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3. Discovery of a New Deeply Eclipsing SU UMa-Type Dwarf Nova, IY UMa (= TmzV85)

Author

Uemura, M., Kato, T., Matsumoto, K., Takamizawa, K., Schmeer, P., Jensen, L. T., Vanmunster, T., Novak, R., Martin, B., Pietz, J., Buczynski, D., Kinnunen, T., Moilanen, M., Oksanen, A., Cook, Lewis M., Watanabe, T., Maehara, H., and Itoh, H.

Subjects
Astrophysics
Abstract

We discovered a new deeply eclipsing SU UMa-type dwarf nova, IY UMa, which experienced a superoutburst in 2000 January. Our monitoring revealed two distinct outbursts, which suggest a superoutburst interval of ~800 d, or its half, and an outburst amplitude of 5.4 mag. From time-series photometry during the superoutburst, we determined a superhump and orbital period of 0.07588 d and 0.0739132 d, respectively., Comment: 5 pages, 3 figures, accepted by PASJ letter

Published
2000
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4. Worldwide Disparities in Recovery of Cardiac Testing 1 Year Into COVID-19

Author

Einstein, A, Hirschfeld, C, Williams, M, Vitola, J, Better, N, Villines, T, Cerci, R, Shaw, L, Choi, A, Dorbala, S, Karthikeyan, G, Lu, B, Sinitsyn, V, Ansheles, A, Kudo, T, Bucciarelli-Ducci, C, Norgaard, B, Maurovich-Horvat, P, Campisi, R, Milan, E, Louw, L, Allam, A, Bhatia, M, Sewanan, L, Malkovskiy, E, Cohen, Y, Randazzo, M, Narula, J, Morozova, O, Pascual, T, Pynda, Y, Dondi, M, Paez, D, Hinterleitner, G, Lu, Y, Xu, Z, Erinne, I, Shetty, M, Lopez-Mattei, J, Parwani, P, Goda, A, Shirka, E, Bouyoucef, S, Chelghoum, L, Mansouri, F, Medjahedi, A, Naili, Q, Ridouh, M, Alasia, D, Alberghina, L, Aramayo, N, Buchara, D, Busso, F, Bustos Rivadero, J, Camilletti, J, Campanelli, H, Castro, R, Daicz, M, del Riego, H, Dragonetti, L, Echazarreta, D, Erriest, J, Faccio, F, Facello, A, Gallegos, H, Geronazzo, R, Glait, H, Hasbani, V, Jager, V, Lewkowicz, J, Lotti, J, Maciel, N, Masoli, O, Mastrovito, E, Medus, M, Merani, M, Molteni, S, Montecinos, M, Parisi, G, Sueldo, C, Perez de Arenaza, D, Quintana, L, Radzinschi, A, Redruello, M, Rodriguez, M, Rojas, H, Acuna, A, Schere, D, Traverso, S, Vazquez, G, Zeffiro, S, Sakanyan, M, Beuzeville, S, Boktor, R, Crowley, M, Downie, D, Dwivedi, G, Elison, B, Farouque, O, Jasper, K, Joshi, S, Lee, J, Lee, K, Lui, E, Mcconachie, P, Meaker, J, Nandurkar, D, Neill, J, O'Rourke, E, O'Sullivan, P, Pandos, G, Premaratne, M, Prior, D, Rutherford, N, Saunders, C, Taubman, K, Tauro, A, Taylor, A, Theuerle, J, Thomas, P, Tow, J, Upton, A, Vamadevan, S, Wayne, V, Wegner, E, Wong, D, Younger, J, Beitzke, D, Feuchtner, G, Sommer, O, Weiss, K, Maroz-Vadalazhskaya, N, Tserakhau, U, Homans, F, Van De Heyning, C, Araujo, R, Soldat-Stankovic, V, Stankovic, S, Almeida, A, Anselmi, C, Azevedo, G, Bittencourt, M, Pianta, D, Cabeda, E, Carreira, L, Coelho, I, de Amorim Fernandes, F, de Lorenzo, A, Delgado, R, Erthal, F, Fernandes, F, Fernandes, J, Ferreira de Souza, T, Foppa, M, Matos Alves, W, Gontijo, C, Gottlieb, I, Grossman, G, Albernaz Siqueira, M, Nomura, C, Koga, K, Lima, R, Lopes, R, Marcal Filho, H, Masiero, P, Mastrocola, L, Menezes de Siqueira, M, Mesquita, C, Naves, D, Penna, F, Pinto, I, Rocha, T, Rocha, J, Rodrigues, A, Salioni, L, Sanches, A, Santos, M, Da Silva, L, Schvartzman, P, Matushita, C, Senra, T, Silva, M, Soares, C, Spiro, B, Suaide Silva, C, Torres, R, Monte, G, Vilela, A, Villa, A, Voss, T, Waltrick, R, Zapparoli, M, Naseer, H, Garcheva-Tsacheva, M, Ouattara, T, Thou, S, Varoeun, S, Abikhzer, G, Beanlands, R, Chetrit, M, Dabreo, D, Dennie, C, Friedrich, M, Hafez, M, Hanneman, K, Miller, R, Oikonomou, A, Roifman, I, Small, G, Tandon, V, Trivedi, A, White, J, Zukotynski, K, Alay, R, Concha, C, Massardo, T, Abad, P, Anzola, K, Arturo, H, Benitez, L, Cadena, A, Zamudio, C, Calderon, A, Gutierrez Villamil, C, Jaimes, C, Londono, J, Lopez, N, Merlano-Gaitan, S, Murgieitio-Cabrera, R, Valencia, M, Vergel, D, Santamaria, A, Solis, F, Batinic, T, Franceschi, M, Paar, M, Prpic, M, Felipe Batista, C, Cabrera, L, Peix, A, Pena, Y, Rochela Vazquez, L, Ntalas, I, Kaminek, M, Kincl, V, Lang, O, Abdulla, J, Bottcher, M, Busk, M, Geisler, U, Gormsen, L, Hansson, N, Hess, S, Hove, J, Jensen, L, Jensen, M, Kragholm, K, Ovrehus, K, Rasmussen, J, Ronnow Sand, N, Sondergaard, H, Zaremba, T, Speckter, H, Amores, N, Velez, M, Alrahman, T, Elsamad, S, Abdelfattah, A, Elkaffas, S, Hassan, M, Hussein, E, Ibrahim, A, Kandeel, A, Ali, M, Shaaban, M, Flores, C, Gomez Leiva, V, Liiver, A, Larikka, M, Uusitalo, V, Agostini, D, Berger, C, Dietz, M, Hyafil, F, Ohana, M, Prigent, K, Regaieg, H, Sarda-Mantel, L, H-Ici, D, Ayetey, H, Angelidis, G, Fragkaki, C, Fragkiadaki, C, Georgoulias, P, Koutelou, M, Kyrozi, E, Lama, N, Prassopoulos, V, Spartalis, M, Zaglavara, T, Gonzalez, C, Gutierrez, G, Maldonado, A, Martinez, Y, Kovacs, A, Szilveszter, B, Banthia, N, Bhat, V, Choudhury, P, Chowdekar, V, Christopher, J, Garg, T, Goyal, N, Gupta, R, Gupta, A, Hephzibah, J, Jain, S, Krupa, J, Kumar, P, Kumar, S, Lalchandani, A, Mishra, A, Mishra, V, Mohan, P, Ozair, A, Pandey, S, Parameswaran, R, Patel, C, Patel, T, Patel, S, Vimala, L, Kumar Sarangi, D, Sengupta, S, Sethi, A, Sharma, A, Sharma, P, Shrigiriwar, A, Singh, S, Singh, H, Sood, A, Verma, A, Vyas, A, Soeriadi, E, Bun, E, Hutomo, F, Syawaluddin, H, Yudistiro, R, Albadr, A, Assadi, M, Emami, F, Emami-Ardekani, A, Farzanehfar, S, Jafari, R, Manafi-Farid, R, Tajik, M, Arnson, Y, Fuchs, S, Goldkorn, R, Kennedy, J, Leitman, M, Shalev, A, Acampa, W, Albano, D, Alongi, P, Arnone, G, Assante, R, Baritussio, A, Bauckneht, M, Bianco, F, Bonfiglioli, R, Bovenzi, F, Bruno, I, Bruno, A, Busnardo, E, Califaretti, E, Casoni, R, Censullo, V, Chierichetti, F, Chiocchi, M, Cittanti, C, Clemente, A, Cuocolo, A, De Rimini, M, De Vincentis, G, Della Tommasina, V, Dellegrottaglie, S, Erba, P, Evangelista, L, Faggi, L, Faragasso, E, Florimonte, L, Frantellizzi, V, Gatti, M, Gaudiano, A, Gelardi, F, Gerali, A, Gimelli, A, Guglielmo, M, Leccisotti, L, Liga, R, Liguori, C, Longo, G, Maffione, M, Marcassa, C, Matassa, G, Mele, D, Mircoli, L, Paccagnella, A, Pacella, S, Padovano, F, Pellegrini, D, Pergola, V, Pugliese, L, Quartuccio, N, Rampin, L, Ricci, F, Rubini, G, Russo, V, Sambuceti, G, Scatteia, A, Sciagra, R, Spidalieri, G, Stefanelli, A, Tedeschi, C, Ventroni, G, Baugh, D, Madu, E, Aikawa, T, Asano, H, Fujimoto, S, Fujise, K, Fukushima, Y, Fukuyama, K, Ichikawa, Y, Ideguchi, R, Iguchi, N, Imai, M, Ishimura, H, Isobe, S, Ito, K, Izawa, Y, Kadokami, T, Kasai, T, Kato, T, Kawamoto, T, Kiryu, S, Kumita, S, Manabe, O, Maruno, H, Matsumoto, N, Miyagawa, M, Moroi, M, Nagamachi, S, Nakajima, K, Nakazato, R, Nanasato, M, Naya, M, Norikane, T, Ohta, Y, Otomi, Y, Otsuka, H, Oyama-Manabe, N, Saito, M, Sarai, M, Sato, J, Sato, D, Shiraishi, S, Takanami, K, Takehana, K, Taniguchi, Y, Teragawa, H, Tomizawa, N, Umeji, K, Wakabayashi, Y, Yamada, S, Yamazaki, S, Yoneyama, T, Rawashdeh, M, Dautov, T, Makhdomi, K, Abass, M, Garashi, M, Siraj, Q, Kalnina, M, Haidar, M, Komiagiene, R, Kviecinskiene, G, Vajauskas, D, Karim, N, Doucoure, M, Reichmuth, L, Samuel, A, Dieng, M, Naojee, A, Hernandez, E, Alducin Tellez, C, Alexanderson-Rosas, E, Barragan, E, Cabada, M, Calderon, D, Carvajal-Juarez, I, Esparza, J, Gama-Moreno, M, Quinto, V, Gonzalez, N, Herrera-Zarza, M, Meave, A, Medina Verdugo, J, Melendez, G, Morales Murguia, R, Navarro Quiroz, C, Ornelas, M, Preciado-Anaya, A, Preciado-Gutierrez, O, Puente, A, Salazar, A, Rosales Uvera, S, Rosales-Uvera, S, Serna Macias, J, Sierra-Galan, L, Tirado Alderete, J, Vallejo, E, Faraggi, M, Sereegotov, E, Ben Rais, N, Alaoui, N, Kyiphyu, T, Oo, S, Win, S, Zar, H, Ghimire, R, Neupane, M, Glaudemans, A, Slart, R, Verschure, D, Allen, B, Edmond, J, Mckenzie, C, Tie, S, Van Pelt, N, Worthington, K, Young, C, Soli, I, Kana, S, Onubogu, U, Sani, M, Braten, A, Jorgensen, A, Vassbotn, H, Al Dhuhli, H, Jawa, Z, Tag, N, Fatima, S, Imran, M, Younis, M, Saadullah, M, Malo, Y, Lenturut-Katal, D, Castillo, M, Ortellado, J, Akhter, A, Cader, F, Hussain, R, Khan, S, Mandal, T, Nasreen, F, An, Y, Cao, D, Gong, L, Hou, Y, Jia, C, Li, T, Li, C, Liu, H, Liu, W, Liu, J, Ng, M, Shi, H, Tang, C, Wang, X, Wang, Z, Wang, Y, Wu, J, Yi, Y, Yuan, L, Zhang, T, Zhang, L, Chavez, E, Cruz, C, Llontop, C, Morales, R, Abrihan, P, Bustos-Barroso, A, Duldulao-Ogbac, M, Eduarte, C, Obaldo, J, Quinon, A, San Juan, B, San Juan, C, Sauler-Gomez, M, Uy, M, Kostkiewicz, M, Kunikowska, J, Teresinska, A, Urbanik, T, Bettencourt, N, Fontes-Carvalho, R, Gavina, C, Goncalves, L, Macedo, F, Moreno, N, Sousa, C, Timoteo, A, Vidigal, M, Al Heidous, M, Ramanathan, S, Arnous, S, Aytani, S, Byrne, A, Gleeson, T, Kerins, D, O'Brien, J, Bang, J, Bom, H, Cheon, M, Cheon, G, Cho, S, Hong, C, Jeong, Y, Kang, W, Kang, Y, Kim, J, Oh, S, So, Y, Song, H, Won, K, Yoo, S, Mitevska, I, Vavlukis, M, Salobir, B, Stalc, M, Benedek, T, Pop, M, Stan, C, Dariy, O, Gagarina, N, Itskovich, I, Karalkin, A, Kokov, A, Marina, G, Migunova, E, Pospelov, V, Ryzhkova, D, Sayfullina, G, Sergienko, V, Shurupova, I, Vakhromeeva, M, Valiullina, N, Zavadovsky, K, Zhuravlev, K, Abazid, R, Al Garni, T, Alasnag, M, Aljizeeri, A, Amer, H, Amro, A, Hamdy, H, Smettei, O, Saranovic, D, Vlajkovic, M, Keng, F, See, J, Berecova, Z, Mistinova, J, Evbuomwan, O, Govender, N, Hack, J, Hadebe, B, Hlongwa, K, Kaplan, M, Lakhi, H, Milos, K, Modiselle, M, More, S, Muambadzi, N, Scholtz, L, Barreiro-Perez, M, Blanco, I, Broncano, J, Camarero, A, Casans-Tormo, I, De Haro, J, Flotats, A, Garcia, E, Mendiguchia, C, Jimenez-Heffernan, A, Leta, R, Diaz, J, Vega, L, Manovel-Sanchez, A, Monzonis, A, Patrut, B, Pubul, V, Perez, R, Zeidan, N, Nanayakkara, D, Suliman, A, Engblom, H, Murtadha, M, Ostenfeld, E, Simonsson, M, Alkadhi, H, Buechel, R, Burger, P, Grani, C, Kamani, C, Kawel-Bohm, N, Klaeser, B, Manka, R, Prior, J, Kaewchur, T, Khiewvan, B, Kositwattanarerk, A, Namwongprom, S, Thientunyakit, T, Sayman, H, Yuksel, M, Sebikali, M, Okello, E, Korol, P, Noverko, I, Satyr, M, Ahmad, T, Alfakih, K, Andrade, I, Buckingham, S, Bularga, A, Carpenter, J, Cole, G, Cusack, D, David, S, Davis, P, Fairbairn, T, Ghosh, A, Ramkumar, P, Hamilton, M, Haque, F, Hudson, B, Johnstone, A, Karthikeyan, V, Kay, M, Khan, M, Kitt, J, Low, C, Mcalindon, E, Mccreavy, D, Morrissey, B, Motwani, M, Na, D, Nicol, E, Patel, D, Rodrigues, J, Rofe, C, Schofield, R, Semple, T, Sheikh, A, Sinha, A, Subedi, D, Topping, W, Tweed, K, Underwood, S, Weir-Mccall, J, Zuhairy, H, Abbasi, T, Abohashem, S, Abramson, S, Al-Mallah, M, Kumar, M, Balmer-Swain, M, Berman, D, Bernheim, A, Bhatti, S, Biederman, R, Bieging, E, Bingham, S, Bloom, S, Blue, S, Borges, A, Branch, K, Bravo, P, Buddhe, S, Budoff, M, Bullock-Palmer, R, Cahill, M, Candela, C, Cao, J, Chatterjee, S, Chatzizisis, Y, Chaudhuri, N, Cheezum, M, Chelliah, A, Chen, T, Chen, M, Chen, L, Chokshi, A, Chung, J, Danciu, S, Desisto, W, Dilorenzo, M, Doukky, R, Duvall, W, Ferencik, M, Foster, C, Fuisz, A, Gannon, M, German, D, Gerson, M, Geske, J, Hage, F, Haider, A, Haider, S, Hamirani, Y, Hassen, K, Hendel, R, Henkel, J, Horgan, S, Hyun, M, Janardhanan, R, Jerome, S, Kalra, D, Kassop, D, Kinkhabwala, M, Kinzfogl, G, Koch, B, Koweek, L, Krepp, J, Kwon, Y, Layer, J, Lesser, J, Leung, S, Lisske, B, Magurany, K, Markowitz, J, Mccullough, B, Moalemi, A, Moffitt, C, Montanez, J, Moore, W, Morayati, S, Mossa-Basha, M, Mrsic, Z, Murthy, V, Nagpal, P, Nelson, K, Nijjar, P, O'Quinn, R, Passen, E, Patil, P, Pursnani, A, Quachang, N, Rabbat, M, Ranjan, P, Lozano, P, Schemmer, M, Seifried, R, Shah, N, Shah, A, Shanbhag, S, Sharma, G, Skotnicki, R, Sobczak, M, Soman, P, Sorrell, V, Srichai, M, Streeter, J, Strickland, L, Suliman, S, Tebyanian, N, Thomas, D, Thompson, R, Uretsky, S, Vallurupalli, S, Vandyck-Acquah, M, Verma, V, Weinstein, J, Wolinsky, D, Zareba, K, Zgaljardic, M, Beretta, M, Ferrando, R, Kapitan, M, Mut, F, Djuraev, O, Rozikhodjaeva, G, Vera, L, Duc, B, Nguyen, X, Hiep Nguyen, P, Einstein A. J., Hirschfeld C., Williams M. C., Vitola J. V., Better N., Villines T. C., Cerci R., Shaw L. J., Choi A. D., Dorbala S., Karthikeyan G., Lu B., Sinitsyn V., Ansheles A. A., Kudo T., Bucciarelli-Ducci C., Norgaard B. L., Maurovich-Horvat P., Campisi R., Milan E., Louw L., Allam A. H., Bhatia M., Sewanan L., Malkovskiy E., Cohen Y., Randazzo M., Narula J., Morozova O., Pascual T. N. B., Pynda Y., Dondi M., Paez D., Hinterleitner G., Lu Y., Xu Z., Hirschfeld C. B., Erinne I., Shetty M., Choi A., Lopez-Mattei J., Parwani P., Goda A., Shirka E., Bouyoucef S., Chelghoum L., Mansouri F., Medjahedi A., Naili Q., Ridouh M., Alasia D., Alberghina L., Aramayo N., Buchara D., Busso F. G., Bustos Rivadero J. J., Camilletti J., Campanelli H., Castro R. B., Daicz M., del Riego H., Dragonetti L., Echazarreta D., Erriest J., Faccio F., Facello A., Gallegos H., Geronazzo R., Glait H., Hasbani V., Jager V., Lewkowicz J. M., Lotti J., Maciel N., Masoli O., Mastrovito E., Medus M., Merani M. F., Molteni S., Montecinos M., Parisi G., Sueldo C. P., Perez de Arenaza D., Quintana L., Radzinschi A., Redruello M., Rodriguez M., Rojas H., Acuna A. R., Schere D., Traverso S., Vazquez G., Zeffiro S., Sakanyan M., Beuzeville S., Boktor R., Crowley M., Downie D. A., Dwivedi G., Elison B., Farouque O., Jasper K., Joshi S., Lee J., Lee K., Lui E., Mcconachie P., Meaker J., Nandurkar D., Neill J., O'Rourke E., O'Sullivan P., Pandos G., Premaratne M., Prior D., Rutherford N., Saunders C., Taubman K., Tauro A., Taylor A., Theuerle J., Thomas P., Tow J., Upton A., Vamadevan S., Wayne V., Wegner E. A., Wong D., Younger J., Beitzke D., Feuchtner G., Sommer O., Weiss K., Maroz-Vadalazhskaya N., Tserakhau U., Homans F., Van De Heyning C. M., Araujo R., Soldat-Stankovic V., Stankovic S., Almeida A., Anselmi C., Azevedo G. S. A., Bittencourt M. S., Pianta D. B., Cabeda E., Carreira L., Coelho I., de Amorim Fernandes F., de Lorenzo A., Delgado R., Erthal F., Fernandes F., Fernandes J., Ferreira de Souza T., Foppa M., Matos Alves W. F., Gontijo C., Gottlieb I., Grossman G., Albernaz Siqueira M. H., Nomura C. H., Koga K. H., Lima R., Lopes R., Marcal Filho H. H., Masiero P., Mastrocola L., Menezes de Siqueira M. E., Mesquita C., Naves D., Penna F., Pinto I., Rocha T., Rocha J. L., Rodrigues A., Salioni L., Sanches A., Santos M., Da Silva L. S., Schvartzman P., Matushita C. S., Senra T., Silva M., Soares C. E., Spiro B., Suaide Silva C. E., Torres R., Monte G. U., Vilela A., Villa A. V., Vitola J., Voss T., Waltrick R., Zapparoli M., Naseer H., Garcheva-Tsacheva M., Ouattara T. F., Thou S., Varoeun S., Abikhzer G., Beanlands R., Chetrit M., Dabreo D., Dennie C., Friedrich M., Hafez M. N., Hanneman K., Miller R., Oikonomou A., Roifman I., Small G., Tandon V., Trivedi A., White J., Zukotynski K., Alay R., Concha C., Massardo T., Abad P., Anzola K., Arturo H., Benitez L., Cadena A., Zamudio C. C., Calderon A., Gutierrez Villamil C. T., Jaimes C., Londono J. L., Lopez N., Merlano-Gaitan S., Murgieitio-Cabrera R., Valencia M., Vergel D., Santamaria A. Z., Solis F., Batinic T., Franceschi M., Paar M. H., Prpic M., Felipe Batista C. J., Cabrera L. O., Peix A., Pena Y., Rochela Vazquez L. M., Ntalas I., Kaminek M., Kincl V., Lang O., Abdulla J., Bottcher M., Busk M., Geisler U., Gormsen L. C., Hansson N., Hess S., Hove J., Jensen L. T., Jensen M. T., Kragholm K. H., Ovrehus K., Rasmussen J., Ronnow Sand N. P., Sondergaard H., Zaremba T., Speckter H., Amores N., Velez M. S., Alrahman T. A., Elsamad S. A., Abdelfattah A., Allam A., Elkaffas S., Hassan M., Hussein E., Ibrahim A., Kandeel A., Ali M. M., Shaaban M., Flores C., Gomez Leiva V. V., Liiver A., Larikka M., Uusitalo V., Agostini D., Berger C., Dietz M., Hyafil F., Ohana M., Prigent K., Regaieg H., Sarda-Mantel L., H-Ici D. O., Ayetey H., Angelidis G., Fragkaki C., Fragkiadaki C., Georgoulias P., Koutelou M., Kyrozi E., Lama N., Prassopoulos V., Spartalis M., Zaglavara T., Gonzalez C., Gutierrez G., Maldonado A., Martinez Y., Kovacs A., Szilveszter B., Banthia N., Bhat V., Choudhury P., Chowdekar V. S., Christopher J., Garg T., Goyal N. K., Gupta R. K., Gupta A., Hephzibah J., Jain S., Krupa J., Kumar P., Kumar S., Lalchandani A., Mishra A., Mishra V. D., Mohan P., Ozair A., Pandey S., Parameswaran R., Patel C., Patel T., Patel S., Vimala L. R., Kumar Sarangi D. P., Sengupta S., Sethi A., Sharma A., Sharma A. K., Sharma P., Shrigiriwar A., Singh S., Singh H., Sood A., Verma A., Vyas A., Soeriadi E. A., Bun E., Hutomo F., Syawaluddin H., Yudistiro R., Albadr A., Assadi M., Emami F., Emami-Ardekani A., Farzanehfar S., Jafari R., Manafi-Farid R., Tajik M., Arnson Y., Fuchs S., Goldkorn R., Kennedy J., Leitman M., Shalev A., Acampa W., Albano D., Alongi P., Arnone G., Assante R., Baritussio A., Bauckneht M., Bianco F., Bonfiglioli R., Bovenzi F., Bruno I., Bruno A., Busnardo E., Califaretti E., Casoni R., Censullo V., Chierichetti F., Chiocchi M., Cittanti C., Clemente A., Cuocolo A., De Rimini M. L., De Vincentis G., Della Tommasina V., Dellegrottaglie S., Erba P. A., Evangelista L., Faggi L., Faragasso E., Florimonte L., Frantellizzi V., Gatti M., Gaudiano A., Gelardi F., Gerali A., Gimelli A., Guglielmo M., Leccisotti L., Liga R., Liguori C., Longo G., Maffione M., Marcassa C., Matassa G., Mele D., Mircoli L., Paccagnella A., Pacella S., Padovano F., Pellegrini D., Pergola V., Pugliese L., Quartuccio N., Rampin L., Ricci F., Rubini G., Russo V., Sambuceti G., Scatteia A., Sciagra R., Spidalieri G., Stefanelli A., Tedeschi C., Ventroni G., Baugh D., Madu E., Aikawa T., Asano H., Fujimoto S., Fujise K., Fukushima Y., Fukuyama K., Ichikawa Y., Ideguchi R., Iguchi N., Imai M., Ishimura H., Isobe S., Ito K., Izawa Y., Kadokami T., Kasai T., Kato T., Kawamoto T., Kiryu S., Kumita S., Manabe O., Maruno H., Matsumoto N., Miyagawa M., Moroi M., Nagamachi S., Nakajima K., Nakazato R., Nanasato M., Naya M., Norikane T., Ohta Y., Otomi Y., Otsuka H., Oyama-Manabe N., Saito M., Sarai M., Sato J., Sato D., Shiraishi S., Takanami K., Takehana K., Taniguchi Y., Teragawa H., Tomizawa N., Umeji K., Wakabayashi Y., Yamada S., Yamazaki S., Yoneyama T., Rawashdeh M., Dautov T., Makhdomi K., Abass M., Garashi M., Siraj Q., Kalnina M., Haidar M., Komiagiene R., Kviecinskiene G., Vajauskas D., Karim N. 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Ahmad, T, Alfakih, K, Andrade, I, Buckingham, S, Bularga, A, Carpenter, J, Cole, G, Cusack, D, David, S, Davis, P, Fairbairn, T, Ghosh, A, Ramkumar, P, Hamilton, M, Haque, F, Hudson, B, Johnstone, A, Karthikeyan, V, Kay, M, Khan, M, Kitt, J, Low, C, Mcalindon, E, Mccreavy, D, Morrissey, B, Motwani, M, Na, D, Nicol, E, Patel, D, Rodrigues, J, Rofe, C, Schofield, R, Semple, T, Sheikh, A, Sinha, A, Subedi, D, Topping, W, Tweed, K, Underwood, S, Weir-Mccall, J, Zuhairy, H, Abbasi, T, Abohashem, S, Abramson, S, Al-Mallah, M, Kumar, M, Balmer-Swain, M, Berman, D, Bernheim, A, Bhatti, S, Biederman, R, Bieging, E, Bingham, S, Bloom, S, Blue, S, Borges, A, Branch, K, Bravo, P, Buddhe, S, Budoff, M, Bullock-Palmer, R, Cahill, M, Candela, C, Cao, J, Chatterjee, S, Chatzizisis, Y, Chaudhuri, N, Cheezum, M, Chelliah, A, Chen, T, Chen, M, Chen, L, Chokshi, A, Chung, J, Danciu, S, Desisto, W, Dilorenzo, M, Doukky, R, Duvall, W, Ferencik, M, Foster, C, Fuisz, A, Gannon, M, German, D, Gerson, M, Geske, 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J., Hirschfeld C., Williams M. C., Vitola J. V., Better N., Villines T. C., Cerci R., Shaw L. J., Choi A. D., Dorbala S., Karthikeyan G., Lu B., Sinitsyn V., Ansheles A. A., Kudo T., Bucciarelli-Ducci C., Norgaard B. L., Maurovich-Horvat P., Campisi R., Milan E., Louw L., Allam A. H., Bhatia M., Sewanan L., Malkovskiy E., Cohen Y., Randazzo M., Narula J., Morozova O., Pascual T. N. B., Pynda Y., Dondi M., Paez D., Hinterleitner G., Lu Y., Xu Z., Hirschfeld C. B., Erinne I., Shetty M., Choi A., Lopez-Mattei J., Parwani P., Goda A., Shirka E., Bouyoucef S., Chelghoum L., Mansouri F., Medjahedi A., Naili Q., Ridouh M., Alasia D., Alberghina L., Aramayo N., Buchara D., Busso F. G., Bustos Rivadero J. J., Camilletti J., Campanelli H., Castro R. B., Daicz M., del Riego H., Dragonetti L., Echazarreta D., Erriest J., Faccio F., Facello A., Gallegos H., Geronazzo R., Glait H., Hasbani V., Jager V., Lewkowicz J. M., Lotti J., Maciel N., Masoli O., Mastrovito E., Medus M., Merani M. F., Molteni S., Montecinos M., Parisi G., Sueldo C. P., Perez de Arenaza D., Quintana L., Radzinschi A., Redruello M., Rodriguez M., Rojas H., Acuna A. R., Schere D., Traverso S., Vazquez G., Zeffiro S., Sakanyan M., Beuzeville S., Boktor R., Crowley M., Downie D. A., Dwivedi G., Elison B., Farouque O., Jasper K., Joshi S., Lee J., Lee K., Lui E., Mcconachie P., Meaker J., Nandurkar D., Neill J., O'Rourke E., O'Sullivan P., Pandos G., Premaratne M., Prior D., Rutherford N., Saunders C., Taubman K., Tauro A., Taylor A., Theuerle J., Thomas P., Tow J., Upton A., Vamadevan S., Wayne V., Wegner E. A., Wong D., Younger J., Beitzke D., Feuchtner G., Sommer O., Weiss K., Maroz-Vadalazhskaya N., Tserakhau U., Homans F., Van De Heyning C. M., Araujo R., Soldat-Stankovic V., Stankovic S., Almeida A., Anselmi C., Azevedo G. S. A., Bittencourt M. S., Pianta D. B., Cabeda E., Carreira L., Coelho I., de Amorim Fernandes F., de Lorenzo A., Delgado R., Erthal F., Fernandes F., Fernandes J., Ferreira de Souza T., Foppa M., Matos Alves W. F., Gontijo C., Gottlieb I., Grossman G., Albernaz Siqueira M. H., Nomura C. H., Koga K. H., Lima R., Lopes R., Marcal Filho H. H., Masiero P., Mastrocola L., Menezes de Siqueira M. E., Mesquita C., Naves D., Penna F., Pinto I., Rocha T., Rocha J. L., Rodrigues A., Salioni L., Sanches A., Santos M., Da Silva L. S., Schvartzman P., Matushita C. S., Senra T., Silva M., Soares C. E., Spiro B., Suaide Silva C. E., Torres R., Monte G. U., Vilela A., Villa A. V., Vitola J., Voss T., Waltrick R., Zapparoli M., Naseer H., Garcheva-Tsacheva M., Ouattara T. F., Thou S., Varoeun S., Abikhzer G., Beanlands R., Chetrit M., Dabreo D., Dennie C., Friedrich M., Hafez M. N., Hanneman K., Miller R., Oikonomou A., Roifman I., Small G., Tandon V., Trivedi A., White J., Zukotynski K., Alay R., Concha C., Massardo T., Abad P., Anzola K., Arturo H., Benitez L., Cadena A., Zamudio C. C., Calderon A., Gutierrez Villamil C. T., Jaimes C., Londono J. L., Lopez N., Merlano-Gaitan S., Murgieitio-Cabrera R., Valencia M., Vergel D., Santamaria A. Z., Solis F., Batinic T., Franceschi M., Paar M. H., Prpic M., Felipe Batista C. J., Cabrera L. O., Peix A., Pena Y., Rochela Vazquez L. M., Ntalas I., Kaminek M., Kincl V., Lang O., Abdulla J., Bottcher M., Busk M., Geisler U., Gormsen L. C., Hansson N., Hess S., Hove J., Jensen L. T., Jensen M. T., Kragholm K. H., Ovrehus K., Rasmussen J., Ronnow Sand N. P., Sondergaard H., Zaremba T., Speckter H., Amores N., Velez M. S., Alrahman T. A., Elsamad S. A., Abdelfattah A., Allam A., Elkaffas S., Hassan M., Hussein E., Ibrahim A., Kandeel A., Ali M. M., Shaaban M., Flores C., Gomez Leiva V. V., Liiver A., Larikka M., Uusitalo V., Agostini D., Berger C., Dietz M., Hyafil F., Ohana M., Prigent K., Regaieg H., Sarda-Mantel L., H-Ici D. O., Ayetey H., Angelidis G., Fragkaki C., Fragkiadaki C., Georgoulias P., Koutelou M., Kyrozi E., Lama N., Prassopoulos V., Spartalis M., Zaglavara T., Gonzalez C., Gutierrez G., Maldonado A., Martinez Y., Kovacs A., Szilveszter B., Banthia N., Bhat V., Choudhury P., Chowdekar V. S., Christopher J., Garg T., Goyal N. K., Gupta R. K., Gupta A., Hephzibah J., Jain S., Krupa J., Kumar P., Kumar S., Lalchandani A., Mishra A., Mishra V. D., Mohan P., Ozair A., Pandey S., Parameswaran R., Patel C., Patel T., Patel S., Vimala L. R., Kumar Sarangi D. P., Sengupta S., Sethi A., Sharma A., Sharma A. K., Sharma P., Shrigiriwar A., Singh S., Singh H., Sood A., Verma A., Vyas A., Soeriadi E. A., Bun E., Hutomo F., Syawaluddin H., Yudistiro R., Albadr A., Assadi M., Emami F., Emami-Ardekani A., Farzanehfar S., Jafari R., Manafi-Farid R., Tajik M., Arnson Y., Fuchs S., Goldkorn R., Kennedy J., Leitman M., Shalev A., Acampa W., Albano D., Alongi P., Arnone G., Assante R., Baritussio A., Bauckneht M., Bianco F., Bonfiglioli R., Bovenzi F., Bruno I., Bruno A., Busnardo E., Califaretti E., Casoni R., Censullo V., Chierichetti F., Chiocchi M., Cittanti C., Clemente A., Cuocolo A., De Rimini M. L., De Vincentis G., Della Tommasina V., Dellegrottaglie S., Erba P. A., Evangelista L., Faggi L., Faragasso E., Florimonte L., Frantellizzi V., Gatti M., Gaudiano A., Gelardi F., Gerali A., Gimelli A., Guglielmo M., Leccisotti L., Liga R., Liguori C., Longo G., Maffione M., Marcassa C., Matassa G., Mele D., Mircoli L., Paccagnella A., Pacella S., Padovano F., Pellegrini D., Pergola V., Pugliese L., Quartuccio N., Rampin L., Ricci F., Rubini G., Russo V., Sambuceti G., Scatteia A., Sciagra R., Spidalieri G., Stefanelli A., Tedeschi C., Ventroni G., Baugh D., Madu E., Aikawa T., Asano H., Fujimoto S., Fujise K., Fukushima Y., Fukuyama K., Ichikawa Y., Ideguchi R., Iguchi N., Imai M., Ishimura H., Isobe S., Ito K., Izawa Y., Kadokami T., Kasai T., Kato T., Kawamoto T., Kiryu S., Kumita S., Manabe O., Maruno H., Matsumoto N., Miyagawa M., Moroi M., Nagamachi S., Nakajima K., Nakazato R., Nanasato M., Naya M., Norikane T., Ohta Y., Otomi Y., Otsuka H., Oyama-Manabe N., Saito M., Sarai M., Sato J., Sato D., Shiraishi S., Takanami K., Takehana K., Taniguchi Y., Teragawa H., Tomizawa N., Umeji K., Wakabayashi Y., Yamada S., Yamazaki S., Yoneyama T., Rawashdeh M., Dautov T., Makhdomi K., Abass M., Garashi M., Siraj Q., Kalnina M., Haidar M., Komiagiene R., Kviecinskiene G., Vajauskas D., Karim N. K. A., Doucoure M., Reichmuth L., Samuel A., Dieng M. L., Naojee A. S., Hernandez E. A., Alducin Tellez C. R., Alexanderson-Rosas E., Barragan E., Cabada M., Calderon D., Carvajal-Juarez I., Esparza J., Gama-Moreno M. G., Quinto V. G., Gonzalez N. C., Herrera-Zarza M. C., Meave A., Medina Verdugo J. G., Melendez G., Morales Murguia R. H., Navarro Quiroz C. S., Ornelas M., Preciado-Anaya A., Preciado-Gutierrez O. U., Puente A., Salazar A. R., Rosales Uvera S. G., Rosales-Uvera S., Serna Macias J. A., Sierra-Galan L., Sierra-Galan L. M., Tirado Alderete J. C., Vallejo E., Faraggi M., Sereegotov E., Ben Rais N., Alaoui N. I., Kyiphyu T., Oo S. T., Win S. M., Zar H., Ghimire R., Neupane M., Glaudemans A., Slart R., Verschure D., Allen B., Edmond J., Mckenzie C., Tie S., Van Pelt N., Worthington K., Young C., Soli I. A., Kana S., Onubogu U., Sani M., Braten A. T., Jorgensen A., Vassbotn H. -E., Al Dhuhli H., Jawa Z., Tag N., Fatima S., Imran M. B., Younis M. N., Saadullah M., Malo Y. H., Lenturut-Katal D., Castillo M., Ortellado J., Akhter A., Cader F. A., Hussain R., Khan S. R., Mandal T., Nasreen F., An Y., Cao D., Gong L., Hou Y., Jia C., Li T., Li C., Liu H., Liu W., Liu J., Ng M. -Y., Shi H., Tang C., Wang X., Wang Z., Wang Y., Wu J., Yi Y., Yuan L., Zhang T., Zhang L., Chavez E., Cruz C., Llontop C., Morales R., Abrihan P., Bustos-Barroso A., Duldulao-Ogbac M., Eduarte C., Obaldo J., Quinon A., San Juan B., San Juan C. J., Sauler-Gomez M. R., Uy M., Kostkiewicz M., Kunikowska J., Teresinska A., Urbanik T., Bettencourt N., Fontes-Carvalho R., Gavina C., Goncalves L., Macedo F., Moreno N., Sousa C., Timoteo A. T., Vidigal M. J., Al Heidous M., Ramanathan S., Arnous S., Aytani S., Byrne A., Gleeson T., Kerins D., O'Brien J., Bang J. -I., Bom H., Cheon M., Cheon G. J., Cho S. -G., Hong C. M., Jeong Y. H., Kang W. J., Kang Y. -K., Kim J. -Y., Oh S. W., So Y., Song H. -C., Won K. S., Yoo S. W., Mitevska I., Vavlukis M., Salobir B. G., Stalc M., Benedek T., Pop M., Stan C., Ansheles A., Dariy O., Gagarina N., Itskovich I., Karalkin A., Kokov A., Marina G., Migunova E., Pospelov V., Ryzhkova D., Sayfullina G., Sergienko V., Shurupova I., Vakhromeeva M., Valiullina N., Zavadovsky K., Zhuravlev K., Abazid R., Al Garni T., Alasnag M., Aljizeeri A., Amer H., Amro A., Hamdy H., Smettei O., Saranovic D. S., Vlajkovic M., Keng F., See J., Berecova Z., Mistinova J. P., Evbuomwan O., Govender N., Hack J., Hadebe B., Hlongwa K., Kaplan M., Lakhi H., Milos K., Modiselle M., More S., Muambadzi N., Scholtz L., Barreiro-Perez M., Blanco I., Broncano J., Camarero A., Casans-Tormo I., De Haro J., Flotats A., Garcia E., Mendiguchia C. G., Jimenez-Heffernan A., Leta R., Diaz J. L., Vega L. L., Manovel-Sanchez A., Monzonis A. M., Patrut B., Pubul V., Perez R. R., Zeidan N., Nanayakkara D., Suliman A., Engblom H., Murtadha M., Ostenfeld E., Simonsson M., Alkadhi H., Buechel R. R., Burger P., Grani C., Kamani C., Kawel-Bohm N., Klaeser B., Manka R., Prior J., Kaewchur T., Khiewvan B., Kositwattanarerk A., Namwongprom S., Thientunyakit T., Sayman H. B., Yuksel M., Sebikali M. J., Okello E., Korol P., Noverko I., Satyr M., Ahmad T., Alfakih K., Andrade I., Buckingham S., Bularga A., Carpenter J. -P., Cole G., Cusack D., David S., Davis P., Fairbairn T., Ghosh A., Ramkumar P. G., Hamilton M., Haque F., Hudson B., Johnstone A., Karthikeyan V. J., Kay M., Khan M. A., Kitt J., Low C. S., Mcalindon E., Mccreavy D., Morrissey B., Motwani M., Na D., Nicol E., Patel D., Rodrigues J., Rofe C., Schofield R., Semple T., Sheikh A., Sinha A., Subedi D., Topping W., Tweed K., Underwood S. R., Weir-Mccall J., Zuhairy H., Abbasi T., Abohashem S., Abramson S., Al-Mallah M., Kumar M. A., Balmer-Swain M., Berman D., Bernheim A., Bhatti S., Biederman R., Bieging E., Bingham S., Bloom S., Blue S., Borges A., Branch K., Bravo P., Buddhe S., Budoff M., Bullock-Palmer R., Cahill M., Candela C., Cao J., Chatterjee S., Chatzizisis Y., Chaudhuri N. R., Cheezum M., Chelliah A., Chen T., Chen M., Chen L., Chokshi A., Chung J., Danciu S., DeSisto W., Dilorenzo M., Doukky R., Duvall W., Ferencik M., Foster C., Fuisz A., Gannon M., German D., Gerson M., Geske J., Hage F., Haider A., Haider S., Hamirani Y., Hassen K., Hendel R., Henkel J., Horgan S., Hyun M., Janardhanan R., Jerome S., Kalra D., Kassop D., Kinkhabwala M., Kinzfogl G., Koch B., Koweek L., Krepp J., Kwon Y., Layer J., Lesser J., Leung S., Lisske B., Magurany K., Markowitz J., Mccullough B., Moalemi A., Moffitt C., Montanez J., Moore W., Morayati S., Mossa-Basha M., Mrsic Z., Murthy V., Nagpal P., Nelson K., Nijjar P., O'Quinn R., Passen E., Patil P., Pursnani A., Quachang N., Rabbat M., Ranjan P., Lozano P. R., Schemmer M., Seifried R., Shah N., Shah A., Shanbhag S., Sharma G., Skotnicki R., Sobczak M., Soman P., Sorrell V., Srichai M., Streeter J., Strickland L., Suliman S., Tebyanian N., Thomas D., Thompson R., Uretsky S., Vallurupalli S., Vandyck-Acquah M., Verma V., Villines T., Weinstein J., Wolinsky D., Zareba K., Zgaljardic M., Beretta M., Ferrando R., Kapitan M., Mut F., Djuraev O., Rozikhodjaeva G., Vera L., Duc B. D., Nguyen X. C., and Hiep Nguyen P. M.

Abstract

Background: The extent to which health care systems have adapted to the COVID-19 pandemic to provide necessary cardiac diagnostic services is unknown. Objectives: The aim of this study was to determine the impact of the pandemic on cardiac testing practices, volumes and types of diagnostic services, and perceived psychological stress to health care providers worldwide. Methods: The International Atomic Energy Agency conducted a worldwide survey assessing alterations from baseline in cardiovascular diagnostic care at the pandemic's onset and 1 year later. Multivariable regression was used to determine factors associated with procedure volume recovery. Results: Surveys were submitted from 669 centers in 107 countries. Worldwide reduction in cardiac procedure volumes of 64% from March 2019 to April 2020 recovered by April 2021 in high- and upper middle-income countries (recovery rates of 108% and 99%) but remained depressed in lower middle- and low-income countries (46% and 30% recovery). Although stress testing was used 12% less frequently in 2021 than in 2019, coronary computed tomographic angiography was used 14% more, a trend also seen for other advanced cardiac imaging modalities (positron emission tomography and magnetic resonance; 22%-25% increases). Pandemic-related psychological stress was estimated to have affected nearly 40% of staff, impacting patient care at 78% of sites. In multivariable regression, only lower-income status and physicians’ psychological stress were significant in predicting recovery of cardiac testing. Conclusions: Cardiac diagnostic testing has yet to recover to prepandemic levels in lower-income countries. Worldwide, the decrease in standard stress testing is offset by greater use of advanced cardiac imaging modalities. Pandemic-related psychological stress among providers is widespread and associated with poor recovery of cardiac testing.

Published
2022

5. Baseline bone turnover marker levels can predict change in bone mineral density during antiresorptive treatment in osteoporotic patients:the Copenhagen bone turnover marker study

Author

Bønløkke, S. E., Rand, M. S., Haddock, B., Arup, S., Smith, C. D., Jensen, J. E.B., Schwarz, P., Hovind, P., Oturai, P. S., Jensen, L. T., Møller, S., Eiken, P., Rubin, K. H., Hitz, M. F., Abrahamsen, B., Jørgensen, N. R., Bønløkke, S. E., Rand, M. S., Haddock, B., Arup, S., Smith, C. D., Jensen, J. E.B., Schwarz, P., Hovind, P., Oturai, P. S., Jensen, L. T., Møller, S., Eiken, P., Rubin, K. H., Hitz, M. F., Abrahamsen, B., and Jørgensen, N. R.

Abstract

Summary: Anti-resorptive osteoporosis treatment might be more effective in patients with high bone turnover. In this registry study including clinical data, high pre-treatment bone turnover measured with biochemical markers was correlated with higher bone mineral density increases. Bone turnover markers may be useful tools to identify patients benefitting most from anti-resorptive treatment. Introduction: In randomized, controlled trials of bisphosphonates, high pre-treatment levels of bone turnover markers (BTM) were associated with a larger increase in bone mineral density (BMD). The purpose of this study was to examine this correlation in a real-world setting. Methods: In this registry-based cohort study of osteoporosis patients (n = 158) receiving antiresorptive therapy, the association between pre-treatment levels of plasma C-telopeptide of type I Collagen (CTX) and/or N-terminal propeptide of type I procollagen (PINP) and change in bone mineral density (BMD) at lumbar spine, total hip, and femoral neck upon treatment was examined. Patients were grouped according to their pre-treatment BTM levels, defined as values above and below the geometric mean for premenopausal women. Results: Pre-treatment CTX correlated with annual increase in total hip BMD, where patients with CTX above the geometric mean experienced a larger annual increase in BMD (p = 0.008) than patients with CTX below the geometric mean. The numerical pre-treatment level of CTX showed a similar correlation at all three skeletal sites (total hip (p = 0.03), femoral neck (p = 0.04), and lumbar spine (p = 0.0003)). A similar association was found for PINP where pre-treatment levels of PINP above the geometric mean correlated with a larger annual increase in BMD for total hip (p = 0.02) and lumbar spine (p = 0.006). Conclusion: Measurement of pre-treatment BTM levels predicts osteoporosis patients’ response to antiresorptive treatment. Patients with high pre-treatment levels of CTX and/or PINP benef

Published
2022

17. RAAS and stress markers in acute ischemic stroke:preliminary findings

Author

Back, C., Thiesen, K L, Olsen, Karsten Skovgaard, Edvinsson, L, Jensen, L T, Larsen, V A, Iversen, H. K., Back, C., Thiesen, K L, Olsen, Karsten Skovgaard, Edvinsson, L, Jensen, L T, Larsen, V A, and Iversen, H. K.

Abstract

OBJECTIVES: Angiotensin II type 1 receptor blockade has neuroprotective effects in animal stroke models, but no effects in clinical stroke trials. We evaluated cerebral and peripheral changes in the renin angiotensin aldosterone system (RAAS) and stress responses in acute ischemic stroke patients.MATERIALS AND METHODS: Blood from a jugular and cubital vein was collected within 48 h of stroke onset, after 24 and 48 h, and renin, angiotensin I, angiotensin II, aldosterone, norepinephrine, epinephrine, and cortisol were measured. Post-stroke cubital vein samples were collected after 8 (4.7-10) months.RESULTS: The acute systolic blood pressure was significantly increased, 148 (141-168) vs 140 (130-147) mmHg post-stroke. Angiotensin I, renin and aldosterone levels were significantly lower, angiotensin II was unchanged, and ACE activity was higher in the acute phase compared to post-stroke. No differences in RAAS were detected between jugular and cubital plasma levels. Jugular venous plasma levels of epinephrine and cortisol were elevated in the acute phase compared to cubital levels (P < 0.05).CONCLUSION: Increased epinephrine and cortisol levels in the jugular vein blood may reflect a higher peripheral turnover. The observed changes in RAAS in the acute stroke phase are consistent with responses to increased blood pressure.

Published
2015

19. Survey of period variations of superhumps in su UMa-type dwarf novae

Author

Kato, T. Imada, A. Uemura, M. Nogami, D. Maehara, H. Ishioka, R. Baba, H. Matsumoto, K. Iwamatsu, H. Kubota, K. Sugiyasu, K. Soejima, Y. Moritani, Y. Ohshima, T. Ohashi, H. Tanaka, J. Sasada, M. Arai, A. Nakajima, K. Kiyota, S. Tanabe, K. Imamura, K. Kunitomi, N. Kunihiro, K. Taguchi, H. Koizumi, M. Yamada, N. Nishi, Y. Kida, M. Tanaka, S. Ueoka, R. Yasui, H. Maruoka, K. Henden, A. Oksanen, A. Moilanen, M. Tikkanen, P. Mika, A.H.O. Monard, B. Itoh, H. Dubovsky, P.A. Kudzej, I. Dancikova, R. Vanmunster, T. Pietz, J. Bolt, G. Boyd, D. Nelson, P. Krajci, T. Cook, L.M. Torii, K. Starkey, D.R. Shears, J. Jensen, L.-T. Masi, G. Hynek, T. Novák, R. Kocián, R. Král, L. Kučáková, H. Kolasa, M. Šťastný, P. Staels, B. Miller, I. Sano, Y. Ponthière, P.D.E. Miyashita, A. Crawford, T. Brady, S. Santallo, R. Richards, T. Martin, B. Buczynski, D. Richmond, M. Kern, J. Davis, S. Crabtree, D. Beaulieu, K. Davis, T. Aggleton, M. Morelle, E. Pavlenko, E.P. Andreev, M. Baklanov, A. Koppelman, M.D. Billings, G. Urbančok, L. Ögmen, Y. Heathcote, B. Gomez, T.L. Voloshina, I. Retter, A. Mularczyk, K. Złoczewski, K. Olech, A. Kedzierski, P. Pickard, R.D. Stockdale, C. Virtanen, J. Morikawa, K. Hambsch, F.-J. Garradd, G. Gualdoni, C. Geary, K. Omodaka, T. Sakai, N. Michel, R. Cárdenas, A.A. Gazeas, K.D. Niarchos, P.G. Yushchenko, A.V. Mallia, F. Fiaschi, M. Good, G.A. Walker, S. James, N. Douzu, K.-I. Julian II, W.M. Butterworth, N.D. Shugarov, S.Yu. Volkov, I. Chochol, D. Katysheva, N. Rosenbush, A.E. Khramtsova, M. Kehusmaa, P. Reszelski, M. Bedient, J. Liller, W. Pojmański, G. Simonsen, M. Stubbings, R. Schmeer, P. Muyllaert, E. Kinnunen, T. Poyner, G. Ripero, J. Kriebel, W.

Abstract

We systematically surveyed period variations of superhumps in SU UMa-type dwarf novae based on newly obtained data and past publications. In many systems, the evolution of the superhump period is found to be composed of three distinct stages: an early evolutionary stage with a longer superhump period, a middle stage with systematically varying periods, and a final stage with a shorter, stable superhump period. During the middle stage, many systems with superhump periods of less than 0.08 d show positive period derivatives. We present observational characteristics of these stages and give greatly improved statistics. Contrary to an earlier claim, we found no clear evidence for a variation of period derivatives among different superoutbursts of the same object. We present an interpretation that the lengthening of the superhump period is a result of the outward propagation of an eccentricity wave, which is limited by the radius near the tidal truncation. We interpret that late-stage superhumps are rejuvenated excitation of a 3:1 resonance when superhumps in the outer disk are effectively quenched. The general behavior of the period variation, particularly in systems with short orbital periods, appears to follow a scenario proposed in Kato, Maehara, and Monard (2008, PASJ, 60, L23). We also present an observational summary of WZ Sge-type dwarf novae. Many of them have shown long-enduring superhumps during a post-superoutburst stage having longer periods than those during the main superoutburst. The period derivatives in WZ Sge-type dwarf novae are found to be strongly correlated with the fractional superhump excess, or consequently with the mass ratio. WZ Sge-type dwarf novae with a long-lasting rebrightening or with multiple rebrightenings tend to have smaller period derivatives, and are excellent candidates for those systems around or after the period minimum of evolution of cataclysmic variables. © 2009. Astronomical Society of Japan.

Published
2009

21. Changes in calcitropic hormones, bone markers and insulin-like growth factor I (IGF-I) during pregnancy and postpartum:a controlled cohort study

Author

Møller, U K, Streym, S, Mosekilde, L, Heickendorff, L, Flyvbjerg, A, Frystyk, J, Jensen, L T, Rejnmark, L, Møller, U K, Streym, S, Mosekilde, L, Heickendorff, L, Flyvbjerg, A, Frystyk, J, Jensen, L T, and Rejnmark, L

Abstract

UNLABELLED: Pregnancy and lactation cause major changes in calcium homeostasis and bone metabolism. This population-based cohort study presents the physiological changes in biochemical indices of calcium homeostasis and bone metabolism during pregnancy and lactationINTRODUCTION: We describe physiological changes in calcium homeostasis, calcitropic hormones and bone metabolism during pregnancy and lactation.METHODS: We studied 153 women planning pregnancy (n=92 conceived) and 52 non-pregnant, age-matched female controls. Samples were collected prior to pregnancy, once each trimester and 2, 16 and 36 weeks postpartum. The controls were followed in parallel.RESULTS: P-estradiol (E2), prolactin and 1,25-dihydroxyvitamin D (1,25(OH)2D) increased (p<0.001) during pregnancy, whereas plasma levels of parathyroid hormone (P-PTH) and calcitonin decreased (p<0.01). Insulin-like growth factor I (IGF-I) was suppressed (p<0.05) in early pregnancy but peaked in the third trimester. Postpartum, E2 was low (p<0.05); prolactin decreased according to lactation status (p<0.05). 1,25(OH)2D was normal and IGF-I was again reduced (p<0.05). P-PTH and calcitonin increased postpartum. From early pregnancy, markers of bone resorption and formation rose and fall, respectively (p<0.001). From the third trimester, bone formation markers increased in association with IGF-I changes (p<0.01). Postpartum increases in bone turnover markers were associated with lactation status (p<0.001). During lactation, plasma phosphate was increased, whereas calcium levels tended to be decreased which may stimulate PTH levels during and after prolonged lactation.CONCLUSION: The increased calcium requirements in early pregnancy are not completely offset by increased intestinal calcium absorption caused by high 1,25(OH)2D since changes in bone markers indicated a negative bone balance. The rise in bone formation in late pregnancy may be initiated by a spike i

Published
2013

22. The antihypertensive effect of fermented milk in individuals with prehypertension or borderline hypertension

Author

Usinger, Lotte, Jensen, L T, Flambard, B, Linneberg, A, Ibsen, H, Usinger, Lotte, Jensen, L T, Flambard, B, Linneberg, A, and Ibsen, H

Abstract

Fermented milk (FM) with putative antihypertensive effect in humans could be an easy applicable lifestyle intervention against hypertension. The mode of action is supposed to be through active milk peptides, shown to possess in vitro ACE-inhibitory effect. Blood pressure (BP) reductions upto 23¿mm¿Hg have been reported in spontaneously hypertensive rats fed FM. Results from human studies of the antihypertensive effect are inconsistent. However, many studies suffer from methodological weaknesses, as insufficient blinding and the use of office BP measurements. We conducted a randomised, double-blind placebo-controlled study of the antihypertensive effect of Lactobacillus helveticus FM in 94 prehypertensive and borderline hypertensive subjects. The participants were randomised into three treatment groups with a daily intake of 150¿ml of FM, 300¿ml of FM or placebo (chemically acidified milk). The primary outcome was repeated 24-h ambulatory BP measurements. There were no statistically significant differences in the outcome between the groups (systolic BP (SBP), P=0.9; diastolic BP (DBP), P=0.2). However, the group receiving 300¿ml FM had reduced BP across the 8-week period in several readings, which could be compatible with a minor antihypertensive effect. Heart rate and lipids remained unchanged between groups. Hence, our study does not support earlier studies measuring office BP-measurements, reporting antihypertensive effect of FM. Based on straight performed 24-h ambulatory BP measurements, milk fermented with Lactobacillus helveticus does not posses significant antihypertensive effect.

Published
2010

23. Changes in cerebral blood flow after acetazolamide: an experimental study comparing near-infrared spectroscopy and SPECT

Author

Schytz, H W, Wienecke, T, Jensen, L T, Selb, J, Boas, D A, Ashina, M, Wienecke, Troels, Jensen, Lars Thorbjørn, Schytz, H W, Wienecke, T, Jensen, L T, Selb, J, Boas, D A, Ashina, M, Wienecke, Troels, and Jensen, Lars Thorbjørn

Abstract

Udgivelsesdato: 2009-Apr, BACKGROUND AND PURPOSE: It is important to find a reliable and bedside method, which can estimate the cerebral blood flow (CBF) of patients in clinical settings. Estimation of CBF by calculating a blood flow index (BFI) using continuous wave near-infrared spectroscopy (CW-NIRS) and indocyanine green (ICG) as an i.v. tracer has been proposed to be a feasible and promising method. To validate if the BFI method can detect relative changes in CBF we compared data with the established method (133)Xenon single photon emission computer tomography ((133)Xe-SPECT). METHODS: Ten healthy subjects were investigated before and after a bolus of acetazolamide. NIRS data were obtained using a multi source detector separation configuration in order to assess a corrected BFI (BFI(corr)) value, which attempts to eliminate contamination of skin blood flow. RESULTS: Data obtained showed no significant correlation between CBF changes measured by (133)Xe-SPECT and BFI(corr) (0.133, P = 0.732). After acetazolamide, a 49% increase in CBF was detected using the (133)Xe-SPECT method, whereas no changes in any ICG variables were observed after acetazolamide. CONCLUSION: The study shows that it is not possible to obtain reliable BFI data, which reflect changes in CBF after acetazolamide infusion, using the CW-NIRS and ICG method.

Published
2009

28. The aminoterminal propeptide of type III procollagen. Studies on physiology and pathophysiology

Author

Jensen, L T and Jensen, L T

Abstract

The aim of the present study was to examine the physiological basis for the clinical use of serum PIIINP as a marker of the deposition rate of type III collagen. The assumption was that the serum concentration of PIIINP would reflect the turnover of type III collagen and thus directly reflect the inflammatory response. For the study we assessed commercially available RIAs and optimised one of them. Porcine PIIINP was purified and compared with human PIIINP. The application of a gentle iodination procedure made it possible to perform tracer studies. An experimental model consisting of a thoracic duct-venous shunt in conscious pigs was developed. Double and triple isotope tracer techniques were used for kinetic studies in the animal model and in cultures of tubule cells. The rat model with the induction of granulation tissue was used to investigate catabolic states. The anabolic state was studied in humans receiving growth hormone therapy. We conclude: 1) That, for our purpose, the best method of determining PIIINP is the PIIINP RIA, owing to the profile of the substances determined. It was possible to improve the quality of the tracer and to increase sensitivity by changing the assay procedure. 2) That porcine PIIINP is similar to human PIIINP, therefore the human assay is suitable for studies in pigs. 3) That PIIINP most likely escapes from the extracellular space by bulk flow, similar to that of albumin. That the major part of the PIIINP synthesised is drained via the lymphatics. That intact PIIINP is not, or only to a minor extent, degraded through the lymphatics. Consequently, peak B is not a product of processes of the lymph system. 4) That in pigs intact PIIINP has a circulatory half-life of about 1 hour, and that it is degraded by at least two intermediary steps. The first step gives rises to peak B, which is found in an almost constant ratio to intact PIIINP. Peak B has a half-life of about 4 hours. Given steady state conditions peaks B and C (intact PIIIN

Published
1997

29. Long-term effects of intravenous 1 alpha (OH)D3 combined with CaCO3 and low-calcium dialysis on secondary hyperparathyroidism and biochemical bone markers in patients on chronic hemodialysis

Author

Brandi, L, Daugaard, H, Nielsen, P K, Jensen, L T, Egsmose, C, Olgaard, K, Brandi, L, Daugaard, H, Nielsen, P K, Jensen, L T, Egsmose, C, and Olgaard, K

Abstract

The effects of intravenous administration of 1 alpha-hydroxycholecalciferol [1 alpha (OH)D3] in combination with CaCO3 and 'low-calcium dialysis' (1.25 mmol/l) on plasma (p) parathyroid hormone (PTH) and biochemical bone markers (osteocalcin, alkaline phosphatase, procollagen type 1 c-terminal extension peptide) were examined in 54 patients on chronic hemodialysis with either normal or elevated PTH. Increasing doses of 1 alpha (OH)D3 were administered intravenously under careful control of p-Ca2+ and inorganic phosphate. Blood samples were obtained 1 week before the start of treatment and then every 2nd week. 20 patients with initially normal PTH levels (23.5 +/- 4.17 pg/ml) and 34 patients with initially elevated PTH levels (301 +/- 45 pg/ml) were followed for up to 88 weeks. The present investigation: demonstrated: (1) 'Low-calcium hemodialysis' (1.25 mmol/l) made it possible to use larger doses of CaCO3 and to reduce the doses of an aluminium-containing oral phosphate binder. A decrease in p-Ca2+ during dialysis was induced, and special care had to focus on the compliance to CaCO3, in order not to aggravate the secondary hyperparathyroidism. (2) The combination of 'low-calcium hemodialysis', CaCO3, and pulse intravenous 1 alpha (OH)D3 prevented the development of secondary hyperparathyroidism in patients with normal PTH levels and induced a long-term suppression of p-PTH (106 +/- 25 pg/ml, 88 weeks) in the patients with secondary hyperparathyroidism. By careful monitoring, severe hypercalcemia and hyperphosphatemia were avoided. There were no indications, clinically or biochemically, of development of adynamic bone disease. (3) Bone lesions were healed and a decrease of the bone mineral content in lumbar spine and femoral neck of patients with both normal and elevated PTH levels prevented. (4) The present results may suggest that PTH might be of influence on that regulation of procollagen type 1 c-terminal extension peptide.

Published
1996

30. Diffusional transport of the aminoterminal propeptide of type III procollagen in the interstitium of the globally ischaemic cat myocardium

Author

Høst, N B, Sejrsen, P, Jensen, L T, Haunsø, S, Høst, N B, Sejrsen, P, Jensen, L T, and Haunsø, S

Abstract

Local repair after acute myocardial infarction appears to be reflected by levels in serum of the aminoterminal propeptide of type III procollagen (serum-PIIINP). Furthermore, serum-PIIINP has recently been reported to provide information on prognosis after acute myocardial infarction. However, no attention has yet been paid to the resistance to diffusion offered by the myocardial interstitium. We determined the diffusion coefficient of PIIINP in the interstitium of the globally ischaemic interstitium of the cat (D'37) by means of a "true transient diffusion' method, and compared with the free diffusion in water (D37). D'37 (in cm2 s-1.10(-5) was 0.0157 +/- 0.0005 (mean +/- SEM) (n = 13), and D37 was 0.0624 +/- 0.0024 (n = 12). The mean diffusive progression during 20 min of the concentration profile of [125I]PIIINP into the tissue was calculated to be 0.19 mm. The D'37 of albumin is practically identical to the D'37 of PIIINP, and the myocardium offers a similar resistance to diffusion of PIIINP and albumin, as expressed from the ratio D37/D'37 of approximately 4 for both molecules. PIIINP has a molecular weight of 42,000 Da, is rod shaped and has an overall negative charge. These characteristics explain the similarity in diffusion coefficients of PIIINP and albumin, which has a molecular weight of 69,000 Da. Albumin is known to pass the membrane of the continuous capillaries of the heart, making it very likely that direct exchange of PIIINP between interstitium and capillary plasma can also occur. During one hour of interstitial diffusion PIIINP will have traversed a distance calculated tp correspond to 15-20 capillaries. Therefore, the results support the concept of serum-PIIINP as a direct marker of events taking place locally in the myocardium following acute myocardial infarction.

Published
1996

31. Insulin-like growth factor-I raises serum procollagen levels in children and adults with Laron syndrome

Author

Klinger, B, Jensen, L T, Silbergeld, A, Laron, Z, Klinger, B, Jensen, L T, Silbergeld, A, and Laron, Z

Abstract

OBJECTIVE: Recombinant IGF-I is now available for the treatment of GH insensitivity (Laron syndrome). We have determined the effects of IGF-I on soft connective tissue and bone metabolism in a group of patients with this disorder.PATIENTS AND DESIGN: Thirteen patients with Laron syndrome (LS) (8 children and 5 adults) were included in the study. The children with LS were treated with IGF-I for 3 years with daily doses of 150-200 micrograms/kg. The adult LS patients were treated for 9 months with daily doses of 50-120 micrograms/kg. Blood samples for procollagens were collected before, during and at the end of IGF-I treatment.MEASUREMENTS: Serum levels of the carboxyterminal propeptide of type I procollagen (PICP), the aminoterminal propeptide of type III procollagen (PIIINP) and of the pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) were determined before and during IGF-I administration.RESULTS: Untreated patients with LS had lower than normal serum levels of PICP and PIIINP for age. IGF-I treatment increased significantly the PIIINP levels in children from 7.2 +/- 2.8 (SD) to 12.5 +/- 2.2 micrograms/l (P < 0.001), and in adults from 2.7 +/- 1.0 to 8.4 +/- 3.6 micrograms/l (P < 0.001); serum PICP increased from 243 +/- 123 to 384 +/- 190 micrograms/l (P < 0.087) in children, and in adults from 43.4 +/- 8.1 to 135.8 +/- 41.9 micrograms/l (P < 0.001). ICTP levels in children increased from 9.7 +/- 3.7 to 14.3 +/- 5.9 micrograms/l (P < 0.001) and in adult patients levels increased from 3.6 +/- 0.9 to 5.5 +/- 2.2 micrograms/l (P < 0.001) during treatment and returned to basal values after stopping IGF-I administration.CONCLUSIONS: Low procollagen levels in untreated Laron syndrome patients and their rise during replacement therapy with IGF-I provide evidence that IGF-I plays an important role in bone and soft connective tissue metabolism and that serum procollagen may serve as a marker to r

Published
1996

32. The aminoterminal propeptide of type III procollagen provides new information on prognosis after acute myocardial infarction

Author

Høst, N B, Jensen, L T, Bendixen, P M, Jensen, S E, Koldkjaer, O G, Simonsen, E E, Høst, N B, Jensen, L T, Bendixen, P M, Jensen, S E, Koldkjaer, O G, and Simonsen, E E

Abstract

The aim of the study was to examine sequential changes in serum levels of the aminoterminal propeptide of type III procollagen (S-PIIINP) after acute myocardial infarction (AMI), and to assess the value of S-PIIINP as a predictor of outcome. The study group comprised 74 patients with AMI, and 24 patients in whom AMI was suspected but disproved. S-PIIINP changed characteristically after AMI, and in patients not receiving thrombolytic therapy or having cardiogenic shock, the changes correlated to peak enzyme values (r = 0.4, p < or = 0.03). S-PIIINP was higher at days 0 to 2 in nonsurviving AMI patients than in survivors (p < 0.05). With use of either the upper quartile for S-PIIINP at day 0 for nonsurviving AMI patients or the mean value of S-PIIINP in a normal population plus 2 SDs as a cutoff, the predictive value of a negative test ranged from 0.79 to 0.87 at days 0 to 2, and the predictive value of a positive test ranged from 0.39 to 0.67. Thus, S-PIIINP on admission and for the following few days after AMI is higher in patients with poor outcome.

Published
1995

33. Effect on collagen metabolism of thrombolytic therapy with tissue-plasminogen activator. A randomized, placebo-controlled study

Author

Høst, N B, Stoltenberg, M B, Jensen, L T, Larsen, O G, Aurup, P, Høst, N B, Stoltenberg, M B, Jensen, L T, Larsen, O G, and Aurup, P

Abstract

This paper assesses alterations in collagen metabolism following thrombolytic therapy of acute myocardial infarction with tissue-plasminogen activator. Sequential serum measurements of the amino-terminal propeptide of type III procollagen (S-PIIINP) and the carboxyterminal propeptide of type I collagen (S-PICP) in patients suspected of acute myocardial infarction randomized to tissue-plasminogen activator or placebo were used. S-PIIINP increased at 3 h in patients with acute myocardial infarction treated with tissue-plasminogen activator (P < 0.05). S-PIIINP was higher in patients treated with tissue-plasminogen activator compared with placebo-treated patients at 3 and 6 h (P < 0.05). S-PICP decreased independently of therapy and diagnosis. Tissue-plasminogen activator, therefore, induces breakdown of collagen, some of which is located in the wall of atheromatous arteries. Vascular patency following thrombolytic therapy may partly be mediated by breakdown of thrombogenic collagen in the vessel wall. The findings may suggest a role for S-PIIINP as a non-invasive indicator of the risk of reocclusion.

Published
1995

34. Collagen metabolism in obesity:the effect of weight loss

Author

Rasmussen, M H, Jensen, L T, Andersen, T, Breum, L, Hilsted, J, Rasmussen, M H, Jensen, L T, Andersen, T, Breum, L, and Hilsted, J

Abstract

OBJECTIVE: To investigate the impact of obesity, fat distribution and weight loss on collagen turnover using serum concentrations of the carboxyterminal propeptide of type I procollagen (S-PICP) and the aminoterminal propeptide of type III pro-collagen (S-PIIINP) as markers for collagen turnover.DESIGN: Blood samples were obtained once at baseline, and after 8 and 16 weeks of dietary treatment (5.0 MJ/day diet).SETTING: Outpatient clinic of Hvidovre University Hospital.MAIN OUTCOME MEASURES: S-PICP, S-PIIINP, fat distribution and weight loss.RESULTS: S-PIIINP was associated with body weight (r = 0.37; P = 0.004), height (r = 0.27; P = 0.04), waist circumference (r = 0.35; P = 0.007), as well as with WHR (r = 0.33; P = 0.01) and was inversely correlated to age (r = -0.40; P = 0.002). Compared with randomly selected controls from a large pool of healthy volunteers, the obese patients had elevated S-PIIINP values before as well as during weight loss, whereas S-PICP levels were within the normal range and did not correlate with any anthropometric measures. The average weight loss after 16 weeks dietary treatment was 8.1 kg (s.d. = 0.8). S-PIIINP decreased during the 16 weeks of energy restriction (P < 0.05) and changes in S-PIIINP was correlated to body weight loss (r = 0.32; P < 0.05) and to changes in waist circumference (r = 0.34; P < 0.05) as well as changes in WHR (r = 0.30; P < 0.05).CONCLUSION: S-PIIINP is elevated in obesity and associated with body fat distribution, suggesting an increased turnover of type III collagen related to obesity in general and to abdominal obesity in particular. S-PIIINP levels decreases during weight loss in obese subjects, whereas S-PICP levels seems un-related to obesity and weight loss.

Published
1995

35. Collagen markers in peritoneal dialysis patients

Author

Graff, J, Joffe, P, Fugleberg, S, Jensen, L T, Graff, J, Joffe, P, Fugleberg, S, and Jensen, L T

Abstract

Possible relationships between the dialysate-to-plasma creatinine equilibration ratio (D/Pcreatinine 4 hour), duration of peritoneal dialysis treatment, number of peritonitis episodes, and mass appearance rates of three connective tissue markers [carboxyterminal propeptide of type I procollagen (PICP), aminoterminal propeptide of type III procollagen (PIIINP), and carboxyterminal telopeptide of type I collagen (ICTP)] were studied in 19 nondiabetic peritoneal dialysis patients. The absence of correlation between the mass appearance rates of the markers and the duration of dialysis treatment as well as the number of peritonitis episodes supports the concept that peritoneal dialysis does not cause persistent changes in the deposition and degradation rates of collagen. A correlation between the D/Pcreatinine 4 hr and the PICP mass appearance rates was found. Since it is unlikely that transperitoneal transport alone is responsible for the appearance of PICP in dialysate, this might reflect an association between a large peritoneal surface area and the amount of submesothelial connective tissue.

Published
1995

36. Collagen derived serum markers in carcinoma of the prostate

Author

Rudnicki, M, Jensen, L T, Iversen, P, Rudnicki, M, Jensen, L T, and Iversen, P

Abstract

Three new collagen markers deriving from the collagenous matrix, e.g. carboxyterminal propeptide of type I procollagen (PICP), carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP), and aminoterminal propeptide of type III procollagen (PIIINP) were used for the diagnose of prostatic bone metastases. Blood samples were obtained prior to biopsy or TURP. Serum PICP, PIIINP and ICTP were measured with commercial available RIAs and PSA by IRMA. Serum PSA was increased in patients with local prostatic cancer compared with patients with hyperplasia (p < 0.05). The level of PIIINP, ICTP, and PICP did not differ between these two groups. In patients with metastatic prostatic cancer all five markers were increased compared to the level measured in patients with localized cancer (p < 0.0001). All variables showed a significant positive relationship with alkaline phosphatase. The sensitivity ranged from 0.53 to 0.62 and specificity from 0.91 to 0.95. The sensitivity for alkaline phosphatase and PSA was 0.69 and 0.66 and specificity 0.91 and 0.68, respectively.

Published
1995

37. Type I procollagen propeptide in patients on CAPD:its relationships with bone histology, osteocalcin, and parathyroid hormone

Author

Joffe, P, Heaf, J G, Jensen, L T, Joffe, P, Heaf, J G, and Jensen, L T

Abstract

Serum procollagen type I carboxyterminal propeptide (PICP) has been shown to be a useful marker of bone formation in patients undergoing haemodialysis. However, PICP levels has not been evaluated in depth in patients maintained on continuous ambulatory peritoneal dialysis (CAPD). Therefore serum and dialysate levels of PICP, its peritoneal clearance (Clp), mass transfer (MTp), and its possible relationship with osteocalcin, parathyroid hormone (PTH), and bone histomorphometry were studied in a group of CAPD patients. Serum PICP was just above the normal range with significant amounts detected in the dialysate but no correlations were found between levels of serum PICP, dialysate PICP, and Clp-PICP. One patient with systemic lupus and osteitis fibrosa had extraordinarily high serum and dialysate levels of PICP. The patient later developed sclerosing peritonitis. No associations were seen between serum PICP and Clp-PICP and any of the 18 bone histomorphometric parameters evaluated. Dialysate level of PICP correlated negatively with mineral appositional rate (r = -0.62, P < 0.01) and mineralization lag time (r = 0.64, P < 0.01). MTp-PICP correlated positively with mineral appositional rate (r = 0.65, P < 0.01). Serum osteocalcin and serum PTH levels did not correlate to serum, dialysate, Clp or MTp measurements of PICP. These results suggest that measurements of PICP in CAPD patients do not give substantial information as an non-invasive marker of bone histology.

Published
1995

38. Selection of Mycoplasma hominis PG21 deletion mutants by cultivation in the presence of monoclonal antibody 552

Author

Jensen, L T, Ladefoged, S, Birkelund, S, Christiansen, G, Jensen, L T, Ladefoged, S, Birkelund, S, and Christiansen, G

Abstract

Three mutants of Mycoplasma hominis PG21 were isolated and shown to contain alterations in the size of a repeat-containing gene encoding a surface-localized 135-kDa antigen designated Lmp1. The mutants were isolated by cultivating M. hominis for a 3-month period in the presence of Lmp1-specific monoclonal antibody (MAb) 552. The epitope for MAb 552 was localized at the repeated part of the protein. The gene encoding Lmp1 is part of a transcriptional complex that contains 9.5 direct repeats of 471 bp each. Pure cultures of mutant strains were obtained by subcloning, and three mutants were characterized. The mutants showed deletions of a various number of repeats. The deletions were accompanied by a decrease in size of the proteins. With increasing size of deletions, agglutination and growth inhibition by MAb 552 became less pronounced. Spontaneous aggregation of the mutant M. hominis cells in culture medium was, however, increased, indicating that the repeated elements may be of importance for repulsion of the cells.

Published
1995

39. The carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen in serum as a marker of bone resorption:the effect of nandrolone decanoate and hormone replacement therapy

Author

Hassager, C, Jensen, L T, Pødenphant, J, Thomsen, K, Christiansen, C, Hassager, C, Jensen, L T, Pødenphant, J, Thomsen, K, and Christiansen, C

Abstract

Carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP) in serum has recently been proposed as a new biochemical marker of bone resorption. In the present study we compared serum ICTP with radiopharmaceutical and histomorphometric measurements of bone turnover in postmenopausal women with mild osteoporosis, and assessed the effect of hormone replacement therapy (HRT) (2 mg 17 beta-estradiol plus 1 mg norethisterone daily) and anabolic steroid therapy (50 mg nandrolone decanoate (ND) i.m. every 3 weeks) on serum ICTP in two double-blind placebo-controlled studies with 55 to 75-year-old women. Serum ICTP measured by radioimmunoassay (RIA) correlated significantly with the 24-hour whole body retention of 99m-technetium diphosphonate (Rho = 0.47, P < 0.001, n = 66), but not with histomorphometric measurements of bone turnover in iliac crest biopsies. One year of HRT (n = 16) versus placebo (n = 15) did not produce significant changes in serum ICTP. Compared with placebo (n = 17), 1 year of ND (n = 19) produced an increase in serum ICTP of 90 +/- 16% (P < 0.0001); 6 months after discontinuation of the treatment, serum ICTP had returned to pretreatment values. We conclude that serum ICTP does reflect bone metabolism in postmenopausal osteoporosis, but it is not a sensitive marker of the changes in bone resorption induced by hormone replacement therapy, and it does not correspond with other measures of bone resorption during anabolic steroid therapy.

Published
1994

40. Acute effect of oral, intraperitoneal, and intravenous 1 alpha-hydroxycholecalciferol on markers of bone metabolism

Author

Joffe, P, Ladefoged, S D, Cintin, C, Jensen, L T, Hyldstrup, L, Joffe, P, Ladefoged, S D, Cintin, C, Jensen, L T, and Hyldstrup, L

Abstract

OBJECTIVE: To study the acute effect of 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) on serum levels of alkaline phosphatase, Ca2+, osteocalcin, parathyroid hormone (PTH), phosphate and type I and III procollagens (PICP and PIIINP respectively) in patients undergoing peritoneal dialysis. Also, 1,25-(OH)2D3 was measured.DESIGN: Single doses of 1 alpha-OHD3 (80 ng/kg body wt) were given in randomized cross-over fashion, orally, intraperitoneally (i.p.) and intravenously (i.v.) on three occasions. Blood was sampled at 0, 1, 6, 12, and 24 h after administration of 1 alpha-OHD3.MAIN RESULTS: Following oral administration of 1 alpha-OHD3, a decrease in serum alkaline phosphatase was seen when levels at 1 and 6 h were compared to baseline (P < 0.05). Oral and i.v. drug administrations resulted in an increasing trend in serum Ca2+ throughout the study (P < 0.05). Moreover, a difference in serum Ca2+ was found when 24-h levels after oral 1 alpha-OHD3 dose was compared to baseline (P < 0.05). Serum osteocalcin at 12 and 24 h after oral 1 alpha-OHD3 compared to baseline were increased (P < 0.05). Intact PTH followed a circadian rhythm after all three routes of drug delivery. After 24 h, significant decreases of intact PTH were observed in the oral and i.v. group. No changes in serum phosphate and serum PICP levels were observed over time after oral, i.p., and i.v. delivery of 1 alpha-OHD3. However, serum PIIINP following oral and i.p. administration of 1 alpha-OHD3 decreased at 1 and 6 h (P < 0.05).CONCLUSION: Oral and i.v. administration of 1 alpha-OHD3 does influence serum levels of osteocalcin, PTH, and PIIINP: Noticeable is the significant increase in serum osteocalcin after oral administration of 1 alpha-OHD3, the remarkable increase (22.6%) in osteocalcin 24 h after i.v. 1 alpha-OHD3, though not statistically significant, the increase in serum PTH levels 12 h following oral and i.v. doses of 1 alpha-OHD3 and the moderate effect on

Published
1994

42. Thrombolytic therapy of acute myocardial infarction alters collagen metabolism

Author

Høst, N B, Hansen, S S, Jensen, L T, Husum, D, Nielsen, J D, Høst, N B, Hansen, S S, Jensen, L T, Husum, D, and Nielsen, J D

Abstract

The objective of the study was to monitor collagen metabolism after thrombolytic therapy. Sequential measurements of serum aminoterminal type-III procollagen propeptide (S-PIIINP) and carboxyterminal type-I procollagen propeptide (S-PICP) were made in 62 patients suspected of acute myocardial infarction and receiving thrombolytic therapy. Regardless of whether acute myocardial infarction was confirmed or not, S-PIIINP increased (94-120%) 4 h after streptokinase therapy (p < or = 0.02), and decreased during the next 20 h with median values at 24 h still above the baseline (p < 0.02). With confirmed acute myocardial infarction, S-PIIINP increased from 24 h towards a plateau reached at day 2-3 (p < 0.01), with values still elevated at 6 months. No similar biphasic pattern was found for S-PICP, but patients with acute myocardial infarction had S-PICP above baseline at 1, 2, and 6 months (p < 0.05). A less pronounced S-PIIINP increase was noted with tissue-plasminogen activator than with streptokinase. Thrombolytic therapy induces collagen breakdown regardless of whether acute myocardial infarction is confirmed or not. With confirmed acute myocardial infarction collagen metabolism is altered for at least 6 months. Furthermore, fibrin-specific and nonspecific thrombolytic agents appear to affect collagen metabolism differently.

Published
1994

43. Collagen metabolism during wound healing in rats. The aminoterminal propeptide of type III procollagen in serum and wound fluid in relation to formation of granulation tissue

Author

Jensen, L T, Garbarsch, C, Hørslev-Petersen, K, Schuppan, D, Kim, K, Lorenzen, I, Jensen, L T, Garbarsch, C, Hørslev-Petersen, K, Schuppan, D, Kim, K, and Lorenzen, I

Abstract

The aminoterminal propeptide of type III procollagen (PIIINP) in serum has been shown to correlate with fibrillogenesis, and thus to be a potential direct marker of type III collagen deposition. The aim of the study was to investigate the correlation between changes in serum PIIINP and formation of granulation tissue during pharmacological suppression. Granulation tissue was induced in rats by the implantation of viscose cellulose sponges. Pharmacological suppression was achieved by cyclophosphamide treatment. To distinguish between the isolated effect of cyclophosphamide and the influence of the weight loss caused by treatment, weight loss caused by starvation was investigated. In untreated rats, serum PIIINP and wound fluid PIIINP were related to formation of granulation tissue (serum: r = 0.58, p < 0.05; wound fluid: r = 0.56, p < 0.05). In rats treated with cyclophosphamide, collagen deposition and formation of granulation tissue were markedly reduced, as compared within the untreated rats (6% vs 33%, p = 0.01). Wound fluid PIIINP reflected the sparse collagen deposition (r = 0.48, p < 0.05), whereas serum PIIINP decreased (-35%, p < 0.01) and was not correlated with the formation of granulation tissue. In starved rats, with a weight loss of 8%, formation of granulation tissue, vascular density, and collagen deposition were not reduced. Wound fluid PIIINP reflected the formation of granulation tissue (r = 0.52, p < 0.05), whereas serum PIIINP remained unchanged despite normal formation of granulation tissue. Starvation of rats without implants caused a decrease in serum PIIINP (-33%(-)-48%, p < 0.01). We conclude that during cyclophosphamide treatment and after a moderate weight loss, serum PIIINP is not a valid marker of fibrillogenesis. However, in normal rats with free access to food, changes in serum PIIINP mirror fibrillogenesis. Furthermore, our study provides experimental evidence consistent with the hypothesis that wound fluid PIIINP

Published
1993

44. Fate of circulating amino-terminal propeptide of type III procollagen in conscious pigs

Author

Jensen, L T, Henriksen, Jens Henrik Sahl, Risteli, J, Olesen, H P, Nielsen, M D, Lorenzen, I, Jensen, L T, Henriksen, Jens Henrik Sahl, Risteli, J, Olesen, H P, Nielsen, M D, and Lorenzen, I

Abstract

Udgivelsesdato: 1993-Jul, The amino-terminal propeptide of type III procollagen (PIIINP, M(r) 42,000) is a promising marker for the formation of type III collagen of granulation tissue in experimental and clinical studies. The disposal kinetics of circulating PIIINP is, however, almost unknown. In conscious pigs with a thoracic duct-venous shunt, 125I-labeled PIIINP was injected intravenously. The initial distribution volume was 2.2 liters, which was 1.7 times the plasma volume (P < 0.01). The disappearance curve was three-phased, with an initial steep decline (t1/2 58 min), followed by two slower phases (t1/2 239 min and 289 h). Consecutive gel filtrations showed that the initial slope of the plasma disappearance curve corresponded to the plasma clearance of the intact PIIINP. The initial plasma clearance was 26.5 ml plasma/min, whereas the urinary clearance was 8.7 ml plasma/min (P < 0.01). The other components of the plasma disappearance curve originated from the formation and disappearance of a high and a low molecular weight (MW) fraction as part of the degradation of PIIINP. The high MW fraction (approximately M(r) 90,000) was similar to a previously described, but not further characterized, PIIINP immunoreactive component. The existence of the low MW fraction (approximately M(r) 20,000) has not been reported before. The lymphatic recirculation of intact PIIINP was rapid, and the lymph-serum ratio was almost constant within 1 h of injection. We conclude that the t1/2 of circulating PIIINP is 58 min, that PIIINP escapes the circulation very quickly, and that the degradation of PIIINP includes at least two intermediary steps.

Published
1993

45. The effects of dietary supplementation with n-3 polyunsaturated fatty acids in patients with rheumatoid arthritis:a randomized, double blind trial

Author

Nielsen, G L, Faarvang, K L, Thomsen, B S, Teglbjaerg, K L, Jensen, L T, Hansen, T M, Lervang, H H, Schmidt, E B, Dyerberg, J, Ernst, E, Nielsen, G L, Faarvang, K L, Thomsen, B S, Teglbjaerg, K L, Jensen, L T, Hansen, T M, Lervang, H H, Schmidt, E B, Dyerberg, J, and Ernst, E

Abstract

STUDY OBJECTIVE: To determine the effect of dietary supplementation with n-3 polyunsaturated fatty acids (n-3 PUFA) on disease variables in patients with rheumatoid arthritis.DESIGN: Multicenter, randomized, placebo controlled, double blind.SETTING: Three Danish hospital Departments of Rheumatology.PATIENTS: Fifty-one patients with active rheumatoid arthritis.INTERVENTION: Random allocation to 12 weeks of treatment with either six n-3 PUFA capsules (3.6 g) or six capsules with fat composition as the average Danish diet.MAIN RESULTS: Significant improvement of morning stiffness and joint tenderness. No significant effect on the four other assessed clinical parameters. No serious side effects.CONCLUSIONS: Dietary supplementation with n-3 PUFA in patients with rheumatoid arthritis improved two out of six patient reported disease parameters. Further studies are needed to clarify the more precise role of n-3 PUFA in the treatment of rheumatoid arthritis.

Published
1992

46. Collagen types I and III propeptides as markers of healing in chronic leg ulcers. A noninvasive method for the determination of procollagen propeptides in wound fluid--influence of growth hormone

Author

Rasmussen, L H, Jensen, L T, Avnstorp, C, Karlsmark, T, Peters, K, Hørslev-Petersen, K, Rasmussen, L H, Jensen, L T, Avnstorp, C, Karlsmark, T, Peters, K, and Hørslev-Petersen, K

Abstract

A noninvasive method allowing measurements of the propeptides of collagen type III (PIIINP) and type I (PICP) in ulcer washings was developed. The response to topical human growth hormone was examined. Fourteen patients with venous ulcers were treated sequentially with human growth hormone (0.1, 0.25, and 1 IU/cm2/day), each dose for 1 week, followed by 1 week washout. On alternate days, three and two times during treatment and washout periods, respectively, the ulcers were washed and incubated for 30 minutes with sterile water. No changes in healing rates in relation to growth hormone application were observed. In contrast, PIIINP increased significantly to 168% (154% to 184%) (mean, 95% confidence interval) and 195% (179% to 218%) 5 and 9 days, respectively, after start of treatment, (p < 0.01). Propeptides of collagen type I reached a significant increase, to 196% (172% to 232%), in the fourth week, (p < 0.01). The areas under the curves of PICP and PIIINP correlated significantly with the healing rates (r = 0.57, p = 0.04; and r = 0.64, p = 0.01, respectively). The authors conclude that propeptide measurements may be useful markers of healing in clinical studies.

Published
1992

47. Metabolism of the aminoterminal propeptide of type III procollagen in cultures of human proximal tubular cells

Author

Jensen, L T, Blaehr, H, Andersen, C B, Risteli, J, Lorenzen, I, Jensen, L T, Blaehr, H, Andersen, C B, Risteli, J, and Lorenzen, I

Abstract

Degradation of the intact form of the aminoterminal propeptide of type III procollagen (PIIINP) has been established in the liver, whereas the col 1 domain of PIIINP is extracted by the kidneys. We used native human PIIINP and col 1 domain of PIIINP to investigate the degradation of PIIINP in cultures of human proximal tubular cells. Normal renal tissue was obtained from the healthy part of kidneys surgically removed and from biopsies from a total of 10 patients. The degradation was characterized by incubation of [125I]-PIIINP followed by gel filtration. We found that in physiological concentrations (4.4 micrograms l-1 and 11.9 micrograms l-1 intact PIIINP was almost totally degraded, but not col 1 domain. High concentrations of PIIINP (20-50 micrograms l-1) had a non-linear, non-monoexponential degradation over time, which suggests several steps. Gel filtration of [125I]-PIIINP after 1 h, 3 h, 6 h and 24 h of incubation confirmed the observation by showing the rapid formation of a high-molecular-weight fraction, followed by the slower formation of a low-molecular-weight fraction. The high-molecular-weight fraction was PIIINP immunoreactive, but not the low-molecular-weight fraction. We conclude that cultures of human proximal tubular cells degrade intact human PIIINP by the formation of high- and low-molecular-weight fractions. Earlier findings that extraction of the PIIINP col 1 domain takes place in the kidneys, cannot be explained by degradation by the proximal tubular cells.

Published
1992

48. Purification of porcine aminoterminal propeptide of type III procollagen from lymph and use for lymphatic clearance studies in pigs

Author

Jensen, L T, Risteli, J, Nielsen, M D, Henriksen, Jens Henrik Sahl, Olesen, H P, Risteli, L, Lorenzen, I, Jensen, L T, Risteli, J, Nielsen, M D, Henriksen, Jens Henrik Sahl, Olesen, H P, Risteli, L, and Lorenzen, I

Abstract

Udgivelsesdato: 1992-Feb, To investigate the lymphatic transport of the aminoterminal propeptide of type III procollagen (PIIINP) we established a thoracic duct-venous shunt in 6 pigs. Porcine PIIINP was purified, characterised, and compared with human PIIINP to ensure the suitability of the radioimmunoassay of human PIIINP for measurements in pigs. SDS-PAGE and radioimmunoinhibition assays show human and porcine PIIINP to be similar, thus indicating that the assay of human PIIINP is also reliable for determinations on pig serum and lymph. Intact PIIINP, as identified by gel filtration, accounted for 60% and 40% of the total PIIINP immunoreactivity in lymph and serum, respectively. The higher amount of total immunoreactivity and proportion of intact PIIINP in lymph compared with serum support the hypothesis that intact PIIINP is transported from peripheral tissue into the circulation by lymph. Two days after the shunt was established, the lymph was collected quantitatively hour-by-hour for 24 h. The flow was higher during the light periods than in the dark (p less than 0.01). The PIIINP concentration varied inversely with the flow, being higher in the dark hours (p less than 0.03). However, the total collected amount of PIIINP in lymph did not differ during the light and dark periods. Serum PIIINP remained unchanged over the 24 h. The lymphatic clearance of total PIIINP immunoreactive components was 6.2 ml serum/min and the lymphatic clearance of intact PIIINP was 9.1 ml serum/min, equal to 7 and 10 times the plasma volume/24 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1992

49. Type I and III procollagen propeptides in growth hormone-deficient patients:effects of increasing doses of GH

Author

Jensen, L T, Jørgensen, J O, Risteli, J, Christiansen, J S, Lorenzen, I, Jensen, L T, Jørgensen, J O, Risteli, J, Christiansen, J S, and Lorenzen, I

Abstract

The effect of increasing doses of growth hormone on collagen synthesis in GH-treated GH-deficient patients was determined in a short-term study. The synthesis of type I and III collagen was estimated by measurements of the carboxyterminal propeptide of type I procollagen and the aminoterminal propeptide of type III procollagen. Type I collagen is mainly found in bone and type III collagen in loose connective tissue. We observed a GH dose dependency of both procollagen propeptides. Serum type I procollagen propeptide was significantly higher following GH doses of 4 and 6 IU/day for 14 days compared with 2 IU/day (normal replacement dose) (p = 0.04). Withdrawal of GH therapy for 14 days resulted in wider variation, but not significantly different from the levels at 2, 4 and 6 IU/day. A dose dependency was found regarding type III procollagen propeptide, showing significantly higher serum concentrations at a GH dose of 4 IU/day compared with 2 IU/day (p = 0.001), and of 6 IU/day compared with 4 IU/day (p = 0.001). Withdrawal of GH therapy resulted in significantly lower type III procollagen propeptide concentrations compared with those at a GH dose of 4 and 6 IU/day (p = 0.03). Serum type III procollagen propeptide increased twice as much as type I procollagen propeptide, by 47 vs 25%, at a GH dose of 6 IU/day compared with 2 IU/day. The differences between the effects on type I and type III collagen may reflect differences in secretion or turn-over rate of collagen in bone and loose connective tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1991

50. Human monocyte elastolytic activity, the propeptides of types I and III procollagen, proteoglycans, and interleukin-6 in synovial fluid from patients with arthritis

Author

Jensen, H S, Jensen, L T, Saxne, T, Diamant, M, Bendtzen, K, Jensen, H S, Jensen, L T, Saxne, T, Diamant, M, and Bendtzen, K

Abstract

Elastolytic activity by live human monocytes (M phi) is mainly caused by cell surface related leucocyte elastase, capable of degrading matrix components. In order to examine the possible correlation between enzyme activity and tissue turnover in the joint, we examined 24 synovial fluids for M phi elastolytic activity, using the levels of synovial fluid interleukin-6 and serum C reactive protein as additional markers of cell activation. Proteoglycan levels were measured as an indication of cartilage degradation and the types I and III procollagen propeptides as markers of synovial membrane turnover. We found that elastolysis by live M phi and the levels of interleukin-6 and C reactive protein correlated significantly with proteoglycan concentrations but not with the procollagen propeptides. These findings suggest that human M phi elastolytic activation is a biologically relevant factor in cartilage degradation, but is unrelated to the collagen metabolism of the synovial membrane.

Published
1991

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