Author: "Hirohata S" / Language: english - Searchworks@Jio Institute Digital Library Search Results

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462 results on '"Hirohata S"'

1. ESICM LIVES 2016: part three: Milan, Italy. 1–5 October 2016

Author: Velasquez, T., Mackey, G., Lusk, J., Kyle, U. G., Fontenot, T., Marshall, P., Shekerdemian, L. S., Coss-Bu, J. A., Nishigaki, A., Yatabe, T., Tamura, T., Yamashita, K., Yokoyama, M., Ruiz-Rodriguez, J. C., Encina, B., Belmonte, R., Troncoso, I., Tormos, P., Riveiro, M., Baena, J., Sanchez, A., Bañeras, J., Cordón, J., Duran, N., Ruiz, A., Caballero, J., Nuvials, X., Riera, J., Serra, J., Rutten, A. M. F., van Ieperen, S. N. M., Der Kinderen, E. P. H. M., Van Logten, T., Kovacikova, L., Skrak, P., Zahorec, M., Kyle, U. G., Akcan-Arikan, A., Silva, J. C., Mackey, G., Lusk, J., Goldsworthy, M., Shekerdemian, L. S., Coss-Bu, J. A., Wood, D., Harrison, D., Parslow, R., Davis, P., Pappachan, J., Goodwin, S., Ramnarayan, P., Chernyshuk, S., Yemets, H., Zhovnir, V., Pulitano’, S. M., De Rosa, S., Mancino, A., Villa, G., Tosi, F., Franchi, P., Conti, G., Patel, B., Khine, H., Shah, A., Sung, D., Singer, L., Haghbin, S., Inaloo, S., Serati, Z., Idei, M., Nomura, T., Yamamoto, N., Sakai, Y., Yoshida, T., Matsuda, Y., Yamaguchi, Y., Takaki, S., Yamaguchi, O., Goto, T., Longani, N., Medar, S., Abdel-Aal, I. R., El Adawy, A. S., Mohammed, H. M. E. H., Mohamed, A. N., Parry, S. M., Knight, L. D., Denehy, L., De Morton, N., Baldwin, C. E., Sani, D., Kayambu, G., da Silva, V. Z. M., Phongpagdi, P., Puthucheary, Z. A., Granger, C. L., Rydingsward, J. E., Horkan, C. M., Christopher, K. B., McWilliams, D., Jones, C., Reeves, E., Atkins, G., Snelson, C., Aitken, L. M., Rattray, J., Kenardy, J., Hull, A. M., Ullman, A., Le Brocque, R., Mitchell, M., Davis, C., Macfarlane, B., Azevedo, J. C., Rocha, L. L., De Freitas, F. F. M., Cavalheiro, A. M., Lucinio, N. M., Lobato, M. S., Ebeling, G., Kraegpoeth, A., Laerkner, E., De Brito-Ashurst, I., White, C., Gregory, S., Forni, L. G., Flowers, E., Curtis, A., Wood, C. A., Siu, K., Venkatesan, K., Muhammad, J. B. H., Ng, L., Seet, E., Baptista, N., Escoval, A., Tomas, E., Agrawal, R., Mathew, R., Varma, A., Dima, E., Charitidou, E., Perivolioti, E., Pratikaki, M., Vrettou, C., Giannopoulos, A., Zakynthinos, S., Routsi, C., Atchade, E., Houzé, S., Jean-Baptiste, S., Thabut, G., Genève, C., Tanaka, S., Lortat-Jacob, B., Augustin, P., Desmard, M., Montravers, P., de Molina, F. J. González, Barbadillo, S., Alejandro, R., Álvarez-Lerma, F., Vallés, J., Catalán, R. M., Palencia, E., Jareño, A., Granada, R. M., Ignacio, M. L., Cui, N., Liu, D., Wang, H., Su, L., Qiu, H., Li, R., Jaffal, K., Rouzé, A., Poissy, J., Sendid, B., Nseir, S., Paramythiotou, E., Rizos, M., Frantzeskaki, F., Antoniadou, A., Vourli, S., Zerva, L., Armaganidis, A., Riera, J., Gottlieb, J., Greer, M., Wiesner, O., Martínez, M., Acuña, M., Rello, J., Welte, T., Atchade, E., Mignot, T., Houzé, S., Jean-Baptiste, S., Thabut, G., Lortat-Jacob, B., Tanaka, S., Augustin, P., Desmard, M., Montravers, P., Soussi, S., Dudoignon, E., Ferry, A., Chaussard, M., Benyamina, M., Alanio, A., Touratier, S., Chaouat, M., Lafaurie, M., Mimoun, M., Mebazaa, A., Legrand, M., Sheils, M. A., Patel, C., Mohankumar, L., Akhtar, N., Noriega, S. K. Pacheco, Aldana, N. Navarrete, León, J. L. Ávila, Baquero, J. Durand, Bernal, F. Fernández, Ahmadnia, E., Hadley, J. S., Millar, M., Hall, D., Hewitt, H., Yasuda, H., Sanui, M., Komuro, T., Kawano, S., Andoh, K., Yamamoto, H., Noda, E., Hatakeyama, J., Saitou, N., Okamoto, H., Kobayashi, A., Takei, T., Matsukubo, S., Rotzel, H. B., Lázaro, A. Serrano, Prada, D. Aguillón, Gimillo, M. Rodriguez, Barinas, O. Diaz, Cortes, M. L. Blasco, Franco, J. Ferreres, Roca, J. M. Segura, Carratalá, A., Gonçalves, B., Turon, R., Mendes, A., Miranda, F., Mata, P. J., Cavalcanti, D., Melo, N., Lacerda, P., Kurtz, P., Righy, C., Rosario, L. E. de la Cruz, Lesmes, S. P. Gómez, Romero, J. C. García, Herrera, A. N. García, Pertuz, E. D. Díaz, Sánchez, M. J. Gómez, Sanz, E. Regidor, Hualde, J. Barado, Hernández, A. Ansotegui, Irazabal, J. M. Guergué, Spatenkova, V., Bradac, O., Suchomel, P., Urli, T., Lazzeri, E. Heusch, Aspide, R., Zanello, M., Perez-Borrero, L., Garcia-Alvarez, J. M., Arias-Verdu, M. D., Aguilar-Alonso, E., Rivera-Fernandez, R., Mora-Ordoñez, J., De La Fuente-Martos, C., Castillo-Lorente, E., Guerrero-Lopez, F., Lesmes, S. P. Gómez, Rosario, L. E. De la Cruz, Pertuz, E. D. Díaz, Hernández, A. Ansotegui, Romero, J. C. García, Sánchez, M. J. Gómez, Herrera, A. N. García, Ramírez, J. Roldán, Sanz, E. Regidor, Hualde, J. Barado, León, J. P. Tirapu, Navarro-Guillamón, L., Cordovilla-Guardia, S., Iglesias-Santiago, A., Guerrero-López, F., Fernández-Mondéjar, E., Vidal, A., Perez, M., Juez, A., Arias, N., Colino, L., Perez, J. L., Pérez, H., Calpe, P., Alcala, M. A., Robaglia, D., Perez, C., Lan, S. K., Cunha, M. M., Moreira, T., Santos, F., Lafuente, E., Fernandes, M. J., Silva, J. G., Rosario, L. E. de la Cruz, Lesmes, S. P. Gómez, Herrera, A. N. García, Romero, J. C. García, Pertuz, E. D. Díaz, Sánchez, M. J. Gómez, Sanz, E. Regidor, Echeverría, J. G. Armando, Hernández, A. Ansotegui, Hualde, J. Barado, Podlepich, V., Sokolova, E., Alexandrova, E., Lapteva, K., Kurtz, P., Shuinotsuka, C., Rabello, L., Vianna, G., Reis, A., Cairus, C., Salluh, J., Bozza, F., Torres, J. C. Barrios, Araujo, N. J. Fernández, García-Olivares, P., Keough, E., Dalorzo, M., Tang, L. K., De Sousa, I., Díaz, M., Marcos-Zambrano, L. J., Guerrero, J. E., Gomez, S. E. Zamora, Lopez, G. D. Hernandez, Cuellar, A. I. Vazquez, Nieto, O. R. Perez, Gonzalez, J. A. Castanon, Bhasin, D., Rai, S., Singh, H., Gupta, O., Bhattal, M. K., Sampley, S., Sekhri, K., Nandha, R., Aliaga, F. A., Olivares, F., Appiani, F., Farias, P., Alberto, F., Hernández, A., Pons, S., Sonneville, R., Bouadma, L., Neuville, M., Mariotte, E., Radjou, A., Lebut, J., Chemam, S., Voiriot, G., Dilly, M. P., Mourvillier, B., Dorent, R., Nataf, P., Wolff, M., Timsit, J. F., Ediboglu, O., Ataman, S., Ozkarakas, H., Kirakli, C., Vakalos, A., Avramidis, V., Obukhova, O., Kurmukov, I. A., Kashiya, S., Golovnya, E., Baikova, V. N., Ageeva, T., Haritydi, T., Kulaga, E. V., Rios-Toro, J. J., Perez-Borrero, L., Aguilar-Alonso, E., Arias-Verdu, M. D., Garcia-Alvarez, J. M., Lopez-Caler, C., De La Fuente-Martos, C., Rodriguez-Fernandez, S., Sanchez-Orézzoli, M. Gomez, Martin-Gallardo, F., Nikhilesh, J., Joshi, V., Villarreal, E., Ruiz, J., Gordon, M., Quinza, A., Gimenez, J., Piñol, M., Castellanos, A., Ramirez, P., Jeon, Y. D., Jeong, W. Y., Kim, M. H., Jeong, I. Y., Ahn, M. Y., Ahn, J. Y., Han, S. H., Choi, J. Y., Song, Y. G., Kim, J. M., Ku, N. S., Shah, H., Kellner, F., Rezai, F., Mistry, N., Yodice, P., Ovnanian, V., Fless, K., Handler, E., Alejos, R. Martínez, Romeu, J. D. Martí, Antón, D. González, Quinart, A., Martí, A. Torres, Llaurado-Serra, M., Lobo-Civico, A., Ventura-Rosado, A., Piñol-Tena, A., Pi-Guerrero, M., Paños-Espinosa, C., Peralvo-Bernat, M., Marine-Vidal, J., Gonzalez-Engroba, R., Montesinos-Cerro, N., Treso-Geira, M., Valeiras-Valero, A., Martinez-Reyes, L., Sandiumenge, A., Jimenez-Herrera, M. F., Helyar, S., Riozzi, P., Noon, A., Hallows, G., Cotton, H., Keep, J., Hopkins, P. A., Taggu, A., Renuka, S., Sampath, S., Rood, P. J. T., Frenzel, T., Verhage, R., Bonn, M., Pickkers, P., van der Hoeven, J. G., van den Boogaard, M., Corradi, F., Melnyk, L., Moggia, F., Pienovi, R., Adriano, G., Brusasco, C., Mariotti, L., Lattuada, M., Bloomer, M. J., Coombs, M., Ranse, K., Endacott, R., Maertens, B., Blot, K., Blot, S., Amerongen, M. P. van Nieuw, van der Heiden, E. S., Twisk, J. W. R., Girbes, A. R. J., Spijkstra, J. J., Riozzi, P., Helyar, S., Cotton, H., Hallows, G., Noon, A., Bell, C., Peters, K., Feehan, A., Keep, J., Hopkins, P. A., Churchill, K., Hawkins, K., Brook, R., Paver, N., Endacott, R., Maistry, N., van Wijk, A., Rouw, N., van Galen, T., Evelein-Brugman, S., Taggu, A., Krishna, B., Sampath, S., Putzu, A., Fang, M., Berto, M. Boscolo, Belletti, A., Cassina, T., Cabrini, L., Mistry, M., Alhamdi, Y., Welters, I., Abrams, S. T., Toh, C. H., Han, H. S., Gil, E. M., Lee, D. S., Park, C. M., Winder-Rhodes, S., Lotay, R., Doyle, J., Ke, M. W., Huang, W. C., Chiang, C. H., Hung, W. T., Cheng, C. C., Lin, K. C., Lin, S. C., Chiou, K. R., Wann, S. R., Shu, C. W., Kang, P. L., Mar, G. Y., Liu, C. P., Dubó, S., Aquevedo, A., Jibaja, M., Berrutti, D., Labra, C., Lagos, R., García, M. F., Ramirez, V., Tobar, M., Picoita, F., Peláez, C., Carpio, D., Alegría, L., Hidalgo, C., Godoy, K., Bakker, J., Hernández, G., Sadamoto, Y., Katabami, K., Wada, T., Ono, Y., Maekawa, K., Hayakawa, M., Sawamura, A., Gando, S., Marin-Mateos, H., Perez-Vela, J. L., Garcia-Gigorro, R., Peiretti, M. A. Corres, Lopez-Gude, M. J., Chacon-Alves, S., Renes-Carreño, E., Montejo-González, J. C., Parlevliet, K. L., Touw, H. R. W., Beerepoot, M., Boer, C., Elbers, P. W. G., Tuinman, P. R., Abdelmonem, S. A., Helmy, T. A., El Sayed, I., Ghazal, S., Akhlagh, S. H., Masjedi, M., Hozhabri, K., Kamali, E., Zýková, I., Paldusová, B., Sedlák, P., Morman, D., Youn, A. M., Ohta, Y., Sakuma, M., Bates, D., Morimoto, T., Su, P. L., Chang, W. Y., Lin, W. C., Chen, C. W., Facchin, F., Zarantonello, F., Panciera, G., De Cassai, A., Venrdramin, A., Ballin, A., Tonetti, T., Persona, P., Ori, C., Del Sorbo, L., Rossi, S., Vergani, G., Cressoni, M., Chiumello, D., Chiurazzi, C., Brioni, M., Algieri, I., Tonetti, T., Guanziroli, M., Colombo, A., Tomic, I., Colombo, A., Crimella, F., Carlesso, E., Gasparovic, V., Gattinoni, L., Neto, A. Serpa, Schmidt, M., Pham, T., Combes, A., de Abreu, M. Gama, Pelosi, P., Schultz, M. J., Katira, B. H., Engelberts, D., Giesinger, R. E., Ackerley, C., Yoshida, T., Zabini, D., Otulakowski, G., Post, M., Kuebler, W. M., McNamara, P. J., Kavanagh, B. P., Pirracchio, R., Rigon, M. Resche, Carone, M., Chevret, S., Annane, D., Eladawy, S., El-Hamamsy, M., Bazan, N., Elgendy, M., De Pascale, G., Vallecoccia, M. S., Cutuli, S. L., Di Gravio, V., Pennisi, M. A., Conti, G., Antonelli, M., Andreis, D. T., Khaliq, W., Singer, M., Hartmann, J., Harm, S., Carmona, S. Alcantara, Almudevar, P. Matia, Abellán, A. Naharro, Ramos, J. Veganzones, Pérez, L. Pérez, Valbuena, B. Lobo, Sanz, N. Martínez, Simón, I. Fernández, Arrigo, M., Feliot, E., Deye, N., Cariou, A., Guidet, B., Jaber, S., Leone, M., Resche-Rigon, M., Baron, A. Vieillard, Legrand, M., Gayat, E., Mebazaa, A., Balik, M., Kolnikova, I., Maly, M., Waldauf, P., Tavazzi, G., Kristof, J., Herpain, A., Su, F., Post, E., Taccone, F., Vincent, J. L., Creteur, J., Lee, C., Hatib, F., Jian, Z., Buddi, S., Cannesson, M., Fileković, S., Turel, M., Knafelj, R., Gorjup, V., Stanić, R., Gradišek, P., Cerović, O., Mirković, T., Noč, M., Tirkkonen, J., Hellevuo, H., Olkkola, K. T., Hoppu, S., Lin, K. C., Hung, W. T., Chiang, C. C., Huang, W. C., Juan, W. C., Lin, S. C., Cheng, C. C., Lin, P. H., Fong, K. Y., Hou, D. S., Kang, P. L., Wann, S. R., Chen, Y. S., Mar, G. Y., Liu, C. P., Paul, M., Bougouin, W., Geri, G., Dumas, F., Champigneulle, B., Legriel, S., Charpentier, J., Mira, J. P., Sandroni, C., Cariou, A., Zimmerman, J., Sullivan, E., Noursadeghi, M., Fox, B., Sampson, D., McHugh, L., Yager, T., Cermelli, S., Seldon, T., Bhide, S., Brandon, R. A., Brandon, R. B., Zwaag, J., Beunders, R., Pickkers, P., Kox, M., Gul, F., Arslantas, M. K., Genc, D., Zibandah, N., Topcu, L., Akkoc, T., Cinel, I., Greco, E., Lauretta, M. P., Andreis, D. T., Singer, M., Garcia, I. Palacios, Cordero, M., Martin, A. Diaz, Pallás, T. Aldabó, Montero, J. Garnacho, Rey, J. Revuelto, Malo, L. Roman, Montoya, A. A. Tanaka, Martinez, A. D. C. Amador, Ayala, L. Y. Delgado, Zepeda, E. Monares, Granillo, J. Franco, Sanchez, J. Aguirre, Alejo, G. Camarena, Cabrera, A. Rugerio, Montenegro, A. Pedraza, Pham, T., Beduneau, G., Schortgen, F., Piquilloud, L., Zogheib, E., Jonas, M., Grelon, F., Runge, I., Terzi, N., Grangé, S., Barberet, G., Guitard, P. G., Frat, J. P., Constan, A., Chrétien, J. M., Mancebo, J., Mercat, A., Richard, J. C. M., Brochard, L., Soilemezi, E., Koco, E., Savvidou, S., Nouris, C., Matamis, D., Di Mussi, R., Spadaro, S., Volta, C. A., Mariani, M., Colaprico, A., Antonio, C., Bruno, F., Grasso, S., Rodriguez, A., Martín-Loeches, I., Díaz, E., Masclans, J. R., Gordo, F., Solé-Violán, J., Bodí, M., Avilés-Jurado, F. X., Trefler, S., Magret, M., Reyes, L. F., Marín-Corral, J., Yebenes, J. C., Esteban, A., Anzueto, A., Aliberti, S., Restrepo, M. I., Larsson, J. Skytte, Redfors, B., Ricksten, S. E., Haines, R., Powell-Tuck, J., Leonard, H., Ostermann, M., Berthelsen, R. E., Itenov, T. S., Perner, A., Jensen, J. U., Ibsen, M., Jensen, A. E. K., Bestle, M. H., Bucknall, T., Dixon, J., Boa, F., MacPhee, I., Philips, B. J., Doyle, J., Saadat, F., Samuels, T., Huddart, S., McCormick, B., DeBrunnar, R., Preece, J., Swart, M., Peden, C., Richardson, S., Forni, L., Kalfon, P., Baumstarck, K., Estagnasie, P., Geantot, M. A., Berric, A., Simon, G., Floccard, B., Signouret, T., Boucekine, M., Fromentin, M., Nyunga, M., Sossou, A., Venot, M., Robert, R., Follin, A., Renault, A., Garrouste, M., Collange, O., Levrat, Q., Villard, I., Thévenin, D., Pottecher, J., Patrigeon, R. G., Revel, N., Vigne, C., Mimoz, O., Auquier, P., Pawar, S., Jacques, T., Deshpande, K., Pusapati, R., Wood, B., Pulham, R. A., Wray, J., Brown, K., Pierce, C., Nadel, S., Ramnarayan, P., Azevedo, J. R., Montenegro, W. S., Rodrigues, D. P., Sousa, S. C., Araujo, V. F., Leitao, A. L., Prazeres, P. H., Mendonca, A. V., Paula, M. P., Das Neves, A., Loudet, C. I., Busico, M., Vazquez, D., Villalba, D., Lischinsky, A., Veronesi, M., Emmerich, M., Descotte, E., Juliarena, A., Bisso, M. Carboni, Grando, M., Tapia, A., Camargo, M., Ulla, D. Villani, Corzo, L., dos Santos, H. Placido, Ramos, A., Doglia, J. A., Estenssoro, E., Carbonara, M., Magnoni, S., Donald, C. L. Mac, Shimony, J. S., Conte, V., Triulzi, F., Stretti, F., Macrì, M., Snyder, A. Z., Stocchetti, N., Brody, D. L., Podlepich, V., Shimanskiy, V., Savin, I., Lapteva, K., Chumaev, A., Tjepkema-Cloostermans, M. C., Hofmeijer, J., Beishuizen, A., Hom, H., Blans, M. J., van Putten, M. J. A. M., Longhi, L., Frigeni, B., Curinga, M., Mingone, D., Beretta, S., Patruno, A., Gandini, L., Vargiolu, A., Ferri, F., Ceriani, R., Rottoli, M. R., Lorini, L., Citerio, G., Pifferi, S., Battistini, M., Cordolcini, V., Agarossi, A., Di Rosso, R., Ortolano, F., Stocchetti, N., Lourido, C. Mora, Cabrera, J. L. Santana, Santana, J. D. Martín, Alzola, L. Melián, del Rosario, C. García, Pérez, H. Rodríguez, Torrent, R. Lorenzo, Eslami, S., Dalhuisen, A., Fiks, T., Schultz, M. J., Hanna, A. Abu, Spronk, P. E., Wood, M., Maslove, D., Muscedere, J., Scott, S. H., Saha, T., Hamilton, A., Petsikas, D., Payne, D., Boyd, J. G., Puthucheary, Z. A., McNelly, A. S., Rawal, J., Connolly, B., McPhail, M. J., Sidhu, P., Rowlerson, A., Moxham, J., Harridge, S. D., Hart, N., Montgomery, H. E., Jovaisa, T., Thomas, B., Gupta, D., Wijayatilake, D. S., Shum, H. P., King, H. S., Chan, K. C., Tang, K. B., Yan, W. W., Arias, C. Castro, Latorre, J., De La Rica, A. Suárez, Garrido, E. Maseda, Feijoo, A. Montero, Gancedo, C. Hernández, Tofiño, A. López, Rodríguez, F. Gilsanz, Gemmell, L. K., Campbell, R., Doherty, P., MacKay, A., Singh, N., Vitaller, S., Nagib, H., Prieto, J., Del Arco, A., Zayas, B., Gomez, C., Tirumala, S., Pasha, S. A., Kumari, B. K., Martinez-Lopez, P., Puerto-Morlán, A., Nuevo-Ortega, P., Pujol, L. Martinez, Dolset, R. Algarte, González, B. Sánchez, Riera, S. Quintana, Álvarez, J. Trenado, Quintana, S., Martínez, L., Algarte, R., Sánchez, B., Trenado, J., Tomas, E., Brock, N., Viegas, E., Filipe, E., Cottle, D., Traynor, T., Martínez, M. V. Trasmonte, Márquez, M. Pérez, Gómez, L. Colino, Martínez, N. Arias, Muñoz, J. M. Milicua, Bellver, B. Quesada, Varea, M. Muñoz, Llorente, M. Á. Alcalá, Calvo, C. Pérez, Hillier, S. D., Faulds, M. C., Hendra, H., Lawrence, N., Maekawa, K., Hayakawa, M., Ono, Y., Kodate, A., Sadamoto, Y., Tominaga, N., Mizugaki, A., Murakami, H., Yoshida, T., Katabami, K., Wada, T., Sawamura, A., Gando, S., Silva, S., Kerhuel, L., Malagurski, B., Citerio, G., Chabanne, R., Laureys, S., Puybasset, L., Nobile, L., Pognuz, E. R., Rossetti, A. O., Verginella, F., Gaspard, N., Creteur, J., Ben-Hamouda, N., Oddo, M., Taccone, F. S., Ono, Y., Hayakawa, M., Iijima, H., Maekawa, K., Kodate, A., Sadamoto, Y., Mizugaki, A., Murakami, H., Katabami, K., Wada, T., Sawamura, A., Gando, S., Kodate, A., Katabami, K., Wada, T., Ono, Y., Maekawa, K., Hayakawa, M., Sawamura, A., Gando, S., Andersen, L. W., Raymond, T., Berg, R., Nadkarni, V., Grossestreuer, A., Kurth, T., Donnino, M., Krüger, A., Ostadal, P., Janotka, M., Vondrakova, D., Kongpolprom, N., Cholkraisuwat, J., Pekkarinen, P. T., Ristagno, G., Masson, S., Latini, R., Bendel, S., Ala-Kokko, T., Varpula, T., Vaahersalo, J., Hoppu, S., Tiainen, M., Mion, M. M., Plebani, M., Pettilä, V., Skrifvars, M.B., Son, Y., Kim, K. S., Suh, G. J., Kwon, W. Y., Ko, J. I., Park, M. J., Cavicchi, F. Zama, Iesu, E., Nobile, L., Vincent, J. L., Creteur, J., Taccone, F. S., Tanaka, H., Otani, N., Ode, S., Ishimatsu, S., Martínez, L., Algarte, R., Sánchez, B., Romero, I., Martínez, F., Quintana, S., Trenado, J., Vondrakova, D., Ostadal, P., Kruger, A., Janotka, M., Malek, F., Neuzil, P., Yeh, Y. C., Chen, Y. S., Wang, C. H., Huang, C. H., Chao, A., Lee, C. T., Lai, C. H., Chan, W. S., Cheng, Y. J., Sun, W. Z., Kaese, S., Horstmann, C., Lebiedz, P., Mourad, M., Gaudard, P., Eliet, J., Zeroual, N., Colson, P., Ostadal, P., Mlcek, M., Hrachovina, M., Kruger, A., Vondrakova, D., Janotka, M., Mates, M., Hala, P., Kittnar, O., Neuzil, P., Jacky, A., Rudiger, A., Spahn, D. R., Bettex, D. A., Kara, A., Akin, S., Dos reis Miranda, D., Struijs, A., Caliskan, K., van Thiel, R. J., Dubois, E. A., de Wilde, W., Zijlstra, F., Gommers, D., Ince, C., Marca, L., Xini, A., Mongkolpun, W., Cordeiro, C. P. R., Leite, R. T., Lheureux, O., Bader, A., Rincon, L., Santacruz, C., Preiser, J. C., Chao, A., Chao, A. S., Chen, Y. S., Kim, W., Ahn, C., Cho, Y., Lim, T. 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Iglesias, Sáez, V. Chica, Ruiz-Ruano, R. de la Chica, González, A. Sánchez, Kunze-Szikszay, N., Wand, S., Klapsing, P., Wetz, A., Heyne, T., Schwerdtfeger, K., Troeltzsch, M., Bauer, M., Quintel, M., Moerer, O., Cook, D. J., Rutherford, W. B., Scales, D. C., Adhikari, N. K., Cuthbertson, B. H., Suzuki, T., Takei, T., Fushimi, K., Iwamoto, M., Nakagawa, S., Mendsaikhan, N., Begzjav, T., Lundeg, G., Dünser, M. W., Romero, D. González, Cabrera, J. L. Santana, Santana, J. D. Martín, Padilla, Y. Santana, Pérez, H. Rodríguez, Torrent, R. Lorenzo, Kleinpell, R., Chouris, I., Radu, V., Stougianni, M., Lavrentieva, A., Lagonidis, D., Price, R. D. T., Day, A., Arora, N., Henderson, M. A., Hickey, S., Costa, M. I. Almeida, Carvalho, J. P., Gomes, A. A., Mergulhão, P. J., Chan, K. K. C., Shum, H. P., Yan, W. W., Maghsoudi, B., Tabei, S. H., Masjedi, M., Sabetian, G., Tabatabaei, H. R., Akbarzadeh, A., Saigal, S., Pakhare, A., Joshi, R., Pattnaik, S. K., Ray, B., Rousseau, A. F., Michel, L., Bawin, M., Cavalier, E., Reginster, J. Y., Damas, P., Bruyere, O., Zhou, J. C., Cauwenberghs, H., De Backer, A., Neels, H., Deblier, I., Berghmans, J., Himpe, D., Barea-Mendoza, J. A., Portillo, I. Prieto, Fernández, M. Valiente, Gigorro, R. Garcia, Vela, J. L. Perez, Mateos, H. Marín, Alves, S. Chacón, Varas, G. Morales, Rodriguez-Biendicho, A., Carreño, E. Renes, González, J. C. Montejo, Yang, J. S., Chiang, C. H., Hung, W. T., Huang, W. C., Cheng, C. C., Lin, K. C., Lin, S. C., Chiou, K. R., Wann, S. R., Lin, K. L., Kang, P. L., Mar, G. Y., Liu, C. P., Zhou, J. C., Choi, Y. J., Yoon, S. Z., Gordillo-Brenes, A., Fernandez-Zamora, M. D., Perez-Borrero, L., Arias-Verdu, M. D., Aguilar-Alonso, E., Herruzo-Aviles, A., Garcia-Delgado, M., Hinojosa-Perez, R., Curiel-Balsera, E., Rivera-Fernandez, R., Lesmes, S. P. Gómez, Rosario, L. E. De la Cruz, Hernández, A. Ansotegui, Herrera, A. N. García, Sanz, E. Regidor, Sánchez, M. J. Gómez, Hualde, J. Barado, Pascual, O. Agudo, León, J. P. Tirapu, Irazabal, J. M. Guergue, Pérez, A. González, Fernández, P. Alvarez, Amor, L. Lopéz, Albaiceta, G. Muñiz, Lesmes, S. P. Gómez, Rosario, L. E. De la Cruz, Hernández, A. Ansotegui, Sanz, E. Regidor, Sánchez, M. J. Gómez, Calvo, S. Aldunate, Herrera, A. N. García, Hualde, J. Barado, Pascual, O. Agudo, León, J. P. Tirapu, Corona, A., Ruffini, C., Spazzadeschi, A., Marrazzo, F., Gandola, A., Sciurti, R., Savi, C., Catena, E., Ke, M. W., Cheng, C. C., Huang, W. C., Chiang, C. H., Hung, W. T., Lin, K. C., Lin, S. C., Wann, S. R., Chiou, K. R., Tseng, C. J., Kang, P. L., Mar, G. Y., Liu, C. P., Bertini, P., De Sanctis, F., Guarracino, F., Bertini, P., Baldassarri, R., Guarracino, F., Buitinck, S. H., van der Voort, P. H. J., Oto, J., Nakataki, E., Tsunano, Y., Izawa, M., Tane, N., Onodera, M., Nishimura, M., Ghosh, S., Gupta, A., De Gasperi, A., Mazza, E., Limuti, R., Prosperi, M., Bissenova, N., Yergaliyeva, A., Talan, L., Yılmaz, G., Güven, G., Yoruk, F., Altıntas, N. D., Mukherjee, D. N., Agarwal, L. K., Mandal, K., Palomar, M., Balsera, B., Vallverdu, M., Martinez, M., Garcia, M., Castellana, D., Lopez, R., Barcenilla, F., Kaminsky, G. E., Carreño, R., Escribá, A., Fuentes, M., Gálvez, V., Del Olmo, R., Nieto, B., Vaquerizo, C., Alvarez, J., De la Torre, M. A., Torres, E., Bogossian, E., Nouer, S. Aranha, Salgado, D. Ribeiro, Brugger, S. Carvalho, Jiménez, G. Jiménez, Torner, M. Miralbés, Vidal, M. Vallverdú, Garrido, B. Balsera, Casals, X. Nuvials, Gaite, F. Barcenilla, Cabello, J. Trujillano, Martínez, M. Palomar, Doganci, M., Izdes, S., Besevli, S. Guzeldag, Alkan, A., Kayaaslan, B., Ramírez, C. Sánchez, Balcázar, L. Caipe, Santana, M. Cabrera, Viera, M. A. Hernández, Escalada, S. Hípola, Vázquez, C. F. Lübbe, Penichet, S. M. Marrero, Campelo, F. Artiles, López, M. A. De La Cal, Santana, P. Saavedra, Santana, S. Ruíz, Repessé, X., Artiguenave, M., Paktoris-Papine, S., Espinasse, F., Dinh, A., El Sayed, F., Charron, C., Géri, G., Vieillard-Baron, A., Marmanidou, K., Oikonomou, M., Nouris, C., Dimitroulakis, K., Soilemezi, E., Matamis, D., Ferré, A., Guillot, M., Teboul, J. L., Lichtenstein, D., Mézière, G., Richard, C., Monnet, X., Pham, T., Beduneau, G., Schortgen, F., Piquilloud, L., Zogheib, E., Jonas, M., Grelon, F., Runge, I., Terzi, N., Grangé, S., Barberet, G., Guitard, P. G., Frat, J. P., Constan, A., Chrétien, J. M., Mancebo, J., Mercat, A., Richard, J. C. M., Brochard, L., Prīdāne, S., Sabeļņikovs, O., Mojoli, F., Orlando, A., Bianchi, I., Torriglia, F., Bianzina, S., Pozzi, M., Iotti, G. A., Braschi, A., Beduneau, G., Pham, T., Schortgen, F., Piquilloud, L., Zogheib, E., Jonas, M., Grelon, F., Runge, I., Terzi, N., Grangé, S., Barberet, G., Guitard, P. G., Frat, J. P., Constan, A., Chrétien, J. M., Mancebo, J., Mercat, A., Richard, J. C. M., Brochard, L., Kondili, E., Psarologakis, C., Kokkini, S., Amargianitakis, V., Babalis, D., Chytas, A., Chouvarda, I., Vaporidi, K., Georgopoulos, D., Trapp, O., Kalenka, A., Mojoli, F., Orlando, A., Bianchi, I., Torriglia, F., Bianzina, S., Pozzi, M., Iotti, G. A., Braschi, A., Lozano, J. A. Benítez, Sánchez, P. Carmona, Francioni, J. E. Barrueco, Ferrón, F. Ruiz, Simón, J. M. Serrano, Spadaro, S., Karbing, D. S., Gioia, A., Moro, F., Corte, F. Dalla, Mauri, T., Volta, C. A., Rees, S. E., Petrova, M. V., Mohan, R., Butrov, A. V., Beeharry, S. D., Vatsik, M. V., Sakieva, F. I., Gobert, F., Yonis, H., Tapponnier, R., Fernandez, R., Labaune, M. A., Burle, J. F., Barbier, J., Vincent, B., Cleyet, M., Richard, J. C., Guérin, C., Shinotsuka, C. Righy, Creteur, J., Taccone, F. S., Törnblom, S., Nisula, S., Vaara, S., Poukkanen, M., Andersson, S., Pettilä, V., Pesonen, E., Xie, Z., Liao, X., Kang, Y., Zhang, J., Kubota, K., Egi, M., Mizobuchi, S., Hegazy, S., El-Keraie, A., El Sayed, E., El Hamid, M. Abd, Rodrigues, N. J., Pereira, M., Godinho, I., Gameiro, J., Neves, M., Gouveia, J., e Silva, Z. Costa, Lopes, J. A., Mckinlay, J., Kostalas, M., Kooner, G., Dudas, G., Horton, A., Kerr, C., Karanjia, N., Creagh-Brown, B., Forni, L., Yamazaki, A., Ganuza, M. Sanz, Molina, J. A. Martinez, Martinez, F. Hidalgo, Freile, M. T. Chiquito, Fernandez, N. Garcia, Travieso, P. Medrano, Bandert, A., Frithiof, R., Lipcsey, M., Smekal, D., Schlaepfer, P., Durovray, J. D., Plouhinec, V., Chiappa, C., Bellomo, R., Schneider, A. G., Mitchell, S., Durrant, J., Street, H., Dunthorne, E., Shears, J., Caballero, C. Hernandez, Hutchison, R., Schwarze, S., Ghabina, S., Thompson, E., Prowle, J. R., Kirwan, C. J., Gonzalez, C. A., Pinto, J. L., Orozco, V., Patiño, J. A., Garcia, P. K., Contreras, K. M., Rodriguez, P., Echeverri, J. E., GETGAG Working Group, JSEPTIC (Japanese Society of Education for Physicians and Trainees in Intensive Care) Clinical Trial Group, CAPCRI Study, for the ReVA Research Network and the PROVE Network Investigators, from the FROG ICU Investigators, The WIND study group, Plug Working Group, GETGAG/SEMICYUC, AKI Research Group, St George’s University of London, IPREA Study Group, FINNRESUSCI Study Group, PICS- HCPA: Programa Intrahospitalar de Combate à Sepse do Hospital de Clínicas de Porto Alegre, ENVIN-HELICS Study Group, ARIAM registry of adult cardiac surgery, The Rapid Diagnosis of Infections in the Critically Ill Team, Tokyo Womens Medical University, PLUG working group, PLUG Working Group, On behalf of Okayama Research Investigation Organizing Network (ORION)investigators, PS-ICU Group, Japan Septic Disseminated Intravascular Coagulation (JSEPTIC DIC) study group, Student Research Committee - Shiraz University of Medical Sciences, ARIAM-ANDALUCIA, The WIND study group, PLUG Working Group, The WIND study group, PLUG Working Group, and Plug working group
Published: 2016
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2. Regulation of mechanical stress-induced MMP-13 and ADAMTS-5 expression by RUNX-2 transcriptional factor in SW1353 chondrocyte-like cells

Author: Tetsunaga, T., Nishida, K., Furumatsu, T., Naruse, K., Hirohata, S., Yoshida, A., Saito, T., and Ozaki, T.
Published: 2011
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3. Migraine in patients with systemic lupus erythematosus is associated with reduced cerebral grey matter volume but not with measures of glial activation or anti-NR2 or anti-P antibodies

Author: Tjensvoll, A. B., Lauvsnes, M. B., Hirohata, S., Beyer, M. K., Greve, O. J., Kvivik, I., Kvaly, J. T., Harboe, E., Gransson, L. G., and Omdal, R.
Published: 2016
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4. Trichostatin A, a histone deacetylase inhibitor, suppresses synovial inflammation and subsequent cartilage destruction in a collagen antibody-induced arthritis mouse model

Author: Nasu, Y., Nishida, K., Miyazawa, S., Komiyama, T., Kadota, Y., Abe, N., Yoshida, A., Hirohata, S., Ohtsuka, A., and Ozaki, T.
Published: 2008
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5. Myocardial infarction caused by rheumatoid vasculitis: histological evidence of the involvement of T lymphocytes

Author: Takayanagi, M., Haraoka, H., Kikuchi, H., and Hirohata, S.
Published: 2003
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6. Bone marrow CD34+ progenitor cells from rheumatoid arthritis patients support spontaneous transformation of peripheral blood B cells from healthy individuals

Author: Hirohata, S., Yanagida, T., Nakamura, H., Yoshino, S., Tomita, T., and Ochi, T.
Published: 2000
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7. Increased differentiation of pre-plasmacytoid dendritic cells in the bone marrow of rheumatoid arthritis: 703782

Author: HIROHATA, S, YOSHIKAWA, H, YANAGIDA, T, and TOMITA, T
Published: 2012

8. CURCUMIN AND BAY 117085 ATTENUATES ADAMTS9 GENE EXPRESSION IN HUMAN CHONDROCYTES: H49

Author: Demircan, K, Hirohata, S, and Gündüz, E
Published: 2010

9. ADAMTS1 INDUCES APOPTOSIS ON ENDOTHELIAL CELLS: 1/06

Author: Hatipoglu, O F, Hirohata, S, Cilek, M Z, Inagaki, J, Ohtsuki, T, Yonezawa, T, Oohashi, T, Kusachi, S, and Ninomiya, Y
Published: 2010

10. ADAMTS1 GENE TRANSFER INHIBITS ANGIOGENESIS AND TUMOR GROWTH: 1/05

Author: Hirohata, S, Obika, M, Hatipoglu, F O, Cilek, M Z, Inagaki, J, Ohtsuki, T, Yonezawa, T, Oohashi, T, Kusachi, S, and Ninomiya, Y
Published: 2010

11. Enhanced expression of mRNA for Krüppel-like factor 5 in CD34+ cells of the bone marrow in rheumatoid arthritis

Author: Hirohata, S, Miura, Y, Tomita, T, and Yoshikawa, H
Published: 2009
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12. Clinical characteristics of cytomegalovirus infection in rheumatic diseases: multicentre survey in a large patient population

Author: Takizawa, Y., Inokuma, S., Tanaka, Y., Saito, K., Atsumi, T., Hirakata, M., Kameda, H., Hirohata, S., Kondo, H., and Kumagai, S.
Published: 2008

13. Autoimmune hepatitis in a patient with systemic lupus erythematosus

Author: Iwai, M., Harada, Y., Ishii, M., Tanaka, S., Muramatsu, A., Mori, T., Nakashima, T., Okanoue, T., and Hirohata, S.
Published: 2003
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14. Cytokine regulation of hemostatic property and IL-6 production of human endothelial cells

Author: Hashimoto, Y., Hirohata, S., Kashiwado, T., Itoh, K., and Ishii, H.
Published: 1992
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15. Differential regulation of Th1 responses and CD154 expression in human CD4+ T cells by IFN-α

Author: SHIBUYA, H., NAGAI, T., ISHII, A., YAMAMOTO, K., and HIROHATA, S.
Published: 2003

16. Inhibition of cyclin A gene expression in human B cells by an immunosuppressant mizoribine

Author: HIROHATA, S., NAKANISHI, K., and YANAGIDA, T.
Published: 2000

17. Human Th1 responses driven by IL-12 are associated with enhanced expression of CD40 ligand

Author: HIROHATA, S.
Published: 1999

18. Abnormal T cell responses to bacterial superantigens in Behçet's disease (BD)

Author: HIROHATA, S. and HASHIMOTO, T.
Published: 1998

19. Synthesis and radical polymerization of N, N-diethyl-α-fluoroacrylamide

Author: Sato, T, Hirohata, S, Fujimoto, T, and Seno, M
Published: 2001
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20. The novel liver X receptor beta agonist, ouabagenin, prevent arterial lipid deposition in SHRSP5/Dmcr rat

Author: Yamamoto, S., Satoh, I., Kakimoto, M., Fujii, M., Matsui, M., Takahashi, Y., Mirokuin, K., Ran, S., Tamura, S., Hirohata, S., and Watanabe, S.
Published: 2020
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21. Obeticholic acid ameliorates non-alcoholic steatohepatitis and atherosclerosis in SHRSP5/Dmcr rats

Author: Satoh, I., Yamamoto, S., Kakimoto, M., Fujii, M., Matsui, M., Takahashi, Y., Mirokuin, K., Ran, S., Hirohata, S., and Watanabe, S.
Published: 2020
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22. ROLE OF INTRATHECAL PRODUCTION OF IL-6 IN THE PATHOGENESIS OF CHRONIC PROGRESSIVE NEURO-BEHCET'S DISEASE.

Author: Hirohata, S. and Kikuchi, H.
Published: 2023
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23. The westernization of life style and atherosclerosis in Japan – the balance of EPA and AA

Author: Matsuo, N., Hayashi, K., Katou, Y., Hasegawa, M., Tanimoto, M., Fujiwara, T., Kagawa, K., Nakano, Y., Oonishi, N., Takaishi, A., Hirohata, S., and Ueeda, M.
Published: 2018
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24. Supplementation of Omega-3 PUFAs could improve long term prognosis after pci in patients without hyperlipidemia and diabetes

Author: Matsuo, N., Hayashi, K., Katou, Y., Hasegawa, M., Tanimoto, M., Fujiwara, T., Kagawa, K., Nakano, Y., Oonishi, N., Takaishi, A., Hirohata, S., and Ueeda, M.
Published: 2018
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25. Accuracy of anti-ribosomal P protein antibody testing for the diagnosis of neuropsychiatric systemic lupus erythematosus - An international meta-analysis

Author: Karassa, FB Afeltra, A Ambrozic, A Chang, DM De Keyser, F Doria, A Galeazzi, M Hirohata, S Hoffman, IEA and Inanc, M Massardo, L Mathieu, A Mok, CC Morozzi, G and Sanna, G Spindler, AJ Tzioufas, AG Yoshio, T Ioannidis, JPA
Abstract: Objective. To quantitatively evaluate the diagnostic accuracy of antibodies to ribosomal P proteins (anti-P) for neuropsychiatric systemic lupus erythematosus (NPSLE) in general, for psychosis, mood disorder, or both, and for other diffuse manifestations. Methods. This international meta-analysis combined standardized data from 1,537 lupus patients contributed by 14 research teams. Weighted estimation of sensitivity and specificity with fixed-effects and random-effects models, as well as summary receiver operating characteristic (SROC) curve analysis, was used to summarize test performance. The robustness of the overall estimates was examined in sensitivity analyses that included additional studies published up to November 1, 2004 in the Medline, EMBase, and Cochrane databases. Results. Combining the data from the 14 teams, the weighted sensitivity and specificity estimates for the diagnosis of NPSLE were 26% (95% confidence interval [95% CI] 15-42%) and 80% (95% CI 74-85%), respectively. For psychosis, mood disorder, or both, the sensitivity and specificity were 27% (95% CI 14-47%) and 80% (95% CI 74-85%), respectively. For other diffuse manifestations, the sensitivity was 24% (95% CI 12-42%), and the specificity was 80% (95% CI 73-85%). The proportion of patients with anti-P antibodies did not vary markedly across different presentations of NPSLE. Between-study heterogeneity was substantial, but the SROC curves were consistent with the weighted estimates. In further analyses that included another 24 published studies, only the sensitivity for psychosis and/or mood disorder was slightly improved, but it was still suboptimal (42% [95% Cl 30-53%]); the specificity remained essentially the same (81% [95% Cl 76-85%]). Conclusion. Anti-P antibody testing has limited diagnostic value for NPSLE, and it is not helpful in differentiating among various disease phenotypes.
Published: 2006

26. IL-6, IL-8, IP-10, MCP-1 and G-CSF are significantly increased in cerebrospinal fluid but not in sera of patients with central neuropsychiatric lupus erythematosus.

Author: Yoshio, T., Okamoto, H., Kurasawa, K., Dei, Y., Hirohata, S., and Minota, S.
Subjects: SYSTEMIC lupus erythematosus, INTERLEUKIN-6, INTERLEUKIN-8, CHEMOKINES, CEREBROSPINAL fluid, GRANULOCYTE-colony stimulating factor, MONOCYTE chemotactic factor
Abstract: Objective To determine whether the intrathecal concentrations of cytokines/chemokines are associated with, or influenced by, serum concentrations in patients with central neuropsychiatric systemic lupus erythematosus (NPSLE), and to ascertain whether the increased production of cytokines/chemokines intrathecally relative to serum levels is associated with the presence of central NPSLE. Methods 52 SLE patients (30 with central NPSLE and 22 with non-NPSLE), for whom the CSF and serum samples were obtained at the same time, were enrolled. 27 kinds of cytokine/chemokine concentrations other than IFN-α in the cerebrospinal fluid (CSF) and serum samples were measured by Bio-Plex Pro Assays. IFN-α concentration and anti-ribosomal P protein antibody (anti-P) titres in CSF and serum samples were measured by ELISA. Results The mean concentrations of IL-6, IL-8, IP-10, MCP-1, G-CSF and GM-CSF were higher in the CSF than in the sera, respectively, while the mean concentrations of other 22 cytokines/chemokines, including RANTES and IFN-α, in the CSF were much lower than those in the sera, respectively. Furthermore, the concentrations of IL-6, IL-8, IP-10, MCP-1 and G-CSF in the CSF of the 30 patients with NPSLE were significantly higher than in the 22 patients with non-NPSLE (p = 6.82 × 10−5, p = 0.00037, p = 0.0028, p = 0.00065, and p = 0.0001, respectively), while the concentration of GM-CSF in the CSF of the 30 patients with NPSLE was not significantly higher than in the 22 patients with non-NPSLE. Most importantly, the largest difference occurred in CSF IL-6 concentrations. A significant positive correlation between CSF anti-P titres and serum anti-P titres in 52 patients with SLE (r = 0.6316, p = 6.44 × 10−6) was found, while no significant positive correlation was observed between CSF levels and serum levels of each cytokine/chemokine in the 52 SLE patients. Conclusion In central NPSLE the production of IL-6, IL-8, IP-10, MCP-1 and G-CSF might take place in the central nervous system (CNS). These increased CSF cytokines/chemokines along with anti-P might have a prerequisite role in the pathogenesis of central NPSLE. [ABSTRACT FROM AUTHOR]
Published: 2016
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27. Association of a single nucleotide polymorphism in the SH2D1A intronic region with systemic lupus erythematosus.

Author: Furukawa, H, Kawasaki, A, Oka, S, Shimada, K, Matsui, T, Ikenaka, T, Hashimoto, A, Okazaki, Y, Takaoka, H, Futami, H, Komiya, A, Kondo, Y, Ito, S, Hayashi, T, Matsumoto, I, Kusaoi, M, Takasaki, Y, Nagai, T, Hirohata, S, and Setoguchi, K
Subjects: SYSTEMIC lupus erythematosus, NUCLEOTIDE sequence, AUTOIMMUNE diseases, GENETIC polymorphisms, LABORATORY mice
Abstract: SH2D1A, also known as signaling lymphocytic activation molecule (SLAM)-associated protein (SAP), is an adaptor protein. Recently, it was reported that SAP deficient mice were protected from systemic lupus erythematosus (SLE). In this study, we postulated SH2D1A gene to be a candidate susceptibility gene for SLE and analyzed its association with SLE. A case-control association study was conducted on 5 tag single nucleotide polymorphisms (SNPs) in SH2D1A region in 506 Japanese female SLE patients and 330 healthy female controls. The luciferase assay was performed to determine the functional role of the SNP associated with SLE. One SNP in the intron 2, rs2049995, showed association with SLE (p = 0.0110, odds ratio (OR) 1.97, 95% confidence interval (CI) 1.16–3.34, under the dominant model). The association of rs2049995 seemed to be stronger in the subset with the age of onset less than 20 years (p = 0.0067, OR 2.65, 95% CI 1.28–5.46). Functional evaluation of rs2049995 showed that reporter gene activity was increased 1.9-fold for the susceptible allele compared with the resistant allele. An intronic SNP of SH2D1A is associated with SLE. [ABSTRACT FROM AUTHOR]
Published: 2013
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28. Semi-Active Vibration Control with Harmonically Varying Damping (Performance Improvement of Base Isolation for SDOF System and Vibration Control of Coupled SDOF Systems).

Author: Hirohata, S., Iba, D., Nakamura, M., and Moriwaki, I.
Subjects: *BASE isolation system, *VIBRATION (Mechanics), *DAMPING (Mechanics), *ACTUATORS, *POWER resources, *ENERGY consumption, *GEOMETRIC rigidity
Abstract: This study demonstrates two types of semi-active vibration control with harmonically varying damping. The first one is performance upgrade of semi-active base isolation method for single-degree-of-freedom system and the other one is a semi-active vibration control method for parallel coupled single-degree-of-freedom system. Recent researches have demonstrated a new method for the utilization of variable damping. In those studies, the damping coefficient was harmonically controlled. Previous studies have confirmed vibration mitigation of a base-isolated structure by interference cancellation with the harmonically varying damping. However the results of previous studies had still room for improvement. Consequently, this study suggests a method for the performance augmentation. However, no such study considering the multi-degree-of-freedom system has been conducted. This paper presents the effect of the harmonically varying damping on the multi-degree-of-freedom system, especially; the influence on two structures in parallel with a variable damper between the structures is discussed. [ABSTRACT FROM AUTHOR]
Published: 2013
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29. Significant relationship between changes in brachial-ankle pulse wave velocity relative to blood pressure elevation and coronary artery disease.

Author: Komatsubara I, Inoue S, Koumoto R, Matano S, Kitawaki T, Hirohata S, Miyoshi T, Ogawa H, Shinohata R, and Kusachi S
Published: 2010
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30. Identification of autoantigens specific for systemic lupus erythematosus with central nervous system involvement.

Author: Iizuka, N., Okamoto, K., Matsushita, R., Kimura, M., Nagai, K., Arito, M., Kurokawa, M. S., Masuko, K., Suematsu, N., Hirohata, S., and Kato, T.
Subjects: ANTIGENS, SYSTEMIC lupus erythematosus, CENTRAL nervous system, PROTEOMICS, NEUROBLASTOMA, ELECTROPHORESIS, BIOLOGICAL transport
Abstract: Using proteomic analysis, we identified candidate autoantigens specific for central nervous system (CNS) involvement in systemic lupus erythematosus (SLE). Proteins, extracted from cultured human neuroblastoma cells, were separated both by SDS-PAGE (1-DE) and two-dimensional electrophoresis (2-DE), and transferred to membranes. Western blot analysis was performed using serum samples from 30 SLE patients with CNS involvement (CNS-Lupus) and from 30 SLE patients without CNS involvement (non-CNS-SLE). The detected autoantigens were identified using MALDI-TOF/TOF MS. On the 1-DE Western blot, we detected 32 antigenic bands in the serum samples from the CNS-Lupus patients. Among them, four bands were detected significantly more frequently in the CNS-Lupus patients than in the non-CNS-SLE patients. Three bands were detected in four or more of the CNS-Lupus patientsbut in only one or none of the non-CNS-SLE patients. We thus selected these seven bands for the next investigations. Next, we detected protein spots corresponding to the selected seven bands by 2-DE Western blot and identified four proteins. They are peroxiredoxin-4, ubiquitin carboxyl-terminal hydrolase isozyme L1, splicing factor arginine/serine-rich 3, and histone H2A type 1. These four candidate autoantigens for the anti-neuronal cell antibodies would be a useful marker for CNS-Lupus. [ABSTRACT FROM AUTHOR]
Published: 2010
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31. Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis.

Author: Ayada, K., Yokota, K., Hirai, K., Fujimoto, K., Kobayashi, K., Ogawa, H., Hatanaka, K., Hirohata, S., Yoshino, T., Shoenfeld, Y., Matsuura, E., and Oguma, K.
Subjects: HELICOBACTER pylori, CELLULAR immunity, ATHEROSCLEROSIS, LABORATORY mice, CELL migration, T cells
Abstract: Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe+/- ldlr+/- mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis. [ABSTRACT FROM AUTHOR]
Published: 2009

32. A prospective comparison of nursing home-acquired pneumonia with hospital-acquired pneumonia in non-intubated elderly.

Author: Maruyama, T., Niederman, M.S., Kobayashi, T., Kobayashi, H., Takagi, T., D'Alessandro-Gabazza, C.N., Fujimoto, H., Gil Bernabe, P., Hirohata, S., Nakayama, S., Nishikubo, K., Yuda, H., Yamaguchi, A., Gabazza, E.C., Noguchi, T., Takei, Y., and Taguchi, O.
Abstract: Summary: There are no prospective comparison of the etiology and clinical outcome between hospital-acquired pneumonia (HAP) and nursing home-acquired pneumonia (NHAP) in non-intubated elderly. This study prospectively evaluated the etiology of HAP and NHAP in non-intubated elderly. A prospective cohort study was carried out in a rural region of Japan where the population over 65 years of age represents 30% of the population. A total of 108 patients were enrolled. There were 33 patients with HAP and 75 with NHAP. Etiologic diagnosis was established in 78.8% of HAP and in 72% of NHAP patients. The most frequent pathogens were Chlamydophila pneumoniae followed by Streptococcus pneumoniae, Staphylococcus aureus and Influenza virus. The frequency of Streptococcus pneumoniae and Influenza virus was significantly higher, whereas the frequency of Staphylococcus aureus and Enterobacteriaceae was significantly lower in NHAP compared to HAP. Performance and nutritional status were significantly worse in patients with HAP than in those with NHAP. Hospital mortality was significantly lower in patients with NHAP compared to those with HAP. This study demonstrated that C. pneumoniae, Streptococcus pneumoniae, Staphylococcus aureus and Influenza virus are frequent causative agents of pneumonia in non-intubated elderly and that the responsible pathogens and clinical outcome differ between NHAP and HAP. [Copyright &y& Elsevier]
Published: 2008
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33. Association of cerebrospinal fluid anti-NR2 glutamate receptor antibodies with diffuse neuropsychiatric systemic lupus erythematosus.

Author: Arinuma Y, Yanagida T, and Hirohata S
Abstract: OBJECTIVE: To explore the association of antibodies directed against N-methyl-D-aspartate receptor subunit NR2 (anti-NR2) in cerebrospinal fluid (CSF) with neuropsychiatric manifestations in systemic lupus erythematosus (NPSLE). METHODS: Paired serum and CSF specimens were obtained from 56 patients with NPSLE (38 with diffuse psychiatric/neuropsychological syndromes [diffuse NPSLE] and 18 with neurologic syndromes or peripheral neuropathy [focal NPSLE]) and from 20 control patients with noninflammatory neurologic diseases. IgG anti-NR2 antibodies were measured by enzyme-linked immunosorbent assay using synthetic peptide containing the extracellular ligand-binding domain of NR2. The binding of affinity-purified anti-NR2 to human neuroblastoma cell line SK-N-MC was examined by flow cytometry. RESULTS: Purified anti-NR2 bound to the surface of SK-N-MC cells. Levels of anti-NR2 antibodies in CSF were significantly elevated in patients with diffuse NPSLE compared with levels in control patients or those with focal NPSLE, whereas there were no significant differences in serum anti-NR2 levels among the 3 groups. In 31 of the 38 patients with diffuse NPSLE (81.6%) and 8 of the 18 patients with focal NPSLE (44.4%), CSF anti-NR2 levels were more than 3 SD above the mean level in the control patients (P=0.0120 by chi-square test). CONCLUSION: These results indicate that anti-NR2 is a constituent of antineuronal antibodies and, more importantly, that anti-NR2 antibodies in CSF, but not in serum, are associated with diffuse NPSLE. [ABSTRACT FROM AUTHOR]
Published: 2008
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34. Higher incidence and serum levels of minor cardiac biomarker elevation in sirolimus-eluting stent (cypher) than bare metal stent implantations.

Author: Seitou T, Murakami M, Komatsubara I, Kawamura H, Yamamoto K, Hina K, Hirohata S, Shinohata R, Ninomiya Y, and Kusachi S
Published: 2008
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35. Association of augmentation index of radial pressure wave form with diurnal variation pattern of blood pressure in untreated patients with essential hypertension.

Author: Shinohata R, Nakatsu T, Yuki Y, Nishitani A, Mashima K, Toyonaga S, Ogawa H, Hirohata S, Usui S, Kitawaki T, and Kusachi S
Published: 2008
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36. Accuracy of anti-ribosomal P protein antibody testing for the diagnosis of neuropsychiatric systemic lupus erythematosus: an international meta-analysis.

Author: Karassa FB, Afeltra A, Ambrozic A, Chang D, De Keyser F, Doria A, Galeazzi M, Hirohata S, Hoffman IEA, Inanc M, Massardo L, Mathieu A, Mok CC, Morozzi G, Sanna G, Spindler AJ, Tzioufas AG, Yoshio T, and Ioannidis JPA
Abstract: OBJECTIVE: To quantitatively evaluate the diagnostic accuracy of antibodies to ribosomal P proteins (anti-P) for neuropsychiatric systemic lupus erythematosus (NPSLE) in general, for psychosis, mood disorder, or both, and for other diffuse manifestations. METHODS: This international meta-analysis combined standardized data from 1,537 lupus patients contributed by 14 research teams. Weighted estimation of sensitivity and specificity with fixed-effects and random-effects models, as well as summary receiver operating characteristic (SROC) curve analysis, was used to summarize test performance. The robustness of the overall estimates was examined in sensitivity analyses that included additional studies published up to November 1, 2004 in the Medline, EMBase, and Cochrane databases. RESULTS: Combining the data from the 14 teams, the weighted sensitivity and specificity estimates for the diagnosis of NPSLE were 26% (95% confidence interval [95% CI] 15-42%) and 80% (95% CI 74-85%), respectively. For psychosis, mood disorder, or both, the sensitivity and specificity were 27% (95% CI 14-47%) and 80% (95% CI 74-85%), respectively. For other diffuse manifestations, the sensitivity was 24% (95% CI 12-42%), and the specificity was 80% (95% CI 73-85%). The proportion of patients with anti-P antibodies did not vary markedly across different presentations of NPSLE. Between-study heterogeneity was substantial, but the SROC curves were consistent with the weighted estimates. In further analyses that included another 24 published studies, only the sensitivity for psychosis and/or mood disorder was slightly improved, but it was still suboptimal (42% [95% CI 30-53%]); the specificity remained essentially the same (81% [95% CI 76-85%]). CONCLUSION: Anti-P antibody testing has limited diagnostic value for NPSLE, and it is not helpful in differentiating among various disease phenotypes. [ABSTRACT FROM AUTHOR]
Published: 2006
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37. Significant correlation of recruitable coronary collateral blood flow determined by coronary wedge pressure with ST-segment elevation during coronary occlusion.

Author: Kamikawa S, Iwasaki K, Yamamoto K, Kusachi S, Hina K, Hirohata S, Murakami M, Hirota M, Murakami T, Shiratori Y, Kamikawa, Shigeshi, Iwasaki, Kohichiro, Yamamoto, Keizo, Kusachi, Shozo, Hina, Kazuyoshi, Hirohata, Satoshi, Murakami, Masaaki, Hirota, Minoru, Murakami, Takashi, and Shiratori, Yasushi
Published: 2005
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38. Elevated levels of soluble fractalkine in active systemic lupus erythematosus: potential involvement in neuropsychiatric manifestations.

Author: Yajima N, Kasama T, Isozaki T, Odai T, Matsunawa M, Negishi M, Ide H, Kameoka Y, Hirohata S, and Adachi M
Abstract: OBJECTIVE: To determine levels of the soluble form of the chemokine fractalkine (sFkn) and its receptor, CX(3)CR1, in patients with systemic lupus erythematosus (SLE) with neuropsychiatric involvement (NPSLE) and in SLE patients without neuropsychiatric involvement, and to assess their relationship with disease activity and organ damage. METHODS: Levels of sFkn in serum and cerebrospinal fluid (CSF) were measured by enzyme-linked immunosorbent assay. Expression of Fkn and CX(3)CR1 was quantified using real-time polymerase chain reaction. Surface expression of CX(3)CR1 on peripheral blood mononuclear cells (PBMCs) was determined by flow cytometry. Disease activity and organ damage were assessed using the SLE Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index, respectively. RESULTS: Serum sFkn levels were significantly higher in patients with SLE than in patients with rheumatoid arthritis (RA) or healthy controls. In addition, significant correlations between serum sFkn levels and the SLEDAI, the SLICC/ACR Damage Index, anti-double-stranded DNA and anti-Sm antibody titers, immune complex levels (C1q), and serum complement levels (CH50) were observed. Expression of CX(3)CR1 was significantly greater in PBMCs from patients with active SLE than in those from RA patients or healthy controls. Levels of sFkn were also significantly higher in CSF from untreated patients with newly diagnosed NPSLE than in SLE patients without neuropsychiatric involvement; treatment reduced both serum and CSF levels of sFkn in patients with SLE. CONCLUSION: Soluble Fkn and CX(3)CR1 may play key roles in the pathogenesis of SLE, including the neuropsychiatric involvement. Soluble Fkn is also a serologic marker of disease activity and organ damage in patients with SLE, and its measurement in CSF may be useful for the diagnosis of NPSLE and followup of patients with NPSLE. [ABSTRACT FROM AUTHOR]
Published: 2005
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39. ADAMTS-9 is synergistically induced by interleukin-1beta and tumor necrosis factor alpha in OUMS-27 chondrosarcoma cells and in human chondrocytes.

Author: Demircan K, Hirohata S, Nishida K, Hatipoglu OF, Oohashi T, Yonezawa T, Apte SS, and Ninomiya Y
Abstract: OBJECTIVE: To compare induction of the aggrecanases (ADAMTS-1, ADAMTS-4, ADAMTS-5, ADAMTS-8, ADAMTS-9, and ADAMTS-15) by interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in chondrocyte-like OUMS-27 cells and human chondrocytes, and to determine the mechanism of induction of the most responsive aggrecanase gene. METHODS: OUMS-27 cells were stimulated for different periods of time and with various concentrations of IL-1beta and/or TNFalpha. Human chondrocytes obtained from osteoarthritic joints and human skin fibroblasts were also stimulated with IL-1beta and/or TNFalpha. Total RNA was extracted, reverse transcribed, and analyzed by quantitative real-time polymerase chain reaction and Northern blotting. ADAMTS-9 protein was examined by Western blotting, and the role of the MAPK signaling pathway for ADAMTS9 induction in IL-1beta-stimulated OUMS-27 cells was investigated. RESULTS: IL-1beta increased messenger RNA (mRNA) levels of ADAMTS4, ADAMTS5, and ADAMTS9 but not ADAMTS1 and ADAMTS8. The fold increase for ADAMTS9 mRNA was greater than that for mRNA of the other aggrecanase genes. The increase of ADAMTS9 mRNA by IL-1beta stimulation was greater in chondrocytes than in fibroblasts. The combination of IL-1beta and TNFalpha had a synergistic effect, resulting in a considerable elevation in the level of ADAMTS9 mRNA. ADAMTS-9 protein was also induced in IL-1beta-stimulated OUMS-27 cells. The MAPK inhibitors SB203580 and PD98059 decreased ADAMTS9 up-regulation in OUMS-27 cells. CONCLUSION: ADAMTS9 is an IL-1beta- and TNFalpha-inducible gene that appears to be more responsive to these proinflammatory cytokines than are other aggrecanase genes. Furthermore, these cytokines had a synergistic effect on ADAMTS9. Together with the known ability of ADAMTS-9 to proteolytically degrade aggrecan and its potential to cleave other cartilage molecules, the data suggest that ADAMTS-9 may have a pathologic role in arthritis. [ABSTRACT FROM AUTHOR]
Published: 2005
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40. Anti-ribosomal P protein antibody in human systemic lupus erythematosus up-regulates the expression of proinflammatory cytokines by human peripheral blood monocytes.

Author: Nagai T, Arinuma Y, Yanagida T, Yamamoto K, and Hirohata S
Abstract: OBJECTIVE: Autoantibodies to ribosomal P proteins (anti-P antibodies) are detected in 12-16% of patients with systemic lupus erythematosus (SLE) and have been found to be associated with some manifestations of the disease, including lupus psychosis and hepatitis. Recent studies have disclosed that anti-P antibodies react with activated T cells but not with B cells, suggesting possible direct effects of anti-P antibodies on immune regulation. The present study was designed to explore the presence of the epitope recognized by anti-P antibodies on human peripheral blood monocytes. METHODS: Highly purified peripheral blood monocytes obtained from healthy donors were cultured with or without interferon-gamma (IFNgamma) in the presence of either anti-P antibodies purified by affinity chromatography from the sera of patients with SLE or control IgG. RESULTS: Flow cytometry analysis disclosed that fresh (day 0) monocytes did not express the ribosomal P epitope, whereas expression of the ribosomal P epitope was induced on annexin V-negative monocytes after activation through plastic adherence for 48 hours. More important, anti-P antibodies (compared with normal IgG or IgG from SLE patients devoid of anti-P antibodies) enhanced the production of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) by activated monocytes. Accordingly, anti-P antibodies also up-regulated the expression of TNFalpha and IL-6 messenger RNA in activated monocytes. Of note, F(ab')(2) fragments of anti-P antibodies, which do not result in Fcgamma receptor (FcgammaR) crosslinking, also effectively up-regulated the expression of TNFalpha and IL-6. CONCLUSION: These results indicate that human peripheral blood monocytes express the ribosomal P epitope upon activation, irrespective of induction of apoptosis. Moreover, the data suggest that anti-P antibodies might modify a variety of inflammatory responses through up-regulation of the expression of proinflammatory cytokines in monocytes, in a manner that does not involve FcgammaR crosslinking. [ABSTRACT FROM AUTHOR]
Published: 2005
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41. Differential regulation of Th1 responses and CD154 expression in human CD4+ T cells by IFN-α.

Author: SHIBUYA, H., NAGAI, T., ISHII, A., YAMAMOTO, K., and HIROHATA, S.
Subjects: TH1 cells, INTERFERONS, INTERLEUKIN-12
Abstract: SUMMARY Like interleukin (IL)-12, interferon (IFN)-α has been shown to play an important role in inducing human Th1 responses. Recent studies have shown that human Th1 responses driven by IL-12 are associated with enhanced expression of CD154. The present study examined the effects of IFN-α on CD154 expression in human CD4+ T cells, with special attention to the relationship with Th1 responses. Highly purified CD4+ T cells from healthy donors were stimulated with immobilized anti-CD3 with or without IFN-α and IL-12 in the complete absence of accessory cells. IFN-α suppressed CD154 protein and mRNA expression in CD4+ T cells at the initial phase of activation with immobilized anti-CD3, but enhanced it in the subsequent maturation phase irrespective of the presence of IL-12. By contrast, IFN-α by itself did not enhance IFN-γ production or mRNA expression in CD4+ T cells in the absence of IL-12 even in the presence of stimulation with anti-CD28, but enhanced it in the presence of IL-12. Accordingly, IFN-α enhanced IL-12Rβ2 mRNA expression in anti-CD3-stimulated CD4+ T cells. Neither IFN-α nor IL-12 influenced the stability of CD154 mRNA in anti-CD3-activated CD4+ T cells. These results indicate that IFN-α by itself enhances CD154 expression in CD4+ T cells independently of the induction of IFN-γ mRNA expression. The data also suggest that the optimal induction of human Th1 responses by IFN-α might require the presence of IL-12 and that the induction of Th1 responses and CD154 expression in human CD4+ T cells might be regulated through different mechanisms. [ABSTRACT FROM AUTHOR]
Published: 2003
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42. Efficacy of Rebamipide as Adjunctive Therapy in the Treatment of Recurrent Oral Aphthous Ulcers in Patients with Behçet's Disease: A Randomised, Double-Blind, Placebo-Controlled Study.

Author: Matsuda, T., Ohno, S., Hirohata, S., Miyanaga, Y., Ujihara, H., Inaba, G., Nakamura, S., Tanaka, S-i., Kogure, M., and Mizushima, Y.
Subjects: BEHCET'S disease, THRUSH (Mouth disease), UVEITIS
Abstract: Background: Behçet's disease (BD) is a recurrent inflammatory disease involving chronic recurrent oral aphthous ulcers (aphthae), uveitis, skin lesions and genital ulcers. We prospectively investigated the efficacy of rebamipide, a gastroprotective drug, against oral aphthous ulcers in BD patients. Methods: In a multicentre, double-blind, placebo-controlled study, 35 patients with BD, having as the main symptom oral aphthosis, were randomised to receive rebamipide 300 mg/day or placebo for 12 to 24 weeks between August 1994 and December 1996. Oral aphthosis must have occurred within 4 weeks prior to enrolment and must have been visible for at least 7 days during that time. Oral aphthae count and pain scores were recorded daily in a diary by the patients themselves. Monthly aphthae count and pain scores were defined as the sum of aphthae count and pain scores for a month, respectively. Investigators rated the global improvement in aphthae count and pain using a 6-point scale. The rate of change in monthly aphthae count and pain scores in the first 3 and last 3 months of treatment were assessed in patients with more severe symptoms whose aphthae count and pain score were >28 at baseline (trial entry). Results: The rate of moderate or marked improvement in aphthae count and pain was 36% (5 of 14 subjects) in the placebo group and 65% (11 of 17 subjects) in the rebamipide group. During months 2 to 6 of treatment, aphthae count tended to increase and reached a peak at month 4 in the placebo group but decreased in the rebamipide group. Pain score decreased to the same extent in both groups for [ABSTRACT FROM AUTHOR]
Published: 2003
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43. Antiribosomal P protein antibody in human systemic lupus erythematosus reacts specifically with activated T cells.

Author: Hirohata, S. and Nakanishi, K.
Subjects: *SYSTEMIC lupus erythematosus treatment, *RIBOSOMES, *T cells, *THERAPEUTICS
Abstract: We examined the presence of the epitope recognized by antiribosomal P protein antibody (anti-P) on the cell surface of human immunocompetent cells. Highly purified CD4+ and CD8+ T cells, and B cells from normal healthy individuals were reacted with affinity-purified IgG anti-P, and were stained with FITC-conjugated F(ab′)2, fragment goat anti-human IgG, followed by analysis on flow cytometry with gating for viable cells by propidium iodide staining. The presence of an epitope that is antigenically related to the carboxyl-terminal 22-amino-acid sequence of ribosomal P protein was not demonstrated on the surface of fresh CD4+ and CD8+ T cells, or fresh B cells. However, the expression of the ribosomal P epitope was induced on CD4+ and CD8+ T cells after activation with immobilized anti-CD3, whereas the epitope was not expressed on activated B cells. These results indicate that anti-P is an antilymphocyte antibody, which reacts specifically with activated T cells but not with resting T cells or B cells, suggesting possible direct effects of anti-P on the immune dysregulation in systemic lupus erythematosus. [ABSTRACT FROM AUTHOR]
Published: 2001
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44. Bone marrow CD34+ progenitor cells from rheumatoid arthritis patients support spontaneous transformation of peripheral blood B cells from healthy individuals.

Author: Hirohata, S., Yanagida, T., Nakamura, H., Yoshino, S., Tomita, T., and Ochi, T.
Subjects: BONE marrow, BLOOD cells, OSTEOARTHRITIS, EPSTEIN-Barr virus, RHEUMATOID arthritis, B cells
Abstract: We show that bone marrow (BM) CD34+ progenitor cells from rheumatoid arthritis (RA) patients have the capacity to support spontaneous transformation of peripheral blood B cells. CD34+ cells purified from BM blood from eight RA patients and eight osteoarthritis (OA) patients were expanded with granulocyte/macrophage colony stimulating factor (GM-CSF) for 4–6 weeks. GM-CSF-stimulated BM CD34+ cells from three of eight RA patients, but none from seven OA patients, gave rise to spontaneous transformation of highly purified B cells of Epstein-Barr virus (EBV)-seronegative healthy donors. GM-CSF-stimulated BM CD34+ cells from four of six RA patients and from one of four OA patients also supported the spontaneous transformation of peripheral blood B cells from EBV-seropositive healthy donors. All the transformed B cell lines were positive for EBV-DNA as determined by PCR. Neither GM-CSF-stimulated BM CD34+ cells alone nor highly purified B cells alone gave rise to spontaneously transformed B cell lines. These results suggest that the capacity of BM CD34+ cells to support survival of B cells might contribute to the pathogenesis of RA by sustaining abnormal B cell responses. [ABSTRACT FROM AUTHOR]
Published: 2000

45. Quantitative analysis of the gastric ulcer healing process using video endoscopic pseudocolor imaging systems.

Author: Tamada, F, Hirohata, S, Honsako, Y, Kumada, H, Kashio, Y, Konishi, M, Fujio, Y, Yamamoto, T, Miura, J, and Miyamoto, M
Published: 1995
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46. Time dependent alterations of serum matrix metalloproteinase-1 and metalloproteinase-1 tissue inhibitor after successful reperfusion of acute myocardial infarction.

Author: Hirohata, S., Kusachi, S., Murakami, M., Murakami, T., Sano, I., Watanabe, T., Komatsubara, I., Kondo, J., and Tsuji, T.
Abstract: Objective: To test the hypothesis that changes in serum matrix metalloproteinase-1 (MMP-1) and tissue inhibitors of metalloproteinase-1 (TIMP-1) after acute myocardial infarction reflect extracellular matrix remodelling and the infarct healing process.Patients: 13 consecutive patients with their first acute myocardial infarction who underwent successful reperfusion.Methods: Blood was sampled on the day of admission, and on days 2, 3, 4, 5, 7, 14, and 28. Serum MMP-1 and TIMP-1 were measured by one step sandwich enzyme immunoassay. Left ventricular volume indices were determined by left ventriculography performed four weeks after the infarct.Results: Serum concentrations of both MMP-1 and TIMP-1 changed over time. The average serum MMP-1 was more than 1 SD below the mean control values during the initial four days, increased thereafter, reaching a peak concentration around day 14, and then returned to the middle control range. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum MMP-1 on day 5, when it began to rise, and for the magnitude of rise in MMP-1 on day 5 compared to admission. Serum TIMP-1 at admission was more than 1 SD below the mean control value, and increased gradually thereafter, reaching a peak on around day 14. Negative correlations with left ventricular end systolic volume index and positive correlations with left ventricular ejection fraction were obtained for serum TIMP-1 on days 5 and 7, and for the magnitude of rise in TIMP-1 on days 5 and 7 compared to admission.Conclusions: Both MMP-1 and TIMP-1 showed significant time dependent alteration after acute myocardial infarction. Thus MMP-1 and TIMP-1 may provide useful information in evaluating the healing process as it affects left ventricular remodelling after acute myocardial infarction. [ABSTRACT FROM AUTHOR]
Published: 1997

47. Tenascin expression in endomyocardial biopsy specimens in patients with dilated cardiomyopathy: distribution along margin of fibrotic lesions.

Author: Tamura, A., Kusachi, S., Nogami, K., Yamanishi, A., Kajikawa, Y., Hirohata, S., and Tsuji, T.
Abstract: Objective: To examine the hypothesis that tenascin, an extracellular matrix glycoprotein, contributes to fibrotic changes in dilated cardiomyopathy.Methods: The localisation of tenascin in biopsy specimens of the hearts obtained from eight patients with dilated cardiomyopathy was examined using staining by the avidin-biotin-peroxidase complex method.Results: (1) Perimysium and endomysium. Although positive staining for tenascin was observed in the enlarged perimysium and endomysium in all patients, moderately intense staining was characteristically observed near the replacement fibrotic lesions. In the narrow perimysium and endomysium of the myocardium not containing replacement fibrotic lesions, tenascin was not present, as in the control specimens. (2) Replacement fibrotic lesions. Non-homogeneous positive staining for tenascin was detected in all replacement fibrotic lesions examined. Intense tenascin deposition was observed in the peripheral portion of the replacement fibrotic lesions. The tenascin staining observed in the small replacement fibrotic lesions was more intense than that in the large lesions.Conclusions: Tenascin contributes to the development of the fibrotic changes seen in the dilated cardiomyopathic heart. Its characteristic location, specifically the distribution along the margin of the fibrosis, suggests that fibrotic change is a continuous process in hearts with dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]
Published: 1996

48. Aberration properties of focused ion-beam induced by space charge effect.

Author: Hirohata, S., Kosugi, T., Sawaragi, H., Aihara, R., and Gamo, K.
Published: 1992
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49. Regulation of Human B Lymphocyte Responsiveness.

Author: Lipsky, P. E., Hirohata, S., Jelinek, D. F., McAnally, L., and Splawski, J. B.
Published: 1988
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50. Familial systemic lupus erythematosus: analysis of extended haplotypes of major histocompatibility complex antigens.

Author: Oguchi, H., Hashimoto, T., and Hirohata, S.
Published: 1995
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