186 results on '"Ishida T."'
Search Results
2. Characterization of mono-chip amplifier-shaper and discriminator FGATI for muon spin imaging spectroscopy.
- Author
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Subhi, Hassan, Takayama, Gen, Kojima, Kenji M., Shoji, M., Miyahara, M., Honda, R., Tanaka, M. M., and Ishida, T.
- Subjects
SPECTRAL imaging ,PULSED lasers ,MUONS ,CAPACITORS ,SPECTROMETRY - Abstract
We report test of a trans-impedance fast amplifier FGATI, using a semiconductor-based photo sensors SiPM and a pulsed laser. The FGATI chip contains 16 channels of amplifier-shaper-discriminator (ASD) circuits which generates low-voltage differentiation signal (LVDS) discriminator digital outputs, readily analyzed its timing by a Time to Digital Converter (TDC). The amplifier gain characteristics are tested using a voltage input pulse supplied through a coupling capacitor to FGATI. The current input from SiPM are characterized with/without the coupling capacitor. The analog signal response as well as the threshold control of the digital pulse output is characterized. The timing resolution achieved by FGATI is less than 50 ps for the saturated laser input. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
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3. Constraint on the matter–antimatter symmetry-violating phase in neutrino oscillations
- Author
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Abe, K., Akutsu, R., Ali, A., Alt, C., Andreopoulos, C., Anthony, L., Antonova, M., Aoki, S., Ariga, A., Arihara, T., Asada, Y., Hiramoto, A., Hogan, M., Holeczek, J., Hong Van, N. T., Iacob, F., Ichikawa, A. K., Ikeda, M., Ishida, T., Ishii, T., Ishitsuka, M., Ashida, Y., Iwamoto, K., Izmaylov, A., Jakkapu, M., Jamieson, B., Jenkins, S. J., Jesús-Valls, C., Jiang, M., Johnson, S., Jonsson, P., Jung, C. K., Atkin, E. T., Junjie, X., Jurj, P. B., Kabirnezhad, M., Kaboth, A. C., Kajita, T., Kakuno, H., Kameda, J., Karlen, D., Kasetti, S. P., Kataoka, Y., Awataguchi, Y., Katori, T., Kato, Y., Kearns, E., Khabibullin, M., Khotjantsev, A., Kikawa, T., Kikutani, H., Kim, H., Kim, J., King, S., Ban, S., Kisiel, J., Knight, A., Knox, A., Kobayashi, T., Koch, L., Koga, T., Konaka, A., Kormos, L. L., Koshio, Y., Kostin, A., Barbi, M., Kowalik, K., Kubo, H., Kudenko, Y., Kukita, N., Kuribayashi, S., Kurjata, R., Kutter, T., Kuze, M., Labarga, L., Lagoda, J., Barker, G. J., Lamoureux, M., Laveder, M., Lawe, M., Licciardi, M., Lindner, T., Litchfield, R. P., Liu, S. L., Li, X., Longhin, A., Ludovici, L., Barr, G., Lu, X., Lux, T., Machado, L. N., Magaletti, L., Mahn, K., Malek, M., Manly, S., Maret, L., Marino, A. D., Marti-Magro, L., Barrow, D., Martin, J. F., Maruyama, T., Matsubara, T., Matsushita, K., Matveev, V., Mavrokoridis, K., Mazzucato, E., McCarthy, M., McCauley, N., McElwee, J., Barry, C., McFarland, K. S., McGrew, C., Mefodiev, A., Metelko, C., Mezzetto, M., Minamino, A., Mineev, O., Mine, S., Miura, M., Molina Bueno, L., Batkiewicz-Kwasniak, M., Moriyama, S., Morrison, J., Mueller, Th. A., Munteanu, L., Murphy, S., Nagai, Y., Nakadaira, T., Nakahata, M., Nakajima, Y., Nakamura, A., Beloshapkin, A., Nakamura, K. G., Nakamura, K., Nakayama, S., Nakaya, T., Nakayoshi, K., Nantais, C., Naseby, C. E. R., Ngoc, T. V., Niewczas, K., Nishikawa, K., Bench, F., Nishimura, Y., Noah, E., Nonnenmacher, T. S., Nova, F., Novella, P., Nowak, J., Nugent, J. C., O’Keeffe, H. M., O’Sullivan, L., Odagawa, T., Berardi, V., Okumura, K., Okusawa, T., Oser, S. M., Owen, R. A., Oyama, Y., Palladino, V., Palomino, J. L., Paolone, V., Pari, M., Parker, W. C., Berkman, S., Parsa, S., Pasternak, J., Paudyal, P., Pavin, M., Payne, D., Penn, G. C., Pickering, L., Pidcott, C., Pintaudi, G., Pinzon Guerra, E. S., Berns, L., Pistillo, C., Popov, B., Porwit, K., Posiadala-Zezula, M., Pritchard, A., Quilain, B., Radermacher, T., Radicioni, E., Radics, B., Ratoff, P. N., Bhadra, S., Reinherz-Aronis, E., Riccio, C., Rondio, E., Roth, S., Rubbia, A., Ruggeri, A. C., Ruggles, C. A., Rychter, A., Sakashita, K., Sánchez, F., Bienstock, S., Santucci, G., Schloesser, C. M., Scholberg, K., Schwehr, J., Scott, M., Seiya, Y., Sekiguchi, T., Sekiya, H., Sgalaberna, D., Shah, R., Blondel, A., Shaikhiev, A., Shaker, F., Shaykina, A., Shiozawa, M., Shorrock, W., Shvartsman, A., Smirnov, A., Smy, M., Sobczyk, J. T., Sobel, H., Bolognesi, S., Soler, F. J. P., Sonoda, Y., Steinmann, J., Suvorov, S., Suzuki, A., Suzuki, S. Y., Suzuki, Y., Sztuc, A. A., Tada, M., Tajima, M., Bourguille, B., Takeda, A., Takeuchi, Y., Tanaka, H. K., Tanaka, H. A., Tanaka, S., Thompson, L. F., Toki, W., Touramanis, C., Towstego, T., Tsui, K. M., Boyd, S. B., Tsukamoto, T., Tzanov, M., Uchida, Y., Uno, W., Vagins, M., Valder, S., Vallari, Z., Vargas, D., Vasseur, G., Vilela, C., Brailsford, D., Vinning, W. G. S., Vladisavljevic, T., Volkov, V. V., Wachala, T., Walker, J., Walsh, J. G., Wang, Y., Wark, D., Wascko, M. O., Weber, A., Bravar, A., Wendell, R., Wilking, M. J., Wilkinson, C., Wilson, J. R., Wilson, R. J., Wood, K., Wret, C., Yamada, Y., Yamamoto, K., Yanagisawa, C., Bravo Berguño, D., Yang, G., Yano, T., Yasutome, K., Yen, S., Yershov, N., Yokoyama, M., Yoshida, T., Yu, M., Zalewska, A., Zalipska, J., Bronner, C., Zaremba, K., Zarnecki, G., Ziembicki, M., Zimmerman, E. D., Zito, M., Zsoldos, S., Zykova, A., The T2K Collaboration, Bubak, A., Buizza Avanzini, M., Calcutt, J., Campbell, T., Cao, S., Cartwright, S. L., Catanesi, M. G., Cervera, A., Chappell, A., Checchia, C., Cherdack, D., Chikuma, N., Cicerchia, M., Christodoulou, G., Coleman, J., Collazuol, G., Cook, L., Coplowe, D., Cudd, A., Dabrowska, A., De Rosa, G., Dealtry, T., Denner, P. F., Dennis, S. R., Densham, C., Di Lodovico, F., Dokania, N., Dolan, S., Doyle, T. A., Drapier, O., Dumarchez, J., Dunne, P., Eguchi, A., Eklund, L., Emery-Schrenk, S., Ereditato, A., Fernandez, P., Feusels, T., Finch, A. J., Fiorentini, G. A., Fiorillo, G., Francois, C., Friend, M., Fujii, Y., Fujita, R., Fukuda, D., Fukuda, R., Fukuda, Y., Fusshoeller, K., Gameil, K., Giganti, C., Golan, T., Gonin, M., Gorin, A., Guigue, M., Hadley, D. R., Haigh, J. T., Hamacher-Baumann, P., Hartz, M., Hasegawa, T., Hassani, S., Hastings, N. C., Hayashino, T., Hayato, Y., Abe, K., Akutsu, R., Ali, A., Alt, C., Andreopoulos, C., Anthony, L., Antonova, M., Aoki, S., Ariga, A., Arihara, T., Asada, Y., Hiramoto, A., Hogan, M., Holeczek, J., Hong Van, N. T., Iacob, F., Ichikawa, A. K., Ikeda, M., Ishida, T., Ishii, T., Ishitsuka, M., Ashida, Y., Iwamoto, K., Izmaylov, A., Jakkapu, M., Jamieson, B., Jenkins, S. J., Jesús-Valls, C., Jiang, M., Johnson, S., Jonsson, P., Jung, C. K., Atkin, E. T., Junjie, X., Jurj, P. B., Kabirnezhad, M., Kaboth, A. C., Kajita, T., Kakuno, H., Kameda, J., Karlen, D., Kasetti, S. P., Kataoka, Y., Awataguchi, Y., Katori, T., Kato, Y., Kearns, E., Khabibullin, M., Khotjantsev, A., Kikawa, T., Kikutani, H., Kim, H., Kim, J., King, S., Ban, S., Kisiel, J., Knight, A., Knox, A., Kobayashi, T., Koch, L., Koga, T., Konaka, A., Kormos, L. L., Koshio, Y., Kostin, A., Barbi, M., Kowalik, K., Kubo, H., Kudenko, Y., Kukita, N., Kuribayashi, S., Kurjata, R., Kutter, T., Kuze, M., Labarga, L., Lagoda, J., Barker, G. J., Lamoureux, M., Laveder, M., Lawe, M., Licciardi, M., Lindner, T., Litchfield, R. P., Liu, S. L., Li, X., Longhin, A., Ludovici, L., Barr, G., Lu, X., Lux, T., Machado, L. N., Magaletti, L., Mahn, K., Malek, M., Manly, S., Maret, L., Marino, A. D., Marti-Magro, L., Barrow, D., Martin, J. F., Maruyama, T., Matsubara, T., Matsushita, K., Matveev, V., Mavrokoridis, K., Mazzucato, E., McCarthy, M., McCauley, N., McElwee, J., Barry, C., McFarland, K. S., McGrew, C., Mefodiev, A., Metelko, C., Mezzetto, M., Minamino, A., Mineev, O., Mine, S., Miura, M., Molina Bueno, L., Batkiewicz-Kwasniak, M., Moriyama, S., Morrison, J., Mueller, Th. A., Munteanu, L., Murphy, S., Nagai, Y., Nakadaira, T., Nakahata, M., Nakajima, Y., Nakamura, A., Beloshapkin, A., Nakamura, K. G., Nakamura, K., Nakayama, S., Nakaya, T., Nakayoshi, K., Nantais, C., Naseby, C. E. R., Ngoc, T. V., Niewczas, K., Nishikawa, K., Bench, F., Nishimura, Y., Noah, E., Nonnenmacher, T. S., Nova, F., Novella, P., Nowak, J., Nugent, J. C., O’Keeffe, H. M., O’Sullivan, L., Odagawa, T., Berardi, V., Okumura, K., Okusawa, T., Oser, S. M., Owen, R. A., Oyama, Y., Palladino, V., Palomino, J. L., Paolone, V., Pari, M., Parker, W. C., Berkman, S., Parsa, S., Pasternak, J., Paudyal, P., Pavin, M., Payne, D., Penn, G. C., Pickering, L., Pidcott, C., Pintaudi, G., Pinzon Guerra, E. S., Berns, L., Pistillo, C., Popov, B., Porwit, K., Posiadala-Zezula, M., Pritchard, A., Quilain, B., Radermacher, T., Radicioni, E., Radics, B., Ratoff, P. N., Bhadra, S., Reinherz-Aronis, E., Riccio, C., Rondio, E., Roth, S., Rubbia, A., Ruggeri, A. C., Ruggles, C. A., Rychter, A., Sakashita, K., Sánchez, F., Bienstock, S., Santucci, G., Schloesser, C. M., Scholberg, K., Schwehr, J., Scott, M., Seiya, Y., Sekiguchi, T., Sekiya, H., Sgalaberna, D., Shah, R., Blondel, A., Shaikhiev, A., Shaker, F., Shaykina, A., Shiozawa, M., Shorrock, W., Shvartsman, A., Smirnov, A., Smy, M., Sobczyk, J. T., Sobel, H., Bolognesi, S., Soler, F. J. P., Sonoda, Y., Steinmann, J., Suvorov, S., Suzuki, A., Suzuki, S. Y., Suzuki, Y., Sztuc, A. A., Tada, M., Tajima, M., Bourguille, B., Takeda, A., Takeuchi, Y., Tanaka, H. K., Tanaka, H. A., Tanaka, S., Thompson, L. F., Toki, W., Touramanis, C., Towstego, T., Tsui, K. M., Boyd, S. B., Tsukamoto, T., Tzanov, M., Uchida, Y., Uno, W., Vagins, M., Valder, S., Vallari, Z., Vargas, D., Vasseur, G., Vilela, C., Brailsford, D., Vinning, W. G. S., Vladisavljevic, T., Volkov, V. V., Wachala, T., Walker, J., Walsh, J. G., Wang, Y., Wark, D., Wascko, M. O., Weber, A., Bravar, A., Wendell, R., Wilking, M. J., Wilkinson, C., Wilson, J. R., Wilson, R. J., Wood, K., Wret, C., Yamada, Y., Yamamoto, K., Yanagisawa, C., Bravo Berguño, D., Yang, G., Yano, T., Yasutome, K., Yen, S., Yershov, N., Yokoyama, M., Yoshida, T., Yu, M., Zalewska, A., Zalipska, J., Bronner, C., Zaremba, K., Zarnecki, G., Ziembicki, M., Zimmerman, E. D., Zito, M., Zsoldos, S., Zykova, A., The T2K Collaboration, Bubak, A., Buizza Avanzini, M., Calcutt, J., Campbell, T., Cao, S., Cartwright, S. L., Catanesi, M. G., Cervera, A., Chappell, A., Checchia, C., Cherdack, D., Chikuma, N., Cicerchia, M., Christodoulou, G., Coleman, J., Collazuol, G., Cook, L., Coplowe, D., Cudd, A., Dabrowska, A., De Rosa, G., Dealtry, T., Denner, P. F., Dennis, S. R., Densham, C., Di Lodovico, F., Dokania, N., Dolan, S., Doyle, T. A., Drapier, O., Dumarchez, J., Dunne, P., Eguchi, A., Eklund, L., Emery-Schrenk, S., Ereditato, A., Fernandez, P., Feusels, T., Finch, A. J., Fiorentini, G. A., Fiorillo, G., Francois, C., Friend, M., Fujii, Y., Fujita, R., Fukuda, D., Fukuda, R., Fukuda, Y., Fusshoeller, K., Gameil, K., Giganti, C., Golan, T., Gonin, M., Gorin, A., Guigue, M., Hadley, D. R., Haigh, J. T., Hamacher-Baumann, P., Hartz, M., Hasegawa, T., Hassani, S., Hastings, N. C., Hayashino, T., and Hayato, Y.
- Published
- 2020
4. Repositioning of the global epicentre of non-optimal cholesterol
- Author
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Taddei, C. (Cristina), Zhou, B. (Bin), Bixby, H. (Honor), Carrillo-Larco, R. M. (Rodrigo M.), Danaei, G. (Goodarz), Jackson, R. T. (Rod T.), Farzadfar, F. (Farshad), Sophiea, M. K. (Marisa K.), Di Cesare, M. (Mariachiara), Iurilli, M. L. (Maria Laura Caminia), Martinez, A. R. (Andrea Rodriguez), Asghari, G. (Golaleh), Dhana, K. (Klodian), Gulayin, P. (Pablo), Kakarmath, S. (Sujay), Santero, M. (Marilina), Voortman, T. (Trudy), Riley, L. M. (Leanne M.), Cowan, M. J. (Melanie J.), Savin, S. (Stefan), Bennett, J. E. (James E.), Stevens, G. A. (Gretchen A.), Paciorek, C. J. (Christopher J.), Aekplakorn, W. (Wichai), Cifkova, R. (Renata), Giampaoli, S. (Simona), Kengne, A. P. (Andre Pascal), Khang, Y.-H. (Young-Ho), Kuulasmaa, K. (Kari), Laxmaiah, A. (Avula), Margozzini, P. (Paula), Mathur, P. (Prashant), Nordestgaard, B. G. (Borge G.), Zhao, D. (Dong), Aadahl, M. (Mette), Abarca-Gomez, L. (Leandra), Rahim, H. A. (Hanan Abdul), Abu-Rmeileh, N. M. (Niveen M.), Acosta-Cazares, B. (Benjamin), Adams, R. J. (Robert J.), Agdeppa, I. A. (Imelda A.), Aghazadeh-Attari, J. (Javad), Aguilar-Salinas, C. A. (Carlos A.), Agyemang, C. (Charles), Ahluwalia, T. S. (Tarunveer S.), Ahmad, N. A. (Noor Ani), Ahmadi, A. (Ali), Ahmadi, N. (Naser), Ahmed, S. H. (Soheir H.), Ahrens, W. (Wolfgang), Ajlouni, K. (Kamel), Alarouj, M. (Monira), AlBuhairan, F. (Fadia), AlDhukair, S. (Shahla), Ali, M. M. (Mohamed M.), Alkandari, A. (Abdullah), Alkerwi, A. (Ala'a), Aly, E. (Eman), Amarapurkar, D. N. (Deepak N.), Amouyel, P. (Philippe), Andersen, L. B. (Lars Bo), Anderssen, S. A. (Sigmund A.), Anjana, R. M. (Ranjit Mohan), Ansari-Moghaddam, A. (Alireza), Aounallah-Skhiri, H. (Hajer), Araujo, J. (Joana), Ariansen, I. (Inger), Aris, T. (Tahir), Arku, R. E. (Raphael E.), Arlappa, N. (Nimmathota), Aryal, K. K. (Krishna K.), Aspelund, T. (Thor), Assuncao, M. C. (Maria Cecilia F.), Auvinen, J. (Juha), Avdicova, M. (Maria), Azevedo, A. (Ana), Azizi, F. (Fereidoun), Azmin, M. (Mehrdad), Balakrishna, N. (Nagalla), Bamoshmoosh, M. (Mohamed), Banach, M. (Maciej), Bandosz, P. (Piotr), Banegas, J. R. (Jose R.), Barbagallo, C. M. (Carlo M.), Barcelo, A. (Alberto), Barkat, A. (Amina), Bata, I. (Iqbal), Batieha, A. M. (Anwar M.), Batyrbek, A. (Assembekov), Baur, L. A. (Louise A.), Beaglehole, R. (Robert), Belavendra, A. (Antonisamy), Ben Romdhane, H. (Habiba), Benet, M. (Mikhail), Benn, M. (Marianne), Berkinbayev, S. (Salim), Bernabe-Ortiz, A. (Antonio), Bernotiene, G. (Gailute), Bettiol, H. (Heloisa), Bhargava, S. K. (Santosh K.), Bi, Y. (Yufang), Bienek, A. (Asako), Bikbov, M. (Mukharram), Bista, B. (Bihungum), Bjerregaard, P. (Peter), Bjertness, E. (Espen), Bjertness, M. B. (Marius B.), Bjorkelund, C. (Cecilia), Bloch, K. V. (Katia, V), Blokstra, A. (Anneke), Bo, S. (Simona), Boehm, B. O. (Bernhard O.), Boggia, J. G. (Jose G.), Boissonnet, C. P. (Carlos P.), Bonaccio, M. (Marialaura), Bongard, V. (Vanina), Borchini, R. (Rossana), Borghs, H. (Herman), Bovet, P. (Pascal), Brajkovich, I. (Imperia), Breckenkamp, J. (Juergen), Brenner, H. (Hermann), Brewster, L. M. (Lizzy M.), Bruno, G. (Graziella), Bugge, A. (Anna), Busch, M. A. (Markus A.), de Leon, A. C. (Antonio Cabrera), Cacciottolo, J. (Joseph), Can, G. (Gunay), Candido, A. P. (Ana Paula C.), Capanzana, M. V. (Mario, V), Capuano, E. (Eduardo), Capuano, V. (Vincenzo), Cardoso, V. C. (Viviane C.), Carvalho, J. (Joana), Casanueva, F. F. (Felipe F.), Censi, L. (Laura), Chadjigeorgiou, C. A. (Charalambos A.), Chamukuttan, S. (Snehalatha), Chaturvedi, N. (Nish), Chen, C.-J. (Chien-Jen), Chen, F. (Fangfang), Chen, S. (Shuohua), Cheng, C.-Y. (Ching-Yu), Cheraghian, B. (Bahman), Chetrit, A. (Angela), Chiou, S.-T. (Shu-Ti), Chirlaque, M.-D. (Maria-Dolores), Cho, B. (Belong), Cho, Y. (Yumi), Chudek, J. (Jerzy), Claessens, F. (Frank), Clarke, J. (Janine), Clays, E. (Els), Concin, H. (Hans), Confortin, S. C. (Susana C.), Cooper, C. (Cyrus), Costanzo, S. (Simona), Cottel, D. (Dominique), Cowell, C. (Chris), Crujeiras, A. B. (Ana B.), Csilla, S. (Semanova), Cui, L. (Liufu), Cureau, F. V. (Felipe, V), D'Arrigo, G. (Graziella), d'Orsi, E. (Eleonora), Dallongeville, J. (Jean), Damasceno, A. (Albertino), Dankner, R. (Rachel), Dantoft, T. M. (Thomas M.), Dauchet, L. (Luc), Davletov, K. (Kairat), De Backer, G. (Guy), De Bacquer, D. (Dirk), de Gaetano, G. (Giovanni), De Henauw, S. (Stefaan), de Oliveira, P. D. (Paula Duarte), De Ridder, D. (David), De Smedt, D. (Delphine), Deepa, M. (Mohan), Deev, A. D. (Alexander D.), Dehghan, A. (Abbas), Delisle, H. (Helene), Dennison, E. (Elaine), Deschamps, V. (Valerie), Dhimal, M. (Meghnath), Di Castelnuovo, A. F. (Augusto F.), Dika, Z. (Zivka), Djalalinia, S. (Shirin), Dobson, A. J. (Annette J.), Donfrancesco, C. (Chiara), Donoso, S. P. (Silvana P.), Doring, A. (Angela), Dorobantu, M. (Maria), Dragano, N. (Nico), Drygas, W. (Wojciech), Du, Y. (Yong), Duante, C. A. (Charmaine A.), Duda, R. B. (Rosemary B.), Dzerve, V. (Vilnis), Dziankowska-Zaborszczyk, E. (Elzbieta), Eddie, R. (Ricky), Eftekhar, E. (Ebrahim), Eggertsen, R. (Robert), Eghtesad, S. (Sareh), Eiben, G. (Gabriele), Ekelund, U. (Ulf), El Ati, J. (Jalila), Eldemire-Shearer, D. (Denise), Eliasen, M. (Marie), Elosua, R. (Roberto), Erasmus, R. T. (Rajiv T.), Erbel, R. (Raimund), Erem, C. (Cihangir), Eriksen, L. (Louise), Eriksson, J. G. (Johan G.), Escobedo-de la Pena, J. (Jorge), Eslami, S. (Saeid), Esmaeili, A. (Ali), Evans, A. (Alun), Faeh, D. (David), Fall, C. H. (Caroline H.), Faramarzi, E. (Elnaz), Farjam, M. (Mojtaba), Fattahi, M. R. (Mohammad Reza), Felix-Redondo, F. J. (Francisco J.), Ferguson, T. S. (Trevor S.), Fernandez-Berges, D. (Daniel), Ferrante, D. (Daniel), Ferrari, M. (Marika), Ferreccio, C. (Catterina), Ferrieres, J. (Jean), Foger, B. (Bernhard), Foo, L. H. (Leng Huat), Forslund, A.-S. (Ann-Sofie), Forsner, M. (Maria), Fouad, H. M. (Heba M.), Francis, D. K. (Damian K.), Franco, M. d. (Maria do Carmo), Franco, O. H. (Oscar H.), Frontera, G. (Guillermo), Fujita, Y. (Yuki), Fumihiko, M. (Matsuda), Furusawa, T. (Takuro), Gaciong, Z. (Zbigniew), Galvano, F. (Fabio), Gao, J. (Jingli), Garcia-de-la-Hera, M. (Manoli), Garnett, S. P. (Sarah P.), Gaspoz, J.-M. (Jean-Michel), Gasull, M. (Magda), Gazzinelli, A. (Andrea), Geleijnse, J. M. (Johanna M.), Ghanbari, A. (Ali), Ghasemi, E. (Erfan), Gheorghe-Fronea, O.-F. (Oana-Florentina), Ghimire, A. (Anup), Gianfagna, F. (Francesco), Gill, T. K. (Tiffany K.), Giovannelli, J. (Jonathan), Gironella, G. (Glen), Giwercman, A. (Aleksander), Goltzman, D. (David), Goncalves, H. (Helen), Gonzalez-Chica, D. A. (David A.), Gonzalez-Gross, M. (Marcela), Gonzalez-Rivas, J. P. (Juan P.), Gonzalez-Villalpando, C. (Clicerio), Gonzalez-Villalpando, M.-E. (Maria-Elena), Gonzalez, A. R. (Angel R.), Gottrand, F. (Frederic), Graff-Iversen, S. (Sidsel), Gregor, R. D. (Ronald D.), Grodzicki, T. (Tomasz), Grontved, A. (Anders), Grosso, G. (Giuseppe), Gruden, G. (Gabriella), Gu, D. (Dongfeng), Guallar-Castillon, P. (Pilar), Guan, O. P. (Ong Peng), Gudmundsson, E. F. (Elias F.), Gudnason, V. (Vilmundur), Guerrero, R. (Ramiro), Guessous, I. (Idris), Gunnlaugsdottir, J. (Johanna), Gupta, R. (Rajeev), Gutierrez, L. (Laura), Gutzwiller, F. (Felix), Ha, S. (Seongjun), Hadaegh, F. (Farzad), Haghshenas, R. (Rosa), Hakimi, H. (Hamid), Hambleton, I. R. (Ian R.), Hamzeh, B. (Behrooz), Hantunen, S. (Sari), Kumar, R. H. (Rachakulla Hari), Hashemi-Shahri, S. M. (Seyed Mohammad), Hata, J. (Jun), Haugsgjerd, T. (Teresa), Hayes, A. J. (Alison J.), He, J. (Jiang), He, Y. (Yuna), Hendriks, M. E. (Marleen Elisabeth), Henriques, A. (Ana), Herrala, S. (Sauli), Heshmat, R. (Ramin), Hill, A. G. (Allan G.), Ho, S. Y. (Sai Yin), Ho, S. C. (Suzanne C.), Hobbs, M. (Michael), Hofman, A. (Albert), Homayounfar, R. (Reza), Hopman, W. M. (Wilma M.), Horimoto, A. R. (Andrea R. V. R.), Hormiga, C. M. (Claudia M.), Horta, B. L. (Bernardo L.), Houti, L. (Leila), Howitt, C. (Christina), Htay, T. T. (Thein Thein), Htet, A. S. (Aung Soe), Htike, M. M. (Maung Maung Than), Huerta, J. M. (Jose Maria), Huhtaniemi, I. T. (Ilpo Tapani), Huisman, M. (Martijn), Hunsberger, M. L. (Monica L.), Husseini, A. S. (Abdullatif S.), Huybrechts, I. (Inge), Hwalla, N. (Nahla), Iacoviello, L. (Licia), Iannone, A. G. (Anna G.), Ibrahim, M. M. (Mohsen M.), Wong, N. I. (Norazizah Ibrahim), Iglesia, I. (Iris), Ikeda, N. (Nayu), Ikram, M. A. (M. Arfan), Iotova, V. (Violeta), Irazola, V. E. (Vilma E.), Ishida, T. (Takafumi), Islam, M. (Muhammad), Ismail, A. A. (Aziz Al-Safi), Iwasaki, M. (Masanori), Jacobs, J. M. (Jeremy M.), Jaddou, H. Y. (Hashem Y.), Jafar, T. (Tazeen), James, K. (Kenneth), Jamrozik, K. (Konrad), Janszky, I. (Imre), Janus, E. (Edward), Järvelin, M.-R. (Marjo-Riitta), Jasienska, G. (Grazyna), Jelakovic, A. (Ana), Jelakovic, B. (Bojan), Jennings, G. (Garry), Jensen, G. B. (Gorm B.), Jeong, S.-l. (Seung-lyeal), Jha, A. K. (Anjani Kumar), Jiang, C. Q. (Chao Qiang), Jimenez, R. O. (Ramon O.), Jockel, K.-H. (Karl-Heinz), Joffres, M. (Michel), Jokelainen, J. J. (Jari J.), Jonas, J. B. (Jost B.), Jorgensen, T. (Torben), Joshi, P. (Pradeep), Joukar, F. (Farahnaz), Jozwiak, J. (Jacek), Juolevi, A. (Anne), Kafatos, A. (Anthony), Kajantie, E. O. (Eero O.), Kalter-Leibovici, O. (Ofra), Kamaruddin, N. A. (Nor Azmi), Kamstrup, P. R. (Pia R.), Karki, K. B. (Khem B.), Katz, J. (Joanne), Kauhanen, J. (Jussi), Kaur, P. (Prabhdeep), Kavousi, M. (Maryam), Kazakbaeva, G. (Gyulli), Keil, U. (Ulrich), Keinanen-Kiukaanniemi, S. (Sirkka), Kelishadi, R. (Roya), Keramati, M. (Maryam), Kerimkulova, A. (Alina), Kersting, M. (Mathilde), Khader, Y. S. (Yousef Saleh), Khalili, D. (Davood), Khateeb, M. (Mohammad), Kheradmand, M. (Motahareh), Khosravi, A. (Alireza), Kiechl-Kohlendorfer, U. (Ursula), Kiechl, S. (Stefan), Killewo, J. (Japhet), Kim, H. C. (Hyeon Chang), Kim, J. (Jeongseon), Kim, Y.-Y. (Yeon-Yong), Klumbiene, J. (Jurate), Knoflach, M. (Michael), Ko, S. (Stephanie), Kohler, H.-P. (Hans-Peter), Kohler, I. V. (Iliana, V), Kolle, E. (Elin), Kolsteren, P. (Patrick), Konig, J. (Jurgen), Korpelainen, R. (Raija), . (), Kos, J. (Jelena), Koskinen, S. (Seppo), Kouda, K. (Katsuyasu), Kowlessur, S. (Sudhir), Kratzer, W. (Wolfgang), Kriemler, S. (Susi), Kristensen, P. L. (Peter Lund), Krokstad, S. (Steiner), Kromhout, D. (Daan), Kujala, U. M. (Urho M.), Kurjata, P. (Pawel), Kyobutungi, C. (Catherine), Laamiri, F. Z. (Fatima Zahra), Laatikainen, T. (Tiina), Lachat, C. (Carl), Laid, Y. (Youcef), Lam, T. H. (Tai Hing), Lambrinou, C.-P. (Christina-Paulina), Lanska, V. (Vera), Lappas, G. (Georg), Larijani, B. (Bagher), Latt, T. S. (Tint Swe), Laugsand, L. E. (Lars E.), Lazo-Porras, M. (Maria), Lee, J. (Jeannette), Lee, J. (Jeonghee), Lehmann, N. (Nils), Lehtimaki, T. (Terho), Levitt, N. S. (Naomi S.), Li, Y. (Yanping), Lilly, C. L. (Christa L.), Lim, W.-Y. (Wei-Yen), Lima-Costa, M. F. (M. Fernanda), Lin, H.-H. (Hsien-Ho), Lin, X. (Xu), Lin, Y.-T. (Yi-Ting), Lind, L. (Lars), Linneberg, A. (Allan), Lissner, L. (Lauren), Liu, J. (Jing), Loit, H.-M. (Helle-Mai), Lopez-Garcia, E. (Esther), Lopez, T. (Tania), Lotufo, P. A. (Paulo A.), Lozano, J. E. (Jose Eugenio), Luksiene, D. (Dalia), Lundqvist, A. (Annamari), Lundqvist, R. (Robert), Lunet, N. (Nuno), Ma, G. (Guansheng), Machado-Coelho, G. L. (George L. L.), Machado-Rodrigues, A. M. (Aristides M.), Machi, S. (Suka), Madar, A. A. (Ahmed A.), Maggi, S. (Stefania), Magliano, D. J. (Dianna J.), Magriplis, E. (Emmanuella), Mahasampath, G. (Gowri), Maire, B. (Bernard), Makdisse, M. (Marcia), Malekzadeh, F. (Fatemeh), Rao, K. M. (Kodavanti Mallikharjuna), Manios, Y. (Yannis), Mann, J. I. (Jim, I), Mansour-Ghanaei, F. (Fariborz), Manzato, E. (Enzo), Marques-Vidal, P. (Pedro), Martorell, R. (Reynaldo), Mascarenhas, L. P. (Luis P.), Mathiesen, E. B. (Ellisiv B.), Matsha, T. E. (Tandi E.), Mavrogianni, C. (Christina), McFarlane, S. R. (Shelly R.), McGarvey, S. T. (Stephen T.), McLachlan, S. (Stela), McLean, R. M. (Rachael M.), McLean, S. B. (Scott B.), McNulty, B. A. (Breige A.), Mediene-Benchekor, S. (Sounnia), Mehdipour, P. (Parinaz), Mehlig, K. (Kirsten), Mehrparvar, A. (AmirHoushang), Meirhaeghe, A. (Aline), Meisinger, C. (Christa), Menezes, A. M. (Ana Maria B.), Menon, G. R. (Geetha R.), Merat, S. (Shahin), Mereke, A. (Alibek), Meshram, I. I. (Indrapal I.), Metcalf, P. (Patricia), Meyer, H. E. (Haakon E.), Mi, J. (Jie), Michels, N. (Nathalie), Miller, J. C. (Jody C.), Minderico, C. S. (Claudia S.), Mini, G. K. (G. K.), Miquel, J. F. (Juan Francisco), Miranda, J. J. (J. Jaime), Mirjalili, M. R. (Mohammad Reza), Mirrakhimov, E. (Erkin), Modesti, P. A. (Pietro A.), Moghaddam, S. S. (Sahar Saeedi), Mohajer, B. (Bahram), Mohamed, M. (MostafaK), Mohammad, K. (Kazem), Mohammadi, Z. (Zahra), Mohammadifard, N. (Noushin), Mohammadpourhodki, R. (Reza), Mohan, V. (Viswanathan), Mohanna, S. (Salim), MohdYusoff, M. F. (Muhammad Fadhli), Mohebbi, I. (Iraj), Mohebi, F. (Farnam), Moitry, M. (Marie), Mollehave, L. T. (Line T.), Mller, N. C. (Niels C.), Molnar, D. (Denes), Momenan, A. (Amirabbas), Mondo, C. K. (Charles K.), Monterrubio-Flores, E. (Eric), Moosazadeh, M. (Mahmood), Morejon, A. (Alain), Moreno, L. A. (Luis A.), Morgan, K. (Karen), Morin, S. N. (Suzanne N.), Moschonis, G. (George), Mossakowska, M. (Malgorzata), Mostafa, A. (Aya), Mota, J. (Jorge), Motlagh, M. E. (Mohammad Esmaeel), Motta, J. (Jorge), Msyamboza, K. P. (Kelias P.), Muiesan, M. L. (Maria L.), Muller-Nurasyid, M. (Martina), Mursu, J. (Jaakko), Mustafa, N. (Norlaila), Nabipour, I. (Iraj), Naderimagham, S. (Shohreh), Nagel, G. (Gabriele), Naidu, B. M. (Balkish M.), Najafi, F. (Farid), Nakamura, H. (Harunobu), Nang, E. E. (Ei Ei K.), Nangia, V. B. (Vinay B.), Nauck, M. (Matthias), Neal, W. A. (William A.), Nejatizadeh, A. (Azim), Nenko, I. (Ilona), Nervi, F. (Flavio), Nguyen, N. D. (Nguyen D.), Nieto-Martinez, R. E. (Ramfis E.), Nihal, T. (Thomas), Niiranen, T. J. (Teemu J.), Ning, G. (Guang), Ninomiya, T. (Toshiharu), Noale, M. (Marianna), Noboa, O. A. (Oscar A.), Noto, D. (Davide), Al Nsour, M. (Mohannad), Nuhoglu, I. (Irfan), O'Neill, T. W. (Terence W.), O'Reilly, D. (Dermot), Ochoa-Aviles, A. M. (Angelica M.), Oh, K. (Kyungwon), Ohtsuka, R. (Ryutaro), Olafsson, O. (Orn), Olie, V. (Valerie), Oliveira, I. O. (Isabel O.), Omar, M. A. (Mohd Azahadi), Onat, A. (Altan), Ong, S. (SokKing), Ordunez, P. (Pedro), Ornelas, R. (Rui), Ortiz, P. J. (Pedro J.), Osmond, C. (Clive), Ostojic, S. M. (Sergej M.), Ostovar, A. (Afshin), Otero, J. A. (Johanna A.), Owusu-Dabo, E. (Ellis), Paccaud, F. M. (Fred Michel), Pahomova, E. (Elena), Pajak, A. (Andrzej), Palmieri, L. (Luigi), Pan, W.-H. (Wen-Harn), Panda-Jonas, S. (Songhomitra), Panza, F. (Francesco), Parnell, W. R. (Winsome R.), Patel, N. D. (Nikhil D.), Peer, N. (Nasheeta), Peixoto, S. V. (Sergio Viana), Peltonen, M. (Markku), Pereira, A. C. (Alexandre C.), Peters, A. (Annette), Petersmann, A. (Astrid), Petkeviciene, J. (Janina), Peykari, N. (Niloofar), Pichardo, R. N. (Rafael N.), Pigeot, I. (Iris), Pilav, A. (Aida), Pilotto, L. (Lorenza), Piwonska, A. (Aleksandra), Pizarro, A. N. (Andreia N.), Plans-Rubio, P. (Pedro), Plata, S. (Silvia), Pohlabeln, H. (Hermann), Porta, M. (Miquel), Portegies, M. L. (Marileen L. P.), Poudyal, A. (Anil), Pourfarzi, F. (Farhad), Poustchi, H. (Hossein), Pradeepa, R. (Rajendra), Price, J. F. (Jacqueline F.), Providencia, R. (Rui), Puder, J. J. (Jardena J.), Puhakka, S. E. (Soile E.), Punab, M. (Margus), Qorbani, M. (Mostafa), Radisauskas, R. (Ricardas), Rahimikazerooni, S. (Salar), Raitakari, O. (Olli), Rao, S. R. (Sudha Ramachandra), Ramachandran, A. (Ambady), Ramos, E. (Elisabete), Ramos, R. (Rafel), Rampal, L. (Lekhraj), Rampal, S. (Sanjay), Redon, J. (Josep), Reganit, P. F. (Paul Ferdinand M.), Revilla, L. (Luis), Rezaianzadeh, A. (Abbas), Ribeiro, R. (Robespierre), Richter, A. (Adrian), Rigo, F. (Fernando), de Wit, T. F. (Tobias F. Rinke), Rodriguez-Artalejo, F. (Fernando), Rodriguez-Perez, M. d. (Maria del Cristo), Rodriguez-Villamizar, L. A. (Laura A.), Roggenbuck, U. (Ulla), Rojas-Martinez, R. (Rosalba), Romaguera, D. (Dora), Romeo, E. L. (Elisabetta L.), Rosengren, A. (Annika), Roy, J. G. (Joel G. R.), Rubinstein, A. (Adolfo), Ruidavets, J.-B. (Jean-Bernard), Ruiz-Betancourt, B. S. (Blanca Sandra), Russo, P. (Paola), Rust, P. (Petra), Rutkowski, M. (Marcin), Sabanayagam, C. (Charumathi), Sachdev, H. S. (Harshpal S.), Sadjadi, A. (Alireza), Safarpour, A. R. (Ali Reza), Safiri, S. (Saeid), Saidi, O. (Olfa), Saki, N. (Nader), Salanave, B. (Benoit), Salmeron, D. (Diego), Salomaa, V. (Veikko), Salonen, J. T. (Jukka T.), Salvetti, M. (Massimo), Sanchez-Abanto, J. (Jose), Sans, S. (Susana), Santaliestra-Pasias, A. M. (Alba M.), Santos, D. A. (Diana A.), Santos, M. (MariaPaula), Santos, R. (Rute), Saramies, J. L. (Jouko L.), Sardinha, L. B. (Luis B.), Sarrafzadegan, N. (Nizal), Saum, K.-U. (Kai-Uwe), Savva, S. C. (Savvas C.), Sawada, N. (Norie), Sbaraini, M. (Mariana), Scazufca, M. (Marcia), Schaan, B. D. (Beatriz D.), Schargrodsky, H. (Herman), Scheidt-Nave, C. (Christa), Schienkiewitz, A. (Anja), Schipf, S. (Sabine), Schmidt, C. O. (Carsten O.), Schottker, B. (Ben), Schramm, S. (Sara), Sebert, S. (Sylvain), Sein, A. A. (Aye Aye), Sen, A. (Abhijit), Sepanlou, S. G. (Sadaf G.), Servais, J. (Jennifer), Shakeri, R. (Ramin), Shalnova, S. A. (Svetlana A.), Shamah-Levy, T. (Teresa), Sharafkhah, M. (Maryam), Sharma, S. K. (Sanjib K.), Shaw, J. E. (Jonathan E.), Shayanrad, A. (Amaneh), Shi, Z. (Zumin), Shibuya, K. (Kenji), Shimizu-Furusawa, H. (Hana), Shin, D. W. (Dong Wook), Shin, Y. (Youchan), Shirani, M. (Majid), Shiri, R. (Rahman), Shrestha, N. (Namuna), Si-Ramlee, K. (Khairil), Siani, A. (Alfonso), Siantar, R. (Rosalynn), Sibai, A. M. (Abla M.), Santos Silva, D. A. (Diego Augusto), Simon, M. (Mary), Simons, J. (Judith), Simons, L. A. (Leon A.), Sjostrom, M. (Michael), Skaaby, T. (Tea), Slowikowska-Hilczer, J. (Jolanta), Slusarczyk, P. (Przemyslaw), Smeeth, L. (Liam), Snijder, M. B. (Marieke B.), Soderberg, S. (Stefan), Soemantri, A. (Agustinus), Sofat, R. (Reecha), Solfrizzi, V. (Vincenzo), Somi, M. H. (Mohammad Hossein), Sonestedt, E. (Emily), Sorensen, T. I. (Thorkild I. A.), Jerome, C. S. (Charles Sossa), Soumare, A. (Aicha), Sozmen, K. (Kaan), Sparrenberger, K. (Karen), Staessen, J. A. (Jan A.), Stathopoulou, M. G. (Maria G.), Stavreski, B. (Bill), Steene-Johannessen, J. (Jostein), Stehle, P. (Peter), Stein, A. D. (Aryeh D.), Stessman, J. (Jochanan), Stevanovic, R. (Ranko), Stieber, J. (Jutta), Stockl, D. (Doris), Stokwiszewski, J. (Jakub), Stronks, K. (Karien), Strufaldi, M. W. (Maria Wany), Suarez-Medina, R. (Ramon), Sun, C.-A. (Chien-An), Sundstrom, J. (Johan), Suriyawongpaisal, P. (Paibul), Sy, R. G. (Rody G.), Sylva, R. C. (Rene Charles), Szklo, M. (Moyses), Tai, E. S. (E. Shyong), Tamosiunas, A. (Abdonas), Tan, E. (EngJoo), Tarawneh, M. R. (Mohammed Rasoul), Tarqui-Mamani, C. B. (Carolina B.), Taylor, A. (Anne), Taylor, J. (Julie), Tell, G. S. (Grethe S.), Tello, T. (Tania), Thankappan, K. R. (K. R.), Thijs, L. (Lutgarde), Thuesen, B. H. (Betina H.), Toft, U. (Ulla), Tolonen, H. K. (Hanna K.), Tolstrup, J. S. (Janne S.), Topbas, M. (Murat), Topor-Madry, R. (Roman), Tormo, M. J. (Maria Jose), Tornaritis, M. J. (Michael J.), Torrent, M. (Maties), Torres-Collado, L. (Laura), Traissac, P. (Pierre), Trinh, O. T. (Oanh T. H.), Truthmann, J. (Julia), Tsugane, S. (Shoichiro), Tulloch-Reid, M. K. (Marshall K.), Tuomainen, T.-P. (Tomi-Pekka), Tuomilehto, J. (Jaakko), Tybjaerg-Hansen, A. (Anne), Tzourio, C. (Christophe), Ueda, P. (Peter), Ugel, E. (Eunice), Ulmer, H. (Hanno), Unal, B. (Belgin), Uusitalo, H. M. (Hannu M. T.), Valdivia, G. (Gonzalo), Valvi, D. (Damaskini), van Dam, R. (RobM), van der Schouw, Y. T. (Yvonne T.), Van Herck, K. (Koen), Rossem, L. (Lenievan), Van Schoor, N. M. (Natasja M.), van Valkengoed, I. G. (Irene G. M.), Vanderschueren, D. (Dirk), Vanuzzo, D. (Diego), Varbo, A. (Anette), Varona-Perez, P. (Patricia), Vasan, S. K. (Senthil K.), Vatten, L. (Lars), Vega, T. (Tomas), Veidebaum, T. (Toomas), Velasquez-Melendez, G. (Gustavo), Venero-Fernandez, S. J. (Silvia J.), Veronesi, G. (Giovanni), MoniqueVerschuren, W. M. (W. M.), Victora, C. G. (Cesar G.), Vidiawati, D. (Dhanasari), Viet, L. (Lucie), Villalpando, S. (Salvador), Vioque, J. (Jesus), Virtanen, J. K. (Jyrki K.), Visvikis-Siest, S. (Sophie), Viswanathan, B. (Bharathi), Vlasoff, T. (Tiina), Vollenweider, P. (Peter), Voutilainen, A. (Ari), Wade, A. N. (Alisha N.), Wagner, A. (Aline), Walton, J. (Janette), Bebakar, W. M. (Wan Mohamad Wan), WanMohamud, W. N. (Wan Nazaimoon), Wang, M.-D. (Ming-Dong), Wang, N. (Ningli), Wang, Q. (Qian), Wang, Y. X. (Ya Xing), Wang, Y.-W. (Ying-Wei), Wannamethee, S. G. (S. Goya), Wedderkopp, N. (Niels), Wei, W. (Wenbin), Whincup, P. H. (Peter H.), Widhalm, K. (Kurt), Widyahening, I. S. (Indah S.), Wiecek, A. (Andrzej), Wijga, A. H. (Alet H.), Wilks, R. J. (Rainford J.), Willeit, J. (Johann), Willeit, P. (Peter), Wilsgaard, T. (Tom), Wojtyniak, B. (Bogdan), Wong-McClure, R. A. (Roy A.), Wong, A. (Andrew), Wong, T. Y. (Tien Yin), Woo, J. (Jean), Woodward, M. (Mark), Wu, F. C. (Frederick C.), Wu, S. (Shouling), Xu, H. (Haiquan), Xu, L. (Liang), Yan, W. (Weili), Yang, X. (Xiaoguang), Yasuharu, T. (Tabara), Ye, X. (Xingwang), Yeow, T. P. (Toh Peng), Yiallouros, P. K. (Panayiotis K.), Yoosefi, M. (Moein), Yoshihara, A. (Akihiro), You, S.-L. (San-Lin), Younger-Coleman, N. O. (Novie O.), Yusoff, A. F. (Ahmad Faudzi), Zainuddin, A. A. (Ahmad A.), Zakavi, S. R. (Seyed Rasoul), Zali, M. R. (Mohammad Reza), Zamani, F. (Farhad), Zambon, S. (Sabina), Zampelas, A. (Antonis), KoZaw, K. (Ko), Zdrojewski, T. (Tomasz), Vrkic, T. Z. (Tajana Zeljkovic), Zhang, Z.-Y. (Zhen-Yu), Zhao, W. (Wenhua), Zhen, S. (Shiqi), Zheng, Y. (Yingfeng), Zholdin, B. (Bekbolat), Zhussupov, B. (Baurzhan), Zoghlami, N. (Nada), Cisneros, J. Z. (Julio Zuniga), Gregg, E. W. (Edward W.), Ezzati, M. (Majid), Taddei, C. (Cristina), Zhou, B. (Bin), Bixby, H. (Honor), Carrillo-Larco, R. M. (Rodrigo M.), Danaei, G. (Goodarz), Jackson, R. T. (Rod T.), Farzadfar, F. (Farshad), Sophiea, M. K. (Marisa K.), Di Cesare, M. (Mariachiara), Iurilli, M. L. (Maria Laura Caminia), Martinez, A. R. (Andrea Rodriguez), Asghari, G. (Golaleh), Dhana, K. (Klodian), Gulayin, P. (Pablo), Kakarmath, S. (Sujay), Santero, M. (Marilina), Voortman, T. (Trudy), Riley, L. M. (Leanne M.), Cowan, M. J. (Melanie J.), Savin, S. (Stefan), Bennett, J. E. (James E.), Stevens, G. A. (Gretchen A.), Paciorek, C. J. (Christopher J.), Aekplakorn, W. (Wichai), Cifkova, R. (Renata), Giampaoli, S. (Simona), Kengne, A. P. (Andre Pascal), Khang, Y.-H. (Young-Ho), Kuulasmaa, K. (Kari), Laxmaiah, A. (Avula), Margozzini, P. (Paula), Mathur, P. (Prashant), Nordestgaard, B. G. (Borge G.), Zhao, D. (Dong), Aadahl, M. (Mette), Abarca-Gomez, L. (Leandra), Rahim, H. A. (Hanan Abdul), Abu-Rmeileh, N. M. (Niveen M.), Acosta-Cazares, B. (Benjamin), Adams, R. J. (Robert J.), Agdeppa, I. A. (Imelda A.), Aghazadeh-Attari, J. (Javad), Aguilar-Salinas, C. A. (Carlos A.), Agyemang, C. (Charles), Ahluwalia, T. S. (Tarunveer S.), Ahmad, N. A. (Noor Ani), Ahmadi, A. (Ali), Ahmadi, N. (Naser), Ahmed, S. H. (Soheir H.), Ahrens, W. (Wolfgang), Ajlouni, K. (Kamel), Alarouj, M. (Monira), AlBuhairan, F. (Fadia), AlDhukair, S. (Shahla), Ali, M. M. (Mohamed M.), Alkandari, A. (Abdullah), Alkerwi, A. (Ala'a), Aly, E. (Eman), Amarapurkar, D. N. (Deepak N.), Amouyel, P. (Philippe), Andersen, L. B. (Lars Bo), Anderssen, S. A. (Sigmund A.), Anjana, R. M. (Ranjit Mohan), Ansari-Moghaddam, A. (Alireza), Aounallah-Skhiri, H. (Hajer), Araujo, J. (Joana), Ariansen, I. (Inger), Aris, T. (Tahir), Arku, R. E. (Raphael E.), Arlappa, N. (Nimmathota), Aryal, K. K. (Krishna K.), Aspelund, T. (Thor), Assuncao, M. C. (Maria Cecilia F.), Auvinen, J. (Juha), Avdicova, M. (Maria), Azevedo, A. (Ana), Azizi, F. (Fereidoun), Azmin, M. (Mehrdad), Balakrishna, N. (Nagalla), Bamoshmoosh, M. (Mohamed), Banach, M. (Maciej), Bandosz, P. (Piotr), Banegas, J. R. (Jose R.), Barbagallo, C. M. (Carlo M.), Barcelo, A. (Alberto), Barkat, A. (Amina), Bata, I. (Iqbal), Batieha, A. M. (Anwar M.), Batyrbek, A. (Assembekov), Baur, L. A. (Louise A.), Beaglehole, R. (Robert), Belavendra, A. (Antonisamy), Ben Romdhane, H. (Habiba), Benet, M. (Mikhail), Benn, M. (Marianne), Berkinbayev, S. (Salim), Bernabe-Ortiz, A. (Antonio), Bernotiene, G. (Gailute), Bettiol, H. (Heloisa), Bhargava, S. K. (Santosh K.), Bi, Y. (Yufang), Bienek, A. (Asako), Bikbov, M. (Mukharram), Bista, B. (Bihungum), Bjerregaard, P. (Peter), Bjertness, E. (Espen), Bjertness, M. B. (Marius B.), Bjorkelund, C. (Cecilia), Bloch, K. V. (Katia, V), Blokstra, A. (Anneke), Bo, S. (Simona), Boehm, B. O. (Bernhard O.), Boggia, J. G. (Jose G.), Boissonnet, C. P. (Carlos P.), Bonaccio, M. (Marialaura), Bongard, V. (Vanina), Borchini, R. (Rossana), Borghs, H. (Herman), Bovet, P. (Pascal), Brajkovich, I. (Imperia), Breckenkamp, J. (Juergen), Brenner, H. (Hermann), Brewster, L. M. (Lizzy M.), Bruno, G. (Graziella), Bugge, A. (Anna), Busch, M. A. (Markus A.), de Leon, A. C. (Antonio Cabrera), Cacciottolo, J. (Joseph), Can, G. (Gunay), Candido, A. P. (Ana Paula C.), Capanzana, M. V. (Mario, V), Capuano, E. (Eduardo), Capuano, V. (Vincenzo), Cardoso, V. C. (Viviane C.), Carvalho, J. (Joana), Casanueva, F. F. (Felipe F.), Censi, L. (Laura), Chadjigeorgiou, C. A. (Charalambos A.), Chamukuttan, S. (Snehalatha), Chaturvedi, N. (Nish), Chen, C.-J. (Chien-Jen), Chen, F. (Fangfang), Chen, S. (Shuohua), Cheng, C.-Y. (Ching-Yu), Cheraghian, B. (Bahman), Chetrit, A. (Angela), Chiou, S.-T. (Shu-Ti), Chirlaque, M.-D. (Maria-Dolores), Cho, B. (Belong), Cho, Y. (Yumi), Chudek, J. (Jerzy), Claessens, F. (Frank), Clarke, J. (Janine), Clays, E. (Els), Concin, H. (Hans), Confortin, S. C. (Susana C.), Cooper, C. (Cyrus), Costanzo, S. (Simona), Cottel, D. (Dominique), Cowell, C. (Chris), Crujeiras, A. B. (Ana B.), Csilla, S. (Semanova), Cui, L. (Liufu), Cureau, F. V. (Felipe, V), D'Arrigo, G. (Graziella), d'Orsi, E. (Eleonora), Dallongeville, J. (Jean), Damasceno, A. (Albertino), Dankner, R. (Rachel), Dantoft, T. M. (Thomas M.), Dauchet, L. (Luc), Davletov, K. (Kairat), De Backer, G. (Guy), De Bacquer, D. (Dirk), de Gaetano, G. (Giovanni), De Henauw, S. (Stefaan), de Oliveira, P. D. (Paula Duarte), De Ridder, D. (David), De Smedt, D. (Delphine), Deepa, M. (Mohan), Deev, A. D. (Alexander D.), Dehghan, A. (Abbas), Delisle, H. (Helene), Dennison, E. (Elaine), Deschamps, V. (Valerie), Dhimal, M. (Meghnath), Di Castelnuovo, A. F. (Augusto F.), Dika, Z. (Zivka), Djalalinia, S. (Shirin), Dobson, A. J. (Annette J.), Donfrancesco, C. (Chiara), Donoso, S. P. (Silvana P.), Doring, A. (Angela), Dorobantu, M. (Maria), Dragano, N. (Nico), Drygas, W. (Wojciech), Du, Y. (Yong), Duante, C. A. (Charmaine A.), Duda, R. B. (Rosemary B.), Dzerve, V. (Vilnis), Dziankowska-Zaborszczyk, E. (Elzbieta), Eddie, R. (Ricky), Eftekhar, E. (Ebrahim), Eggertsen, R. (Robert), Eghtesad, S. (Sareh), Eiben, G. (Gabriele), Ekelund, U. (Ulf), El Ati, J. (Jalila), Eldemire-Shearer, D. (Denise), Eliasen, M. (Marie), Elosua, R. (Roberto), Erasmus, R. T. (Rajiv T.), Erbel, R. (Raimund), Erem, C. (Cihangir), Eriksen, L. (Louise), Eriksson, J. G. (Johan G.), Escobedo-de la Pena, J. (Jorge), Eslami, S. (Saeid), Esmaeili, A. (Ali), Evans, A. (Alun), Faeh, D. (David), Fall, C. H. (Caroline H.), Faramarzi, E. (Elnaz), Farjam, M. (Mojtaba), Fattahi, M. R. (Mohammad Reza), Felix-Redondo, F. J. (Francisco J.), Ferguson, T. S. (Trevor S.), Fernandez-Berges, D. (Daniel), Ferrante, D. (Daniel), Ferrari, M. (Marika), Ferreccio, C. (Catterina), Ferrieres, J. (Jean), Foger, B. (Bernhard), Foo, L. H. (Leng Huat), Forslund, A.-S. (Ann-Sofie), Forsner, M. (Maria), Fouad, H. M. (Heba M.), Francis, D. K. (Damian K.), Franco, M. d. (Maria do Carmo), Franco, O. H. (Oscar H.), Frontera, G. (Guillermo), Fujita, Y. (Yuki), Fumihiko, M. (Matsuda), Furusawa, T. (Takuro), Gaciong, Z. (Zbigniew), Galvano, F. (Fabio), Gao, J. (Jingli), Garcia-de-la-Hera, M. (Manoli), Garnett, S. P. (Sarah P.), Gaspoz, J.-M. (Jean-Michel), Gasull, M. (Magda), Gazzinelli, A. (Andrea), Geleijnse, J. M. (Johanna M.), Ghanbari, A. (Ali), Ghasemi, E. (Erfan), Gheorghe-Fronea, O.-F. (Oana-Florentina), Ghimire, A. (Anup), Gianfagna, F. (Francesco), Gill, T. K. (Tiffany K.), Giovannelli, J. (Jonathan), Gironella, G. (Glen), Giwercman, A. (Aleksander), Goltzman, D. (David), Goncalves, H. (Helen), Gonzalez-Chica, D. A. (David A.), Gonzalez-Gross, M. (Marcela), Gonzalez-Rivas, J. P. (Juan P.), Gonzalez-Villalpando, C. (Clicerio), Gonzalez-Villalpando, M.-E. (Maria-Elena), Gonzalez, A. R. (Angel R.), Gottrand, F. (Frederic), Graff-Iversen, S. (Sidsel), Gregor, R. D. (Ronald D.), Grodzicki, T. (Tomasz), Grontved, A. (Anders), Grosso, G. (Giuseppe), Gruden, G. (Gabriella), Gu, D. (Dongfeng), Guallar-Castillon, P. (Pilar), Guan, O. P. (Ong Peng), Gudmundsson, E. F. (Elias F.), Gudnason, V. (Vilmundur), Guerrero, R. (Ramiro), Guessous, I. (Idris), Gunnlaugsdottir, J. (Johanna), Gupta, R. (Rajeev), Gutierrez, L. (Laura), Gutzwiller, F. (Felix), Ha, S. (Seongjun), Hadaegh, F. (Farzad), Haghshenas, R. (Rosa), Hakimi, H. (Hamid), Hambleton, I. R. (Ian R.), Hamzeh, B. (Behrooz), Hantunen, S. (Sari), Kumar, R. H. (Rachakulla Hari), Hashemi-Shahri, S. M. (Seyed Mohammad), Hata, J. (Jun), Haugsgjerd, T. (Teresa), Hayes, A. J. (Alison J.), He, J. (Jiang), He, Y. (Yuna), Hendriks, M. E. (Marleen Elisabeth), Henriques, A. (Ana), Herrala, S. (Sauli), Heshmat, R. (Ramin), Hill, A. G. (Allan G.), Ho, S. Y. (Sai Yin), Ho, S. C. (Suzanne C.), Hobbs, M. (Michael), Hofman, A. (Albert), Homayounfar, R. (Reza), Hopman, W. M. (Wilma M.), Horimoto, A. R. (Andrea R. V. R.), Hormiga, C. M. (Claudia M.), Horta, B. L. (Bernardo L.), Houti, L. (Leila), Howitt, C. (Christina), Htay, T. T. (Thein Thein), Htet, A. S. (Aung Soe), Htike, M. M. (Maung Maung Than), Huerta, J. M. (Jose Maria), Huhtaniemi, I. T. (Ilpo Tapani), Huisman, M. (Martijn), Hunsberger, M. L. (Monica L.), Husseini, A. S. (Abdullatif S.), Huybrechts, I. (Inge), Hwalla, N. (Nahla), Iacoviello, L. (Licia), Iannone, A. G. (Anna G.), Ibrahim, M. M. (Mohsen M.), Wong, N. I. (Norazizah Ibrahim), Iglesia, I. (Iris), Ikeda, N. (Nayu), Ikram, M. A. (M. Arfan), Iotova, V. (Violeta), Irazola, V. E. (Vilma E.), Ishida, T. (Takafumi), Islam, M. (Muhammad), Ismail, A. A. (Aziz Al-Safi), Iwasaki, M. (Masanori), Jacobs, J. M. (Jeremy M.), Jaddou, H. Y. (Hashem Y.), Jafar, T. (Tazeen), James, K. (Kenneth), Jamrozik, K. (Konrad), Janszky, I. (Imre), Janus, E. (Edward), Järvelin, M.-R. (Marjo-Riitta), Jasienska, G. (Grazyna), Jelakovic, A. (Ana), Jelakovic, B. (Bojan), Jennings, G. (Garry), Jensen, G. B. (Gorm B.), Jeong, S.-l. (Seung-lyeal), Jha, A. K. (Anjani Kumar), Jiang, C. Q. (Chao Qiang), Jimenez, R. O. (Ramon O.), Jockel, K.-H. (Karl-Heinz), Joffres, M. (Michel), Jokelainen, J. J. (Jari J.), Jonas, J. B. (Jost B.), Jorgensen, T. (Torben), Joshi, P. (Pradeep), Joukar, F. (Farahnaz), Jozwiak, J. (Jacek), Juolevi, A. (Anne), Kafatos, A. (Anthony), Kajantie, E. O. (Eero O.), Kalter-Leibovici, O. (Ofra), Kamaruddin, N. A. (Nor Azmi), Kamstrup, P. R. (Pia R.), Karki, K. B. (Khem B.), Katz, J. (Joanne), Kauhanen, J. (Jussi), Kaur, P. (Prabhdeep), Kavousi, M. (Maryam), Kazakbaeva, G. (Gyulli), Keil, U. (Ulrich), Keinanen-Kiukaanniemi, S. (Sirkka), Kelishadi, R. (Roya), Keramati, M. (Maryam), Kerimkulova, A. (Alina), Kersting, M. (Mathilde), Khader, Y. S. (Yousef Saleh), Khalili, D. (Davood), Khateeb, M. (Mohammad), Kheradmand, M. (Motahareh), Khosravi, A. (Alireza), Kiechl-Kohlendorfer, U. (Ursula), Kiechl, S. (Stefan), Killewo, J. (Japhet), Kim, H. C. (Hyeon Chang), Kim, J. (Jeongseon), Kim, Y.-Y. (Yeon-Yong), Klumbiene, J. (Jurate), Knoflach, M. (Michael), Ko, S. (Stephanie), Kohler, H.-P. (Hans-Peter), Kohler, I. V. (Iliana, V), Kolle, E. (Elin), Kolsteren, P. (Patrick), Konig, J. (Jurgen), Korpelainen, R. (Raija), . (), Kos, J. (Jelena), Koskinen, S. (Seppo), Kouda, K. (Katsuyasu), Kowlessur, S. (Sudhir), Kratzer, W. (Wolfgang), Kriemler, S. (Susi), Kristensen, P. L. (Peter Lund), Krokstad, S. (Steiner), Kromhout, D. (Daan), Kujala, U. M. (Urho M.), Kurjata, P. (Pawel), Kyobutungi, C. (Catherine), Laamiri, F. Z. (Fatima Zahra), Laatikainen, T. (Tiina), Lachat, C. (Carl), Laid, Y. (Youcef), Lam, T. H. (Tai Hing), Lambrinou, C.-P. (Christina-Paulina), Lanska, V. (Vera), Lappas, G. (Georg), Larijani, B. (Bagher), Latt, T. S. (Tint Swe), Laugsand, L. E. (Lars E.), Lazo-Porras, M. (Maria), Lee, J. (Jeannette), Lee, J. (Jeonghee), Lehmann, N. (Nils), Lehtimaki, T. (Terho), Levitt, N. S. (Naomi S.), Li, Y. (Yanping), Lilly, C. L. (Christa L.), Lim, W.-Y. (Wei-Yen), Lima-Costa, M. F. (M. Fernanda), Lin, H.-H. (Hsien-Ho), Lin, X. (Xu), Lin, Y.-T. (Yi-Ting), Lind, L. (Lars), Linneberg, A. (Allan), Lissner, L. (Lauren), Liu, J. (Jing), Loit, H.-M. (Helle-Mai), Lopez-Garcia, E. (Esther), Lopez, T. (Tania), Lotufo, P. A. (Paulo A.), Lozano, J. E. (Jose Eugenio), Luksiene, D. (Dalia), Lundqvist, A. (Annamari), Lundqvist, R. (Robert), Lunet, N. (Nuno), Ma, G. (Guansheng), Machado-Coelho, G. L. (George L. L.), Machado-Rodrigues, A. M. (Aristides M.), Machi, S. (Suka), Madar, A. A. (Ahmed A.), Maggi, S. (Stefania), Magliano, D. J. (Dianna J.), Magriplis, E. (Emmanuella), Mahasampath, G. (Gowri), Maire, B. (Bernard), Makdisse, M. (Marcia), Malekzadeh, F. (Fatemeh), Rao, K. M. (Kodavanti Mallikharjuna), Manios, Y. (Yannis), Mann, J. I. (Jim, I), Mansour-Ghanaei, F. (Fariborz), Manzato, E. (Enzo), Marques-Vidal, P. (Pedro), Martorell, R. (Reynaldo), Mascarenhas, L. P. (Luis P.), Mathiesen, E. B. (Ellisiv B.), Matsha, T. E. (Tandi E.), Mavrogianni, C. (Christina), McFarlane, S. R. (Shelly R.), McGarvey, S. T. (Stephen T.), McLachlan, S. (Stela), McLean, R. M. (Rachael M.), McLean, S. B. (Scott B.), McNulty, B. A. (Breige A.), Mediene-Benchekor, S. (Sounnia), Mehdipour, P. (Parinaz), Mehlig, K. (Kirsten), Mehrparvar, A. (AmirHoushang), Meirhaeghe, A. (Aline), Meisinger, C. (Christa), Menezes, A. M. (Ana Maria B.), Menon, G. R. (Geetha R.), Merat, S. (Shahin), Mereke, A. (Alibek), Meshram, I. I. (Indrapal I.), Metcalf, P. (Patricia), Meyer, H. E. (Haakon E.), Mi, J. (Jie), Michels, N. (Nathalie), Miller, J. C. (Jody C.), Minderico, C. S. (Claudia S.), Mini, G. K. (G. K.), Miquel, J. F. (Juan Francisco), Miranda, J. J. (J. Jaime), Mirjalili, M. R. (Mohammad Reza), Mirrakhimov, E. (Erkin), Modesti, P. A. (Pietro A.), Moghaddam, S. S. (Sahar Saeedi), Mohajer, B. (Bahram), Mohamed, M. (MostafaK), Mohammad, K. (Kazem), Mohammadi, Z. (Zahra), Mohammadifard, N. (Noushin), Mohammadpourhodki, R. (Reza), Mohan, V. (Viswanathan), Mohanna, S. (Salim), MohdYusoff, M. F. (Muhammad Fadhli), Mohebbi, I. (Iraj), Mohebi, F. (Farnam), Moitry, M. (Marie), Mollehave, L. T. (Line T.), Mller, N. C. (Niels C.), Molnar, D. (Denes), Momenan, A. (Amirabbas), Mondo, C. K. (Charles K.), Monterrubio-Flores, E. (Eric), Moosazadeh, M. (Mahmood), Morejon, A. (Alain), Moreno, L. A. (Luis A.), Morgan, K. (Karen), Morin, S. N. (Suzanne N.), Moschonis, G. (George), Mossakowska, M. (Malgorzata), Mostafa, A. (Aya), Mota, J. (Jorge), Motlagh, M. E. (Mohammad Esmaeel), Motta, J. (Jorge), Msyamboza, K. P. (Kelias P.), Muiesan, M. L. (Maria L.), Muller-Nurasyid, M. (Martina), Mursu, J. (Jaakko), Mustafa, N. (Norlaila), Nabipour, I. (Iraj), Naderimagham, S. (Shohreh), Nagel, G. (Gabriele), Naidu, B. M. (Balkish M.), Najafi, F. (Farid), Nakamura, H. (Harunobu), Nang, E. E. (Ei Ei K.), Nangia, V. B. (Vinay B.), Nauck, M. (Matthias), Neal, W. A. (William A.), Nejatizadeh, A. (Azim), Nenko, I. (Ilona), Nervi, F. (Flavio), Nguyen, N. D. (Nguyen D.), Nieto-Martinez, R. E. (Ramfis E.), Nihal, T. (Thomas), Niiranen, T. J. (Teemu J.), Ning, G. (Guang), Ninomiya, T. (Toshiharu), Noale, M. (Marianna), Noboa, O. A. (Oscar A.), Noto, D. (Davide), Al Nsour, M. (Mohannad), Nuhoglu, I. (Irfan), O'Neill, T. W. (Terence W.), O'Reilly, D. (Dermot), Ochoa-Aviles, A. M. (Angelica M.), Oh, K. (Kyungwon), Ohtsuka, R. (Ryutaro), Olafsson, O. (Orn), Olie, V. (Valerie), Oliveira, I. O. (Isabel O.), Omar, M. A. (Mohd Azahadi), Onat, A. (Altan), Ong, S. (SokKing), Ordunez, P. (Pedro), Ornelas, R. (Rui), Ortiz, P. J. (Pedro J.), Osmond, C. (Clive), Ostojic, S. M. (Sergej M.), Ostovar, A. (Afshin), Otero, J. A. (Johanna A.), Owusu-Dabo, E. (Ellis), Paccaud, F. M. (Fred Michel), Pahomova, E. (Elena), Pajak, A. (Andrzej), Palmieri, L. (Luigi), Pan, W.-H. (Wen-Harn), Panda-Jonas, S. (Songhomitra), Panza, F. (Francesco), Parnell, W. R. (Winsome R.), Patel, N. D. (Nikhil D.), Peer, N. (Nasheeta), Peixoto, S. V. (Sergio Viana), Peltonen, M. (Markku), Pereira, A. C. (Alexandre C.), Peters, A. (Annette), Petersmann, A. (Astrid), Petkeviciene, J. (Janina), Peykari, N. (Niloofar), Pichardo, R. N. (Rafael N.), Pigeot, I. (Iris), Pilav, A. (Aida), Pilotto, L. (Lorenza), Piwonska, A. (Aleksandra), Pizarro, A. N. (Andreia N.), Plans-Rubio, P. (Pedro), Plata, S. (Silvia), Pohlabeln, H. (Hermann), Porta, M. (Miquel), Portegies, M. L. (Marileen L. P.), Poudyal, A. (Anil), Pourfarzi, F. (Farhad), Poustchi, H. (Hossein), Pradeepa, R. (Rajendra), Price, J. F. (Jacqueline F.), Providencia, R. (Rui), Puder, J. J. (Jardena J.), Puhakka, S. E. (Soile E.), Punab, M. (Margus), Qorbani, M. (Mostafa), Radisauskas, R. (Ricardas), Rahimikazerooni, S. (Salar), Raitakari, O. (Olli), Rao, S. R. (Sudha Ramachandra), Ramachandran, A. (Ambady), Ramos, E. (Elisabete), Ramos, R. (Rafel), Rampal, L. (Lekhraj), Rampal, S. (Sanjay), Redon, J. (Josep), Reganit, P. F. (Paul Ferdinand M.), Revilla, L. (Luis), Rezaianzadeh, A. (Abbas), Ribeiro, R. (Robespierre), Richter, A. (Adrian), Rigo, F. (Fernando), de Wit, T. F. (Tobias F. Rinke), Rodriguez-Artalejo, F. (Fernando), Rodriguez-Perez, M. d. (Maria del Cristo), Rodriguez-Villamizar, L. A. (Laura A.), Roggenbuck, U. (Ulla), Rojas-Martinez, R. (Rosalba), Romaguera, D. (Dora), Romeo, E. L. (Elisabetta L.), Rosengren, A. (Annika), Roy, J. G. (Joel G. R.), Rubinstein, A. (Adolfo), Ruidavets, J.-B. (Jean-Bernard), Ruiz-Betancourt, B. S. (Blanca Sandra), Russo, P. (Paola), Rust, P. (Petra), Rutkowski, M. (Marcin), Sabanayagam, C. (Charumathi), Sachdev, H. S. (Harshpal S.), Sadjadi, A. (Alireza), Safarpour, A. R. (Ali Reza), Safiri, S. (Saeid), Saidi, O. (Olfa), Saki, N. (Nader), Salanave, B. (Benoit), Salmeron, D. (Diego), Salomaa, V. (Veikko), Salonen, J. T. (Jukka T.), Salvetti, M. (Massimo), Sanchez-Abanto, J. (Jose), Sans, S. (Susana), Santaliestra-Pasias, A. M. (Alba M.), Santos, D. A. (Diana A.), Santos, M. (MariaPaula), Santos, R. (Rute), Saramies, J. L. (Jouko L.), Sardinha, L. B. (Luis B.), Sarrafzadegan, N. (Nizal), Saum, K.-U. (Kai-Uwe), Savva, S. C. (Savvas C.), Sawada, N. (Norie), Sbaraini, M. (Mariana), Scazufca, M. (Marcia), Schaan, B. D. (Beatriz D.), Schargrodsky, H. (Herman), Scheidt-Nave, C. (Christa), Schienkiewitz, A. (Anja), Schipf, S. (Sabine), Schmidt, C. O. (Carsten O.), Schottker, B. (Ben), Schramm, S. (Sara), Sebert, S. (Sylvain), Sein, A. A. (Aye Aye), Sen, A. (Abhijit), Sepanlou, S. G. (Sadaf G.), Servais, J. (Jennifer), Shakeri, R. (Ramin), Shalnova, S. A. (Svetlana A.), Shamah-Levy, T. (Teresa), Sharafkhah, M. (Maryam), Sharma, S. K. (Sanjib K.), Shaw, J. E. (Jonathan E.), Shayanrad, A. (Amaneh), Shi, Z. (Zumin), Shibuya, K. (Kenji), Shimizu-Furusawa, H. (Hana), Shin, D. W. (Dong Wook), Shin, Y. (Youchan), Shirani, M. (Majid), Shiri, R. (Rahman), Shrestha, N. (Namuna), Si-Ramlee, K. (Khairil), Siani, A. (Alfonso), Siantar, R. (Rosalynn), Sibai, A. M. (Abla M.), Santos Silva, D. A. (Diego Augusto), Simon, M. (Mary), Simons, J. (Judith), Simons, L. A. (Leon A.), Sjostrom, M. (Michael), Skaaby, T. (Tea), Slowikowska-Hilczer, J. (Jolanta), Slusarczyk, P. (Przemyslaw), Smeeth, L. (Liam), Snijder, M. B. (Marieke B.), Soderberg, S. (Stefan), Soemantri, A. (Agustinus), Sofat, R. (Reecha), Solfrizzi, V. (Vincenzo), Somi, M. H. (Mohammad Hossein), Sonestedt, E. (Emily), Sorensen, T. I. (Thorkild I. A.), Jerome, C. S. (Charles Sossa), Soumare, A. (Aicha), Sozmen, K. (Kaan), Sparrenberger, K. (Karen), Staessen, J. A. (Jan A.), Stathopoulou, M. G. (Maria G.), Stavreski, B. (Bill), Steene-Johannessen, J. (Jostein), Stehle, P. (Peter), Stein, A. D. (Aryeh D.), Stessman, J. (Jochanan), Stevanovic, R. (Ranko), Stieber, J. (Jutta), Stockl, D. (Doris), Stokwiszewski, J. (Jakub), Stronks, K. (Karien), Strufaldi, M. W. (Maria Wany), Suarez-Medina, R. (Ramon), Sun, C.-A. (Chien-An), Sundstrom, J. (Johan), Suriyawongpaisal, P. (Paibul), Sy, R. G. (Rody G.), Sylva, R. C. (Rene Charles), Szklo, M. (Moyses), Tai, E. S. (E. Shyong), Tamosiunas, A. (Abdonas), Tan, E. (EngJoo), Tarawneh, M. R. (Mohammed Rasoul), Tarqui-Mamani, C. B. (Carolina B.), Taylor, A. (Anne), Taylor, J. (Julie), Tell, G. S. (Grethe S.), Tello, T. (Tania), Thankappan, K. R. (K. R.), Thijs, L. (Lutgarde), Thuesen, B. H. (Betina H.), Toft, U. (Ulla), Tolonen, H. K. (Hanna K.), Tolstrup, J. S. (Janne S.), Topbas, M. (Murat), Topor-Madry, R. (Roman), Tormo, M. J. (Maria Jose), Tornaritis, M. J. (Michael J.), Torrent, M. (Maties), Torres-Collado, L. (Laura), Traissac, P. (Pierre), Trinh, O. T. (Oanh T. H.), Truthmann, J. (Julia), Tsugane, S. (Shoichiro), Tulloch-Reid, M. K. (Marshall K.), Tuomainen, T.-P. (Tomi-Pekka), Tuomilehto, J. (Jaakko), Tybjaerg-Hansen, A. (Anne), Tzourio, C. (Christophe), Ueda, P. (Peter), Ugel, E. (Eunice), Ulmer, H. (Hanno), Unal, B. (Belgin), Uusitalo, H. M. (Hannu M. T.), Valdivia, G. (Gonzalo), Valvi, D. (Damaskini), van Dam, R. (RobM), van der Schouw, Y. T. (Yvonne T.), Van Herck, K. (Koen), Rossem, L. (Lenievan), Van Schoor, N. M. (Natasja M.), van Valkengoed, I. G. (Irene G. M.), Vanderschueren, D. (Dirk), Vanuzzo, D. (Diego), Varbo, A. (Anette), Varona-Perez, P. (Patricia), Vasan, S. K. (Senthil K.), Vatten, L. (Lars), Vega, T. (Tomas), Veidebaum, T. (Toomas), Velasquez-Melendez, G. (Gustavo), Venero-Fernandez, S. J. (Silvia J.), Veronesi, G. (Giovanni), MoniqueVerschuren, W. M. (W. M.), Victora, C. G. (Cesar G.), Vidiawati, D. (Dhanasari), Viet, L. (Lucie), Villalpando, S. (Salvador), Vioque, J. (Jesus), Virtanen, J. K. (Jyrki K.), Visvikis-Siest, S. (Sophie), Viswanathan, B. (Bharathi), Vlasoff, T. (Tiina), Vollenweider, P. (Peter), Voutilainen, A. (Ari), Wade, A. N. (Alisha N.), Wagner, A. (Aline), Walton, J. (Janette), Bebakar, W. M. (Wan Mohamad Wan), WanMohamud, W. N. (Wan Nazaimoon), Wang, M.-D. (Ming-Dong), Wang, N. (Ningli), Wang, Q. (Qian), Wang, Y. X. (Ya Xing), Wang, Y.-W. (Ying-Wei), Wannamethee, S. G. (S. Goya), Wedderkopp, N. (Niels), Wei, W. (Wenbin), Whincup, P. H. (Peter H.), Widhalm, K. (Kurt), Widyahening, I. S. (Indah S.), Wiecek, A. (Andrzej), Wijga, A. H. (Alet H.), Wilks, R. J. (Rainford J.), Willeit, J. (Johann), Willeit, P. (Peter), Wilsgaard, T. (Tom), Wojtyniak, B. (Bogdan), Wong-McClure, R. A. (Roy A.), Wong, A. (Andrew), Wong, T. Y. (Tien Yin), Woo, J. (Jean), Woodward, M. (Mark), Wu, F. C. (Frederick C.), Wu, S. (Shouling), Xu, H. (Haiquan), Xu, L. (Liang), Yan, W. (Weili), Yang, X. (Xiaoguang), Yasuharu, T. (Tabara), Ye, X. (Xingwang), Yeow, T. P. (Toh Peng), Yiallouros, P. K. (Panayiotis K.), Yoosefi, M. (Moein), Yoshihara, A. (Akihiro), You, S.-L. (San-Lin), Younger-Coleman, N. O. (Novie O.), Yusoff, A. F. (Ahmad Faudzi), Zainuddin, A. A. (Ahmad A.), Zakavi, S. R. (Seyed Rasoul), Zali, M. R. (Mohammad Reza), Zamani, F. (Farhad), Zambon, S. (Sabina), Zampelas, A. (Antonis), KoZaw, K. (Ko), Zdrojewski, T. (Tomasz), Vrkic, T. Z. (Tajana Zeljkovic), Zhang, Z.-Y. (Zhen-Yu), Zhao, W. (Wenhua), Zhen, S. (Shiqi), Zheng, Y. (Yingfeng), Zholdin, B. (Bekbolat), Zhussupov, B. (Baurzhan), Zoghlami, N. (Nada), Cisneros, J. Z. (Julio Zuniga), Gregg, E. W. (Edward W.), and Ezzati, M. (Majid)
- Abstract
High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world³ and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol—which is a marker of cardiovascular risk—changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million–4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions t
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- 2020
5. Response of river water chemistry to changing atmospheric environment and sulfur dynamics in a forested catchment in central Japan.
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Sase, Hiroyuki, Takahashi, M., Matsuda, K., Sato, K., Tanikawa, T., Yamashita, N., Ohizumi, T., Ishida, T., Kamisako, M., Kobayashi, R., Uchiyama, S., Saito, T., Morohashi, M., Fukuhara, H., Kaneko, S., Inoue, T., Yamada, T., Takenaka, C., Tayasu, I., and Nakano, T.
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ATMOSPHERIC sulfur dioxide ,WATER chemistry ,RESERVOIRS ,CRYSTAL structure ,NANOPARTICLES - Abstract
Reduction of atmospheric sulfur (S) deposition and recovery of terrestrial ecosystems from acidification are matters of concerns in Asia. The Lake Ijira catchment (IJR) is located in the downwind region of the Chukyo Industrial Area in central Japan and has historically experienced large-scale deposition of S and nitrogen (N) from the atmosphere. Long-term monitoring data on the river water (RW) chemistry since 1988 were assessed with intensive-survey datasets on the input-output material budgets and S isotopic analysis (δ
34 S). Previous studies have suggested that IJR was acidified and N-saturated, which was triggered by climatic anomalies (cold summer and drought summer) in the mid-1990s. Analysis shows that with a decline in NO3- concentrations, RW pH recovered to its original level in the early 2000s. Reductions in atmospheric deposition, diminished effects of climatic anomalies, and forest management practices, have all contributed to RW chemistry recovery. Although the SO42- concentration in the RW has declined continuously after the peak in 1994, the mean SO42- output significantly exceeded the input; the 5-year means from 2010 to 2014 are 2.5 kmolc ha−1 year−1 and 0.86 kmolc ha−1 year−1 , respectively. The mean δ34 S values of SO42- in rainwater and soil solution at 20 cm depth were 4.3 ‰ and 3.5 ‰, respectively, and that in the RW was −13.2‰. The contributions of groundwater S to the RW S were estimated to range from 75 to 91%. Geological S with significantly low δ34 S values largely contributed to the discrepancy of the input-output budget, while atmospheric S appeared to accumulate in soil as organic S. The tree-ring δ34 S profile recorded historical changes in the atmospheric inputs in the region. With recovery of the RW, the relative contribution of atmospheric S became smaller. However, most of the atmospheric S is still retained in soil. Over the last few decades, RW chemistry has sensitively responded to changes in the atmospheric environment, including the atmospheric deposition of S and N and climatic anomalies, and as future changes are likely, long-term monitoring is essential. [ABSTRACT FROM AUTHOR]- Published
- 2019
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6. Non-traumatic hemorrhage is controlled with REBOA in acute phase then mortality increases gradually by non-hemorrhagic causes: DIRECT-IABO registry in Japan.
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Matsumura, Y., Matsumoto, J., Idoguchi, K., Kondo, H., Ishida, T., Kon, Y., Tomita, K., Ishida, K., Hirose, T., Umakoshi, K., Funabiki, T., and DIRECT-IABO investigators
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HEMORRHAGIC shock treatment ,CRITICAL care medicine ,REPORTING of diseases ,RESUSCITATION ,TIME ,KAPLAN-Meier estimator - Abstract
Purpose: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is now a feasible and less invasive resuscitation procedure. This study aimed to compare the clinical course of trauma and non-trauma patients undergoing REBOA.Methods: Patient demographics, etiology, bleeding sites, hemodynamic response, length of critical care, and cause of death were recorded. Characteristics and outcomes were compared between non-trauma and trauma patients. Kaplan-Meier survival analysis was then conducted.Results: Between August 2011 and December 2015, 142 (36 non-trauma; 106 trauma) cases were analyzed. Non-traumatic etiologies included gastrointestinal bleeding, obstetrics and gynecology-derived events, visceral aneurysm, abdominal aortic aneurysm, and post-abdominal surgery. The abdomen was a common bleeding site (69%), followed by the pelvis or extra-pelvic retroperitoneum. None of the non-trauma patients had multiple bleeding sites, whereas 45% of trauma patients did (P < 0.001). No non-trauma patients required resuscitative thoracotomy compared with 28% of the trauma patients (P < 0.001). Non-trauma patients presented a lower 24-h mortality than trauma patients (19 vs. 51%, P = 0.001). The non-trauma cases demonstrated a gradual but prolonged increased mortality, whereas survival in trauma cases rapidly declined (P = 0.009) with similar hospital mortality (68 vs. 64%). Non-trauma patients who survived for 24 h had 0 ventilator-free days and 0 ICU-free days vs. a median of 19 and 12, respectively, for trauma patients (P = 0.33 and 0.39, respectively). Non-hemorrhagic death was more common in non-trauma vs. trauma patients (83 vs. 33%, P < 0.001).Conclusions: Non-traumatic hemorrhagic shock often resulted from a single bleeding site, and resulted in better 24-h survival than traumatic hemorrhage among Japanese patients who underwent REBOA. However, hospital mortality increased steadily in non-trauma patients affected by non-hemorrhagic causes after a longer period of critical care. [ABSTRACT FROM AUTHOR]
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- 2018
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7. The use of aortic balloon occlusion in traumatic shock: first report from the ABO trauma registry.
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Sadeghi, M., Nilsson, K. F., Larzon, T., Pirouzram, A., Toivola, A., Skoog, P., Idoguchi, K., Kon, Y., Ishida, T., Matsumara, Y., Matsumoto, J., Reva, V., Maszkowski, M., Bersztel, A., Caragounis, E., Falkenberg, M., Handolin, L., Kessel, B., Hebron, D., and Coccolini, F.
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TRAUMATIC shock (Pathology) treatment ,CATHETERIZATION ,REPORTING of diseases ,INTERNATIONAL relations ,MEDICAL cooperation ,REPORT writing ,RESEARCH ,TIME ,TREATMENT effectiveness - Abstract
Purpose: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a technique for temporary stabilization of patients with non-compressible torso hemorrhage. This technique has been increasingly used worldwide during the past decade. Despite the good outcomes of translational studies, clinical studies are divided. The aim of this multicenter-international study was to capture REBOA-specific data and outcomes.Methods: REBOA practicing centers were invited to join this online register, which was established in September 2014. REBOA cases were reported, both retrospective and prospective. Demographics, injury patterns, hemodynamic variables, REBOA-specific data, complications and 30-days mortality were reported.Results: Ninety-six cases from 6 different countries were reported between 2011 and 2016. Mean age was 52 ± 22 years and 88% of the cases were blunt trauma with a median injury severity score (ISS) of 41 (IQR 29-50). In the majority of the cases, Zone I REBOA was used. Median systolic blood pressure before balloon inflation was 60 mmHg (IQR 40-80), which increased to 100 mmHg (IQR 80-128) after inflation. Continuous occlusion was applied in 52% of the patients, and 48% received non-continuous occlusion. Occlusion time longer than 60 min was reported as 38 and 14% in the non-continuous and continuous groups, respectively. Complications, such as extremity compartment syndrome (n = 3), were only noted in the continuous occlusion group. The 30-day mortality for non-continuous REBOA was 48%, and 64% for continuous occlusion.Conclusions: This observational multicenter study presents results regarding continuous and non-continuous REBOA with favorable outcomes. However, further prospective studies are needed to be able to draw conclusions on morbidity and mortality. [ABSTRACT FROM AUTHOR]
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- 2018
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8. 18F-fluorodeoxyglucose specimen-positron emission mammography delineates tumour extension in breast-conserving surgery: Preliminary results.
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Watanabe, Gou, Itoh, M., Duan, X., Watabe, H., Mori, N., Tada, H., Suzuki, A., Miyashita, M., Ohuchi, N., and Ishida, T.
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FLUORODEOXYGLUCOSE F18 ,BREAST tumors ,HISTOPATHOLOGY ,CANCER chemotherapy ,BREAST surgery ,BREAST tumor diagnosis ,MAMMOGRAMS ,CANCER invasiveness ,DEOXY sugars ,RADIOPHARMACEUTICALS ,POSITRON emission tomography ,LUMPECTOMY ,PHARMACODYNAMICS - Abstract
Objectives: We aimed to determine whether high-resolution specimen-positron emission mammography (PEM) using fluorodeoxyglucose (18F-FDG) can reveal extension of breast cancer in breast-conserving surgery (BCS), and assess the safety of radiation exposure to medical staff.Methods: Sixteen patients underwent positron emission tomography, and then BCS with intraoperative frozen section analysis on the same day. Resected specimens with remaining 18F-FDG accumulation were scanned by high-resolution PEM. At least 1 day after surgery, tumour extension was evaluated by three independent experienced readers and by binarized images from the specimen-PEM data. Intraoperative exposure of medical staff to 18F-FDG was measured.Results: Specimen-PEM evaluations of binarized images and the three investigators detected all (100 %, 12/12) invasive lesions and 94.4 % (17/18) of in situ lesions using both methods. The positive predictive value of the accumulated lesions was 74.4 % (29/39) for the binarized images and 82.9 % (29/35) for the three investigators. Analysis of intraoperative frozen sections detected 100 % (2/2) of the margin-positive cases, also detected by both specimen-PEM evaluation methods with no false-positive margin cases. The mean exposure of the medical staff to 18F was 18 μSv.Conclusions: Specimen-PEM detected invasive and in situ lesions with high accuracy and allowable radiation exposure.Key Points: • Specimen-PEM detected invasive and in situ lesions with high accuracy. • Specimen-PEM predicted complete resection with the same accuracy as frozen section analysis. • Breast-conserving surgery after fluorodeoxyglucose injection was performed with low medical staff exposure. [ABSTRACT FROM AUTHOR]- Published
- 2018
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9. Clinical significance of Aspergillus species isolated from respiratory specimens in patients with Mycobacterium avium complex lung disease.
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Furuuchi, K., Ito, A., Hashimoto, T., Kumagai, S., and Ishida, T.
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ASPERGILLUS ,MYCOBACTERIUM avium ,PULMONARY aspergillosis ,LUNG diseases ,DIAGNOSTIC specimens - Abstract
Chronic pulmonary aspergillosis (CPA) is associated with mortality in patients with Mycobacterium avium complex lung disease (MAC-LD). An Aspergillus-positive respiratory specimen often reflects colonization, and thus the clinical significance of Aspergillus isolation in MAC-LD patients is not well understood. The objective of this study was to investigate the clinical characteristics and outcomes of MAC-LD patients in whom Aspergillus was isolated from respiratory specimens. We performed a retrospective review of the medical records of 329 MAC-LD patients. We compared the characteristics and mortality rates between patients with Aspergillus isolation and those without. All Aspergillus species detected from respiratory specimens within the follow-up period were reviewed. Aspergillus was detected in 40 (12.2%) of the 329 patients. There were no significant differences in the clinical characteristics and mortality rates between patients with and without Aspergillus isolation. Among the 40 patients with Aspergillus isolation, 9 (22.5%) developed CPA. CPA was most often caused by A. fumigatus. In the 40 Aspergillus-positive patients, patients with A. fumigatus isolation had a significantly higher mortality rate than those without ( P < 0.001). The multivariate Cox proportional hazards model showed older age ( P = 0.050), presence of respiratory comorbidities ( P = 0.008), hypoalbuminemia ( P < 0.001), and isolation of A. fumigatus ( P = 0.005) to be prognostic factors for mortality in MAC-LD patients. There was no significant difference in the mortality rates between patients with Aspergillus isolation and those without. However, isolation of A. fumigatus may be associated with poor prognosis in MAC-LD patients. [ABSTRACT FROM AUTHOR]
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- 2018
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10. A functional SNP upstream of the beta-2 adrenergic receptor gene (ADRB2) is associated with obesity in Oceanic populations
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Naka, I, Hikami, K, Nakayama, K, Koga, M, Nishida, N, Kimura, R, Furusawa, T, Natsuhara, K, Yamauchi, T, Nakazawa, M, Ataka, Y, Ishida, T, Inaoka, T, Iwamoto, S, Matsumura, Y, Ohtsuka, R, Tsuchiya, N, Ohashi, J, Naka, I, Hikami, K, Nakayama, K, Koga, M, Nishida, N, Kimura, R, Furusawa, T, Natsuhara, K, Yamauchi, T, Nakazawa, M, Ataka, Y, Ishida, T, Inaoka, T, Iwamoto, S, Matsumura, Y, Ohtsuka, R, Tsuchiya, N, and Ohashi, J
- Abstract
OBJECTIVE:Obesity is a growing health concern in the Oceanic populations. To investigate the genetic factors associated with adult obesity in the Oceanic populations, the association of single nucleotide polymorphisms (SNPs) of the beta-2 adrenergic receptor (ADRB2) gene with obesity was examined in 694 adults living in Tonga and Solomon Islands. RESULTS:A screening for variation in 16 Oceanic subjects detected 17 SNPs in the entire region of ADRB2, of which nine SNPs including two non-synonymous ones, rs1042713 (Arg16Gly) and rs1042714 (Gln27Glu), were further genotyped for all subjects. The rs34623097-A allele, at a SNP located upstream of ADRB2, showed the strongest association with risk for obesity in a logistic regression analysis adjusted for age, sex, and population (P=5.6 × 10^<−4>, odds ratio [OR]=2.5, 95% confidence interval [CI]=1.5–4.2). The 27Glu was also significantly associated with obesity in the single-point association analysis (P=0.013, OR=2.0, 95%CI=1.2–3.4); however, this association was no longer significant after adjustment for rs34623097 since these SNPs were in linkage disequilibrium with each other. A copy of the obesity-risk allele, rs34623097-A, led to a 1.6 kg/m^2 increase in body mass index (BMI; defined as weight in kilograms divided by height in meters squared) (P=0.0019). A luciferase reporter assay indicated that rs34623097-A reduced the transcriptional activity of the luciferase reporter gene by approximately 10% compared with rs34623097-G. An electrophoretic mobility shift assay demonstrated that rs34623097 modulated the binding affinity with nuclear factors. An evolutionary analysis implies that a G>A mutation at rs34623097 occurred in the Neandertal genome and then the rs34623097-A allele flowed into the ancestors of present-day humans. CONCLUSION:The present results suggest that rs34623097-A, which would lead to lower expression of ADRB2, contributes to the onset of obesity in the Oceanic populations.
- Published
- 2012
11. Impact of bacterial coinfection on clinical outcomes in pneumococcal pneumonia.
- Author
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Kumagai, S., Ishida, T., Tachibana, H., Ito, Y., Ito, A., and Hashimoto, T.
- Subjects
- *
MIXED infections , *PNEUMOCOCCAL pneumonia , *HAEMOPHILUS influenzae , *COHORT analysis , *REGRESSION analysis , *PATIENTS - Abstract
The aim of this study was to investigate the influence of bacterial coinfection on patients with pneumococcal pneumonia. We retrospectively analyzed the incidence, clinical features, microbial distributions, and outcomes of patients with bacterial coinfection in a cohort of 433 hospitalized patients with pneumococcal pneumonia. Eighty-five patients (19.6 %) were diagnosed with bacterial coinfection; the most frequent pathogens were Haemophilus influenzae (25 patients, 33.3 %), methicillin-susceptible Staphylococcus aureus (MSSA) (15 patients, 20.0 %), and Moraxella catarrhalis (13 patients, 17.3 %). The CURB-65 score and pneumonia severity index (PSI) were significantly higher in patients with bacterial coinfection (both P < 0.001). In addition, the proportion of patients with bacterial coinfection who met the Infectious Disease Society of America (IDSA)/American Thoracic Society (ATS) severe pneumonia criteria was significantly higher ( P < 0.001). Multivariate logistic regression analysis identified three risk factors for bacterial coinfection in patients with pneumococcal pneumonia: alcoholism (odds ratio [OR], 5.12; 95 % confidence interval (95 % CI), 1.60-16.4; P = 0.006), hospitalization for 2 days or more within 90 days preceding admission (OR, 2.02; 95 % CI, 1.03-3.98; P = 0.041), and residence in a nursing home or extended care facility (OR, 3.22; 95 % CI, 1.48-6.97; P = 0.003). Multivariate analysis for 30-day mortality showed that bacterial coinfection was a significant adverse prognostic factor (OR, 2.50; 95 % CI, 1.13-5.53; P = 0.023), independent of IDSA/ATS severe pneumonia, PSI, or healthcare-associated pneumonia. In conclusion, bacterial coinfection may have an adverse impact on severity and outcomes of pneumococcal pneumonia. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
12. Theoretical investigation for isomerization of allylic alcohols over Au cluster.
- Author
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Sakata, K., Koga, H., Ishida, T., Aimoto, J., Tokunaga, M., and Okumura, M.
- Subjects
ALLYL alcohol ,ISOMERIZATION ,GOLD nanoparticles ,MANUFACTURING processes ,ALDEHYDES ,SUBSTRATES (Materials science) ,PROTON transfer reactions - Abstract
Transformation of allylic alcohols to corresponding saturated carbonyl compounds is one of the important reactions for industrial processes. Lately, Au-supported catalysts exhibit the catalytic activity for the isomerization of allylic alcohols to saturated aldehydes. However, the detail catalytic mechanism of this reaction was not elucidated in detail. Thus, theoretical calculations were carried out for the isomerization of 2-hexen-1-ol over isolated Au cluster in order to elucidate the reaction over Au catalysts. From these calculation results, it was found that the rate determining step of the reaction process was the hydrogen elimination from OH group of allylic alcohol, and the substrate was converted to 1-hexen-1-ol on Au cluster. Finally, it was also confirmed that 1-hexen-1-ol was converted to the corresponding aldehyde, and its activation barrier was much smaller than that of the deprotonation from OH group of allylic alcohol. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
13. On the Decay of Isotropic Turbulence.
- Author
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Oberlack, Martin, Khujadze, George, Günther, Silke, Weller, Tanja, Frewer, Michael, Peinke, Joachim, Barth, Stephan, Davidson, P. A., Kaneda, Y., and Ishida, T.
- Abstract
We investigate the decay of freely-evolving, isotropic turbulence whose spectrum takes the form E(k→0)∼Ik4, I being Loitsyansky's integral. We report numerical simulations in a periodic domain whose dimensions, lbox, are much larger than the integral scale of the turbulence, l. We find that, provided lbox≫l and Re≫1, the turbulence evolves to a state in which Loitsyansky's integral is approximately constant and Kolmogorov's decay law, u2∼t−10/7, holds true. The approximate conservation of I in fully-developed turbulence implies that the long-range interactions between remote eddies, as measured by the triple correlations, are very weak. [ABSTRACT FROM AUTHOR]
- Published
- 2007
- Full Text
- View/download PDF
14. Current Sensitivity Enhancement of a Quasi-One-Junction SQUID Comparator as an Input Circuit of SFQ Readout Circuit for a Superconducting Detector.
- Author
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Miyajima, S., Ito, K., Kita, Y., Ishida, T., and Fujimaki, A.
- Subjects
JOSEPHSON junctions ,SENSITIVITY analysis ,ONE-dimensional conductors ,COMPARATOR circuits ,SUPERCONDUCTING junction devices ,PARTICLE detectors - Abstract
We evaluated the current sensitivity of a quasi-one-junction SQUID (QOS) comparator with an input transformer at 4.2 K. A comparator based on a QOS is promising for constructing the single flux quantum (SFQ) readout circuits of an array system of multiple superconducting detectors.The QOS comparator is made of three Nb/AlO $$_x$$ /Nb Josephson junctions, senses an output signal of a superconductor detector, and generates the SFQ pulses.There are strong demands for enhancing the current sensitivity of the QOS comparator because an output current from superconducting detector typically remains at the magnitude of a few $$\upmu $$ A. We fabricated the QOS comparator with an input transformer using AIST Standard Process 2, where the critical current density of the Josephson junctions is chosen as high as 2.5 kA/cm $$^{2}$$ . We designed the input transformer to enhance the current sensitivity under the conditions of 200 $$\upmu $$ m $$\times $$ 200 $$\upmu $$ m in size and 20:1 in turn ratio. Consequently, we succeeded in reducing a gray zone width of the comparator, and achieved the current sensitivity of 400 nA at 4.2 K in the low frequency range. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
15. Four-Channel Current-Biased Kinetic Inductance Detectors Using MgB $$_2$$ Nanowires for Sensing Pulsed Laser Irradiation.
- Author
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Yoshioka, N., Narukami, Y., Miyajima, S., Shishido, H., Fujimaki, A., Miki, S., Wang, Z., and Ishida, T.
- Subjects
ELECTRIC inductance ,NANOWIRES ,PULSED lasers ,IRRADIATION ,NEUTRON counters ,COLD neutrons ,SUPERCONDUCTING junction devices - Abstract
We recently proposed the idea of a novel sort of superconducting detector, i.e., a current-biased kinetic inductance detector (CB-KID). This detector is different from a current-biased transition edge detector studied previously, and is able to sense a change in kinetic inductance $$L_k$$ given by $$L_{k} = \Lambda _{k}l/S = m_{s}l/n_{s}{q_{s}}^{2}S$$ ( $$\Lambda _{k}$$ ; kinetic inductivity, $$m_s$$ ; mass of Cooper pair, $$n_s$$ ; density of Cooper pairs, $$q_s$$ ; charge of Cooper pair, $$l$$ ; length of device, $$S$$ ; cross sectional area) under a constant dc bias current $$I_b$$ . In the present work, we first extend this idea to construct a multi-channel CB-KIDs array made of 200-nm-thick MgB $$_2$$ thin-film meanderline with 3- $$\upmu $$ m thin wire. We succeeded in observing clear signals for imaging from the four-channel CB-KIDs at 4 K by irradiating focused pulsed laser. A scanning laser spot can be achieved by an XYZ piezo-driven stage and an optical fiber with an aspheric focused lens. We can see typical signals from all 4 channels at 4 K, and obtain the positional dependence of the signal as the contour in XY plane. Our CB-KIDs can be used as neutron detectors by utilizing energy released from a nuclear reaction between $$^{10}$$ B and cold neutron. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
16. Activation of TLR9 by incorporated pDNA within PEG-coated lipoplex enhances anti-PEG IgM production.
- Author
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Hashimoto, Y, Uehara, Y, Abu Lila, A S, Ishida, T, and Kiwada, H
- Subjects
TOLL-like receptors ,IMMUNOGLOBULIN M ,LIPOSOMES ,GENE therapy ,BLOOD circulation ,POLYETHYLENE glycol ,SURFACE coatings - Abstract
Cationic liposome represents a promising alternative to viral vectors for the delivery of therapeutic genes. For in vivo use, surface modification of the liposome with polyethylene glycol (PEG) is frequently applied to achieve gene-expression in the targeted tissue. However, we have reported that PEG-coated liposomes have induced anti-PEG IgM, which has caused subsequent doses of PEG-coated liposome to be rapidly cleared from blood circulation, and the complexation of pDNA electrostatically associated with liposome surface has enhanced this antibody response. In this study, we investigated how a Toll-like receptor (TLR) might enhance anti-PEG IgM production. PEG-coated pDNA-lipoplex (PDCL) was injected into either wild type, MyD88 (all TLR adaptor protein, independent of TLR3) knock out (KO) or TLR9 KO mice, and the anti-PEG IgM production levels were detected. Attenuated anti-PEG IgM production following the injection of PDCL was observed in both MyD88 and TLR9 KO mice compared to wild type mice, probably due to the abolished induction of cytokines in both MyD88 and TLR9 KO mice. Our results suggest that TLR, exclusively TLR9, signaling plays a potential role in the enhanced anti-PEG IgM production following the injection of PDCL. This result may have important implications for the design and development of an efficient PEG-coated non-viral gene vector. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
17. A functional SNP upstream of the beta-2 adrenergic receptor gene (ADRB2) is associated with obesity in Oceanic populations.
- Author
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Naka, I, Hikami, K, Nakayama, K, Koga, M, Nishida, N, Kimura, R, Furusawa, T, Natsuhara, K, Yamauchi, T, Nakazawa, M, Ataka, Y, Ishida, T, Inaoka, T, Iwamoto, S, Matsumura, Y, Ohtsuka, R, Tsuchiya, N, and Ohashi, J
- Subjects
OBESITY genetics ,OVERWEIGHT persons ,BETA adrenoceptors ,SINGLE nucleotide polymorphisms ,LUCIFERASE genetics ,ELECTROPHORESIS ,ALLELES ,GENE expression - Abstract
OBJECTIVE:Obesity is a growing health concern in the Oceanic populations. To investigate the genetic factors associated with adult obesity in the Oceanic populations, the association of single nucleotide polymorphisms (SNPs) of the beta-2 adrenergic receptor (ADRB2) gene with obesity was examined in 694 adults living in Tonga and Solomon Islands.RESULTS:A screening for variation in 16 Oceanic subjects detected 17 SNPs in the entire region of ADRB2, of which nine SNPs including two non-synonymous ones, rs1042713 (Arg16Gly) and rs1042714 (Gln27Glu), were further genotyped for all subjects. The rs34623097-A allele, at a SNP located upstream of ADRB2, showed the strongest association with risk for obesity in a logistic regression analysis adjusted for age, sex, and population (P=5.6 × 10
−4 , odds ratio [OR]=2.5, 95% confidence interval [CI]=1.5-4.2). The 27Glu was also significantly associated with obesity in the single-point association analysis (P=0.013, OR=2.0, 95%CI=1.2-3.4); however, this association was no longer significant after adjustment for rs34623097 since these SNPs were in linkage disequilibrium with each other. A copy of the obesity-risk allele, rs34623097-A, led to a 1.6 kg/m2 increase in body mass index (BMI; defined as weight in kilograms divided by height in meters squared) (P=0.0019). A luciferase reporter assay indicated that rs34623097-A reduced the transcriptional activity of the luciferase reporter gene by approximately 10% compared with rs34623097-G. An electrophoretic mobility shift assay demonstrated that rs34623097 modulated the binding affinity with nuclear factors. An evolutionary analysis implies that a G>A mutation at rs34623097 occurred in the Neandertal genome and then the rs34623097-A allele flowed into the ancestors of present-day humans.CONCLUSION:The present results suggest that rs34623097-A, which would lead to lower expression of ADRB2, contributes to the onset of obesity in the Oceanic populations. [ABSTRACT FROM AUTHOR]- Published
- 2013
- Full Text
- View/download PDF
18. Intratumoral concentration of estrogens and clinicopathological changes in ductal carcinoma in situ following aromatase inhibitor letrozole treatment.
- Author
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Takagi, K, Ishida, T, Miki, Y, Hirakawa, H, Kakugawa, Y, Amano, G, Ebata, A, Mori, N, Nakamura, Y, Watanabe, M, Amari, M, Ohuchi, N, Sasano, H, and Suzuki, T
- Abstract
Background: Estrogens have important roles in ductal carcinoma in situ (DCIS) of the breast. However, the significance of presurgical aromatase inhibitor treatment remains unclear. Therefore, we examined intratumoral concentration of estrogens and changes of clinicopathological factors in DCIS after letrozole treatment.Methods: Ten cases of postmenopausal oestrogen receptor (ER)-positive DCIS were examined. They received oral letrozole before the surgery, and the tumour size was evaluated by ultrasonography. Surgical specimens and corresponding biopsy samples were used for immunohistochemistry. Snap-frozen specimens were also available in a subset of cases, and used for hormone assays and microarray analysis.Results: Intratumoral oestrogen levels were significantly lower in DCIS treated with letrozole compared with that in those without the therapy. A great majority of oestrogen-induced genes showed low expression levels in DCIS treated with letrozole by microarray analysis. Moreover, letrozole treatment reduced the greatest dimension of DCIS, and significantly decreased Ki-67 and progesterone receptor immunoreactivity in DCIS tissues.Conclusion: These results suggest that estrogens are mainly produced by aromatase in DCIS tissues, and aromatase inhibitors potently inhibit oestrogen actions in postmenopausal ER-positive DCIS through rapid deprivation of intratumoral estrogens. [ABSTRACT FROM AUTHOR]- Published
- 2013
- Full Text
- View/download PDF
19. Nutrient export and material recycling using aquatic plants: Lake Kitagata case study.
- Author
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Takashima, M., Nanbu, H., Kato, K., Kataya, C., Ogawa, A., and Ishida, T.
- Abstract
Lake Kitagata in Fukui Prefecture, Japan, was examined to collect fundamental data on nutrient export and material recycling using the native aquatic plants, common reed and wild rice. Common reed was located all over the lake shore, while wild rice was in the upper part of the lake. On average, the nutrient content was nitrogen: 2.1 and 2.6 %, PO: 0.38 and 0.64 %, KO: 2.1 and 2.4 % for common reed and wild rice, respectively, and decreased along with their growth. If harvested in October, the nitrogen and phosphorus exported from the lake were estimated to be only 1.1 and 1.9 % of the inflow, respectively. Methane fermentation of these plants showed an average of 134 and 150 mL-CH/g-VS added for common reed and wild rice, respectively, indicating possible use as an auxiliary source. The composting of these plants mixed with chicken manure, bean curd and rice bran was successful, and the products were rich in the major nutrients and well-balanced. A pretreatment method combining sulfuric acid and thermal treatment was able to convert about 50 % of cellulose in common reed to glucose, the precursor for bioethanol production. Therefore, these technologies are demonstrated to be helpful for the beneficial use of the biomass. [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
20. Does the 'hikikomori' syndrome of social withdrawal exist outside Japan? A preliminary international investigation.
- Author
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Kato TA, Tateno M, Shinfuku N, Fujisawa D, Teo AR, Sartorius N, Akiyama T, Ishida T, Choi TY, Balhara YP, Matsumoto R, Umene-Nakano W, Fujimura Y, Wand A, Chang JP, Chang RY, Shadloo B, Ahmed HU, Lerthattasilp T, and Kanba S
- Abstract
Purpose: To explore whether the 'hikikomori' syndrome (social withdrawal) described in Japan exists in other countries, and if so, how patients with the syndrome are diagnosed and treated.Methods: Two hikikomori case vignettes were sent to psychiatrists in Australia, Bangladesh, India, Iran, Japan, Korea, Taiwan, Thailand and the USA. Participants rated the syndrome's prevalence in their country, etiology, diagnosis, suicide risk, and treatment.Results: Out of 247 responses to the questionnaire (123 from Japan and 124 from other countries), 239 were enrolled in the analysis. Respondents' felt the hikikomori syndrome is seen in all countries examined and especially in urban areas. Biopsychosocial, cultural, and environmental factors were all listed as probable causes of hikikomori, and differences among countries were not significant. Japanese psychiatrists suggested treatment in outpatient wards and some did not think that psychiatric treatment is necessary. Psychiatrists in other countries opted for more active treatment such as hospitalization.Conclusions: Patients with the hikikomori syndrome are perceived as occurring across a variety of cultures by psychiatrists in multiple countries. Our results provide a rational basis for study of the existence and epidemiology of hikikomori in clinical or community populations in international settings. [ABSTRACT FROM AUTHOR]- Published
- 2012
- Full Text
- View/download PDF
21. Development of Laboratory Experimental System to Clarify Solar Wind Charge Exchange Mechanism with TES Microcalorimeter.
- Author
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Enoki, T., Ishisaki, Y., Akamatsu, H., Ezoe, Y., Ohashi, T., Kanda, T., Ishida, T., Tanuma, H., Ohashi, H., Shinozaki, K., and Mitsuda, K.
- Subjects
SOLAR wind ,CHARGE exchange ,CALORIMETERS ,DIFFUSION ,ARTIFICIAL satellites ,NUCLEAR counters ,X-ray astronomy - Abstract
Significant fraction of the cosmic diffuse soft X-ray emission (0.1-1 keV) is caused by the Solar Wind Charge eXchange (SWCX) process between the solar wind ion (C, N, O etc.) and the interplanetary neutral matter. It is difficult to identify spectral features of SWCX with the spectral resolution of existing X-ray astronomy satellites. We are developing a laboratory experimental system with transition edge sensor (TES) X-ray microcalorimeters, in order to clarify the SWCX mechanism. This experiment is designed to measure Charge eXchange (CX) X-rays using Electron Cyclotron Resonance Ion Source (ECRIS) that generates multi-charged ions. Emission lines (O: 2p→1s; 654 eV) by CX between O and neutral He atom is aimed to be measured with energy resolution better than 10 eV. The TES microcalorimeter is cooled by a double-stage adiabatic demagnetization refrigerator (DADR), however, our TES microcalorimeter are not working potentially due to magnetic field contamination. This paper reports our experimental system, present results, and future prospects. [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
22. Medical cost analysis for antifungal prophylaxis in neutropenic patients with hematological malignancies: a systematic simulation analysis.
- Author
-
Imataki O, Kubota Y, Ohnishi H, Kitanaka A, Ishida T, Tanaka T, Imataki, Osamu, Kubota, Yoshitsugu, Ohnishi, Hiroaki, Kitanaka, Akira, Ishida, Toshihiko, and Tanaka, Terukazu
- Abstract
Goals Of Work: We assessed the medical costs of different antifungal agents for prophylaxis of invasive fungal infections in neutropenic patients in Japan with a cost simulation model designed for the study.Patients and Methods: We used probabilities of prophylaxis failure, possible cases for empiric therapy, probable proportions of infections caused by fungus species among prophylaxis failure patients, and incidence of adverse events caused by any reason, based on systematic analysis of previously reported randomized trials identified by a computerized search of the PubMed database. Antifungal agents were limited to oral fluconazole, oral itraconazole, micafungin, and liposomal amphotericin B. The range of the expected medical cost was simulated as a sensitivity analysis using 95% of confidence interval of a mean.Main Results: Fifteen studies were identified for our analysis. The prophylactic efficacy was comparable between the four agents. The simulated expected cost for invasive fungal infection prophylaxis and treatment of the infection was $1,035.74 when oral itraconazole was used for prophylaxis, $1,552.81 with oral fluconazole, $2,245.96 with micafungin, and $3,028.10 with liposomal amphotericin B. The total cost including treatment cost for adverse events related to each drug was $2,742.14, $3,547.91, $3,034.57, and $3,028.10, respectively. This result was confirmed in a sensitivity analysis in which IFI incidence and therapy duration were tested as parameters.Conclusions: Our analysis results suggest that oral itraconazole is the most cost-effective prophylactic antifungal agent for invasive fungal infections in neutropenic patients with hematological malignancies, and this result was robust by sensitivity analysis. [ABSTRACT FROM AUTHOR]- Published
- 2011
- Full Text
- View/download PDF
23. Adiposity, adult weight change and breast cancer risk in postmenopausal Japanese women: the Miyagi Cohort Study.
- Author
-
Kawai, M., Minami, Y., Kuriyama, S., Kakizaki, M., Kakugawa, Y., Nishino, Y., Ishida, T., Fukao, A., Tsuji, I., and Ohuchi, N.
- Subjects
OBESITY in women ,COHORT analysis ,BREAST cancer risk factors ,POSTMENOPAUSE ,BODY mass index - Abstract
Background: The role of adult weight change in breast cancer (BC) risk is unclear in Japanese women.Methods: A total of 10,106 postmenopausal women aged 40-64 years (the Miyagi Cohort) were followed from 1990 to 2003, and 108 BC cases were identified. Hazard ratios (HRs) were estimated according to body mass index (BMI) at the current age and at the of age 20 years, and weight change since age 20 years.Results: Higher current BMI was associated with an increased risk of BC (P for trend=0.02), whereas higher BMI at the age 20 years was inversely associated with this risk (P for trend=0.002). There was a significant association between weight change since age 20 years and BC risk (P for trend=0.0086). Compared with stable weight, HR was 0.35 for weight loss of 5 kg or more (P for weight loss trend=0.04) and 1.55 for weight gain of 12 kg or more (P for weight gain trend=0.05).Conclusion: Adiposity at younger and current age has differential effects on BC risk among postmenopausal women; weight gain in adulthood being associated with an increased, and weight loss with a decreased risk. [ABSTRACT FROM AUTHOR]- Published
- 2010
- Full Text
- View/download PDF
24. Bortezomib-resistant myeloma cell lines: a role for mutated PSMB5 in preventing the accumulation of unfolded proteins and fatal ER stress.
- Author
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Ri, M., Iida, S., Nakashima, T., Miyazaki, H., Mori, F., Ito, A., Inagaki, A., Kusumoto, S., Ishida, T., Komatsu, H., Shiotsu, Y., and Ueda, R.
- Subjects
CELL lines ,MULTIPLE myeloma ,APOPTOSIS ,CELL death ,DRUGS - Abstract
Bortezomib is an effective agent for treating multiple myeloma (MM). To investigate the underlying mechanisms associated with acquired resistance to this agent, we established two bortezomib-resistant MM cell lines, KMS-11/BTZ and OPM-2/BTZ, the 50% inhibitory concentration values of which were respectively 24.7- and 16.6-fold higher than their parental cell lines. No activation of caspase and BH3-only proteins such as Noxa was noted in bortezomib-resistant cells after exposure to the drug. The accumulation of polyubiquitinated proteins was reduced in bortezomib-resistant cells compared with the parental cells, associated with avoidance of catastrophic ER stress as assessed by downregulation of CHOP expression. These resistant MM cells have a unique point mutation, G322A, in the gene encoding the proteasome β5 subunit (PSMB5), likely resulting in conformational changes to the bortezomib-binding pocket of this subunit. KMS-11 parental cells transfected to express mutated PSMB5 also showed reduced bortezomib-induced apoptosis compared with those expressing wild-type PSMB5 or the parental cells. Expression of mutated PSMB5 was associated with the prevention of the accumulation of unfolded proteins. Thus, a fraction of MM cells may acquire bortezomib resistance by suppressing apoptotic signals through the inhibition of unfolded protein accumulation and subsequent excessive ER stress by a mutation of the PSMB5 gene. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
25. Molecular characterization of quinolone resistance-determining regions and their correlation with serotypes and genotypes among Streptococcus pneumoniae isolates in Japan.
- Author
-
Osawa, M., Ito, Y., Ishida, T., Imai, S., Ichiyama, S., and Mishima, M.
- Subjects
MOLECULAR genetics ,MOLECULAR cloning ,STREPTOCOCCUS pneumoniae ,QUINOLONE antibacterial agents ,SEROTYPES ,AMINO acids ,GENETICS - Abstract
We established the distribution of amino acid alterations in quinolone resistance-determining regions (QRDRs) of Streptococcus pneumoniae isolates in Japan and described the correlation of these alterations with serotypes determined by multilocus sequencing typing. Among 141 S. pneumoniae isolates, five levofloxacin-resistant isolates harbored mutations in both gyrA and parC and/or parE and were clonally unrelated. Among 136 levofloxacin-susceptible isolates, one isolate (MIC = 2 mg/l) had a first-step parC mutation at Asp78. Twenty isolates had Lys137Asp in parC and Ile460Val in parE and contained nine serotypes and eight clonal complexes (CCs), including all eight Colombia
23F -26 (CC138) isolates. Eighty-one isolates had Ile460Val in parE alone and contained 14 serotypes and 16 CCs, including 36 of 37 Netherlands3 -31 (CC180) isolates and all 22 Taiwan19F -14 (CC271) isolates. In contrast, seven of ten Taiwan23F -15 (CC242) isolates were wild-type. Although each QRDR genotype contained various serotypes and CCs, prevalent clones were mostly associated with a single QRDR genotype. [ABSTRACT FROM AUTHOR]- Published
- 2010
- Full Text
- View/download PDF
26. Usefulness of lesion image mapping with multidetector-row helical computed tomography using a dedicated skin marker in breast-conserving surgery.
- Author
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Harada-Shoji N, Yamada T, Ishida T, Amari M, Suzuki A, Moriya T, Ohuchi N, Harada-Shoji, Narumi, Yamada, Takayuki, Ishida, Takanori, Amari, Masakazu, Suzuki, Akihiko, Moriya, Takuya, and Ohuchi, Noriaki
- Abstract
To investigate the usefulness of computed tomography (CT) with skin-marker placement in determining the excision area and decreasing the positive or close margin rates in breast-conserving surgery (BCS). Multidetector-row helical computed tomography (MDCT) mapping images were reconstructed in subjects (n = 117) diagnosed with primary breast cancer who had undergone MDCT using CT skin markers. Serial 5-mm-thick slices prepared from the surgical specimen were used for pathological analyses. A "positive margin" was defined as the presence of malignant cells at the surgical margin, and a "close margin" as a tumor within 5 mm of the surgical margin. The rates of positive and close margins were calculated. We identified the lesions in 111 of 117 cases (94.9%) on MDCT. Of these, 93 underwent BCS under the guidance of MDCT mapping and the remaining 18 underwent mastectomy. Among the 93 cases, 6 (6.5%) had positive or close margins and were diagnosed with ductal carcinoma in situ of low nuclear grade. MDCT mapping with a CT skin marker is feasible for simulating surgical positioning and determining the excision area. MDCT mapping could decrease the positive and close margin rates in BCS. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
27. Measurements of the inclusive pd breakup cross section at low and intermediate energies.
- Author
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Kuroita, S., Sagara, K., Kudoh, T., Sueta, T., Sugimoto, T., Shimoda, H., Yamada, Y., Wakasa, T., Noro, T., Tameshige, Y., Shimizu, Y., Ishida, T., Kamiya, J., Sakemi, Y., Tamii, A., and Hatanaka, K.
- Subjects
FORCE & energy ,MEASUREMENT ,NUCLEAR reactions ,COLLISIONS (Nuclear physics) ,NUCLEAR physics ,NUCLEON-nucleon scattering ,NUCLEAR energy ,MATHEMATICAL analysis - Abstract
Inclusive measurements of the D( p, p) pn reaction were made at incident proton energies of 248 MeV and 13 MeV, to investigate the global feature of the pd breakup reaction at intermediate and low energies. At 248 MeV, the cross section and analyzing power A
y were measured at four angles from 7° to 20°. The data largely disagree with Faddeev calculations even if 2π-exchange three-nucleon force (2π3NF) or Δ-isobar is included, and the disagreement increases at forward angles. At 13 MeV, the cross section was measured at eight angles from 10° to 70°. The data are well reproduced by a recent pd Faddeev calculation, and the effects of Δ-isobar at 13 MeV are very small. [ABSTRACT FROM AUTHOR]- Published
- 2008
- Full Text
- View/download PDF
28. EML4-ALK fusion transcript is not found in gastrointestinal and breast cancers.
- Author
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Fukuyoshi, Y., Inoue, H., Kita, Y., Utsunomiya, T., Ishida, T., and Mori, M.
- Subjects
BREAST cancer ,GASTROINTESTINAL cancer ,LUNG cancer ,LYMPHOMAS ,LEUKEMIA ,ETIOLOGY of diseases - Abstract
Fusion genes have been identified as chromosomal rearrangements in certain cancers, such as leukaemia, lymphoma, and sarcoma. The EML4-ALK (EML4: echinoderm microtubule-associated-protein-like 4; ALK: anaplastic lymphoma kinase) fusion gene has been identified as an oncogene in non-small-cell lung cancer (NSCLC). This study examined the presence of this fusion transcript in gastrointestinal and breast cancers. We evaluated the expression of the EML4-ALK transcript in 104 lung cancer cases and in 645 gastrointestinal and breast cancer samples. Only one of the lung cancer samples tested positive for the EML4-ALK fusion transcript, whereas none were detected in 555 gastrointestinal and 90 breast cancer cases. Our data suggest that the EML4-ALK fusion transcript is not present in gastrointestinal or breast cancers and is specific to NSCLC. [ABSTRACT FROM AUTHOR]
- Published
- 2008
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29. Study of energy dependence of pion production by proton on copper target near 350 MeV.
- Author
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Karpechev, E. V., Kurepin, A. B., Reshetin, A. I., Karavicheva, T. L., Fujita, K., Hatanaka, K., Kamiya, J., Sakemi, Y., Wakasa, T., Yoshida, H. P., Shimizu, Y., Fukuda, T., Saha, P. K., Tamura, K., and Ishida, T.
- Subjects
PARTICLES (Nuclear physics) ,PROTONS ,NUCLEAR energy ,PION production ,NUCLEAR physics - Abstract
New measurement of the energy dependence of pion production on a copper target near 350-MeV proton energy has been performed. The E-170 experiment has been carried out at the Ring Cyclotron Facility of the Research Center for Nuclear Physics, Osaka University, Japan. A small enhancement of the low-energy pion production cross section was observed near the incident proton energy of 352 MeV. [ABSTRACT FROM AUTHOR]
- Published
- 2008
- Full Text
- View/download PDF
30. Pneumococcal surface protein A family types of Streptococcus pneumoniae from community-acquired pneumonia patients in Japan.
- Author
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Ito, Y., Osawa, M., Isozumi, R., Imai, S., Ito, I., Hirai, T., Ishida, T., Ichiyama, S., and Mishima, M.
- Subjects
PNEUMOCOCCAL vaccines ,STREPTOCOCCUS pneumoniae ,PNEUMONIA ,DRUG resistance in microorganisms ,EFFECT of drugs on microorganisms ,ERYTHROMYCIN ,ANTI-infective agents ,CLINICAL trials ,CLINICAL medicine research ,PATIENTS - Abstract
We assessed pneumococcal surface protein A (PspA) family types of 141 isolates of Streptococcus pneumoniae from community-acquired pneumonia patients in Japan. Families 1 and 2 were expressed in 78 (55.3%) and 58 (41.1%) isolates, respectively. Five isolates were not typed either as family 1 or 2. PspA family types were not associated with age, sex, or pneumonia severity. Penicillin-resistant S. pneumoniae was more likely to belong to family 2 whereas organisms highly resistant to erythromycin and positive for ermB were more prevalent in family 1. The association of PspA type with antimicrobial resistance was possibly affected by prevalent serotypes or resistance clones. It would therefore be necessary to include both family 1 and 2 proteins in a PspA-containing vaccine to cover the major PspA families and to reduce antimicrobial resistance. [ABSTRACT FROM AUTHOR]
- Published
- 2007
- Full Text
- View/download PDF
31. Drying induced moisture losses from mortar to the environment. Part II: numerical implementation.
- Author
-
Azenha, M., Maekawa, K., Ishida, T., and Faria, R.
- Abstract
Copyright of Materials & Structures is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2007
- Full Text
- View/download PDF
32. Drying induced moisture losses from mortar to the environment. Part I: experimental research.
- Author
-
Azenha, M., Maekawa, K., Ishida, T., and Faria, R.
- Abstract
Copyright of Materials & Structures is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2007
- Full Text
- View/download PDF
33. The CCR4 as a novel-specific molecular target for immunotherapy in Hodgkin lymphoma.
- Author
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Ishida, T., Ishii, T., Inagaki, A., Yano, H., Kusumoto, S., Ri, M., Komatsu, H., Iida, S., Inagaki, H., and Ueda, R.
- Subjects
- *
TUMORS , *HODGKIN'S disease , *CHEMOKINES , *MONOCLONAL antibodies , *LABORATORY mice , *MONOCYTES - Abstract
Here, we report that tumor cells from some patients (23.8%) with Hodgkin lymphoma (HL) are positive for CC chemokine receptor 4 (CCR4). We therefore tested the chimeric anti-CCR4 monoclonal antibody (mAb), KM2760, the Fc region of which is defucosylated to enhance antibody-dependent cellular cytotoxicity (ADCC), as a novel immunotherapy for refractory HL. KM2760 demonstrated a promising antitumor activity in the CCR4-positive HL-bearing mouse model in the therapeutic setting. Although KM2760 did not induce any ADCC mediated by mouse natural killer (NK) cells, it significantly enhanced phagocytosis mediated by mouse monocytes/macrophages against the CCR4-positive HL cell line in vitro. Together with the findings that KM2760 did not exhibit any complement-dependent cytotoxicity or direct antiproliferation activity in vitro, these data indicated that KM2760 exerted its robust in vivo antitumor activity via monocytes/macrophages in mice. In the human system, KM2760 enhanced phagocytic activity mediated by monocytes/macrophages. Furthermore, it induced robust ADCC mediated by NK cells against the CCR4-positive HL cell line in vitro. Thus, it is conceivable that KM2760 would have much more potent antitumor activity in humans than in mice. Collectively, this study strongly indicates that anti-CCR4 mAb could be a novel treatment modality for patients with CCR4-positive HL.Leukemia (2006) 20, 2162–2168. doi:10.1038/sj.leu.2404415; published online 12 October 2006 [ABSTRACT FROM AUTHOR]
- Published
- 2006
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34. A phase II trial of gefitinib as first-line therapy for advanced non-small cell lung cancer with epidermal growth factor receptor mutations.
- Author
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Asahina, H., Yamazaki, K., Kinoshita, I., Sukoh, N., Harada, M., Yokouchi, H., Ishida, T., Ogura, S., Kojima, T., Okamoto, Y., Fujita, Y., Dosaka-Akita, H., Isobe, H., and Nishimura, M.
- Subjects
GENETIC mutation ,ANTINEOPLASTIC agents ,SMALL cell lung cancer ,DRUG efficacy ,EXONS (Genetics) ,EPIDERMAL growth factor ,CANCER treatment ,CLINICAL trials - Abstract
Retrospective analysis has shown that activating mutations in exons 18-21 of the epidermal growth factor receptor (EGFR) gene are a predictor of response to gefitinib. We conducted a phase II trial to evaluate the efficacy and safety of gefitinib as first-line therapy for advanced non-small cell lung cancer (NSCLC) with EGFR mutations. Patients with stage IIIB or IV chemotherapy-naïve NSCLC with EGFR mutation were treated with 250 mg gefitinib daily. For mutational analysis, DNA was extracted from paraffin-embedded tissues and EGFR mutations were analysed by direct sequence of PCR products. Twenty (24%) of the 82 patients analysed had EGFR mutations (deletions in or near E746-A750, n=16; L858R, n=4). Sixteen patients were enrolled and treated with gefitinib. Twelve patients had objective response and response rate was 75% (95% CI, 48-93%). After a median follow-up of 12.7 months (range, 3.1-16.8 months), 10 patients demonstrated disease progression, with median progression-free survival of 8.9 months (95% CI, 6.7-11.1 months). The median overall survival time has not yet been reached. Most of the toxicities were mild. This study showed that gefitinib is very active and well tolerated as first-line therapy for advanced NSCLC with EGFR mutations. [ABSTRACT FROM AUTHOR]
- Published
- 2006
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- View/download PDF
35. Prolactin regulatory element binding protein as a potential transcriptional factor for the insulin gene in response to glucose stimulation.
- Author
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Ohtsuka, S., Murao, K., Imachi, H., Cao, W. M., Yu, X., Li, J., Iwama, H., Wong, N. C. W., Bancroft, C., and Ishida, T.
- Subjects
PROLACTIN ,INSULIN ,GLUCOSE ,LABORATORY rats ,CELL lines ,PANCREATIC beta cells ,GENE expression - Abstract
Aims/hypothesis: Prolactin regulatory element binding (PREB) protein has been identified as a factor that regulates prolactin promoter activity in rat anterior pituitary. PREB is located not only in the anterior pituitary but also in pancreas; however its role in the pancreas is not known. We therefore examined the role of PREB in insulin gene expression. Materials and methods: To analyse the effects of PREB on insulin gene transcription, we employed the luciferase reporter gene assay and electrophoretic mobility shift assay (EMSA). In cells expressing or knocked down for PREB, insulin expression and secretion were determined. Results: PREB was located mainly in nuclei of rat pancreatic beta cells and its cell line, INS-1. A nuclear extract of INS-1 cells contained material that was recognised by PREB antiserum. This nuclear extract also showed insulin promoter binding activity that was super-shifted by PREB antiserum in EMSA studies. In the INS-1 cells, co-expression of PREB and the insulin promoter induced activity of the latter. The addition of glucose to the cells increased PREB expression. Deletional analysis of the insulin promoter showed that A3, a glucose-responsive cis-element in the insulin promoter, mediated the transcriptional effect of PREB. In addition, synthesised PREB bound the A3 element by EMSA, while a mutant of this motif in the insulin promoter abrogated the effect of PREB. Cells expressing or knocked down for PREB exhibited increased or decreased insulin expression, respectively. Conclusions/interpretation: These results demonstrate that PREB may contribute to the regulation of insulin gene transcription and insulin secretion in response to glucose stimulation. [ABSTRACT FROM AUTHOR]
- Published
- 2006
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36. Nonspecific interstitial pneumonia pattern as pulmonary involvement of rheumatoid arthritis.
- Author
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Yoshinouchi, T., Ohtsuki, Y., Fujita, J., Yamadori, I., Bandoh, S., Ishida, T., and Ueda, R.
- Subjects
HONEYCOMBS ,TOMOGRAPHY ,RHEUMATOID arthritis ,FIBROSIS ,PULMONARY fibrosis ,PNEUMONIA - Abstract
The pathologic patterns of lung involvement were evaluated in 16 patients with rheumatoid arthritis (RA). They consisted of six females and ten males, with a median age of 67.5 years and diagnosed according to the American Rheumatism Association revised criteria. High-resolution computed tomography (HRCT) of the lungs was performed in all patients, and honeycomb formation was apparent in seven. Histopathologically, seven patients were diagnosed with usual interstitial pneumonia (UIP) pattern, seven with nonspecific interstitial pneumonia/fibrosis (NSIP) pattern, and two with UIP/NSIP hybrid pattern. There were no apparent honeycomb formations on HRCT in patients diagnosed with NSIP pattern. In conclusion, the present study demonstrates that NSIP pattern is also a significant histologic classification of interstitial pneumonia associated with RA. [ABSTRACT FROM AUTHOR]
- Published
- 2005
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37. Orally active antioxidative copper(II) aspirinate: synthesis, structure characterization, superoxide scavenging activity, and in vitro and in vivo antioxidative evaluations.
- Author
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Fujimori, T., Yamada, S., Yasui, H., Sakurai, H., In, Y., and Ishida, T.
- Subjects
COPPER ,SALICYLATES ,ACETATES ,FIBROBLASTS ,CONNECTIVE tissue cells ,REACTIVE oxygen species ,SKIN ,CARCINOGENESIS ,ASPIRIN - Abstract
Ever since it was proposed that reactive oxygen species (ROS) are involved in the pathogeneses of various diseases, superoxide dismutase (SOD)-mimetic complexes have been intensively studied. We prepared copper(II) aspirinate [Cu
2 (asp)4 ] from Cu(II) and aspirin, which has been in use for many years as an antipyretic, an analgesic, and an anti-inflammatory agent. However, Cu2 (asp)4 has been found to have additional activities, including anti-inflammatory, antiulcer, anti-ischemic/reperfusion agent, anticancer, antimutagenic, and antimicrobial activities. The activity of copper salicylate [Cu(sal)2 ] was also compared with that of Cu2 (asp)4 . The structure of the Cu2 (asp)4 was determined using X-ray structure analysis. Its SOD-mimetic activity was determined using cytochrome c, electron spin resonance (ESR) spectroscopy, and ESR spin trap methods. The activity of Cu2 (asp)4 was slightly greater than CuSO4 and copper acetate [Cu(ace)2 ] and slightly less than that of Cu(sal)2 . The in vitro antioxidant activity, evaluated in human epithelial or transformed neoplastic keratinocyte cells, HaCaT, and normal dermal fibroblasts in terms of cell survival following ultraviolet B (UVB) irradiation, was significantly increased in the presence of Cu2 (asp)4 , Cu(sal)2 , and CuSO4 . Further, ROS generation following UVA irradiation in the skin of hairless mice following oral treatment with Cu2 (asp)4 for three consecutive days was significantly suppressed compared to the vehicle- or Cu(ace)2 -treated mice. On the basis of these results, Cu2 (asp)4 was observed to be a potent antioxidative compound possessing antioxidative activity in biological systems. In conclusion, Cu2 (asp)4 is a potent antioxidative agent that may be useful for future treatment of diseases resulting from ROS. [ABSTRACT FROM AUTHOR]- Published
- 2005
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38. The more efficacious acupoints of Zusanli and Sanyinjiao than that of non-acupoints on bone mass in osteopenic ovariectomized rats.
- Author
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Zhang W, Kanehara M, Zhang Y, Yu Z, Zhang G, Yang Y, Sun Y, Zhang J, and Ishida T
- Abstract
OBJECTIVE: To clarify whether the acupoints of Zusanli (ST36) and Sanyinjiao (SP6) have specific actions other than non-acupoints to bone. METHODS: Forty Sprague-Dawley female rats were divided into five groups: Sham operated (sham) group; Ovariectomized (OVX, model) group; non-acupuncture group; OVX, needling on Zusanli and Sanyinjiao (Acp-A) group; OVX, needling on the reverse sides of Zusanli and Sanyinjiao (Acp-B) group; OVX, periostineal stimulation on the same height as points of Zusanli and Sanyinjiao (Acp-C) group. The experiment was continued for 23 weeks and then all animals were sacrificed. RESULTS: OVX had a significantly higher body weight and lower bone mineral density (BMD) on the lumbar vertebrae, total femora and tibiae than sham rats, however, Acp-A showed a higher BMD compared with the other OVX groups. On the other hand, bone weights, bone strength and bone morphometry such as trabecular volume, trabecular separation, labeled width and bone formation rate also showed the same improvements in Acp-A as compared to the other OVX rats. CONCLUSION: The stimulation on Zusanli and Sanyinjiao specifically prevented the development of osteopenic rats compared with non-acupoints. [ABSTRACT FROM AUTHOR]
- Published
- 2005
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39. Multiple myeloma oncogene 1 (MUM1)/interferon regulatory factor 4 (IRF4) upregulates monokine induced by interferon-γ (MIG) gene expression in B-cell malignancy.
- Author
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Uranishi, M., Iida, S., Sanda, T., Ishida, T., Tajima, E., Ito, M., Komatsu, H., Inagaki, H., and Ueda, R.
- Subjects
B cell lymphoma ,ONCOGENES ,MULTIPLE myeloma ,INTERFERONS ,GENE expression ,GENETIC regulation - Abstract
MUM1 (multiple myeloma oncogene 1)/IRF4 (interferon regulatory factor 4) is a transcription factor that is activated as a result of t(6;14)(p25;q32) in multiple myeloma. MUM1 expression is seen in various B-cell lymphomas and predicts an unfavorable outcome in some lymphoma subtypes. To elucidate its role in B-cell malignancies, we prepared MUM1-expressing Ba/F3 cells, which proliferated until higher cellular density than the parental cells, and performed cDNA microarray analysis to identify genes whose expression is regulated by MUM1. We found that the expression of four genes including FK506-binding protein 3 (FKBP3), the monokine induced by interferon-γ(MIG), Fas apoptotic inhibitory molecule (Faim) and Zinc-finger protein 94 was altered in the MUM1-expressing cells. We then focused on MIG since its expression was immediately upregulated by MUM1. In reporter assays, MUM1 activated the MIG promoter in cooperation with PU.1, and the interaction between MUM1 and the MIG promoter sequence was confirmed. The expression of MIG was correlated with that of MUM1 in B-CLL cell lines, and treatment with neutralizing antibodies against MIG and its receptor, CXCR3, slightly inhibited the proliferation of two MUM1-expressing lines. These results suggest that MUM1 plays roles in the progression of B-cell lymphoma/leukemia by regulating the expression of various genes including MIG.Leukemia (2005) 19, 1471–1478. doi:10.1038/sj.leu.2403833; published online 16 June 2005 [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
40. Antimyeloma effects of a novel synthetic retinoid Am80 (Tamibarotene) through inhibition of angiogenesis.
- Author
-
Sanda, T., Kuwano, T., Nakao, S., Iida, S., Ishida, T., Komatsu, H., Shudo, K., Kuwano, M., Ono, M., and Ueda, R.
- Subjects
MULTIPLE myeloma ,B cell lymphoma ,NEOVASCULARIZATION ,VASCULAR endothelial growth factors ,TRETINOIN ,BLOOD-vessel development - Abstract
In multiple myeloma (MM), the interaction between myeloma cells and bone marrow microenvironment has an important role in the pathogenesis of MM. We first examined the inducing effect of myeloma cells on migration of human umbilical vein vascular endothelial cells (HUVECs). Five myeloma cell lines produced varying amounts of VEGF, and migration of HUVECs was induced by coculture with myeloma cells. We next examined the inhibitory effect of a novel synthetic retinoid Am80 (Tamibarotene) on both myeloma cells and HUVECs. Am80 is specific for the retinoic-acid receptor-a/ß, and has therapeutic effects in all-trans retinoic acid resistant acute promyelocytic leukemia. Am80 slightly inhibited the growth of both myeloma cells and HUVECs, and remarkably inhibited the growth of HUVECs stimulated by VEGF. Am80 showed little growth inhibition of bone marrow stromal cells (BMSCs), but it markedly inhibited migration of HUVECs by cocultured myeloma cells. Am80 inhibited VEGF-induced phosphorylation of VEGF receptor. In addition, VEGF-induced formation of tube-like structures in vitro and neovascularization in mouse corneas were significantly inhibited by Am80. These findings clearly demonstrate that Am80 is a potential inhibitor of angiogenesis caused by the interaction between vascular endothelial cells and myeloma cells, and might be a useful therapeutic agent against MM.Leukemia (2005) 19, 901-909. doi:10.1038/sj.leu.2403754 Published online 21 April 2005 [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
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41. Aberrant DNA methylation associated with silencing BNIP3 gene expression in haematopoietic tumours.
- Author
-
Murai, M., Toyota, M., Satoh, A., Suzuki, H., Akino, K., Mita, H., Sasaki, Y., Ishida, T., Shen, L., Garcia-Manero, G., Issa, J.-P. J., Hinoda, Y., Tokino, T., and Imai, K.
- Subjects
METHYLATION ,GENE expression ,HYPOXEMIA ,LYMPHOCYTIC leukemia ,DRUG therapy ,CELL death ,METHYLTRANSFERASES ,MYELOID leukemia - Abstract
Hypoxia is a key factor contributing to the progression of human neoplasias and to the development of resistance to chemotherapy. BNIP3 is a proapoptotic member of the Bcl-2 protein family involved in hypoxia-induced cell death. We evaluated the expression and methylation status of BNIP3 gene to better understand the role of epigenetic alteration of its expression in haematopoietic tumours. Methylation of the region around the BNIP3 transcription start site was detected in four acute lymphocytic leukaemia, one multiple myeloma and one Burkitt lymphoma cell lines, and was closely associated with silencing the gene. That expression of BNIP3 was restored by treatment with 5-aza2'-deoxycytidine (5-aza-dC), a methyltransferase inhibitor, which confirmed the gene to be epigenetically inactivated by methylation. Notably, re-expression of BNIP3 using 5-aza2-dC also restored hypoxia-mediated cell death in methylated cell lines. Acetylation of histone H3 in the 5'region of the gene, which was assessed using chromatin immunoprecipitation assays, correlated directly with gene expression and inversely with DNA methylation. Among primary tumours, methylation of BNIP3 was detected in five of 34 (15%) acute lymphocytic leukaemias, six of 35 (17%) acute myelogenous leukaemias and three of 14 (21%) multiple myelomas. These results suggest that aberrant DNA methylation of the 5'CpG island and histone deacetylation play key roles in silencing BNIP3 expression in haematopoietic tumours.British Journal of Cancer (2005) 92, 1165-1172. doi:10.1038/sj.bjc.6602422 www.bjcancer.com Published online 8 March 2005 [ABSTRACT FROM AUTHOR]
- Published
- 2005
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42. Cis-acting effect of the IL1B C-31T polymorphism on IL-1ßmRNA expression.
- Author
-
Kimura, R., Nishioka, T., Soemantri, A., and Ishida, T.
- Subjects
GENETIC polymorphisms ,INTERLEUKINS ,CYTOKINES ,MESSENGER RNA ,GENETIC transcription ,GENE expression - Abstract
Since the effect of IL1B polymorphisms on IL-1ßproduction is still controversial, we selected two polymorphisms to test their cis-acting effect on IL-1ßmRNA expression by means of the allele-specific transcript quantification and the haplotype analysis. As for the C-31T polymorphism, we found that expression of the-31T allele was 2.2 times of the-31C allele. This higher transcription efficiency may correspond to the fact that C-31T is located in a TATA box. The other polymorphism, C+3954T, did not alter the levels of transcription. The use of the allele-specific transcript quantification enables us to exclude trans-acting effects of polymorphisms on the gene expression and contributes to understanding the roles of the IL1B polymorphisms in susceptibility to multifactorial diseases.Genes and Immunity (2004) 5, 572-575. doi:10.1038/sj.gene.6364128 Published online 9 September 2004 [ABSTRACT FROM AUTHOR]
- Published
- 2004
- Full Text
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43. Constitutively activated phosphatidylinositol 3-kinase primes platelets from patients with chronic myelogenous leukemia for thrombopoietin-induced aggregation.
- Author
-
Kubota, Y., Tanaka, T., Ohnishi, H., Kitanaka, A., Okutani, Y., Taminato, T., Ishida, T., and Kamano, H.
- Subjects
THROMBOPOIETIN ,BLOOD platelets ,MYELOPROLIFERATIVE neoplasms ,MYELOID leukemia ,AMINO acids ,LEUKEMIA ,TYROSINE metabolism ,BIOCHEMISTRY ,BLOOD platelet aggregation ,COLONY-stimulating factors (Physiology) ,DOSE-effect relationship in pharmacology ,ENZYME inhibitors ,HETEROCYCLIC compounds ,PHENOMENOLOGY ,PHOSPHORYLATION ,PHOSPHOTRANSFERASES ,STEROIDS ,CHRONIC myeloid leukemia ,CHROMONES ,IN vitro studies ,CHEMICAL inhibitors ,PHARMACODYNAMICS ,PHYSIOLOGY - Abstract
In this study, we examined the effect of thrombopoietin (TPO) on the aggregation of platelets from 40 patients with myeloproliferative disorders (MPDs), including 17 patients with chronic myelogenous leukemia in the chronic phase (CML-CP), 10 with polycythemia vera, 10 with essential thrombocythemia, and three with myelofibrosis. TPO by itself dose-dependently induced the aggregation of platelets from patients with CML-CP but not from those with other MPDs or with CML-CP in cytogenetical complete remission. The expression of CD63 in CML-CP platelets was induced by TPO treatment. Phosphatidylinositol 3-kinase (PI3-kinase) was constitutively activated in CML-CP platelets. Pretreatment with PI3-kinase inhibitors (wortmannin and LY294002) dose-dependently inhibited TPO-induced aggregation of CML-CP platelets. The Abl kinase inhibitor imatinib mesylate and the Jak inhibitor AG490 suppressed TPO-induced aggregation of CML-CP platelets. Pretreatment with imatinib mesylate, but not with AG490, inhibited the activity of PI3-kinase in CML-CP platelets. In addition, tyrosine phosphorylation of Jak2 was undetected in CML-CP platelets before TPO treatment. These findings indicate that the constitutive activation of PI3-kinase primes CML-CP platelets for the aggregation induced by TPO, and that Bcr-Abl, but not Jak family protein tyrosine kinases, are involved in the constitutive activation of PI3-kinase in CML-CP platelets. [ABSTRACT FROM AUTHOR]
- Published
- 2004
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44. Inactivation of class II transactivator by DNA methylation and histone deacetylation associated with absence of HLA-DR induction by interferon-? in haematopoietic tumour cells.
- Author
-
Morimoto, Y., Toyota, M., Satoh, A., Murai, M., Mita, H., Suzuki, H., Takamura, Y., Ikeda, H., Ishida, T., Sato, N., Tokino, T., and Imai, K.
- Subjects
CANCER cells ,DNA ,INTERFERONS ,CELL membranes ,METHYLATION ,MAJOR histocompatibility complex ,PEPTIDES ,HISTONES - Abstract
By presenting immunogenic peptides at the cell surface, major histocompatibility complex (MHC) class II molecules play a key role in the control of adaptive immune responses. Whether expressed constitutively or induced by interferon-?, expression of MHC class II molecules is regulated via coactivator class II transactivator (CIITA); moreover, suppression of their expression is one mechanism by which cancer cells escape host immunity. In this study, we surveyed the relationship between the expression of one MHC class II antigen, HLA-DR, and its coactivators in a group of haematopoietic cell lines, and explored the role of the aberrant DNA methylation in silencing HLA-DR expression. Among 26 cell lines studied, HLA-DR expression was lost from eight T-cell and two myeloid leukaemia cell lines, and this loss was closely associated with suppression of CIITA-PIV expression. Notably, nine of the 10 cell lines that lost CIITA-PIV expression showed methylation of the gene's 5' CpG island. Thus, DNA methylation is believed to inhibit the expression of MHC class II molecules in haematopoietic tumour cells by silencing its coactivator, CIITA-PIV. Furthermore, methylation of CIITA-PIV was detected in seven of 32 primary acute myeloid leukaemia specimens, indicating that epigenetic alteration is not a cell line-specific phenomenon. Collectively, these data suggest that, by suppressing expression of MHC class II molecules, epigenetic inactivation of CIITA provides a survival advantage to a subset of haematopoietic tumours.British Journal of Cancer (2004) 90, 844-852. doi:10.1038/sj.bjc.6601602 www.bjcancer.com [ABSTRACT FROM AUTHOR]
- Published
- 2004
- Full Text
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45. The SDF1-G801A polymorphism is not associated with SDF1 gene expression in Epstein-Barr virus-transformed lymphoblastoid cells.
- Author
-
Kimura, R, Nishioka, T, and Ishida, T
- Subjects
GENETIC polymorphisms ,RNA ,CELLS ,GENE expression - Abstract
The effects of the SDF1-3′ A on AIDS progression have been attributed to the altered amount of stromal cell-derived factor 1 (SDF-1). However, the contribution of the SDF1-G801A polymorphism to SDF-1 expression is still unclear. In contrast to fresh peripheral blood mononuclear cells (PBMCs), Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs) express the SDF-1 mRNA. Using EBV-transformed LCLs from 42 individuals with different genotypes, we investigated the SDF-1 mRNA levels and methylation status in the SDF1 gene. Both in PBMCs and in EBV-transformed LCLs, CpG dinucleotides in the 5′ region of the SDF1 gene were unmethylated. As for the 3′ untranslated region (3′UTR), by contrast, CpG dinucleotides were methylated in PBMCs, whereas site-specific demethylation around the polymorphic site was detected in EBV-transformed LCLs. The levels of the demethylation were correlated with the SDF-1 mRNA levels. However, the genotype for the SDF1-G801A polymorphism did not significantly alter the SDF-1 mRNA levels. The allele preferences in transcription and methylation were also absent in the heterozygous cells. In conclusion, this study suggested a contribution of site-specific demethylation in the 3′ UTR to the SDF1 gene expression, but did not show any evidence for the contribution of the SDF1-G801A polymorphism to the amount of the SDF-1 mRNA. [ABSTRACT FROM AUTHOR]
- Published
- 2003
- Full Text
- View/download PDF
46. Photoreaction of a ZnO gel film chemically modified with β-diketones.
- Author
-
Kawahara, T., Ishida, T., Tada, H., Noma, N., Tohge, N., and Ito, S.
- Subjects
- *
CHELATES , *ABSORPTION , *IONS , *IRRADIATION , *CHEMICAL decomposition , *CARBONYL compounds , *ELECTRONICS - Abstract
Chelate formation is confirmed by a red shift of the n → π* absorption peak of benzoylacetone (BzAcH) from 309 to 336 nm with its addition to a sol containing Zn2+ ions. The chelate bonds between Zn2+ and BzAc- are mostly maintained in the gel film prepared from the sol. Irradiation of the gel film by a Xe lamp with a cut filter (λex > 300 nm) in the presence of H2O leads to decomposition of the chelate ring. As a result of the photolysis, ZnO–H groups, CH3CHO and other carbonyl compounds are generated with the lost of CH3 groups of the BzAc- ligand and H2O involved in the film. INDO/S calculations on a model complex (Zn(BzAc)(OEt)) assign the n → π* absorption to the electronic transition from a non-bonding molecular orbital (MO) distributed mainly at the phenyl group to an anti-bonding MO localized at the CO bonds. On the basis of these results, a photo-induced hydrolysis mechanism was presented to explain the formation of positive-type patterned ZnO films. [ABSTRACT FROM AUTHOR]
- Published
- 2003
- Full Text
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47. Modeling of structural performances under coupled environmental and weather actions.
- Author
-
Maekawa, K. and Ishida, T.
- Abstract
Copyright of Materials & Structures is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2002
- Full Text
- View/download PDF
48. Nonspecific interstitial pneumonia as pulmonary involvement of primary Sjögren's syndrome NSIP in patients with Sjögren's syndrome.
- Author
-
Yamadori, I., Fujita, J., Bandoh, S., Tokuda, M., Tanimoto, Y., Kataoka, M., Yamasaki, Y., Yoshinouchi, T., Ohtsuki, Y., and Ishida, T.
- Subjects
LUNG diseases ,PNEUMONIA ,RESPIRATORY organs ,PATIENTS ,PATHOLOGY ,DIAGNOSIS - Abstract
The pathologic patterns of lung involvement in nine patients with Sjögren's syndrome (SjS) are evaluated. The patients consisted of three males and six females, with a median age of 59 years. The SjS was diagnosed according to the criteria of the First International Seminar on SjS. In all patients, high-resolution computed radiographic scanning (HRCT) of the lungs was performed, and apparent honeycomb or microhoneycomb formation was observed in six patients. Pathologically, six patients were diagnosed with usual interstitial pneumonia (UIP), and three were diagnosed with nonspecific interstitial pneumonia/fibrosis (NSIP) (group II). There were no apparent honeycomb formations on HRCT in patients diagnosed with NSIP. In conclusion, NSIP is also a possible histologic classification of interstitial pneumonia associated with SjS. [ABSTRACT FROM AUTHOR]
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- 2002
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49. Effect of monomer sequence on the polymer durability in the copolymers of chlorotrifluoroethylene with an alkyl vinyl ester or an alkyl vinyl ether.
- Author
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Ishida, T., Suzuki, T., Takimoto, Y., Sasakura, H., and Jitsugiri, Y.
- Abstract
Copyright of Surface Coatings International Part B: Coatings Transactions is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2002
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50. Anthropological implication of the SDF1-3′A allele distribution in Southeast Asia and Melanesia.
- Author
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Kimura, R., Soemantri, A., Settheetham-Ishida, W., Ohtsuka, R., Inaoka, T., Pookajorn, S., Tiwawech, D., Duanchang, P., and Ishida, T.
- Subjects
ALLELES ,GENETIC epidemiology - Abstract
The distribution of the SDF1-3′A allele among 1848 individuals in Southeast Asia and Melanesia was studied with the polymerase chain reaction-restriction fragment length polymorphism assay. The SDF1-3′A allele frequency in the populations of mainland Southeast Asia ranged from 0.0 to 0.355, whereas in the populations of insular Southeast Asia and Melanesia, it ranged from 0.233 to 0.733, with an increasing cline from west to east. Correlation between SDF1-3′A frequency and longitude values was highly significant for the populations in the Pacific region (r = 0.867, P < 0.001). The geographic distribution of the SDF1-3′A frequencies in the Pacific region was interpreted by an admixture of Austronesians with the aboriginal people in situ. In addition, this study found high proportions of SDF1-3′A/3′A homozygous individuals in several populations, which will enable us to evaluate roles of the SDF1 genotypes in SDF-1 expression. [ABSTRACT FROM AUTHOR]
- Published
- 2002
- Full Text
- View/download PDF
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