamamoto, Yuta, Kohjitani, Hirohiko, Hirose, Sayako, Chen, Jiarong, Kawamura, Mihoko, Ohno, Seiko, Itoh, Hideki, Takeuchi, Ayako, Matsuoka, Satoshi, Miura, Masaru, Sumitomo, Naokata, Horie, Minoru, Yamanaka, Shinya, Kimura, Takeshi, 30528302, 20447965, 90823013, 10295694, 80359786, Sasaki, Kenichi, Makiyama, Takeru, Yoshida, Yoshinori, Wuriyanghai, Yimin, Kamakura, Tsukasa, Nishiuchi, Suguru, Hayano, Mamoru, Harita, Takeshi, Yamamoto, Yuta, Kohjitani, Hirohiko, Hirose, Sayako, Chen, Jiarong, Kawamura, Mihoko, Ohno, Seiko, Itoh, Hideki, Takeuchi, Ayako, Matsuoka, Satoshi, Miura, Masaru, Sumitomo, Naokata, Horie, Minoru, Yamanaka, Shinya, and Kimura, Takeshi

Published
2016

49. Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Sasaki, Kenichi, primary, Makiyama, Takeru, additional, Yoshida, Yoshinori, additional, Wuriyanghai, Yimin, additional, Kamakura, Tsukasa, additional, Nishiuchi, Suguru, additional, Hayano, Mamoru, additional, Harita, Takeshi, additional, Yamamoto, Yuta, additional, Kohjitani, Hirohiko, additional, Hirose, Sayako, additional, Chen, Jiarong, additional, Kawamura, Mihoko, additional, Ohno, Seiko, additional, Itoh, Hideki, additional, Takeuchi, Ayako, additional, Matsuoka, Satoshi, additional, Miura, Masaru, additional, Sumitomo, Naokata, additional, Horie, Minoru, additional, Yamanaka, Shinya, additional, and Kimura, Takeshi, additional

Published
2016
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