58 results on '"Rosenthal, N"'
Search Results
2. Myofiber development and survival
- Author
-
Musaro', Antonio and Rosenthal, N.
- Published
- 2002
3. Search for heavy long-lived charged R-hadrons with the ATLAS detector in 3.2 fb−1 of proton–proton collision data at s=13 TeV
- Author
-
Aaboud, M., Aad, G., Abbott, B., Abdallah, J., Abdinov, O., Abeloos, B., Aben, R., Abouzeid, O. S., Abraham, N. L., Abramowicz, H., Abreu, H., Abreu, R., Abulaiti, Y., Acharya, B. S., Adamczyk, L., Adams, D. L., Adelman, J., Adersberger, M., Adomeit, S., Adye, T., Affolder, A. A., Agatonovic Jovin, T., Agricola, J., Aguilar Saavedra, J. A., Ahlen, S. P., Ahmadov, F., Aielli, G., Akerstedt, H., Åkesson, T. P. A., Akimov, A. V., Alberghi, G. L., Albert, J., Albrand, S., Alconada Verzini, M. J., Aleksa, M., Aleksandrov, I. N., Alexa, C., Alexander, G., Alexopoulos, T., Alhroob, M., Ali, B., Aliev, M., Alimonti, G., Alison, J., Alkire, S. P., Allbrooke, B. M. M., Allen, B. W., Allport, P. P., Aloisio, A., Alonso, A., Alonso, F., Alpigiani, C., Alstaty, M., Alvarez Gonzalez, B., Álvarez Piqueras, D., Alviggi, M. G., Amadio, B. T., Amako, K., Amaral Coutinho, Y., Amelung, C., Amidei, D., Amor Dos Santos, S. P., Amorim, A., Amoroso, S., Amundsen, G., Anastopoulos, C., Ancu, L. S., Andari, N., Andeen, T., Anders, C. F., Anders, G., Anders, J. K., Anderson, K. J., Andreazza, A., Andrei, V., Angelidakis, S., Angelozzi, I., Anger, P., Angerami, A., Anghinolfi, F., Anisenkov, A. V., Anjos, N., Annovi, A., Antel, C., Antonelli, M., Antonov, A., Anulli, F., Aoki, M., Aperio Bella, L., Arabidze, G., Arai, Y., Araque, J. P., Arce, A. T. H., Arduh, F. A., Arguin, J. F., Argyropoulos, S., Arik, M., Armbruster, A. J., Armitage, L. J., Arnaez, O., Arnold, H., Arratia, M., Arslan, O., Artamonov, A., Artoni, G., Artz, S., Asai, S., Asbah, N., Ashkenazi, A., Åsman, B., Asquith, L., Assamagan, K., Astalos, R., Atkinson, M., Atlay, N. B., Augsten, K., Avolio, G., Axen, B., Ayoub, M. K., Azuelos, G., Baak, M. A., Baas, A. E., Baca, M. J., Bachacou, H., Bachas, K., Backes, M., Backhaus, M., Bagiacchi, P., Bagnaia, P., Bai, Y., Baines, J. T., Baker, O. K., Baldin, E. M., Balek, P., Balestri, T., Balli, F., Balunas, W. K., Banas, E., Banerjee, S. w., Bannoura, A. A. E., Barak, L., Barberio, E. L., Barberis, D., Barbero, M., Barillari, T., Barisits, M. S, Barklow, T., Barlow, N., Barnes, S. L., Barnett, B. M., Barnett, R. M., Barnovska, Z., Baroncelli, A., Barone, G., Barr, A. J., Barranco Navarro, L., Barreiro, F., Barreiro Guimarães da Costa, J., Bartoldus, R., Barton, A. E., Bartos, P., Basalaev, A., Bassalat, A., Bates, R. L., Batista, S. J., Batley, J. R., Battaglia, M., Bauce, M., Bauer, F., Bawa, H. S., Beacham, J. B., Beattie, M. D., Beau, T., Beauchemin, P. H., Bechtle, P., Beck, H. P., Becker, K., Becker, M., Beckingham, M., Becot, C., Beddall, A. J., Beddall, A., Bednyakov, V. A., Bedognetti, M., Bee, C. P., Beemster, L. J., Beermann, T. A., Begel, M., Behr, J. K., Belanger Champagne, C., Bell, A. S., Bella, G., Bellagamba, L., Bellerive, A., Bellomo, M., Belotskiy, K., Beltramello, O., Belyaev, N. L., Benary, O., Benchekroun, D., Bender, M., Bendtz, K., Benekos, N., Benhammou, Y., Benhar Noccioli, E., Benitez, J., Benjamin, D. P., Bensinger, J. R., Bentvelsen, S., Beresford, L., Beretta, M., Berge, D., Bergeaas Kuutmann, E., Berger, N., Beringer, J., Berlendis, S., Bernard, N. R., Bernius, C., Bernlochner, F. U., Berry, T., Berta, P., Bertella, C., Bertoli, G., Bertolucci, F., Bertram, I. A., Bertsche, C., Bertsche, D., Besjes, G. J., Bessidskaia Bylund, O., Bessner, M., Besson, N., Betancourt, C., Bethke, S., Bevan, A. J., Bianchi, R. M., Bianchini, L., Bianco, M., Biebel, O., Biedermann, D., Bielski, R., Biesuz, N. V., Biglietti, M., Bilbao De Mendizabal, J., Billoud, T. R. V., Bilokon, H., Bindi, M., Binet, S., Bingul, A., Bini, C., Biondi, S., Bjergaard, D. M., Black, C. W., Black, J. E., Black, K. M., Blackburn, D., Blair, R. E., Blanchard, J. B., Blazek, T., Bloch, I., Blocker, C., Blum, W., Blumenschein, U., Blunier, S., Bobbink, G. J., Bobrovnikov, V. S., Bocchetta, S. S., Bocci, A., Bock, C., Boehler, M., Boerner, D., Bogaerts, J. A., Bogavac, D., Bogdanchikov, A. G., Bohm, C., Boisvert, V., Bokan, P., Bold, T., Boldyrev, A. S., Bomben, M., Bona, M., Boonekamp, M., Borisov, A., Borissov, G., Bortfeldt, J., Bortoletto, D., Bortolotto, V., Bos, K., Boscherini, D., Bosman, M., Bossio Sola, J. D., Boudreau, J., Bouffard, J., Bouhova Thacker, E. V., Boumediene, D., Bourdarios, C., Boutle, S. K., Boveia, A., Boyd, J., Boyko, I. R., Bracinik, J., Brandt, A., Brandt, G., Brandt, O., Bratzler, U., Brau, B., Brau, J. E., Braun, H. M., Breaden Madden, W. D., Brendlinger, K., Brennan, A. J., Brenner, L., Brenner, R., Bressler, S., Bristow, T. M., Britton, D., Britzger, D., Brochu, F. M., Brock, I., Brock, R., Brooijmans, G., Brooks, T., Brooks, W. K., Brosamer, J., Brost, E., Broughton, J. H., Bruckman de Renstrom, P. A., Bruncko, D., Bruneliere, R., Bruni, A., Bruni, G., Bruni, L. S., Brunt, B. H., Bruschi, M., Bruscino, N., Bryant, P., Bryngemark, L., Buanes, T., Buat, Q., Buchholz, P., Buckley, A. G., Budagov, I. A., Buehrer, F., Bugge, M. K., Bulekov, O., Bullock, D., Burckhart, H., Burdin, S., Burgard, C. D., Burghgrave, B., Burka, K., Burke, S., Burmeister, I., Burr, J. T. P., Busato, E., Büscher, D., Büscher, V., Bussey, P., Butler, J. M., Buttar, C. M., Butterworth, J. M., Butti, P., Buttinger, W., Buzatu, A., Buzykaev, A. R., Cabrera Urbán, S., Caforio, D., Cairo, V. M., Cakir, O., Calace, N., Calafiura, P., Calandri, A., Calderini, G., Calfayan, P., Callea, G., Caloba, L. P., Calvente Lopez, S., Calvet, D., Calvet, S., Calvet, T. P., Camacho Toro, R., Camarda, S., Camarri, P., Cameron, D., Caminal Armadans, R., Camincher, C., Campana, S., Campanelli, M., Camplani, A., Campoverde, A., Canale, V., Canepa, A., Cano Bret, M., Cantero, J., Cantrill, R., Cao, T., Capeans Garrido, M. D. M., Caprini, I., Caprini, M., Capua, M., Caputo, R., Carbone, R. M., Cardarelli, R., Cardillo, F., Carli, I., Carli, T., Carlino, G., Carminati, L., Caron, S., Carquin, E., Carrillo Montoya, G. D., Carter, J. R., Carvalho, J., Casadei, D., Casado, M. P., Casolino, M., Casper, D. W., Castaneda Miranda, E., Castelijn, R., Castelli, A., Castillo Gimenez, V., Castro, N. F., Catinaccio, A., Catmore, J. R., Cattai, A., Caudron, J., Cavaliere, V., Cavallaro, E., Cavalli, D., Cavalli Sforza, M., Cavasinni, Vincenzo, Ceradini, F., Cerda Alberich, L., Cerio, B. C., Cerqueira, A. S., Cerri, A., Cerrito, L., Cerutti, F., Cerv, M., Cervelli, A., Cetin, S. A., Chafaq, A., Chakraborty, D., Chan, S. K., Chan, Y. L., Chang, P., Chapman, J. D., Charlton, D. G., Chatterjee, A., Chau, C. C., Chavez Barajas, C. A., Che, S., Cheatham, S., Chegwidden, A., Chekanov, S., Chekulaev, S. V., Chelkov, G. A., Chelstowska, M. A., Chen, C., Chen, H., Chen, K., Chen, S., Chen, X., Chen, Y., Cheng, H. C., Cheng, H. J., Cheng, Y., Cheplakov, A., Cheremushkina, E., Cherkaoui El Moursli, R., Chernyatin, V., Cheu, E., Chevalier, L., Chiarella, V., Chiarelli, G., Chiodini, G., Chisholm, A. S., Chitan, A., Chizhov, M. V., Choi, K., Chomont, A. R., Chouridou, S., Chow, B. K. B., Christodoulou, V., Chromek Burckhart, D., Chudoba, J., Chuinard, A. J., Chwastowski, J. J., Chytka, L., Ciapetti, G., Ciftci, A. K., Cinca, D., Cindro, V., Cioara, I. A., Ciocca, C., Ciocio, A., Cirotto, F., Citron, Z. H., Citterio, M., Ciubancan, M., Clark, A., Clark, B. L., Clark, M. R., Clark, P. J., Clarke, R. N., Clement, C., Coadou, Y., Cobal, M., Coccaro, A., Cochran, J., Colasurdo, L., Cole, B., Colijn, A. P., Collot, J., Colombo, T., Compostella, G., Conde Muiño, P., Coniavitis, E., Connell, S. H., Connelly, I. A., Consorti, V., Constantinescu, S., Conti, G., Conventi, F., Cooke, M., Cooper, B. D., Cooper Sarkar, A. M., Cormier, K. J. R., Cornelissen, T., Corradi, M., Corriveau, F., Corso Radu, A., Cortes Gonzalez, A., Cortiana, G., Costa, G., Costa, M. J., Costanzo, D., Cottin, G., Cowan, G., Cox, B. E., Cranmer, K., Crawley, S. J., Cree, G., Crépé Renaudin, S., Crescioli, F., Cribbs, W. A., Crispin Ortuzar, M., Cristinziani, M., Croft, V., Crosetti, G., Cueto, A., Cuhadar Donszelmann, T., Cummings, J., Curatolo, M., Cúth, J., Czirr, H., Czodrowski, P., D'Amen, G., D'Auria, S., D'Onofrio, M., Da Cunha Sargedas De Sousa, M. J., Da Via, C., Dabrowski, W., Dado, T., Dai, T., Dale, O., Dallaire, F., Dallapiccola, C., Dam, M., Dandoy, J. R., Dang, N. P., Daniells, A. C., Dann, N. S., Danninger, M., Dano Hoffmann, M., Dao, V., Darbo, G., Darmora, S., Dassoulas, J., Dattagupta, A., Davey, W., David, C., Davidek, T., Davies, M., Davison, P., Dawe, E., Dawson, I., Daya Ishmukhametova, R. K., De, K., de Asmundis, R., De Benedetti, A., De Castro, S., De Cecco, S., De Groot, N., de Jong, P., De la Torre, H., De Lorenzi, F., De Maria, A., De Pedis, D., De Salvo, A., De Sanctis, U., De Santo, A., De Vivie De Regie, J. B., Dearnaley, W. J., Debbe, R., Debenedetti, C., Dedovich, D. V., Dehghanian, N., Deigaard, I., Del Gaudio, M., Del Peso, J., Del Prete, T., Delgove, D., Deliot, F., Delitzsch, C. M., Deliyergiyev, M., Dell'Acqua, A., Dell'Asta, L., Dell'Orso, Mauro, Della Pietra, M., della Volpe, D., Delmastro, M., Delsart, P. A., Demarco, D. A., Demers, S., Demichev, M., Demilly, A., Denisov, S. P., Denysiuk, D., Derendarz, D., Derkaoui, J. E., Derue, F., Dervan, P., Desch, K., Deterre, C., Dette, K., Deviveiros, P. O., Dewhurst, A., Dhaliwal, S., Di Ciaccio, A., Di Ciaccio, L., Di Clemente, W. K., Di Donato, C., Di Girolamo, A., Di Girolamo, B., Di Micco, B., Di Nardo, R., Di Simone, A., Di Sipio, R., Di Valentino, D., Diaconu, C., Diamond, M., Dias, F. A., Diaz, M. A., Diehl, E. B., Dietrich, J., Diglio, S., Dimitrievska, A., Dingfelder, J., Dita, P., Dita, S., Dittus, F., Djama, F., Djobava, T., Djuvsland, J. I., do Vale, M. A. B., Dobos, D., Dobre, M., Doglioni, C., Dolejsi, J., Dolezal, Z., Dolgoshein, B. A., Donadelli, M., Donati, Simone, Dondero, P., Donini, J., Dopke, J., Doria, A., Dova, M. T., Doyle, A. T., Drechsler, E., Dris, M., Du, Y., Duarte Campderros, J., Duchovni, E., Duckeck, G., Ducu, O. A., Duda, D., Dudarev, A., Duffield, E. M., Duflot, L., Dührssen, M., Dumancic, M., Dunford, M., Duran Yildiz, H., Düren, M., Durglishvili, A., Duschinger, D., Dutta, B., Dyndal, M., Eckardt, C., Ecker, K. M., Edgar, R. C., Edwards, N. C., Eifert, T., Eigen, G., Einsweiler, K., Ekelof, T., El Kacimi, M., Ellajosyula, V., Ellert, M., Elles, S., Ellinghaus, F., Elliot, A. A., Ellis, N., Elmsheuser, J., Elsing, M., Emeliyanov, D., Enari, Y., Endner, O. C., Ennis, J. S., Erdmann, J., Ereditato, A., Ernis, G., Ernst, J., Ernst, M., Errede, S., Ertel, E., Escalier, M., Esch, H., Escobar, C., Esposito, B., Etienvre, A. I., Etzion, E., Evans, H., Ezhilov, A., Fabbri, F., Fabbri, L., Facini, G., Fakhrutdinov, R. M., Falciano, S., Falla, R. J., Faltova, J., Fang, Y., Fanti, M., Farbin, A., Farilla, A., Farina, C., Farina, E. M., Farooque, T., Farrell, S., Farrington, S. M., Farthouat, P., Fassi, F., Fassnacht, P., Fassouliotis, D., Faucci Giannelli, M., Favareto, A., Fawcett, W. J., Fayard, L., Fedin, O. L., Fedorko, W., Feigl, S., Feligioni, L., Feng, C., Feng, E. J., Feng, H., Fenyuk, A. B., Feremenga, L., Fernandez Martinez, P., Fernandez Perez, S., Ferrando, J., Ferrari, A., Ferrari, P., Ferrari, R., Ferreira de Lima, D. E., Ferrer, A., Ferrere, D., Ferretti, C., Ferretto Parodi, A., Fiedler, F., Filipčič, A., Filipuzzi, M., Filthaut, F., Fincke Keeler, M., Finelli, K. D., Fiolhais, M. C. N., Fiorini, L., Firan, A., Fischer, A., Fischer, C., Fischer, J., Fisher, W. C., Flaschel, N., Fleck, I., Fleischmann, P., Fletcher, G. T., Fletcher, R. R. M., Flick, T., Floderus, A., Flores Castillo, L. R., Flowerdew, M. J., Forcolin, G. T., Formica, A., Forti, A., Foster, A. G., Fournier, D., Fox, H., Fracchia, S., Francavilla, P., Franchini, M., Francis, D., Franconi, L., Franklin, M., Frate, M., Fraternali, M., Freeborn, D., Fressard Batraneanu, S. M., Friedrich, F., Froidevaux, D., Frost, J. A., Fukunaga, C., Fullana Torregrosa, E., Fusayasu, T., Fuster, J., Gabaldon, C., Gabizon, O., Gabrielli, A., Gach, G. P., Gadatsch, S., Gadomski, S., Gagliardi, G., Gagnon, L. G., Gagnon, P., Galea, C., Galhardo, B., Gallas, E. J., Gallop, B. J., Gallus, P., Galster, G., Gan, K. K., Gao, J., Gao, Y., Gao, Y. S., Garay Walls, F. M., García, C., García Navarro, J. E., Garcia Sciveres, M., Gardner, R. W., Garelli, N., Garonne, V., Gascon Bravo, A., Gasnikova, K., Gatti, C., Gaudiello, A., Gaudio, G., Gauthier, L., Gavrilenko, I. L., Gay, C., Gaycken, G., Gazis, E. N., Gecse, Z., Gee, C. N. P., Geich Gimbel, C. h., Geisen, M., Geisler, M. P., Gemme, C., Genest, M. H., Geng, C., Gentile, S., Gentsos, C., George, S., Gerbaudo, D., Gershon, A., Ghasemi, S., Ghazlane, H., Ghneimat, M., Giacobbe, B., Giagu, S., Giannetti, P., Gibbard, B., Gibson, S. M., Gignac, M., Gilchriese, M., Gillam, T. P. S., Gillberg, D., Gilles, G., Gingrich, D. M., Giokaris, N., Giordani, M. P., Giorgi, F. M., Giraud, P. F., Giromini, P., Giugni, D., Giuli, F., Giuliani, C., Giulini, M., Gjelsten, B. K., Gkaitatzis, S., Gkialas, I., Gkougkousis, E. L., Gladilin, L. K., Glasman, C., Glatzer, J., Glaysher, P. C. F., Glazov, A., Goblirsch Kolb, M., Godlewski, J., Goldfarb, S., Golling, T., Golubkov, D., Gomes, A., Gonçalo, R., Goncalves Pinto Firmino Da Costa, J., Gonella, G., Gonella, L., Gongadze, A., González de la Hoz, S., Gonzalez Parra, G., Gonzalez Sevilla, S., Goossens, L., Gorbounov, P. A., Gordon, H. A., Gorelov, I., Gorini, B., Gorini, E., Gorišek, A., Gornicki, E., Goshaw, A. T., Gössling, C., Gostkin, M. I., Goudet, C. R., Goujdami, D., Goussiou, A. G., Govender, N., Gozani, E., Graber, L., Grabowska Bold, I., Gradin, P. O. J., Grafström, P., Gramling, J., Gramstad, E., Grancagnolo, S., Gratchev, V., Gravila, P. M., Gray, H. M., Graziani, E., Greenwood, Z. D., Grefe, C., Gregersen, K., Gregor, I. M., Grenier, P., Grevtsov, K., Griffiths, J., Grillo, A. A., Grimm, K., Grinstein, S., Gris, P. h., Grivaz, J. F., Groh, S., Grohs, J. P., Gross, E., Grosse Knetter, J., Grossi, G. C., Grout, Z. J., Guan, L., Guan, W., Guenther, J., Guescini, F., Guest, D., Gueta, O., Guido, E., Guillemin, T., Guindon, S., Gul, U., Gumpert, C., Guo, J., Guo, Y., Gupta, R., Gupta, S., Gustavino, G., Gutierrez, P., Gutierrez Ortiz, N. G., Gutschow, C., Guyot, C., Gwenlan, C., Gwilliam, C. B., Haas, A., Haber, C., Hadavand, H. K., Haddad, N., Hadef, A., Haefner, P., Hageböck, S., Hajduk, Z., Hakobyan, H., Haleem, M., Haley, J., Halladjian, G., Hallewell, G. D., Hamacher, K., Hamal, P., Hamano, K., Hamilton, A., Hamity, G. N., Hamnett, P. G., Han, L., Hanagaki, K., Hanawa, K., Hance, M., Haney, B., Hanisch, S., Hanke, P., Hanna, R., Hansen, J. B., Hansen, J. D., Hansen, M. C., Hansen, P. H., Hara, K., Hard, A. S., Harenberg, T., Hariri, F., Harkusha, S., Harrington, R. D., Harrison, P. F., Hartjes, F., Hartmann, N. M., Hasegawa, M., Hasegawa, Y., Hasib, A., Hassani, S., Haug, S., Hauser, R., Hauswald, L., Havranek, M., Hawkes, C. M., Hawkings, R. J., Hayakawa, D., Hayden, D., Hays, C. P., Hays, J. M., Hayward, H. S., Haywood, S. J., Head, S. J., Heck, T., Hedberg, V., Heelan, L., Heim, S., Heim, T., Heinemann, B., Heinrich, J. J., Heinrich, L., Heinz, C., Hejbal, J., Helary, L., Hellman, S., Helsens, C., Henderson, J., Henderson, R. C. W., Heng, Y., Henkelmann, S., Henriques Correia, A. M., Henrot Versille, S., Herbert, G. H., Hernández Jiménez, Y., Herten, G., Hertenberger, R., Hervas, L., Hesketh, G. G., Hessey, N. P., Hetherly, J. W., Hickling, R., Higón Rodriguez, E., Hill, E., Hill, J. C., Hiller, K. H., Hillier, S. J., Hinchliffe, I., Hines, E., Hinman, R. R., Hirose, M., Hirschbuehl, D., Hobbs, J., Hod, N., Hodgkinson, M. C., Hodgson, P., Hoecker, A., Hoeferkamp, M. R., Hoenig, F., Hohn, D., Holmes, T. R., Homann, M., Hong, T. M., Hooberman, B. H., Hopkins, W. H., Horii, Y., Horton, A. J., Hostachy, J. Y., Hou, S., Hoummada, A., Howarth, J., Hrabovsky, M., Hristova, I., Hrivnac, J., Hryn'Ova, T., Hrynevich, A., Hsu, C., Hsu, P. J., Hsu, S. C., Hu, D., Hu, Q., Hu, S., Huang, Y., Hubacek, Z., Hubaut, F., Huegging, F., Huffman, T. B., Hughes, E. W., Hughes, G., Huhtinen, M., Huo, P., Huseynov, N., Huston, J., Huth, J., Iacobucci, G., Iakovidis, G., Ibragimov, I., Iconomidou Fayard, L., Ideal, E., Idrissi, Z., Iengo, P., Igonkina, O., Iizawa, T., Ikegami, Y., Ikeno, M., Ilchenko, Y., Iliadis, D., Ilic, N., Ince, T., Introzzi, G., Ioannou, P., Iodice, M., Iordanidou, K., Ippolito, V., Ishijima, N., Ishino, M., Ishitsuka, M., Ishmukhametov, R., Issever, C., Istin, S., Ito, F., Iturbe Ponce, J. M., Iuppa, R., Iwanski, W., Iwasaki, H., Izen, J. M., Izzo, V., Jabbar, S., Jackson, B., Jackson, P., Jain, V., Jakobi, K. B., Jakobs, K., Jakobsen, S., Jakoubek, T., Jamin, D. O., Jana, D. K., Jansen, E., Jansky, R., Janssen, J., Janus, M., Jarlskog, G., Javadov, N., Javůrek, T., Jeanneau, F., Jeanty, L., Jejelava, J., Jeng, G. Y., Jennens, D., Jenni, P., Jeske, C., Jézéquel, S., Ji, H., Jia, J., Jiang, H., Jiang, Y., Jiggins, S., Jimenez Pena, J., Jin, S., Jinaru, A., Jinnouchi, O., Johansson, P., Johns, K. A., Johnson, W. J., Jon And, K., Jones, G., Jones, R. W. L., Jones, S., Jones, T. J., Jongmanns, J., Jorge, P. M., Jovicevic, J., Ju, X., Juste Rozas, A., Köhler, M. K., Kaczmarska, A., Kado, M., Kagan, H., Kagan, M., Kahn, S. J., Kaji, T., Kajomovitz, E., Kalderon, C. W., Kaluza, A., Kama, S., Kamenshchikov, A., Kanaya, N., Kaneti, S., Kanjir, L., Kantserov, V. A., Kanzaki, J., Kaplan, B., Kaplan, L. S., Kapliy, A., Kar, D., Karakostas, K., Karamaoun, A., Karastathis, N., Kareem, M. J., Karentzos, E., Karnevskiy, M., Karpov, S. N., Karpova, Z. M., Karthik, K., Kartvelishvili, V., Karyukhin, A. N., Kasahara, K., Kashif, L., Kass, R. D., Kastanas, A., Kataoka, Y., Kato, C., Katre, A., Katzy, J., Kawagoe, K., Kawamoto, T., Kawamura, G., Kazanin, V. F., Keeler, R., Kehoe, R., Keller, J. S., Kempster, J. J., Kentaro, K., Keoshkerian, H., Kepka, O., Kerševan, B. P., Kersten, S., Keyes, R. A., Khader, M., Khalil zada, F., Khanov, A., Kharlamov, A. G., Khoo, T. J., Khovanskiy, V., Khramov, E., Khubua, J., Kido, S., Kilby, C. R., Kim, H. Y., Kim, S. H., Kim, Y. K., Kimura, N., Kind, O. M., King, B. T., King, M., King, S. B., Kirk, J., Kiryunin, A. E., Kishimoto, T., Kisielewska, D., Kiss, F., Kiuchi, K., Kivernyk, O., Kladiva, E., Klein, M. H., Klein, M., Klein, U., Kleinknecht, K., Klimek, P., Klimentov, A., Klingenberg, R., Klinger, J. A., Klioutchnikova, T., Kluge, E. E., Kluit, P., Kluth, S., Knapik, J., Kneringer, E., Knoops, E. B. F. G., Knue, A., Kobayashi, A., Kobayashi, D., Kobayashi, T., Kobel, M., Kocian, M., Kodys, P., Koehler, N. M., Koffas, T., Koffeman, E., Koi, T., Kolanoski, H., Kolb, M., Koletsou, I., Komar, A. A., Komori, Y., Kondo, T., Kondrashova, N., Köneke, K., König, A. C., Kono, T., Konoplich, R., Konstantinidis, N., Kopeliansky, R., Koperny, S., Köpke, L., Kopp, A. K., Korcyl, K., Kordas, K., Korn, A., Korol, A. A., Korolkov, I., Korolkova, E. V., Kortner, O., Kortner, S., Kosek, T., Kostyukhin, V. V., Kotwal, A., Kourkoumeli Charalampidi, A., Kourkoumelis, C., Kouskoura, V., Kowalewska, A. B., Kowalewski, R., Kowalski, T. Z., Kozakai, C., Kozanecki, W., Kozhin, A. S., Kramarenko, V. A., Kramberger, G., Krasnopevtsev, D., Krasny, M. W., Krasznahorkay, A., Kravchenko, A., Kretz, M., Kretzschmar, J., Kreutzfeldt, K., Krieger, P., Krizka, K., Kroeninger, K., Kroha, H., Kroll, J., Kroseberg, J., Krstic, J., Kruchonak, U., Krüger, H., Krumnack, N., Kruse, A., Kruse, M. C., Kruskal, M., Kubota, T., Kucuk, H., Kuday, S., Kuechler, J. T., Kuehn, S., Kugel, A., Kuger, F., Kuhl, A., Kuhl, T., Kukhtin, V., Kukla, R., Kulchitsky, Y., Kuleshov, S., Kuna, M., Kunigo, T., Kupco, A., Kurashige, H., Kurochkin, Y. A., Kus, V., Kuwertz, E. S., Kuze, M., Kvita, J., Kwan, T., Kyriazopoulos, D., La Rosa, A., La Rosa Navarro, J. L., La Rotonda, L., Lacasta, C., Lacava, F., Lacey, J., Lacker, H., Lacour, D., Lacuesta, V. R., Ladygin, E., Lafaye, R., Laforge, B., Lagouri, T., Lai, S., Lammers, S., Lampl, W., Lançon, E., Landgraf, U., Landon, M. P. J., Lanfermann, M. C., Lang, V. S., Lange, J. C., Lankford, A. J., Lanni, F., Lantzsch, K., Lanza, A., Laplace, S., Lapoire, C., Laporte, J. F., Lari, T., Lasagni Manghi, F., Lassnig, M., Laurelli, P., Lavrijsen, W., Law, A. T., Laycock, P., Lazovich, T., Lazzaroni, M., Le, B., Le Dortz, O., Le Guirriec, E., Le Quilleuc, E. P., Leblanc, M., Lecompte, T., Ledroit Guillon, F., Lee, C. A., Lee, S. C., Lee, L., Lefebvre, B., Lefebvre, G., Lefebvre, M., Legger, F., Leggett, C., Lehan, A., Lehmann Miotto, G., Lei, X., Leight, W. A., Leisos, A., Leister, A. G., Leite, M. A. L., Leitner, R., Lellouch, D., Lemmer, B., Leney, K. J. C., Lenz, T., Lenzi, B., Leone, R., Leone, S., Leonidopoulos, C., Leontsinis, S., Lerner, G., Leroy, C., Lesage, A. A. J., Lester, C. G., Levchenko, M., Levêque, J., Levin, D., Levinson, L. J., Levy, M., Lewis, D., Leyko, A. M., Leyton, M., Li, B., Li, H., H. L., Li, Li, L., Li, Q., Li, S., Li, X., Li, Y., Liang, Z., Liberti, B., Liblong, A., Lichard, P., Lie, K., Liebal, J., Liebig, W., Limosani, A., Lin, S. C., Lin, T. H., Lindquist, B. E., Lionti, A. E., Lipeles, E., Lipniacka, A., Lisovyi, M., Liss, T. M., Lister, A., Litke, A. M., Liu, B., Liu, D., Liu, H., Liu, J., Liu, J. B., Liu, K., Liu, L., Liu, M., Liu, Y. L., Liu, Y., Livan, M., Lleres, A., Llorente Merino, J., Lloyd, S. L., Lo Sterzo, F., Lobodzinska, E., Loch, P., Lockman, W. S., Loebinger, F. K., Loevschall Jensen, A. E., Loew, K. M., Loginov, A., Lohse, T., Lohwasser, K., Lokajicek, M., Long, B. A., Long, J. D., Long, R. E., Longo, L., Looper, K. A., Lopes, L., Lopez Mateos, D., Lopez Paredes, B., Lopez Paz, I., Lopez Solis, A., Lorenz, J., Lorenzo Martinez, N., Losada, M., Lösel, P. J., Lou, X., Lounis, A., Love, J., Love, P. A., Lu, H., Lu, N., Lubatti, H. J., Luci, C., Lucotte, A., Luedtke, C., Luehring, F., Lukas, W., Luminari, L., Lundberg, O., Lund Jensen, B., Luzi, P. M., Lynn, D., Lysak, R., Lytken, E., Lyubushkin, V., Ma, H., L. L., Ma, Ma, Y., Maccarrone, G., Macchiolo, A., Macdonald, C. M., Maček, B., Machado Miguens, J., Madaffari, D., Madar, R., Maddocks, H. J., Mader, W. F., Madsen, A., Maeda, J., Maeland, S., Maeno, T., Maevskiy, A., Magradze, E., Mahlstedt, J., Maiani, C., Maidantchik, C., Maier, A. A., Maier, T., Maio, A., Majewski, S., Makida, Y., Makovec, N., Malaescu, B., Malecki, P. a., Maleev, V. P., Malek, F., Mallik, U., Malon, D., Malone, C., Maltezos, S., Malyukov, S., Mamuzic, J., Mancini, G., Mandelli, B., Mandelli, L., Mandić, I., Maneira, J., Manhaes de Andrade Filho, L., Manjarres Ramos, J., Mann, A., Manousos, A., Mansoulie, B., Mansour, J. D., Mantifel, R., Mantoani, M., Manzoni, S., Mapelli, L., Marceca, G., March, L., Marchiori, G., Marcisovsky, M., Marjanovic, M., Marley, D. E., Marroquim, F., Marsden, S. P., Marshall, Z., Marti Garcia, S., Martin, B., Martin, T. A., Martin, V. J., Martin dit Latour, B., Martinez, M., Martinez Outschoorn, V. I., Martin Haugh, S., Martoiu, V. S., Martyniuk, A. C., Marx, M., Marzin, A., Masetti, L., Mashimo, T., Mashinistov, R., Masik, J., Maslennikov, A. L., Massa, I., Massa, L., Mastrandrea, P., Mastroberardino, A., Masubuchi, T., Mättig, P., Mattmann, J., Maurer, J., Maxfield, S. J., Maximov, D. A., Mazini, R., Mazza, S. M., Mc Fadden, N. C., Mc Goldrick, G., Mc Kee, S. P., Mccarn, A., Mccarthy, R. L., Mccarthy, T. G., Mcclymont, L. I., Mcdonald, E. F., Mcfayden, J. A., Mchedlidze, G., Mcmahon, S. J., Mcpherson, R. A., Medinnis, M., Meehan, S., Mehlhase, S., Mehta, A., Meier, K., Meineck, C., Meirose, B., Melini, D., Mellado Garcia, B. R., Melo, M., Meloni, F., Mengarelli, A., Menke, S., Meoni, E., Mergelmeyer, S., Mermod, P., Merola, L., Meroni, C., Merritt, F. S., Messina, A., Metcalfe, J., Mete, A. S., Meyer, C., Meyer, J. P., Meyer, J., Meyer Zu Theenhausen, H., Miano, F., Middleton, R. P., Miglioranzi, S., Mijović, L., Mikenberg, G., Mikestikova, M., Mikuž, M., Milesi, M., Milic, A., Miller, D. W., Mills, C., Milov, A., Milstead, D. A., Minaenko, A. A., Minami, Y., Minashvili, I. A., Mincer, A. I., Mindur, B., Mineev, M., Ming, Y., Mir, L. M., Mistry, K. P., Mitani, T., Mitrevski, J., Mitsou, V. A., Miucci, A., Miyagawa, P. S., Mjörnmark, J. U., Moa, T., Mochizuki, K., Mohapatra, S., Molander, S., Moles Valls, R., Monden, R., Mondragon, M. C., Mönig, K., Monk, J., Monnier, E., Montalbano, A., Montejo Berlingen, J., Monticelli, F., Monzani, S., Moore, R. W., Morange, N., Moreno, D., Moreno Llácer, M., Morettini, P., Mori, D., Mori, T., Morii, M., Morinaga, M., Morisbak, V., Moritz, S., Morley, A. K., Mornacchi, G., Morris, J. D., Mortensen, S. S., Morvaj, L., Mosidze, M., Moss, J., Motohashi, K., Mount, R., Mountricha, E., Mouraviev, S. V., Moyse, E. J. W., Muanza, S., Mudd, R. D., Mueller, F., Mueller, J., Mueller, R. S. P., Mueller, T., Muenstermann, D., Mullen, P., Mullier, G. A., Munoz Sanchez, F. J., Murillo Quijada, J. A., Murray, W. J., Musheghyan, H., Muškinja, M., Myagkov, A. G., Myska, M., Nachman, B. P., Nackenhorst, O., Nagai, K., Nagai, R., Nagano, K., Nagasaka, Y., Nagata, K., Nagel, M., Nagy, E., Nairz, A. M., Nakahama, Y., Nakamura, K., Nakamura, T., Nakano, I., Namasivayam, H., Naranjo Garcia, R. F., Narayan, R., Narrias Villar, D. I., Naryshkin, I., Naumann, T., Navarro, G., Nayyar, R., Neal, H. A., Nechaeva, P. Y. u., Neep, T. J., Negri, A., Negrini, M., Nektarijevic, S., Nellist, C., Nelson, A., Nemecek, S., Nemethy, P., Nepomuceno, A. A., Nessi, M., Neubauer, M. S., Neumann, M., Neves, R. M., Nevski, P., Newman, P. R., Nguyen, D. H., Nguyen Manh, T., Nickerson, R. B., Nicolaidou, R., Nielsen, J., Nikiforov, A., Nikolaenko, V., Nikolic Audit, I., Nikolopoulos, K., Nilsen, J. K., Nilsson, P., Ninomiya, Y., Nisati, A., Nisius, R., Nobe, T., Nomachi, M., Nomidis, I., Nooney, T., Norberg, S., Nordberg, M., Norjoharuddeen, N., Novgorodova, O., Nowak, S., Nozaki, M., Nozka, L., Ntekas, K., Nurse, E., Nuti, F., O'Grady, F., O'Neil, D. C., O'Rourke, A. A., O'Shea, V., Oakham, F. G., Oberlack, H., Obermann, T., Ocariz, J., Ochi, A., Ochoa, I., Ochoa Ricoux, J. P., Oda, S., Odaka, S., Ogren, H., Oh, A., S. H., Oh, Ohm, C. C., Ohman, H., Oide, H., Okawa, H., Okumura, Y., Okuyama, T., Olariu, A., Oleiro Seabra, L. F., Olivares Pino, S. A., Oliveira Damazio, D., Olszewski, A., Olszowska, J., Onofre, A., Onogi, K., Onyisi, P. U. E., Oreglia, M. J., Oren, Y., Orestano, D., Orlando, N., Orr, R. S., Osculati, B., Ospanov, R., Otero y. Garzon, G., Otono, H., Ouchrif, M., Ould Saada, F., Ouraou, A., Oussoren, K. P., Ouyang, Q., Owen, M., Owen, R. E., Ozcan, V. E., Ozturk, N., Pachal, K., Pacheco Pages, A., Pacheco Rodriguez, L., Padilla Aranda, C., Pagáčová, M., Pagan Griso, S., Paige, F., Pais, P., Pajchel, K., Palacino, G., Palazzo, S., Palestini, S., Palka, M., Pallin, D., Panagiotopoulou, E. S. t., Pandini, C. E., Panduro Vazquez, J. G., Pani, P., Panitkin, S., Pantea, D., Paolozzi, L., Papadopoulou, T. h. D., Papageorgiou, K., Paramonov, A., Paredes Hernandez, D., Parker, A. J., Parker, M. A., Parker, K. A., Parodi, F., Parsons, J. A., Parzefall, U., Pascuzzi, V. R., Pasqualucci, E., Passaggio, S., Pastore, F. r., Pásztor, G., Pataraia, S., Pater, J. R., Pauly, T., Pearce, J., Pearson, B., Pedersen, L. E., Pedersen, M., Pedraza Lopez, S., Pedro, R., Peleganchuk, S. V., Penc, O., Peng, C., Peng, H., Penwell, J., Peralva, B. S., Perego, M. M., Perepelitsa, D. V., Perez Codina, E., Perini, L., Pernegger, H., Perrella, S., Peschke, R., Peshekhonov, V. D., Peters, K., Peters, R. F. Y., Petersen, B. A., Petersen, T. C., Petit, E., Petridis, A., Petridou, C., Petroff, P., Petrolo, E., Petrov, M., Petrucci, F., Pettersson, N. E., Peyaud, A., Pezoa, R., Phillips, P. W., Piacquadio, G., Pianori, E., Picazio, A., Piccaro, E., Piccinini, M., Pickering, M. A., Piegaia, R., Pilcher, J. E., Pilkington, A. D., Pin, A. W. J., Pinamonti, M., Pinfold, J. L., Pingel, A., Pires, S., Pirumov, H., Pitt, M., Plazak, L., Pleier, M. A., Pleskot, V., Plotnikova, E., Plucinski, P., Pluth, D., Poettgen, R., Poggioli, L., Pohl, D., Polesello, G., Poley, A., Policicchio, A., Polifka, R., Polini, A., Pollard, C. S., Polychronakos, V., Pommès, K., Pontecorvo, L., Pope, B. G., Popeneciu, G. A., Popovic, D. S., Poppleton, A., Pospisil, S., Potamianos, K., Potrap, I. N., Potter, C. J., Potter, C. T., Poulard, G., Poveda, J., Pozdnyakov, V., Pozo Astigarraga, M. E., Pralavorio, P., Pranko, A., Prell, S., Price, D., Price, L. E., Primavera, M., Prince, S., Prokofiev, K., Prokoshin, F., Protopopescu, S., Proudfoot, J., Przybycien, M., Puddu, D., Purohit, M., Puzo, P., Qian, J., Qin, G., Qin, Y., Quadt, A., Quayle, W. B., Queitsch Maitland, M., Quilty, D., Raddum, S., Radeka, V., Radescu, V., Radhakrishnan, S. K., Radloff, P., Rados, P., Ragusa, F., Rahal, G., Raine, J. A., Rajagopalan, S., Rammensee, M., Rangel Smith, C., Ratti, M. G., Rauscher, F., Rave, S., Ravenscroft, T., Ravinovich, I., Raymond, M., Read, A. L., Readioff, N. P., Reale, M., Rebuzzi, D. M., Redelbach, A., Redlinger, G., Reece, R., Reeves, K., Rehnisch, L., Reichert, J., Reisin, H., Rembser, C., Ren, H., Rescigno, M., Resconi, S., Rezanova, O. L., Reznicek, P., Rezvani, R., Richter, R., Richter, S., Richter Was, E., Ricken, O., Ridel, M., Rieck, P., Riegel, C. J., Rieger, J., Rifki, O., Rijssenbeek, M., Rimoldi, A., Rimoldi, M., Rinaldi, L., Ristić, B., Ritsch, E., Riu, I., Rizatdinova, F., Rizvi, E., Rizzi, C., Robertson, S. H., Robichaud Veronneau, A., Robinson, D., Robinson, J. E. M., Robson, A., Roda, CHIARA MARIA ANGELA, Rodina, Y., Rodriguez Perez, A., Rodriguez Rodriguez, D., Roe, S., Rogan, C. S., Røhne, O., Romaniouk, A., Romano, M., Romano Saez, S. M., Romero Adam, E., Rompotis, N., Ronzani, M., Roos, L., Ros, E., Rosati, S., Rosbach, K., Rose, P., Rosenthal, O., Rosien, N. A., Rossetti, V., Rossi, E., Rossi, L. P., Rosten, J. H. N., Rosten, R., Rotaru, M., Roth, I., Rothberg, J., Rousseau, D., Royon, C. R., Rozanov, A., Rozen, Y., Ruan, X., Rubbo, F., Rudolph, M. S., Rühr, F., Ruiz Martinez, A., Rurikova, Z., Rusakovich, N. A., Ruschke, A., Russell, H. L., Rutherfoord, J. P., Ruthmann, N., Ryabov, Y. F., Rybar, M., Rybkin, G., Ryu, S., Ryzhov, A., Rzehorz, G. F., Saavedra, A. F., Sabato, G., Sacerdoti, S., Sadrozinski, H. F. W., Sadykov, R., Safai Tehrani, F., Saha, P., Sahinsoy, M., Saimpert, M., Saito, T., Sakamoto, H., Sakurai, Y., Salamanna, G., Salamon, A., Salazar Loyola, J. E., Salek, D., Sales De Bruin, P. H., Salihagic, D., Salnikov, A., Salt, J., Salvatore, D., Salvatore, F., Salvucci, A., Salzburger, A., Sammel, D., Sampsonidis, D., Sanchez, A., Sánchez, J., Sanchez Martinez, V., Sandaker, H., Sandbach, R. L., Sander, H. G., Sandhoff, M., Sandoval, C., Sandstroem, R., Sankey, D. P. C., Sannino, M., Sansoni, A., Santoni, C., Santonico, R., Santos, H., Santoyo Castillo, I., Sapp, K., Sapronov, A., Saraiva, J. G., Sarrazin, B., Sasaki, O., Sasaki, Y., Sato, K., Sauvage, G., Sauvan, E., Savage, G., Savard, P., Savic, N., Sawyer, C., Sawyer, L., Saxon, J., Sbarra, C., Sbrizzi, A., Scanlon, T., Scannicchio, D. A., Scarcella, M., Scarfone, V., Schaarschmidt, J., Schacht, P., Schachtner, B. M., Schaefer, D., Schaefer, R., Schaeffer, J., Schaepe, S., Schaetzel, S., Schäfer, U., Schaffer, A. C., Schaile, D., Schamberger, R. D., Scharf, V., Schegelsky, V. A., Scheirich, D., Schernau, M., Schiavi, C., Schier, S., Schillo, C., Schioppa, M., Schlenker, S., Schmidt Sommerfeld, K. R., Schmieden, K., Schmitt, C., Schmitt, S., Schmitz, S., Schneider, B., Schnoor, U., Schoeffel, L., Schoening, A., Schoenrock, B. D., Schopf, E., Schott, M., Schovancova, J., Schramm, S., Schreyer, M., Schuh, N., Schulte, A., Schultens, M. J., Schultz Coulon, H. C., Schulz, H., Schumacher, M., Schumm, B. A., Schune, P. h., Schwartzman, A., Schwarz, T. A., Schweiger, H., Schwemling, P. h., Schwienhorst, R., Schwindling, J., Schwindt, T., Sciolla, G., Scuri, F., Scutti, F., Searcy, J., Seema, P., Seidel, S. C., Seiden, A., Seifert, F., Seixas, J. M., Sekhniaidze, G., Sekhon, K., Sekula, S. J., Seliverstov, D. M., Semprini Cesari, N., Serfon, C., Serin, L., Serkin, L., Sessa, M., Seuster, R., Severini, H., Sfiligoj, T., Sforza, F., Sfyrla, A., Shabalina, E., Shaikh, N. W., Shan, L. Y., Shang, R., Shank, J. T., Shapiro, M., Shatalov, P. B., Shaw, K., Shaw, S. M., Shcherbakova, A., Shehu, C. Y., Sherwood, P., Shi, L., Shimizu, S., Shimmin, C. O., Shimojima, M., Shiyakova, M., Shmeleva, A., Shoaleh Saadi, D., Shochet, M. J., Shojaii, S., Shrestha, S., Shulga, E., Shupe, M. A., Sicho, P., Sickles, A. M., Sidebo, P. E., Sidiropoulou, O., Sidorov, D., Sidoti, A., Siegert, F., Sijacki, D. j., Silva, J., Silverstein, S. B., Simak, V., Simic, L. j., Simion, S., Simioni, E., Simmons, B., Simon, D., Simon, M., Sinervo, P., Sinev, N. B., Sioli, M., Siragusa, G., Sivoklokov, S. Y. u., Sjölin, J., Skinner, M. B., Skottowe, H. P., Skubic, P., Slater, M., Slavicek, T., Slawinska, M., Sliwa, K., Slovak, R., Smakhtin, V., Smart, B. H., Smestad, L., Smiesko, J., Smirnov, S. Y. u., Smirnov, Y., Smirnova, L. N., Smirnova, O., Smith, M. N. K., Smith, R. W., Smizanska, M., Smolek, K., Snesarev, A. A., Snyder, S., Sobie, R., Socher, F., Soffer, A., Soh, D. A., Sokhrannyi, G., Solans Sanchez, C. A., Solar, M., Soldatov, E. Y. u., Soldevila, U., Solodkov, A. A., Soloshenko, A., Solovyanov, O. V., Solovyev, V., Sommer, P., Son, H., Song, H. Y., Sood, A., Sopczak, A., Sopko, V., Sorin, V., Sosa, D., Sotiropoulou, C. L., Soualah, R., Soukharev, A. M., South, D., Sowden, B. C., Spagnolo, S., Spalla, M., Spangenberg, M., Spanò, F., Sperlich, D., Spettel, F., Spighi, R., Spigo, G., Spiller, L. A., Spousta, M., R. D., S. t. Denis, Stabile, A., Stamen, R., Stamm, S., Stanecka, E., Stanek, R. W., Stanescu, C., Stanescu Bellu, M., Stanitzki, M. M., Stapnes, S., Starchenko, E. A., Stark, G. H., Stark, J., Staroba, P., Starovoitov, P., Stärz, S., Staszewski, R., Steinberg, P., Stelzer, B., Stelzer, H. J., Stelzer Chilton, O., Stenzel, H., Stewart, G. A., Stillings, J. A., Stockton, M. C., Stoebe, M., Stoicea, G., Stolte, P., Stonjek, S., Stradling, A. R., Straessner, A., Stramaglia, M. E., Strandberg, J., Strandberg, S., Strandlie, A., Strauss, M., Strizenec, P., Ströhmer, R., Strom, D. M., Stroynowski, R., Strubig, A., Stucci, S. A., Stugu, B., Styles, N. A., Su, D., Su, J., Suchek, S., Sugaya, Y., Suk, M., Sulin, V. V., Sultansoy, S., Sumida, T., Sun, S., Sun, X., Sundermann, J. E., Suruliz, K., Susinno, G., Sutton, M. R., Suzuki, S., Svatos, M., Swiatlowski, M., Sykora, I., Sykora, T., Ta, D., Taccini, C., Tackmann, K., Taenzer, J., Taffard, A., Tafirout, R., Taiblum, N., Takai, H., Takashima, R., Takeshita, T., Takubo, Y., Talby, M., Talyshev, A. A., Tan, K. G., Tanaka, J., Tanaka, M., Tanaka, R., Tanaka, S., Tannenwald, B. B., Tapia Araya, S., Tapprogge, S., Tarem, S., Tartarelli, G. F., Tas, P., Tasevsky, M., Tashiro, T., Tassi, E., Tavares Delgado, A., Tayalati, Y., Taylor, A. C., Taylor, G. N., Taylor, P. T. E., Taylor, W., Teischinger, F. A., Teixeira Dias, P., Temming, K. K., Temple, D., Ten Kate, H., Teng, P. K., Teoh, J. J., Tepel, F., Terada, S., Terashi, K., Terron, J., Terzo, S., Testa, M., Teuscher, R. J., Theveneaux Pelzer, T., Thomas, J. P., Thomas Wilsker, J., Thompson, E. N., Thompson, P. D., Thompson, A. S., Thomsen, L. A., Thomson, E., Thomson, M., Tibbetts, M. J., Ticse Torres, R. E., Tikhomirov, V. O., Tikhonov, Y. u. A., Timoshenko, S., Tipton, P., Tisserant, S., Todome, K., Todorov, T., Todorova Nova, S., Tojo, J., Tokár, S., Tokushuku, K., Tolley, E., Tomlinson, L., Tomoto, M., Tompkins, L., Toms, K., Tong, B., Torrence, E., Torres, H., Torró Pastor, E., Toth, J., Touchard, F., Tovey, D. R., Trefzger, T., Tricoli, A., Trigger, I. M., Trincaz Duvoid, S., Tripiana, M. F., Trischuk, W., Trocmé, B., Trofymov, A., Troncon, C., Trottier McDonald, M., Trovatelli, M., Truong, L., Trzebinski, M., Trzupek, A., Tseng, J. C. L., Tsiareshka, P. V., Tsipolitis, G., Tsirintanis, N., Tsiskaridze, S., Tsiskaridze, V., Tskhadadze, E. G., Tsui, K. M., Tsukerman, I. I., Tsulaia, V., Tsuno, S., Tsybychev, D., Tu, Y., Tudorache, A., Tudorache, V., Tuna, A. N., Tupputi, S. A., Turchikhin, S., Turecek, D., Turgeman, D., Turra, R., Turvey, A. J., Tuts, P. M., Tyndel, M., Ucchielli, G., Ueda, I., Ughetto, M., Ukegawa, F., Unal, G., Undrus, A., Unel, G., Ungaro, F. C., Unno, Y., Unverdorben, C., Urban, J., Urquijo, P., Urrejola, P., Usai, G., Usanova, A., Vacavant, L., Vacek, V., Vachon, B., Valderanis, C., Valdes Santurio, E., Valencic, N., Valentinetti, S., Valero, A., Valery, L., Valkar, S., Valls Ferrer, J. A., Van Den Wollenberg, W., Van Der Deijl, P. C., van der Graaf, H., van Eldik, N., van Gemmeren, P., Van Nieuwkoop, J., van Vulpen, I., van Woerden, M. C., Vanadia, M., Vandelli, W., Vanguri, R., Vaniachine, A., Vankov, P., Vardanyan, G., Vari, R., Varnes, E. W., Varol, T., Varouchas, D., Vartapetian, A., Varvell, K. E., Vasquez, J. G., Vazeille, F., Vazquez Schroeder, T., Veatch, J., Veeraraghavan, V., Veloce, L. M., Veloso, F., Veneziano, S., Ventura, A., Venturi, M., Venturi, N., Venturini, A., Vercesi, V., Verducci, M., Verkerke, W., Vermeulen, J. C., Vest, A., Vetterli, M. C., Viazlo, O., Vichou, I., Vickey, T., Vickey Boeriu, O. E., Viehhauser, G. H. A., Viel, S., Vigani, L., Villa, M., Villaplana Perez, M., Vilucchi, E., Vincter, M. G., Vinogradov, V. B., Vittori, C., Vivarelli, I., Vlachos, S., Vlasak, M., Vogel, M., Vokac, P., Volpi, G., Volpi, M., von der Schmitt, H., von Toerne, E., Vorobel, V., Vorobev, K., Vos, M., Voss, R., Vossebeld, J. H., Vranjes, N., Vranjes Milosavljevic, M., Vrba, V., Vreeswijk, M., Vuillermet, R., Vukotic, I., Vykydal, Z., Wagner, P., Wagner, W., Wahlberg, H., Wahrmund, S., Wakabayashi, J., Walder, J., Walker, R., Walkowiak, W., Wallangen, V., Wang, C., Wang, F., Wang, H., Wang, J., Wang, K., Wang, R., Wang, S. M., Wang, T., Wang, W., Wang, X., Wanotayaroj, C., Warburton, A., Ward, C. P., Wardrope, D. R., Washbrook, A., Watkins, P. M., Watson, A. T., Watson, M. F., Watts, G., Watts, S., Waugh, B. M., Webb, S., Weber, M. S., Weber, S. W., Webster, J. S., Weidberg, A. R., Weinert, B., Weingarten, J., Weiser, C., Weits, H., Wells, P. S., Wenaus, T., Wengler, T., Wenig, S., Wermes, N., Werner, M., Werner, M. D., Werner, P., Wessels, M., Wetter, J., Whalen, K., Whallon, N. L., Wharton, A. M., White, A., White, M. J., White, R., Whiteson, D., Wickens, F. J., Wiedenmann, W., Wielers, M., Wienemann, P., Wiglesworth, C., Wiik Fuchs, L. A. M., Wildauer, A., Wilk, F., Wilkens, H. G., Williams, H. H., Williams, S., Willis, C., Willocq, S., Wilson, J. A., Wingerter Seez, I., Winklmeier, F., Winston, O. J., Winter, B. T., Wittgen, M., Wittkowski, J., Wolf, T. M. H., Wolter, M. W., Wolters, H., Worm, S. D., Wosiek, B. K., Wotschack, J., Woudstra, M. J., Wozniak, K. W., Wu, M., S. L., Wu, Wu, X., Wu, Y., Wyatt, T. R., Wynne, B. M., Xella, S., Xu, D., Xu, L., Yabsley, B., Yacoob, S., Yamaguchi, D., Yamaguchi, Y., Yamamoto, A., Yamamoto, S., Yamanaka, T., Yamauchi, K., Yamazaki, Y., Yan, Z., Yang, H., Yang, Y., Yang, Z., Yao, W. M., Yap, Y. C., Yasu, Y., Yatsenko, E., Yau Wong, K. H., Ye, J., Ye, S., Yeletskikh, I., Yen, A. L., Yildirim, E., Yorita, K., Yoshida, R., Yoshihara, K., Young, C., Young, C. J. S., Youssef, S., D. R., Yu, Yu, J., J. M., Yu, Yuan, L., Yuen, S. P. Y., Yusuff, I., Zabinski, B., Zaidan, R., Zaitsev, A. M., Zakharchuk, N., Zalieckas, J., Zaman, A., Zambito, S., Zanello, L., Zanzi, D., Zeitnitz, C., Zeman, M., Zemla, A., Zeng, J. C., Zeng, Q., Zengel, K., Zenin, O., Ženiš, T., Zerwas, D., Zhang, D., Zhang, F., Zhang, G., Zhang, H., Zhang, J., Zhang, L., Zhang, R., Zhang, X., Zhang, Z., Zhao, X., Zhao, Y., Zhao, Z., Zhemchugov, A., Zhong, J., Zhou, B., Zhou, C., Zhou, L., Zhou, M., Zhou, N., Zhu, C. G., Zhu, H., Zhu, J., Zhu, Y., Zhuang, X., Zhukov, K., Zibell, A., Zieminska, D., Zimine, N. I., Zimmermann, C., Zimmermann, S., Zinonos, Z., Zinser, M., Ziolkowski, M., Živković, L., Zobernig, G., Zoccoli, A., zur Nedden, M., Zwalinski, L., and M. Aaboud, G. Aad, B. Abbott, J. Abdallah, O. Abdinov, B. Abeloos, R. Aben, O.S. AbouZeid, N.L. Abraham, H. Abramowicz, H. Abreu, R. Abreu, Y. Abulaiti, B.S. Acharya, L. Adamczyk, D.L. Adams, J. Adelman, M. Adersberger, S. Adomeit, T. Adye, A.A. Affolder, T. Agatonovic-Jovin, J. Agricola, J.A. Aguilar-Saavedra, S.P. Ahlen, F. Ahmadov, G. Aielli, H. Akerstedt, T.P.A. Åkesson, A.V. Akimov, G.L. Alberghi, J. Albert, S. Albrand, M.J. Alconada Verzini, M. Aleksa, I.N. Aleksandrov, C. Alexa, G. Alexander, T. Alexopoulos, M. Alhroob, B. Ali, M. Aliev, G. Alimonti, J. Alison, S.P. Alkire, B.M.M. Allbrooke, B.W. Allen, P.P. Allport, A. Aloisio, A. Alonso, F. Alonso, C. Alpigiani, M. Alstaty, B. Alvarez Gonzalez, D. Álvarez Piqueras, M.G. Alviggi, B.T. Amadio, K. Amako, Y. Amaral Coutinho, C. Amelung, D. Amidei, S.P. Amor Dos Santos, A. Amorim, S. Amoroso, G. Amundsen, C. Anastopoulos, L.S. Ancu, N. Andari, T. Andeen, C.F. Anders, G. Anders, J.K. Anders, K.J. Anderson, A. Andreazza, V. Andrei, S. Angelidakis, I. Angelozzi, P. Anger, A. Angerami, F. Anghinolfi, A.V. Anisenkov, N. Anjos, A. Annovi, C. Antel, M. Antonelli, A. Antonov, F. Anulli, M. Aoki, L. Aperio Bella, G. Arabidze, Y. Arai, J.P. Araque, A.T.H. Arce, F.A. Arduh, J-F. Arguin, S. Argyropoulos, M. Arik, A.J. Armbruster, L.J. Armitage, O. Arnaez, H. Arnold, M. Arratia, O. Arslan, A. Artamonov, G. Artoni, S. Artz, S. Asai, N. Asbah, A. Ashkenazi, B. Åsman, L. Asquith, K. Assamagan, R. Astalos, M. Atkinson, N.B. Atlay, K. Augsten, G. Avolio, B. Axen, M.K. Ayoub, G. Azuelos, M.A. Baak, A.E. Baas, M.J. Baca, H. Bachacou, K. Bachas, M. Backes, M. Backhaus, P. Bagiacchi, P. Bagnaia, Y. Bai, J.T. Baines, O.K. Baker, E.M. Baldin, P. Balek, T. Balestri, F. Balli, W.K. Balunas, E. Banas, Sw. Banerjee, A.A.E. Bannoura, L. Barak, E.L. Barberio, D. Barberis, M. Barbero, T. Barillari, M-S Barisits, T. Barklow, N. Barlow, S.L. Barnes, B.M. Barnett, R.M. Barnett, Z. Barnovska, A. Baroncelli, G. Barone, A.J. Barr, L. Barranco Navarro, F. Barreiro, J. Barreiro Guimarães da Costa, R. Bartoldus, A.E. Barton, P. Bartos, A. Basalaev, A. Bassalat, R.L. Bates, S.J. Batista, J.R. Batley, M. Battaglia, M. Bauce, F. Bauer, H.S. Bawa, J.B. Beacham, M.D. Beattie, T. Beau, P.H. Beauchemin, P. Bechtle, H.P. Beck, K. Becker, M. Becker, M. Beckingham, C. Becot, A.J. Beddall, A. Beddall, V.A. Bednyakov, M. Bedognetti, C.P. Bee, L.J. Beemster, T.A. Beermann, M. Begel, J.K. Behr, C. Belanger-Champagne, A.S. Bell, G. Bella, L. Bellagamba, A. Bellerive, M. Bellomo, K. Belotskiy, O. Beltramello, N.L. Belyaev, O. Benary, D. Benchekroun, M. Bender, K. Bendtz, N. Benekos, Y. Benhammou, E. Benhar Noccioli, J. Benitez, D.P. Benjamin, J.R. Bensinger, S. Bentvelsen, L. Beresford, M. Beretta, D. Berge, E. Bergeaas Kuutmann, N. Berger, J. Beringer, S. Berlendis, N.R. Bernard, C. Bernius, F.U. Bernlochner, T. Berry, P. Berta, C. Bertella, G. Bertoli, F. Bertolucci, I.A. Bertram, C. Bertsche, D. Bertsche, G.J. Besjes, O. Bessidskaia Bylund, M. Bessner, N. Besson, C. Betancourt, S. Bethke, A.J. Bevan, R.M. Bianchi, L. Bianchini, M. Bianco, O. Biebel, D. Biedermann, R. Bielski, N.V. Biesuz, M. Biglietti, J. Bilbao De Mendizabal, T.R.V. Billoud, H. Bilokon, M. Bindi, S. Binet, A. Bingul, C. Bini, S. Biondi, D.M. Bjergaard, C.W. Black, J.E. Black, K.M. Black, D. Blackburn, R.E. Blair, J.-B. Blanchard, T. Blazek, I. Bloch, C. Blocker, W. Blum, U. Blumenschein, S. Blunier, G.J. Bobbink, V.S. Bobrovnikov, S.S. Bocchetta, A. Bocci, C. Bock, M. Boehler, D. Boerner, J.A. Bogaerts, D. Bogavac, A.G. Bogdanchikov, C. Bohm, V. Boisvert, P. Bokan, T. Bold, A.S. Boldyrev, M. Bomben, M. Bona, M. Boonekamp, A. Borisov, G. Borissov, J. Bortfeldt, D. Bortoletto, V. Bortolotto, K. Bos, D. Boscherini, M. Bosman, J.D. Bossio Sola, J. Boudreau, J. Bouffard, E.V. Bouhova-Thacker, D. Boumediene, C. Bourdarios, S.K. Boutle, A. Boveia, J. Boyd, I.R. Boyko, J. Bracinik, A. Brandt, G. Brandt, O. Brandt, U. Bratzler, B. Brau, J.E. Brau, H.M. Braun, W.D. Breaden Madden, K. Brendlinger, A.J. Brennan, L. Brenner, R. Brenner, S. Bressler, T.M. Bristow, D. Britton, D. Britzger, F.M. Brochu, I. Brock, R. Brock, G. Brooijmans, T. Brooks, W.K. Brooks, J. Brosamer, E. Brost, J.H Broughton, P.A. Bruckman de Renstrom, D. Bruncko, R. Bruneliere, A. Bruni, G. Bruni, L.S. Bruni, BH Brunt, M. Bruschi, N. Bruscino, P. Bryant, L. Bryngemark, T. Buanes, Q. Buat, P. Buchholz, A.G. Buckley, I.A. Budagov, F. Buehrer, M.K. Bugge, O. Bulekov, D. Bullock, H. Burckhart, S. Burdin, C.D. Burgard, B. Burghgrave, K. Burka, S. Burke, I. Burmeister, J.T.P. Burr, E. Busato, D. Büscher, V. Büscher, P. Bussey, J.M. Butler, C.M. Buttar, J.M. Butterworth, P. Butti, W. Buttinger, A. Buzatu, A.R. Buzykaev, S. Cabrera Urbán, D. Caforio, V.M. Cairo, O. Cakir, N. Calace, P. Calafiura, A. Calandri, G. Calderini, P. Calfayan, G. Callea, L.P. Caloba, S. Calvente Lopez, D. Calvet, S. Calvet, T.P. Calvet, R. Camacho Toro, S. Camarda, P. Camarri, D. Cameron, R. Caminal Armadans, C. Camincher, S. Campana, M. Campanelli, A. Camplani, A. Campoverde, V. Canale, A. Canepa, M. Cano Bret, J. Cantero, R. Cantrill, T. Cao, M.D.M. Capeans Garrido, I. Caprini, M. Caprini, M. Capua, R. Caputo, R.M. Carbone, R. Cardarelli, F. Cardillo, I. Carli, T. Carli, G. Carlino, L. Carminati, S. Caron, E. Carquin, G.D. Carrillo-Montoya, J.R. Carter, J. Carvalho, D. Casadei, M.P. Casado, M. Casolino, D.W. Casper, E. Castaneda-Miranda, R. Castelijn, A. Castelli, V. Castillo Gimenez, N.F. Castro, A. Catinaccio, J.R. Catmore, A. Cattai, J. Caudron, V. Cavaliere, E. Cavallaro, D. Cavalli, M. Cavalli-Sforza, V. Cavasinni, F. Ceradini, L. Cerda Alberich, B.C. Cerio, A.S. Cerqueira, A. Cerri, L. Cerrito, F. Cerutti, M. Cerv, A. Cervelli, S.A. Cetin, A. Chafaq, D. Chakraborty, S.K. Chan, Y.L. Chan, P. Chang, J.D. Chapman, D.G. Charlton, A. Chatterjee, C.C. Chau, C.A. Chavez Barajas, S. Che, S. Cheatham, A. Chegwidden, S. Chekanov, S.V. Chekulaev, G.A. Chelkov, M.A. Chelstowska, C. Chen, H. Chen, K. Chen, S. Chen, S. Chen, X. Chen, Y. Chen, H.C. Cheng, H.J Cheng, Y. Cheng, A. Cheplakov, E. Cheremushkina, R. Cherkaoui El Moursli, V. Chernyatin, E. Cheu, L. Chevalier, V. Chiarella, G. Chiarelli, G. Chiodini, A.S. Chisholm, A. Chitan, M.V. Chizhov, K. Choi, A.R. Chomont, S. Chouridou, B.K.B. Chow, V. Christodoulou, D. Chromek-Burckhart, J. Chudoba, A.J. Chuinard, J.J. Chwastowski, L. Chytka, G. Ciapetti, A.K. Ciftci, D. Cinca, V. Cindro, I.A. Cioara, C. Ciocca, A. Ciocio, F. Cirotto, Z.H. Citron, M. Citterio, M. Ciubancan, A. Clark, B.L. Clark, M.R. Clark, P.J. Clark, R.N. Clarke, C. Clement, Y. Coadou, M. Cobal, A. Coccaro, J. Cochran, L. Colasurdo, B. Cole, A.P. Colijn, J. Collot, T. Colombo, G. Compostella, P. Conde Muiño, E. Coniavitis, S.H. Connell, I.A. Connelly, V. Consorti, S. Constantinescu, G. Conti, F. Conventi, M. Cooke, B.D. Cooper, A.M. Cooper-Sarkar, K.J.R. Cormier, T. Cornelissen, M. Corradi, F. Corriveau, A. Corso-Radu, A. Cortes-Gonzalez, G. Cortiana, G. Costa, M.J. Costa, D. Costanzo, G. Cottin, G. Cowan, B.E. Cox, K. Cranmer, S.J. Crawley, G. Cree, S. Crépé-Renaudin, F. Crescioli, W.A. Cribbs, M. Crispin Ortuzar, M. Cristinziani, V. Croft, G. Crosetti, A. Cueto, T. Cuhadar Donszelmann, J. Cummings, M. Curatolo, J. Cúth, H. Czirr, P. Czodrowski, G. D'amen, S. D'Auria, M. D'Onofrio, M.J. Da Cunha Sargedas De Sousa, C. Da Via, W. Dabrowski, T. Dado, T. Dai, O. Dale, F. Dallaire, C. Dallapiccola, M. Dam, J.R. Dandoy, N.P. Dang, A.C. Daniells, N.S. Dann, M. Danninger, M. Dano Hoffmann, V. Dao, G. Darbo, S. Darmora, J. Dassoulas, A. Dattagupta, W. Davey, C. David, T. Davidek, M. Davies, P. Davison, E. Dawe, I. Dawson, R.K. Daya-Ishmukhametova, K. De, R. de Asmundis, A. De Benedetti, S. De Castro, S. De Cecco, N. De Groot, P. de Jong, H. De la Torre, F. De Lorenzi, A. De Maria, D. De Pedis, A. De Salvo, U. De Sanctis, A. De Santo, J.B. De Vivie De Regie, W.J. Dearnaley, R. Debbe, C. Debenedetti, D.V. Dedovich, N. Dehghanian, I. Deigaard, M. Del Gaudio, J. Del Peso, T. Del Prete, D. Delgove, F. Deliot, C.M. Delitzsch, M. Deliyergiyev, A. Dell'Acqua, L. Dell'Asta, M. Dell'Orso, M. Della Pietra, D. della Volpe, M. Delmastro, P.A. Delsart, D.A. DeMarco, S. Demers, M. Demichev, A. Demilly, S.P. Denisov, D. Denysiuk, D. Derendarz, J.E. Derkaoui, F. Derue, P. Dervan, K. Desch, C. Deterre, K. Dette, P.O. Deviveiros, A. Dewhurst, S. Dhaliwal, A. Di Ciaccio, L. Di Ciaccio, W.K. Di Clemente, C. Di Donato, A. Di Girolamo, B. Di Girolamo, B. Di Micco, R. Di Nardo, A. Di Simone, R. Di Sipio, D. Di Valentino, C. Diaconu, M. Diamond, F.A. Dias, M.A. Diaz, E.B. Diehl, J. Dietrich, S. Diglio, A. Dimitrievska, J. Dingfelder, P. Dita, S. Dita, F. Dittus, F. Djama, T. Djobava, J.I. Djuvsland, M.A.B. do Vale, D. Dobos, M. Dobre, C. Doglioni, J. Dolejsi, Z. Dolezal, B.A. Dolgoshein, M. Donadelli, S. Donati, P. Dondero, J. Donini, J. Dopke, A. Doria, M.T. Dova, A.T. Doyle, E. Drechsler, M. Dris, Y. Du, J. Duarte-Campderros, E. Duchovni, G. Duckeck, O.A. Ducu, D. Duda, A. Dudarev, E.M. Duffield, L. Duflot, M. Dührssen, M. Dumancic, M. Dunford, H. Duran Yildiz, M. Düren, A. Durglishvili, D. Duschinger, B. Dutta, M. Dyndal, C. Eckardt, K.M. Ecker, R.C. Edgar, N.C. Edwards, T. Eifert, G. Eigen, K. Einsweiler, T. Ekelof, M. El Kacimi, V. Ellajosyula, M. Ellert, S. Elles, F. Ellinghaus, A.A. Elliot, N. Ellis, J. Elmsheuser, M. Elsing, D. Emeliyanov, Y. Enari, O.C. Endner, J.S. Ennis, J. Erdmann, A. Ereditato, G. Ernis, J. Ernst, M. Ernst, S. Errede, E. Ertel, M. Escalier, H. Esch, C. Escobar, B. Esposito, A.I. Etienvre, E. Etzion, H. Evans, A. Ezhilov, F. Fabbri, L. Fabbri, G. Facini, R.M. Fakhrutdinov, S. Falciano, R.J. Falla, J. Faltova, Y. Fang, M. Fanti, A. Farbin, A. Farilla, C. Farina, E.M. Farina, T. Farooque, S. Farrell, S.M. Farrington, P. Farthouat, F. Fassi, P. Fassnacht, D. Fassouliotis, M. Faucci Giannelli, A. Favareto, W.J. Fawcett, L. Fayard, O.L. Fedin, W. Fedorko, S. Feigl, L. Feligioni, C. Feng, E.J. Feng, H. Feng, A.B. Fenyuk, L. Feremenga, P. Fernandez Martinez, S. Fernandez Perez, J. Ferrando, A. Ferrari, P. Ferrari, R. Ferrari, D.E. Ferreira de Lima, A. Ferrer, D. Ferrere, C. Ferretti, A. Ferretto Parodi, F. Fiedler, A. Filipčič, M. Filipuzzi, F. Filthaut, M. Fincke-Keeler, K.D. Finelli, M.C.N. Fiolhais, L. Fiorini, A. Firan, A. Fischer, C. Fischer, J. Fischer, W.C. Fisher, N. Flaschel, I. Fleck, P. Fleischmann, G.T. Fletcher, R.R.M. Fletcher, T. Flick, A. Floderus, L.R. Flores Castillo, M.J. Flowerdew, G.T. Forcolin, A. Formica, A. Forti, A.G. Foster, D. Fournier, H. Fox, S. Fracchia, P. Francavilla, M. Franchini, D. Francis, L. Franconi, M. Franklin, M. Frate, M. Fraternali, D. Freeborn, S.M. Fressard-Batraneanu, F. Friedrich, D. Froidevaux, J.A. Frost, C. Fukunaga, E. Fullana Torregrosa, T. Fusayasu, J. Fuster, C. Gabaldon, O. Gabizon, A. Gabrielli, A. Gabrielli, G.P. Gach, S. Gadatsch, S. Gadomski, G. Gagliardi, L.G. Gagnon, P. Gagnon, C. Galea, B. Galhardo, E.J. Gallas, B.J. Gallop, P. Gallus, G. Galster, K.K. Gan, J. Gao, Y. Gao, Y.S. Gao, F.M. Garay Walls, C. García, J.E. García Navarro, M. Garcia-Sciveres, R.W. Gardner, N. Garelli, V. Garonne, A. Gascon Bravo, K. Gasnikova, C. Gatti, A. Gaudiello, G. Gaudio, L. Gauthier, I.L. Gavrilenko, C. Gay, G. Gaycken, E.N. Gazis, Z. Gecse, C.N.P. Gee, Ch. Geich-Gimbel, M. Geisen, M.P. Geisler, C. Gemme, M.H. Genest, C. Geng, S. Gentile, C. Gentsos, S. George, D. Gerbaudo, A. Gershon, S. Ghasemi, H. Ghazlane, M. Ghneimat, B. Giacobbe, S. Giagu, P. Giannetti, B. Gibbard, S.M. Gibson, M. Gignac, M. Gilchriese, T.P.S. Gillam, D. Gillberg, G. Gilles, D.M. Gingrich, N. Giokaris, M.P. Giordani, F.M. Giorgi, F.M. Giorgi, P.F. Giraud, P. Giromini, D. Giugni, F. Giuli, C. Giuliani, M. Giulini, B.K. Gjelsten, S. Gkaitatzis, I. Gkialas, E.L. Gkougkousis, L.K. Gladilin, C. Glasman, J. Glatzer, P.C.F. Glaysher, A. Glazov, M. Goblirsch-Kolb, J. Godlewski, S. Goldfarb, T. Golling, D. Golubkov, A. Gomes, R. Gonçalo, J. Goncalves Pinto Firmino Da Costa, G. Gonella, L. Gonella, A. Gongadze, S. González de la Hoz, G. Gonzalez Parra, S. Gonzalez-Sevilla, L. Goossens, P.A. Gorbounov, H.A. Gordon, I. Gorelov, B. Gorini, E. Gorini, A. Gorišek, E. Gornicki, A.T. Goshaw, C. Gössling, M.I. Gostkin, C.R. Goudet, D. Goujdami, A.G. Goussiou, N. Govender, E. Gozani, L. Graber, I. Grabowska-Bold, P.O.J. Gradin, P. Grafström, J. Gramling, E. Gramstad, S. Grancagnolo, V. Gratchev, P.M. Gravila, H.M. Gray, E. Graziani, Z.D. Greenwood, C. Grefe, K. Gregersen, I.M. Gregor, P. Grenier, K. Grevtsov, J. Griffiths, A.A. Grillo, K. Grimm, S. Grinstein, Ph. Gris, J.-F. Grivaz, S. Groh, J.P. Grohs, E. Gross, J. Grosse-Knetter, G.C. Grossi, Z.J. Grout, L. Guan, W. Guan, J. Guenther, F. Guescini, D. Guest, O. Gueta, E. Guido, T. Guillemin, S. Guindon, U. Gul, C. Gumpert, J. Guo, Y. Guo, R. Gupta, S. Gupta, G. Gustavino, P. Gutierrez, N.G. Gutierrez Ortiz, C. Gutschow, C. Guyot, C. Gwenlan, C.B. Gwilliam, A. Haas, C. Haber, H.K. Hadavand, N. Haddad, A. Hadef, P. Haefner, S. Hageböck, Z. Hajduk, H. Hakobyan, M. Haleem, J. Haley, G. Halladjian, G.D. Hallewell, K. Hamacher, P. Hamal, K. Hamano, A. Hamilton, G.N. Hamity, P.G. Hamnett, L. Han, K. Hanagaki, K. Hanawa, M. Hance, B. Haney, S. Hanisch, P. Hanke, R. Hanna, J.B. Hansen, J.D. Hansen, M.C. Hansen, P.H. Hansen, K. Hara, A.S. Hard, T. Harenberg, F. Hariri, S. Harkusha, R.D. Harrington, P.F. Harrison, F. Hartjes, N.M. Hartmann, M. Hasegawa, Y. Hasegawa, A. Hasib, S. Hassani, S. Haug, R. Hauser, L. Hauswald, M. Havranek, C.M. Hawkes, R.J. Hawkings, D. Hayakawa, D. Hayden, C.P. Hays, J.M. Hays, H.S. Hayward, S.J. Haywood, S.J. Head, T. Heck, V. Hedberg, L. Heelan, S. Heim, T. Heim, B. Heinemann, J.J. Heinrich, L. Heinrich, C. Heinz, J. Hejbal, L. Helary, S. Hellman, C. Helsens, J. Henderson, R.C.W. Henderson, Y. Heng, S. Henkelmann, A.M. Henriques Correia, S. Henrot-Versille, G.H. Herbert, Y. Hernández Jiménez, G. Herten, R. Hertenberger, L. Hervas, G.G. Hesketh, N.P. Hessey, J.W. Hetherly, R. Hickling, E. Higón-Rodriguez, E. Hill, J.C. Hill, K.H. Hiller, S.J. Hillier, I. Hinchliffe, E. Hines, R.R. Hinman, M. Hirose, D. Hirschbuehl, J. Hobbs, N. Hod, M.C. Hodgkinson, P. Hodgson, A. Hoecker, M.R. Hoeferkamp, F. Hoenig, D. Hohn, T.R. Holmes, M. Homann, T.M. Hong, B.H. Hooberman, W.H. Hopkins, Y. Horii, A.J. Horton, J-Y. Hostachy, S. Hou, A. Hoummada, J. Howarth, M. Hrabovsky, I. Hristova, J. Hrivnac, T. Hryn'ova, A. Hrynevich, C. Hsu, P.J. Hsu, S.-C. Hsu, D. Hu, Q. Hu, S. Hu, Y. Huang, Z. Hubacek, F. Hubaut, F. Huegging, T.B. Huffman, E.W. Hughes, G. Hughes, M. Huhtinen, P. Huo, N. Huseynov, J. Huston, J. Huth, G. Iacobucci, G. Iakovidis, I. Ibragimov, L. Iconomidou-Fayard, E. Ideal, Z. Idrissi, P. Iengo, O. Igonkina, T. Iizawa, Y. Ikegami, M. Ikeno, Y. Ilchenko, D. Iliadis, N. Ilic, T. Ince, G. Introzzi, P. Ioannou, M. Iodice, K. Iordanidou, V. Ippolito, N. Ishijima, M. Ishino, M. Ishitsuka, R. Ishmukhametov, C. Issever, S. Istin, F. Ito, J.M. Iturbe Ponce, R. Iuppa, W. Iwanski, H. Iwasaki, J.M. Izen, V. Izzo, S. Jabbar, B. Jackson, P. Jackson, V. Jain, K.B. Jakobi, K. Jakobs, S. Jakobsen, T. Jakoubek, D.O. Jamin, D.K. Jana, E. Jansen, R. Jansky, J. Janssen, M. Janus, G. Jarlskog, N. Javadov, T. Javůrek, F. Jeanneau, L. Jeanty, J. Jejelava, G.-Y. Jeng, D. Jennens, P. Jenni, C. Jeske, S. Jézéquel, H. Ji, J. Jia, H. Jiang, Y. Jiang, S. Jiggins, J. Jimenez Pena, S. Jin, A. Jinaru, O. Jinnouchi, P. Johansson, K.A. Johns, W.J. Johnson, K. Jon-And, G. Jones, R.W.L. Jones, S. Jones, T.J. Jones, J. Jongmanns, P.M. Jorge, J. Jovicevic, X. Ju, A. Juste Rozas, M.K. Köhler, A. Kaczmarska, M. Kado, H. Kagan, M. Kagan, S.J. Kahn, T. Kaji, E. Kajomovitz, C.W. Kalderon, A. Kaluza, S. Kama, A. Kamenshchikov, N. Kanaya, S. Kaneti, L. Kanjir, V.A. Kantserov, J. Kanzaki, B. Kaplan, L.S. Kaplan, A. Kapliy, D. Kar, K. Karakostas, A. Karamaoun, N. Karastathis, M.J. Kareem, E. Karentzos, M. Karnevskiy, S.N. Karpov, Z.M. Karpova, K. Karthik, V. Kartvelishvili, A.N. Karyukhin, K. Kasahara, L. Kashif, R.D. Kass, A. Kastanas, Y. Kataoka, C. Kato, A. Katre, J. Katzy, K. Kawagoe, T. Kawamoto, G. Kawamura, V.F. Kazanin, R. Keeler, R. Kehoe, J.S. Keller, J.J. Kempster, K Kentaro, H. Keoshkerian, O. Kepka, B.P. Kerševan, S. Kersten, R.A. Keyes, M. Khader, F. Khalil-zada, A. Khanov, A.G. Kharlamov, T.J. Khoo, V. Khovanskiy, E. Khramov, J. Khubua, S. Kido, C.R. Kilby, H.Y. Kim, S.H. Kim, Y.K. Kim, N. Kimura, O.M. Kind, B.T. King, M. King, S.B. King, J. Kirk, A.E. Kiryunin, T. Kishimoto, D. Kisielewska, F. Kiss, K. Kiuchi, O. Kivernyk, E. Kladiva, M.H. Klein, M. Klein, U. Klein, K. Kleinknecht, P. Klimek, A. Klimentov, R. Klingenberg, J.A. Klinger, T. Klioutchnikova, E.-E. Kluge, P. Kluit, S. Kluth, J. Knapik, E. Kneringer, E.B.F.G. Knoops, A. Knue, A. Kobayashi, D. Kobayashi, T. Kobayashi, M. Kobel, M. Kocian, P. Kodys, N.M. Koehler, T. Koffas, E. Koffeman, T. Koi, H. Kolanoski, M. Kolb, I. Koletsou, A.A. Komar, Y. Komori, T. Kondo, N. Kondrashova, K. Köneke, A.C. König, T. Kono, R. Konoplich, N. Konstantinidis, R. Kopeliansky, S. Koperny, L. Köpke, A.K. Kopp, K. Korcyl, K. Kordas, A. Korn, A.A. Korol, I. Korolkov, E.V. Korolkova, O. Kortner, S. Kortner, T. Kosek, V.V. Kostyukhin, A. Kotwal, A. Kourkoumeli-Charalampidi, C. Kourkoumelis, V. Kouskoura, A.B. Kowalewska, R. Kowalewski, T.Z. Kowalski, C. Kozakai, W. Kozanecki, A.S. Kozhin, V.A. Kramarenko, G. Kramberger, D. Krasnopevtsev, M.W. Krasny, A. Krasznahorkay, A. Kravchenko, M. Kretz, J. Kretzschmar, K. Kreutzfeldt, P. Krieger, K. Krizka, K. Kroeninger, H. Kroha, J. Kroll, J. Kroseberg, J. Krstic, U. Kruchonak, H. Krüger, N. Krumnack, A. Kruse, M.C. Kruse, M. Kruskal, T. Kubota, H. Kucuk, S. Kuday, J.T. Kuechler, S. Kuehn, A. Kugel, F. Kuger, A. Kuhl, T. Kuhl, V. Kukhtin, R. Kukla, Y. Kulchitsky, S. Kuleshov, M. Kuna, T. Kunigo, A. Kupco, H. Kurashige, Y.A. Kurochkin, V. Kus, E.S. Kuwertz, M. Kuze, J. Kvita, T. Kwan, D. Kyriazopoulos, A. La Rosa, J.L. La Rosa Navarro, L. La Rotonda, C. Lacasta, F. Lacava, J. Lacey, H. Lacker, D. Lacour, V.R. Lacuesta, E. Ladygin, R. Lafaye, B. Laforge, T. Lagouri, S. Lai, S. Lammers, W. Lampl, E. Lançon, U. Landgraf, M.P.J. Landon, M.C. Lanfermann, V.S. Lang, J.C. Lange, A.J. Lankford, F. Lanni, K. Lantzsch, A. Lanza, S. Laplace, C. Lapoire, J.F. Laporte, T. Lari, F. Lasagni Manghi, M. Lassnig, P. Laurelli, W. Lavrijsen, A.T. Law, P. Laycock, T. Lazovich, M. Lazzaroni, B. Le, O. Le Dortz, E. Le Guirriec, E.P. Le Quilleuc, M. LeBlanc, T. LeCompte, F. Ledroit-Guillon, C.A. Lee, S.C. Lee, L. Lee, B. Lefebvre, G. Lefebvre, M. Lefebvre, F. Legger, C. Leggett, A. Lehan, G. Lehmann Miotto, X. Lei, W.A. Leight, A. Leisos, A.G. Leister, M.A.L. Leite, R. Leitner, D. Lellouch, B. Lemmer, K.J.C. Leney, T. Lenz, B. Lenzi, R. Leone, S. Leone, C. Leonidopoulos, S. Leontsinis, G. Lerner, C. Leroy, A.A.J. Lesage, C.G. Lester, M. Levchenko, J. Levêque, D. Levin, L.J. Levinson, M. Levy, D. Lewis, A.M. Leyko, M. Leyton, B. Li, H. Li, H.L. Li, L. Li, L. Li, Q. Li, S. Li, X. Li, Y. Li, Z. Liang, B. Liberti, A. Liblong, P. Lichard, K. Lie, J. Liebal, W. Liebig, A. Limosani, S.C. Lin, T.H. Lin, B.E. Lindquist, A.E. Lionti, E. Lipeles, A. Lipniacka, M. Lisovyi, T.M. Liss, A. Lister, A.M. Litke, B. Liu, D. Liu, H. Liu, H. Liu, J. Liu, J.B. Liu, K. Liu, L. Liu, M. Liu, M. Liu, Y.L. Liu, Y. Liu, M. Livan, A. Lleres, J. Llorente Merino, S.L. Lloyd, F. Lo Sterzo, E. Lobodzinska, P. Loch, W.S. Lockman, F.K. Loebinger, A.E. Loevschall-Jensen, K.M. Loew, A. Loginov, T. Lohse, K. Lohwasser, M. Lokajicek, B.A. Long, J.D. Long, R.E. Long, L. Longo, K.A. Looper, L. Lopes, D. Lopez Mateos, B. Lopez Paredes, I. Lopez Paz, A. Lopez Solis, J. Lorenz, N. Lorenzo Martinez, M. Losada, P.J. Lösel, X. Lou, A. Lounis, J. Love, P.A. Love, H. Lu, N. Lu, H.J. Lubatti, C. Luci, A. Lucotte, C. Luedtke, F. Luehring, W. Lukas, L. Luminari, O. Lundberg, B. Lund-Jensen, P.M. Luzi, D. Lynn, R. Lysak, E. Lytken, V. Lyubushkin, H. Ma, L.L. Ma, Y. Ma, G. Maccarrone, A. Macchiolo, C.M. Macdonald, B. Maček, J. Machado Miguens, D. Madaffari, R. Madar, H.J. Maddocks, W.F. Mader, A. Madsen, J. Maeda, S. Maeland, T. Maeno, A. Maevskiy, E. Magradze, J. Mahlstedt, C. Maiani, C. Maidantchik, A.A. Maier, T. Maier, A. Maio, S. Majewski, Y. Makida, N. Makovec, B. Malaescu, Pa. Malecki, V.P. Maleev, F. Malek, U. Mallik, D. Malon, C. Malone, S. Maltezos, S. Malyukov, J. Mamuzic, G. Mancini, B. Mandelli, L. Mandelli, I. Mandić, J. Maneira, L. Manhaes de Andrade Filho, J. Manjarres Ramos, A. Mann, A. Manousos, B. Mansoulie, J.D. Mansour, R. Mantifel, M. Mantoani, S. Manzoni, L. Mapelli, G. Marceca, L. March, G. Marchiori, M. Marcisovsky, M. Marjanovic, D.E. Marley, F. Marroquim, S.P. Marsden, Z. Marshall, S. Marti-Garcia, B. Martin, T.A. Martin, V.J. Martin, B. Martin dit Latour, M. Martinez, V.I. Martinez Outschoorn, S. Martin-Haugh, V.S. Martoiu, A.C. Martyniuk, M. Marx, A. Marzin, L. Masetti, T. Mashimo, R. Mashinistov, J. Masik, A.L. Maslennikov, I. Massa, L. Massa, P. Mastrandrea, A. Mastroberardino, T. Masubuchi, P. Mättig, J. Mattmann, J. Maurer, S.J. Maxfield, D.A. Maximov, R. Mazini, S.M. Mazza, N.C. Mc Fadden, G. Mc Goldrick, S.P. Mc Kee, A. McCarn, R.L. McCarthy, T.G. McCarthy, L.I. McClymont, E.F. McDonald, J.A. Mcfayden, G. Mchedlidze, S.J. McMahon, R.A. McPherson, M. Medinnis, S. Meehan, S. Mehlhase, A. Mehta, K. Meier, C. Meineck, B. Meirose, D. Melini, B.R. Mellado Garcia, M. Melo, F. Meloni, A. Mengarelli, S. Menke, E. Meoni, S. Mergelmeyer, P. Mermod, L. Merola, C. Meroni, F.S. Merritt, A. Messina, J. Metcalfe, A.S. Mete, C. Meyer, C. Meyer, J-P. Meyer, J. Meyer, H. Meyer Zu Theenhausen, F. Miano, R.P. Middleton, S. Miglioranzi, L. Mijović, G. Mikenberg, M. Mikestikova, M. Mikuž, M. Milesi, A. Milic, D.W. Miller, C. Mills, A. Milov, D.A. Milstead, A.A. Minaenko, Y. Minami, I.A. Minashvili, A.I. Mincer, B. Mindur, M. Mineev, Y. Ming, L.M. Mir, K.P. Mistry, T. Mitani, J. Mitrevski, V.A. Mitsou, A. Miucci, P.S. Miyagawa, J.U. Mjörnmark, T. Moa, K. Mochizuki, S. Mohapatra, S. Molander, R. Moles-Valls, R. Monden, M.C. Mondragon, K. Mönig, J. Monk, E. Monnier, A. Montalbano, J. Montejo Berlingen, F. Monticelli, S. Monzani, R.W. Moore, N. Morange, D. Moreno, M. Moreno Llácer, P. Morettini, D. Mori, T. Mori, M. Morii, M. Morinaga, V. Morisbak, S. Moritz, A.K. Morley, G. Mornacchi, J.D. Morris, S.S. Mortensen, L. Morvaj, M. Mosidze, J. Moss, K. Motohashi, R. Mount, E. Mountricha, S.V. Mouraviev, E.J.W. Moyse, S. Muanza, R.D. Mudd, F. Mueller, J. Mueller, R.S.P. Mueller, T. Mueller, D. Muenstermann, P. Mullen, G.A. Mullier, F.J. Munoz Sanchez, J.A. Murillo Quijada, W.J. Murray, H. Musheghyan, M. Muškinja, A.G. Myagkov, M. Myska, B.P. Nachman, O. Nackenhorst, K. Nagai, R. Nagai, K. Nagano, Y. Nagasaka, K. Nagata, M. Nagel, E. Nagy, A.M. Nairz, Y. Nakahama, K. Nakamura, T. Nakamura, I. Nakano, H. Namasivayam, R.F. Naranjo Garcia, R. Narayan, D.I. Narrias Villar, I. Naryshkin, T. Naumann, G. Navarro, R. Nayyar, H.A. Neal, P.Yu. Nechaeva, T.J. Neep, A. Negri, M. Negrini, S. Nektarijevic, C. Nellist, A. Nelson, S. Nemecek, P. Nemethy, A.A. Nepomuceno, M. Nessi, M.S. Neubauer, M. Neumann, R.M. Neves, P. Nevski, P.R. Newman, D.H. Nguyen, T. Nguyen Manh, R.B. Nickerson, R. Nicolaidou, J. Nielsen, A. Nikiforov, V. Nikolaenko, I. Nikolic-Audit, K. Nikolopoulos, J.K. Nilsen, P. Nilsson, Y. Ninomiya, A. Nisati, R. Nisius, T. Nobe, M. Nomachi, I. Nomidis, T. Nooney, S. Norberg, M. Nordberg, N. Norjoharuddeen, O. Novgorodova, S. Nowak, M. Nozaki, L. Nozka, K. Ntekas, E. Nurse, F. Nuti, F. O'grady, D.C. O'Neil, A.A. O'Rourke, V. O'Shea, F.G. Oakham, H. Oberlack, T. Obermann, J. Ocariz, A. Ochi, I. Ochoa, J.P. Ochoa-Ricoux, S. Oda, S. Odaka, H. Ogren, A. Oh, S.H. Oh, C.C. Ohm, H. Ohman, H. Oide, H. Okawa, Y. Okumura, T. Okuyama, A. Olariu, L.F. Oleiro Seabra, S.A. Olivares Pino, D. Oliveira Damazio, A. Olszewski, J. Olszowska, A. Onofre, K. Onogi, P.U.E. Onyisi, M.J. Oreglia, Y. Oren, D. Orestano, N. Orlando, R.S. Orr, B. Osculati, R. Ospanov, G. Otero y Garzon, H. Otono, M. Ouchrif, F. Ould-Saada, A. Ouraou, K.P. Oussoren, Q. Ouyang, M. Owen, R.E. Owen, V.E. Ozcan, N. Ozturk, K. Pachal, A. Pacheco Pages, L. Pacheco Rodriguez, C. Padilla Aranda, M. Pagáčová, S. Pagan Griso, F. Paige, P. Pais, K. Pajchel, G. Palacino, S. Palazzo, S. Palestini, M. Palka, D. Pallin, E.St. Panagiotopoulou, C.E. Pandini, J.G. Panduro Vazquez, P. Pani, S. Panitkin, D. Pantea, L. Paolozzi, Th.D. Papadopoulou, K. Papageorgiou, A. Paramonov, D. Paredes Hernandez, A.J. Parker, M.A. Parker, K.A. Parker, F. Parodi, J.A. Parsons, U. Parzefall, V.R. Pascuzzi, E. Pasqualucci, S. Passaggio, Fr. Pastore, G. Pásztor, S. Pataraia, J.R. Pater, T. Pauly, J. Pearce, B. Pearson, L.E. Pedersen, M. Pedersen, S. Pedraza Lopez, R. Pedro, S.V. Peleganchuk, O. Penc, C. Peng, H. Peng, J. Penwell, B.S. Peralva, M.M. Perego, D.V. Perepelitsa, E. Perez Codina, L. Perini, H. Pernegger, S. Perrella, R. Peschke, V.D. Peshekhonov, K. Peters, R.F.Y. Peters, B.A. Petersen, T.C. Petersen, E. Petit, A. Petridis, C. Petridou, P. Petroff, E. Petrolo, M. Petrov, F. Petrucci, N.E. Pettersson, A. Peyaud, R. Pezoa, P.W. Phillips, G. Piacquadio, E. Pianori, A. Picazio, E. Piccaro, M. Piccinini, M.A. Pickering, R. Piegaia, J.E. Pilcher, A.D. Pilkington, A.W.J. Pin, M. Pinamonti, J.L. Pinfold, A. Pingel, S. Pires, H. Pirumov, M. Pitt, L. Plazak, M.-A. Pleier, V. Pleskot, E. Plotnikova, P. Plucinski, D. Pluth, R. Poettgen, L. Poggioli, D. Pohl, G. Polesello, A. Poley, A. Policicchio, R. Polifka, A. Polini, C.S. Pollard, V. Polychronakos, K. Pommès, L. Pontecorvo, B.G. Pope, G.A. Popeneciu, D.S. Popovic, A. Poppleton, S. Pospisil, K. Potamianos, I.N. Potrap, C.J. Potter, C.T. Potter, G. Poulard, J. Poveda, V. Pozdnyakov, M.E. Pozo Astigarraga, P. Pralavorio, A. Pranko, S. Prell, D. Price, L.E. Price, M. Primavera, S. Prince, K. Prokofiev, F. Prokoshin, S. Protopopescu, J. Proudfoot, M. Przybycien, D. Puddu, M. Purohit, P. Puzo, J. Qian, G. Qin, Y. Qin, A. Quadt, W.B. Quayle, M. Queitsch-Maitland, D. Quilty, S. Raddum, V. Radeka, V. Radescu, S.K. Radhakrishnan, P. Radloff, P. Rados, F. Ragusa, G. Rahal, J.A. Raine, S. Rajagopalan, M. Rammensee, C. Rangel-Smith, M.G. Ratti, F. Rauscher, S. Rave, T. Ravenscroft, I. Ravinovich, M. Raymond, A.L. Read, N.P. Readioff, M. Reale, D.M. Rebuzzi, A. Redelbach, G. Redlinger, R. Reece, K. Reeves, L. Rehnisch, J. Reichert, H. Reisin, C. Rembser, H. Ren, M. Rescigno, S. Resconi, O.L. Rezanova, P. Reznicek, R. Rezvani, R. Richter, S. Richter, E. Richter-Was, O. Ricken, M. Ridel, P. Rieck, C.J. Riegel, J. Rieger, O. Rifki, M. Rijssenbeek, A. Rimoldi, M. Rimoldi, L. Rinaldi, B. Ristić, E. Ritsch, I. Riu, F. Rizatdinova, E. Rizvi, C. Rizzi, S.H. Robertson, A. Robichaud-Veronneau, D. Robinson, J.E.M. Robinson, A. Robson, C. Roda, Y. Rodina, A. Rodriguez Perez, D. Rodriguez Rodriguez, S. Roe, C.S. Rogan, O. Røhne, A. Romaniouk, M. Romano, S.M. Romano Saez, E. Romero Adam, N. Rompotis, M. Ronzani, L. Roos, E. Ros, S. Rosati, K. Rosbach, P. Rose, O. Rosenthal, N.-A. Rosien, V. Rossetti, E. Rossi, L.P. Rossi, J.H.N. Rosten, R. Rosten, M. Rotaru, I. Roth, J. Rothberg, D. Rousseau, C.R. Royon, A. Rozanov, Y. Rozen, X. Ruan, F. Rubbo, M.S. Rudolph, F. Rühr, A. Ruiz-Martinez, Z. Rurikova, N.A. Rusakovich, A. Ruschke, H.L. Russell, J.P. Rutherfoord, N. Ruthmann, Y.F. Ryabov, M. Rybar, G. Rybkin, S. Ryu, A. Ryzhov, G.F. Rzehorz, A.F. Saavedra, G. Sabato, S. Sacerdoti, H.F-W. Sadrozinski, R. Sadykov, F. Safai Tehrani, P. Saha, M. Sahinsoy, M. Saimpert, T. Saito, H. Sakamoto, Y. Sakurai, G. Salamanna, A. Salamon, J.E. Salazar Loyola, D. Salek, P.H. Sales De Bruin, D. Salihagic, A. Salnikov, J. Salt, D. Salvatore, F. Salvatore, A. Salvucci, A. Salzburger, D. Sammel, D. Sampsonidis, A. Sanchez, J. Sánchez, V. Sanchez Martinez, H. Sandaker, R.L. Sandbach, H.G. Sander, M. Sandhoff, C. Sandoval, R. Sandstroem, D.P.C. Sankey, M. Sannino, A. Sansoni, C. Santoni, R. Santonico, H. Santos, I. Santoyo Castillo, K. Sapp, A. Sapronov, J.G. Saraiva, B. Sarrazin, O. Sasaki, Y. Sasaki, K. Sato, G. Sauvage, E. Sauvan, G. Savage, P. Savard, N. Savic, C. Sawyer, L. Sawyer, J. Saxon, C. Sbarra, A. Sbrizzi, T. Scanlon, D.A. Scannicchio, M. Scarcella, V. Scarfone, J. Schaarschmidt, P. Schacht, B.M. Schachtner, D. Schaefer, R. Schaefer, J. Schaeffer, S. Schaepe, S. Schaetzel, U. Schäfer, A.C. Schaffer, D. Schaile, R.D. Schamberger, V. Scharf, V.A. Schegelsky, D. Scheirich, M. Schernau, C. Schiavi, S. Schier, C. Schillo, M. Schioppa, S. Schlenker, K.R. Schmidt-Sommerfeld, K. Schmieden, C. Schmitt, S. Schmitt, S. Schmitz, B. Schneider, U. Schnoor, L. Schoeffel, A. Schoening, B.D. Schoenrock, E. Schopf, M. Schott, J. Schovancova, S. Schramm, M. Schreyer, N. Schuh, A. Schulte, M.J. Schultens, H.-C. Schultz-Coulon, H. Schulz, M. Schumacher, B.A. Schumm, Ph. Schune, A. Schwartzman, T.A. Schwarz, H. Schweiger, Ph. Schwemling, R. Schwienhorst, J. Schwindling, T. Schwindt, G. Sciolla, F. Scuri, F. Scutti, J. Searcy, P. Seema, S.C. Seidel, A. Seiden, F. Seifert, J.M. Seixas, G. Sekhniaidze, K. Sekhon, S.J. Sekula, D.M. Seliverstov, N. Semprini-Cesari, C. Serfon, L. Serin, L. Serkin, M. Sessa, R. Seuster, H. Severini, T. Sfiligoj, F. Sforza, A. Sfyrla, E. Shabalina, N.W. Shaikh, L.Y. Shan, R. Shang, J.T. Shank, M. Shapiro, P.B. Shatalov, K. Shaw, S.M. Shaw, A. Shcherbakova, C.Y. Shehu, P. Sherwood, L. Shi, S. Shimizu, C.O. Shimmin, M. Shimojima, M. Shiyakova, A. Shmeleva, D. Shoaleh Saadi, M.J. Shochet, S. Shojaii, S. Shrestha, E. Shulga, M.A. Shupe, P. Sicho, A.M. Sickles, P.E. Sidebo, O. Sidiropoulou, D. Sidorov, A. Sidoti, F. Siegert, Dj. Sijacki, J. Silva, S.B. Silverstein, V. Simak, Lj. Simic, S. Simion, E. Simioni, B. Simmons, D. Simon, M. Simon, P. Sinervo, N.B. Sinev, M. Sioli, G. Siragusa, S.Yu. Sivoklokov, J. Sjölin, M.B. Skinner, H.P. Skottowe, P. Skubic, M. Slater, T. Slavicek, M. Slawinska, K. Sliwa, R. Slovak, V. Smakhtin, B.H. Smart, L. Smestad, J. Smiesko, S.Yu. Smirnov, Y. Smirnov, L.N. Smirnova, O. Smirnova, M.N.K. Smith, R.W. Smith, M. Smizanska, K. Smolek, A.A. Snesarev, S. Snyder, R. Sobie, F. Socher, A. Soffer, D.A. Soh, G. Sokhrannyi, C.A. Solans Sanchez, M. Solar, E.Yu. Soldatov, U. Soldevila, A.A. Solodkov, A. Soloshenko, O.V. Solovyanov, V. Solovyev, P. Sommer, H. Son, H.Y. Song, A. Sood, A. Sopczak, V. Sopko, V. Sorin, D. Sosa, C.L. Sotiropoulou, R. Soualah, A.M. Soukharev, D. South, B.C. Sowden, S. Spagnolo, M. Spalla, M. Spangenberg, F. Spanò, D. Sperlich, F. Spettel, R. Spighi, G. Spigo, L.A. Spiller, M. Spousta, R.D. St. Denis, A. Stabile, R. Stamen, S. Stamm, E. Stanecka, R.W. Stanek, C. Stanescu, M. Stanescu-Bellu, M.M. Stanitzki, S. Stapnes, E.A. Starchenko, G.H. Stark, J. Stark, P. Staroba, P. Starovoitov, S. Stärz, R. Staszewski, P. Steinberg, B. Stelzer, H.J. Stelzer, O. Stelzer-Chilton, H. Stenzel, G.A. Stewart, J.A. Stillings, M.C. Stockton, M. Stoebe, G. Stoicea, P. Stolte, S. Stonjek, A.R. Stradling, A. Straessner, M.E. Stramaglia, J. Strandberg, S. Strandberg, A. Strandlie, M. Strauss, P. Strizenec, R. Ströhmer, D.M. Strom, R. Stroynowski, A. Strubig, S.A. Stucci, B. Stugu, N.A. Styles, D. Su, J. Su, S. Suchek, Y. Sugaya, M. Suk, V.V. Sulin, S. Sultansoy, T. Sumida, S. Sun, X. Sun, J.E. Sundermann, K. Suruliz, G. Susinno, M.R. Sutton, S. Suzuki, M. Svatos, M. Swiatlowski, I. Sykora, T. Sykora, D. Ta, C. Taccini, K. Tackmann, J. Taenzer, A. Taffard, R. Tafirout, N. Taiblum, H. Takai, R. Takashima, T. Takeshita, Y. Takubo, M. Talby, A.A. Talyshev, K.G. Tan, J. Tanaka, M. Tanaka, R. Tanaka, S. Tanaka, B.B. Tannenwald, S. Tapia Araya, S. Tapprogge, S. Tarem, G.F. Tartarelli, P. Tas, M. Tasevsky, T. Tashiro, E. Tassi, A. Tavares Delgado, Y. Tayalati, A.C. Taylor, G.N. Taylor, P.T.E. Taylor, W. Taylor, F.A. Teischinger, P. Teixeira-Dias, K.K. Temming, D. Temple, H. Ten Kate, P.K. Teng, J.J. Teoh, F. Tepel, S. Terada, K. Terashi, J. Terron, S. Terzo, M. Testa, R.J. Teuscher, T. Theveneaux-Pelzer, J.P. Thomas, J. Thomas-Wilsker, E.N. Thompson, P.D. Thompson, A.S. Thompson, L.A. Thomsen, E. Thomson, M. Thomson, M.J. Tibbetts, R.E. Ticse Torres, V.O. Tikhomirov, Yu.A. Tikhonov, S. Timoshenko, P. Tipton, S. Tisserant, K. Todome, T. Todorov, S. Todorova-Nova, J. Tojo, S. Tokár, K. Tokushuku, E. Tolley, L. Tomlinson, M. Tomoto, L. Tompkins, K. Toms, B. Tong, E. Torrence, H. Torres, E. Torró Pastor, J. Toth, F. Touchard, D.R. Tovey, T. Trefzger, A. Tricoli, I.M. Trigger, S. Trincaz-Duvoid, M.F. Tripiana, W. Trischuk, B. Trocmé, A. Trofymov, C. Troncon, M. Trottier-McDonald, M. Trovatelli, L. Truong, M. Trzebinski, A. Trzupek, J.C-L. Tseng, P.V. Tsiareshka, G. Tsipolitis, N. Tsirintanis, S. Tsiskaridze, V. Tsiskaridze, E.G. Tskhadadze, K.M. Tsui, I.I. Tsukerman, V. Tsulaia, S. Tsuno, D. Tsybychev, Y. Tu, A. Tudorache, V. Tudorache, A.N. Tuna, S.A. Tupputi, S. Turchikhin, D. Turecek, D. Turgeman, R. Turra, A.J. Turvey, P.M. Tuts, M. Tyndel, G. Ucchielli, I. Ueda, M. Ughetto, F. Ukegawa, G. Unal, A. Undrus, G. Unel, F.C. Ungaro, Y. Unno, C. Unverdorben, J. Urban, P. Urquijo, P. Urrejola, G. Usai, A. Usanova, L. Vacavant, V. Vacek, B. Vachon, C. Valderanis, E. Valdes Santurio, N. Valencic, S. Valentinetti, A. Valero, L. Valery, S. Valkar, J.A. Valls Ferrer, W. Van Den Wollenberg, P.C. Van Der Deijl, H. van der Graaf, N. van Eldik, P. van Gemmeren, J. Van Nieuwkoop, I. van Vulpen, M.C. van Woerden, M. Vanadia, W. Vandelli, R. Vanguri, A. Vaniachine, P. Vankov, G. Vardanyan, R. Vari, E.W. Varnes, T. Varol, D. Varouchas, A. Vartapetian, K.E. Varvell, J.G. Vasquez, F. Vazeille, T. Vazquez Schroeder, J. Veatch, V. Veeraraghavan, L.M. Veloce, F. Veloso, S. Veneziano, A. Ventura, M. Venturi, N. Venturi, A. Venturini, V. Vercesi, M. Verducci, W. Verkerke, J.C. Vermeulen, A. Vest, M.C. Vetterli, O. Viazlo, I. Vichou, T. Vickey, O.E. Vickey Boeriu, G.H.A. Viehhauser, S. Viel, L. Vigani, M. Villa, M. Villaplana Perez, E. Vilucchi, M.G. Vincter, V.B. Vinogradov, C. Vittori, I. Vivarelli, S. Vlachos, M. Vlasak, M. Vogel, P. Vokac, G. Volpi, M. Volpi, H. von der Schmitt, E. von Toerne, V. Vorobel, K. Vorobev, M. Vos, R. Voss, J.H. Vossebeld, N. Vranjes, M. Vranjes Milosavljevic, V. Vrba, M. Vreeswijk, R. Vuillermet, I. Vukotic, Z. Vykydal, P. Wagner, W. Wagner, H. Wahlberg, S. Wahrmund, J. Wakabayashi, J. Walder, R. Walker, W. Walkowiak, V. Wallangen, C. Wang, C. Wang, F. Wang, H. Wang, H. Wang, J. Wang, J. Wang, K. Wang, R. Wang, S.M. Wang, T. Wang, T. Wang, W. Wang, X. Wang, C. Wanotayaroj, A. Warburton, C.P. Ward, D.R. Wardrope, A. Washbrook, P.M. Watkins, A.T. Watson, M.F. Watson, G. Watts, S. Watts, B.M. Waugh, S. Webb, M.S. Weber, S.W. Weber, J.S. Webster, A.R. Weidberg, B. Weinert, J. Weingarten, C. Weiser, H. Weits, P.S. Wells, T. Wenaus, T. Wengler, S. Wenig, N. Wermes, M. Werner, M.D. Werner, P. Werner, M. Wessels, J. Wetter, K. Whalen, N.L. Whallon, A.M. Wharton, A. White, M.J. White, R. White, D. Whiteson, F.J. Wickens, W. Wiedenmann, M. Wielers, P. Wienemann, C. Wiglesworth, L.A.M. Wiik-Fuchs, A. Wildauer, F. Wilk, H.G. Wilkens, H.H. Williams, S. Williams, C. Willis, S. Willocq, J.A. Wilson, I. Wingerter-Seez, F. Winklmeier, O.J. Winston, B.T. Winter, M. Wittgen, J. Wittkowski, T.M.H. Wolf, M.W. Wolter, H. Wolters, S.D. Worm, B.K. Wosiek, J. Wotschack, M.J. Woudstra, K.W. Wozniak, M. Wu, M. Wu, S.L. Wu, X. Wu, Y. Wu, T.R. Wyatt, B.M. Wynne, S. Xella, D. Xu, L. Xu, B. Yabsley, S. Yacoob, D. Yamaguchi, Y. Yamaguchi, A. Yamamoto, S. Yamamoto, T. Yamanaka, K. Yamauchi, Y. Yamazaki, Z. Yan, H. Yang, H. Yang, Y. Yang, Z. Yang, W-M. Yao, Y.C. Yap, Y. Yasu, E. Yatsenko, K.H. Yau Wong, J. Ye, S. Ye, I. Yeletskikh, A.L. Yen, E. Yildirim, K. Yorita, R. Yoshida, K. Yoshihara, C. Young, C.J.S. Young, S. Youssef, D.R. Yu, J. Yu, J.M. Yu, J. Yu, L. Yuan, S.P.Y. Yuen, I. Yusuff, B. Zabinski, R. Zaidan, A.M. Zaitsev, N. Zakharchuk, J. Zalieckas, A. Zaman, S. Zambito, L. Zanello, D. Zanzi, C. Zeitnitz, M. Zeman, A. Zemla, J.C. Zeng, Q. Zeng, K. Zengel, O. Zenin, T. Ženiš, D. Zerwas, D. Zhang, F. Zhang, G. Zhang, H. Zhang, J. Zhang, L. Zhang, R. Zhang, R. Zhang, X. Zhang, Z. Zhang, X. Zhao, Y. Zhao, Z. Zhao, A. Zhemchugov, J. Zhong, B. Zhou, C. Zhou, L. Zhou, L. Zhou, M. Zhou, N. Zhou, C.G. Zhu, H. Zhu, J. Zhu, Y. Zhu, X. Zhuang, K. Zhukov, A. Zibell, D. Zieminska, N.I. Zimine, C. Zimmermann, S. Zimmermann, Z. Zinonos, M. Zinser, M. Ziolkowski, L. Živković, G. Zobernig, A. Zoccoli, M. zur Nedden, L. Zwalinski
- Subjects
Nuclear and High Energy Physics ,High Energy Physics::Phenomenology ,High Energy Physics::Experiment ,Nuclear Experiment ,lcsh:Physics ,lcsh:QC1-999 - Abstract
A search for heavy long-lived charged R-hadrons is reported using a data sample corresponding to 3.2 fb−1 of proton–proton collisions at s=13 TeV collected by the ATLAS experiment at the Large Hadron Collider at CERN. The search is based on observables related to large ionisation losses and slow propagation velocities, which are signatures of heavy charged particles travelling significantly slower than the speed of light. No significant deviations from the expected background are observed. Upper limits at 95% confidence level are provided on the production cross section of long-lived R-hadrons in the mass range from 600 GeV to 2000 GeV and gluino, bottom and top squark masses are excluded up to 1580 GeV, 805 GeV and 890 GeV, respectively.
- Published
- 2016
4. In-hospital mortality, length of stay, and hospitalization cost of COVID-19 patients with and without hyperkalemia.
- Author
-
Amin A, Moon R, Agiro A, Rosenthal N, Brown H, Legg R, and Pottorf W
- Subjects
- Aged, Hospital Mortality, Hospitalization, Humans, Intensive Care Units, Length of Stay, Male, Potassium, Retrospective Studies, COVID-19 epidemiology, COVID-19 therapy, Hyperkalemia epidemiology
- Abstract
Background: Hyperkalemia (HK) may be associated with poor clinical outcomes among COVID-19 patients. This study aimed to describe the prevalence of HK and evaluate the associations between HK and in-hospital mortality, intensive care unit (ICU) admission, length of hospital stay (LOS), and hospitalization cost among COVID-19 inpatients., Methods: A retrospective cohort study was conducted using a large hospital discharge database (PINC AI Healthcare Database) for COVID-19 inpatients discharged between April 1 and August 31, 2020. HK was defined with discharge diagnosis and potassium binder use., Results: Of 192,182 COVID-19 inpatients, 12% (n = 22,702) had HK. HK patients were more likely to be older (median age 67 vs 63 years), male (63% vs 50%), black (30% vs 22%), and have a history of chronic kidney disease (45% vs 16%) or diabetes mellitus (55% vs 35%) than non-HK patients (all p<.001). A significantly higher proportion of patients with HK had in-hospital mortality (42% vs 11%, p<.001) than those without HK; this was persistent after adjusting for confounders (adjusted odds ratio [
a OR] 1.69, 95% confidence interval [CI]1.62-1.77). Patients with HK were also more likely to be admitted to ICU (a OR 1.05, 95% CI 1.01-1.09), incur higher cost of care (adjusted mean difference $5,389) and have longer LOS (adjusted mean difference 1.3 days) than non-HK patients., Conclusions: Presence of HK was independently associated with higher in-hospital mortality, LOS, and cost of care among COVID-19 inpatients. Detecting and closely monitoring HK are recommended to improve clinical outcomes and reduce LOS and healthcare cost among COVID-19 patients., Competing Interests: Declaration of Competing Interest A. Amin served as a principal investigator or co-investigator of clinical trials sponsored by NIH/NIAID, NeuroRx Pharma, Pulmotect, Blade Therpeutics, Novartis, Takeda, Humanigen, Eli Lilly, PTC Therapeutics, OctaPharma, Fulcrum Therapeutics, Alexion. He served as a speaker and/or consultant for BMS, Pfizer, BI, Portola, Sunovion, Mylan, Salix, Alexion, AstraZeneca, Novartis, Nabriva, Paratek, Bayer, Tetraphase, Achogen LaJolla, Millenium, PeraHealth, HeartRite, Aseptiscope, Sprightly. R.M. worked on the study as a full-time employee of Premier, Inc. N.R. and H.B. worked on the study as full-time employees and stockholders of Premier, Inc. A. Agiro, R.L., and W.P. worked on the study as full-time employees and stockholders of AstraZeneca., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2022
- Full Text
- View/download PDF
5. Healthcare Resource Utilization of Patients With COVID-19 Visiting US Hospitals.
- Author
-
Moon RC, Brown H, and Rosenthal N
- Subjects
- Adolescent, Adult, Delivery of Health Care, Female, Hospitalization, Hospitals, Humans, Male, Middle Aged, Retrospective Studies, United States epidemiology, COVID-19 epidemiology, COVID-19 therapy
- Abstract
Objectives: Severe cases of COVID-19 have overwhelmed hospital systems across the nation. This study aimed to describe the healthcare resource utilization of patients with COVID-19 from hospital visit to 30 days after discharge for inpatients and hospital-based outpatients in the United States., Methods: A retrospective cohort study was conducted using Premier Healthcare Database COVID-19 Special Release, a large geographically diverse all-payer hospital administrative database. Adult patients (age ≥ 18 years) were identified by their first, or "index," visit between April 1, 2020, and February 28, 2021, with a principal or secondary discharge diagnosis of COVID-19., Results: Of 1 454 780 adult patients with COVID-19, 33% (n = 481 216) were inpatients and 67% (n = 973 564) were outpatients. Among inpatients, mean age was 64.4 years and comorbidities were common. Most patients (80%) originated from home, 10% from another acute care facility, and 95% were admitted through the emergency department. Of these patients, 23% (n = 108 120) were admitted to intensive care unit and 14% (n = 66 706) died during index hospitalization; 44% were discharged home, 15% to nursing or rehabilitation facility, and 12% to home health. Among outpatients, mean age was 48.8 years, 44% were male, and 60% were emergency department outpatients (n = 586 537). During index outpatient visit, 79% were sent home but 10% had another outpatient visit and 4% were hospitalized within 30 days., Conclusions: COVID-19 is associated with high level of healthcare resource utilization and in-hospital mortality. More than one-third of inpatients required post hospital healthcare services. Such information may help healthcare providers better allocate resources for patients with COVID-19 during the pandemic., (Copyright © 2022. Published by Elsevier Inc.)
- Published
- 2022
- Full Text
- View/download PDF
6. Insights from CREDENCE trial indicate an acute drop in estimated glomerular filtration rate during treatment with canagliflozin with implications for clinical practice.
- Author
-
Oshima M, Jardine MJ, Agarwal R, Bakris G, Cannon CP, Charytan DM, de Zeeuw D, Edwards R, Greene T, Levin A, Lim SK, Mahaffey KW, Neal B, Pollock C, Rosenthal N, Wheeler DC, Zhang H, Zinman B, Perkovic V, and Heerspink HJL
- Subjects
- Canagliflozin adverse effects, Glomerular Filtration Rate, Humans, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Diabetes Mellitus, Type 2 drug therapy, Renal Insufficiency, Chronic diagnosis, Sodium-Glucose Transporter 2 Inhibitors adverse effects
- Abstract
Canagliflozin slows the progression of chronic kidney disease in patients with type 2 diabetes and induces a reversible acute drop in estimated glomerular filtration rate (eGFR), believed to be a hemodynamic effect. Predictors of the initial drop and its association with long-term eGFR trajectories and safety outcomes are unknown. To assess this, we performed a post-hoc analysis of 4289 participants in the CREDENCE trial with type 2 diabetes and chronic kidney disease equally split into treatment and placebo groups who had eGFR measured at both baseline and week three. The eGFR was categorized at week three as greater than a 10% decline; between 0 and 10% decline; and no decline. Long-term eGFR trajectories and safety outcomes were estimated in each category of acute eGFR change by linear mixed effects models and Cox regression after adjustment for baseline characteristics and medications use. Significantly more participants in the canagliflozin (45%) compared to the placebo (21%) group experienced an acute drop in eGFR over 10%. An over 30% drop occurred infrequently (4% of participants with canagliflozin and 2% with placebo). The odds ratio for a drop in eGFR over 10% with canagliflozin compared to placebo was significant at 3.03 (95% confidence interval 2.65, 3.47). Following the initial drop in eGFR, multivariable adjusted long-term eGFR trajectories, as well as overall and kidney safety profiles, in those treated with canagliflozin were similar across eGFR decline categories. Thus, although acute drops in eGFR over 10% occurred in nearly half of all participants following initiation of canagliflozin, the clinical benefit of canagliflozin was observed regardless. Additionally, safety outcomes were similar among subgroups of acute eGFR drop., (Copyright © 2021 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2021
- Full Text
- View/download PDF
7. Clinical Outcomes in Patients With Heart Failure Hospitalized With COVID-19.
- Author
-
Bhatt AS, Jering KS, Vaduganathan M, Claggett BL, Cunningham JW, Rosenthal N, Signorovitch J, Thune JJ, Vardeny O, and Solomon SD
- Subjects
- Aged, Comorbidity, Female, Heart Failure therapy, Hospital Mortality trends, Humans, Male, Risk Factors, United States epidemiology, COVID-19 epidemiology, Heart Failure epidemiology, Hospitalization statistics & numerical data, Pandemics, SARS-CoV-2
- Abstract
Objectives: The purpose of this study was to evaluate in-hospital outcomes among patients with a history of heart failure (HF) hospitalized with coronavirus disease-2019 (COVID-19)., Background: Cardiometabolic comorbidities are common in patients with severe COVID-19. Patients with HF may be particularly susceptible to COVID-19 complications., Methods: The Premier Healthcare Database was used to identify patients with at least 1 HF hospitalization or 2 HF outpatient visits between January 1, 2019, and March 31, 2020, who were subsequently hospitalized between April and September 2020. Baseline characteristics, health care resource utilization, and mortality rates were compared between those hospitalized with COVID-19 and those hospitalized with other causes. Predictors of in-hospital mortality were identified in HF patients hospitalized with COVID-19 by using multivariate logistic regression., Results: Among 1,212,153 patients with history of HF, 132,312 patients were hospitalized from April 1, 2020, to September 30, 2020. A total of 23,843 patients (18.0%) were hospitalized with acute HF, 8,383 patients (6.4%) were hospitalized with COVID-19, and 100,068 patients (75.6%) were hospitalized with alternative reasons. Hospitalization with COVID-19 was associated with greater odds of in-hospital mortality as compared with hospitalization with acute HF; 24.2% of patients hospitalized with COVID-19 died in-hospital compared to 2.6% of those hospitalized with acute HF. This association was strongest in April (adjusted odds ratio [OR]: 14.48; 95% confidence interval [CI]:12.25 to 17.12) than in subsequent months (adjusted OR: 10.11; 95% CI: 8.95 to 11.42; p
interaction <0.001). Among patients with HF hospitalized with COVID-19, male sex (adjusted OR: 1.26; 95% CI: 1.13 to 1.40) and morbid obesity (adjusted OR: 1.25; 95% CI: 1.07 to 1.46) were associated with greater odds of in-hospital mortality, along with age (adjusted OR: 1.35; 95% CI: 1.29 to 1.42 per 10 years) and admission earlier in the pandemic., Conclusions: Patients with HF hospitalized with COVID-19 are at high risk for complications, with nearly 1 in 4 dying during hospitalization., Competing Interests: Author Disclosures Dr. Bhatt has received speaker fees from Sanofi Pasteur; and is supported by National Heart, Lung, and Blood Institute T32 post-doctoral training grant T32HL007604. Dr. Jering is supported by National Heart, Lung, and Blood Institute T32 post-doctoral training grant T32HL007604. Dr. Vaduganathan has received grants from Harvard Catalyst, grants and personal fees from Amgen, and personal fees from AstraZeneca, Baxter HealthCare, Bayer AG, Boehringer Ingelheim, Cytokinetics, and Relypsa outside the submitted work. Dr. Claggett has received personal fees from Amgen, Boehringer Ingelheim, Corvia, MyoKardia, and Novartis outside the submitted work. Dr. Cunningham is supported by National Heart, Lung, and Blood Institute T32 post-doctoral training grant T32HL007604. Dr. Rosenthal is an employee of Premier Inc., which curates the Premier Healthcare Database. Dr. Signorovitch is an employee of Analysis Group, Inc. Dr. Thune has received lecture fees from Bristol-Myers Squibb; and has received personal fees and travel support from Novartis. Dr. Vardeny has received research support from U.S. National Institutes of Health; and is a consultant for Sanofi-Pasteur. Dr. Solomon has received grants from Alnylam, Amgen, AstraZeneca, Bellerophon, Bayer, Bristol-Myers Squibb, Celladon, Cytokinetics, Eidos, Gilead, GlaxoSmithKline, Ionis, Lone Star Heart, Mesoblast, MyoKardia, Neurotronik, National Institutes of Health/National Heart, Lung, and Blood Institute, Novartis, Respicardia, Sanofi Pasteur, and Theracos; and has received personal fees from Akros, Alnylam, Amgen, Arena, AstraZeneca, Bayer, Bristol-Meyers Squibb, Cardior, Cardurion, Corvia, Cytokinetics, Daiichi-Sankyo, Gilead, GlaxoSmithKline, Ironwood, Merck, Myokardia, Novartis, Roche, Takeda, Theracos, Quantum Genetics, Cardurion, AoBiome, Janssen, Cardiac Dimensions, Sanofi-Pasteur, Tenaya, Dinaqor, Tremeau, CellProThera, and Moderna outside the submitted work., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)- Published
- 2021
- Full Text
- View/download PDF
8. The effects of combination canagliflozin and glucagon-like peptide-1 receptor agonist therapy on intermediate markers of cardiovascular risk in the CANVAS program.
- Author
-
Arnott C, Neuen BL, Heerspink HJL, Figtree GA, Kosiborod M, Lam CS, Cannon CP, Rosenthal N, Shaw W, Mahaffey KW, Jardine MJ, Perkovic V, and Neal B
- Subjects
- Canagliflozin, Glucagon-Like Peptide-1 Receptor, Heart Disease Risk Factors, Humans, Hypoglycemic Agents, Risk Factors, Cardiovascular Diseases diagnosis, Cardiovascular Diseases epidemiology, Diabetes Mellitus, Type 2 diagnosis, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 epidemiology
- Abstract
Background: Sodium glucose co-transporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP1-RA) reduce cardiovascular events, and improve intermediate markers of cardiometabolic health, in those with type 2 diabetes. We investigated these effects in the CANVAS Program., Methods and Results: The CANVAS Program comprised 2 double-blind, randomized, placebo-controlled trials (CANVAS and CANVAS-R) done in patients with type 2 diabetes and elevated cardiovascular risk. Effects were estimated using mixed-effects models for continuous measures and Cox regression models for other outcomes. Randomized treatment by subgroup interaction terms were used to compare effects of canagliflozin versus placebo across subgroups defined by baseline use of GLP1-RA. There were 10,142 participants, of whom 407 (4%) were using GLP1-RA therapy at baseline. Those using GLP1-RA at baseline were less likely to have a history of cardiovascular disease (60.4% vs 65.8%), had a longer duration of diabetes (15.2 vs 13.5 years) and a higher body mass index (BMI; 35.6 vs 31.8 kg/m
2 ) but were otherwise similar. There were greater reductions with canagliflozin versus placebo for HbA1c (-0.75% versus -0.58%; P = .0091), SBP (-6.26 versus -3.83 mmHg; P = .0018), and body weight (-3.79 versus -2.18 kg; P < .0001) in those on baseline GLP1-RA therapy. Effects across subgroups were similar for UACR (P = .21), eGFR slope (P = .72), major adverse cardiac events (P = .94) and total serious adverse events (P = .74)., Conclusions: There may be a synergistic effect of SGLT2 inhibition when used on a background of GLP1-RA for intermediate cardiometabolic markers., Competing Interests: Disclosures C. Arnott is an employee of the George Institute for Global Health. B.L. Neuen is supported by an Australian National Health and Medical Research Council Postgraduate Scholarship and a University Postgraduate Award from the University of New South Wales; he has received travel support from Janssen. H.J.L. Heerspink has served as a consultant for Abbvie, Astellas, AstraZeneca, Boehringer Ingelheim, Fresenius, Gilead, Janssen, Merck, and Mitsubishi-Tanabe; and has received grant support from Abbvie, AstraZeneca, Boehringer Ingelheim, and Janssen. G.A. Figtree has received research support from the cofunded Australian National Health and Medical Research Council and Heart Foundation fellowship and Heart Research Australia; and has received compensation from Janssen for serving on the adjudication panel of the CANVAS Program. M. Kosiborod has received research grants from AstraZeneca and Boehringer Ingelheim; has served as a consultant or on advisory boards for Amarin, Amgen, Applied Therapeutics, AstraZeneca, Bayer, Boehringer Ingelheim, Eisai, Eli Lilly, GlaxoSmithKline, Glytec, Intarcia, Janssen, Merck (Diabetes), Novartis, Novo Nordisk, Sanofi, and Vifor Pharma; has received other research support from AstraZeneca; and has received honoraria from AstraZeneca, Boehringer Ingelheim, and Novo Nordisk. C.S. Lam is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, and Vifor Pharma; has served as consultant or on the advisory board, steering committee, or executive committee for Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, Vifor Pharma, Novartis, Amgen, Merck, Janssen Research & Development LLC, Menarini, Boehringer Ingelheim, Novo Nordisk, Abbott Diagnostics, Corvia, Stealth BioTherapeutics, JanaCare, Biofourmis, Darma, Applied Therapeutics, MyoKardia, Cytokinetics, WebMD Global LLC, Radcliffe Group Ltd. and Corpus; and serves as co-founder and non-executive director of eKo.ai. C.P. Cannon has received research grants from Amgen, Boehringer-Ingelheim (BI), Bristol-Myers Squibb (BMS), Daiichi Sankyo, Janssen, Merck, and Pfizer, and consulting fees from Aegerion, Alnylam, Amarin, Amgen, Applied Therapeutics, Ascendia, BI, BMS, Corvidia, HLS Therapeutics, Innovent, Janssen, Kowa, Merck, Pfizer, and Sanofi. N. Rosenthal and W. Shaw are full-time employees of Janssen Research & Development, LLC. K.W. Mahaffey has received research support from Afferent, Amgen, Apple, Inc., AstraZeneca, Cardiva Medical, Inc., Daiichi, Ferring, Google (Verily), Johnson & Johnson, Luitpold, Medtronic, Merck, NIH, Novartis, Sanofi, St. Jude, and Tenax; and has served as a consultant (speaker fees for CME events only) for Abbott, Ablynx, AstraZeneca, Baim Institute, Boehringer Ingelheim, Bristol Myers Squibb, Elsevier, GlaxoSmithKline, Johnson & Johnson, MedErgy, Medscape, Mitsubishi, Myokardia, NIH, Novartis, Novo Nordisk, Portola, Radiometer, Regeneron, Springer Publishing, and UCSF. M.J. Jardine is supported by a Medical Research Future Fund Next Generation Clinical Researchers Program Career Development Fellowship; is responsible for research projects that have received unrestricted funding from Baxter, Amgen, Eli Lilly, and Merck Sharpe Dohme; serves on a Steering Committee sponsored by CSL; has served on advisory boards sponsored by Akebia, Baxter, Boehringer Ingelheim, and Vifor; and has spoken at scientific meetings sponsored by Janssen, with any consultancy, honoraria, or travel support paid to her institution. V. Perkovic has received fees for Advisory Boards, Steering Committee roles, or Scientific Presentations from Abbvie, Astellas, AstraZeneca, Bayer, Baxter, BMS, Boehringer Ingelheim, Dimerix, Durect, Eli Lilly, Gilead, GSK, Janssen, Merck, Mitsubishi Tanabe, Mundipharma, Novartis, Novo Nordisk, Pfizer, Pharmalink, Relypsa, Retrophin, Sanofi, Servier, Vifor, and Tricida. B. Neal is supported by an Australian National Health and Medical Research Council Principal Research Fellowship; holds a research grant for this study from Janssen; and has held research grants for other large-scale cardiovascular outcome trials from Roche, Servier, and Merck Schering Plough; and his institution has received consultancy, honoraria, or travel support for contributions he has made to advisory boards and/or the continuing medical education programs of Abbott, Janssen, Novartis, Pfizer, Roche, and Servier., (Copyright © 2020 Elsevier B.V. All rights reserved.)- Published
- 2020
- Full Text
- View/download PDF
9. Cost of managing meningitis and encephalitis among adult patients in the United States of America.
- Author
-
Balada-Llasat JM, Rosenthal N, Hasbun R, Zimmer L, Ginocchio CC, Duff S, Allison J, and Bozzette S
- Subjects
- Adult, Encephalitis economics, Female, Hospital Costs, Humans, Intensive Care Units economics, Male, Meningitis economics, Retrospective Studies, Spinal Puncture economics, United States, Encephalitis therapy, Health Care Costs, Meningitis therapy
- Abstract
Objective: To determine the associated costs related to the diagnosis and treatment of meningitis and encephalitis (ME) in adult patients in the USA., Methods: A retrospective observational study design was used to assess the use and costs of diagnostic tests and antimicrobial treatment and the total hospitalization costs for adult patients with suspected ME, who received a lumbar puncture procedure during an emergency department visit or during the first two service days of an inpatient stay. Related costs were calculated by timing of lumbar puncture performed and infectious etiology., Results: A total 26429 adult patients with suspected ME diagnosed between 2011 and 2014 were included in the study. The mean hospitalization cost was $15 572±27168, with antimicrobial medication cost of $1144±4052 and laboratory test cost of $210±244. The total visit cost increased with delayed lumbar puncture procedure, intensive care unit stay, and if the etiology was fungi, arbovirus, or bacteria., Conclusions: Higher diagnostic and treatment costs are associated with a delayed lumbar puncture procedure, the etiological agent, and the requirement for an intensive care unit stay., (Copyright © 2018 BioMerieux, Inc. Published by Elsevier Ltd.. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
10. Genome Wide Conditional Mouse Knockout Resources.
- Author
-
Kaloff C, Anastassiadis K, Ayadi A, Baldock R, Beig J, Birling MC, Bradley A, Brown S, Bürger A, Bushell W, Chiani F, Collins FS, Doe B, Eppig JT, Finnel RH, Fletcher C, Flicek P, Fray M, Friedel RH, Gambadoro A, Gates H, Hansen J, Herault Y, Hicks GG, Hörlein A, Hrabé de Angelis M, Iyer V, de Jong PJ, Koscielny G, Kühn R, Liu P, Lloyd KC, Lopez RG, Marschall S, Martínez S, McKerlie C, Meehan T, von Melchner H, Moore M, Murray SA, Nagy A, Nutter L, Pavlovic G, Pombero A, Prosser H, Ramirez-Solis R, Ringwald M, Rosen B, Rosenthal N, Rossant J, Ruiz Noppinger P, Ryder E, Skarnes WC, Schick J, Schnütgen F, Schofield P, Seisenberger C, Selloum M, Smedley D, Simpson EM, Stewart AF, Teboul L, Tocchini Valentini GP, Valenzuela D, West A, and Wurst W
- Abstract
The International Knockout Mouse Consortium (IKMC) developed high throughput gene trapping and gene targeting pipelines that produced mostly conditional mutations of more than 18,500 genes in C57BL/6N mouse embryonic stem (ES) cells which have been archived and are freely available to the research community as a frozen resource. From this unprecedented resource more than 6,000 mutant mouse strains have been produced by the IKMC and mostly the International Mouse Phenotyping Consortium (IMPC). In addition, a cre-driver resource was established including 250 inducible cre-driver mouse strains in a C57BL/6 background. Complementing the cre-driver resource, a collection of comprising 27 cre-driver rAAVs has also been produced. The resources can be easily accessed at the IKMC/IMPC web portal (www.mousephenotype.org). The IKMC/IMPC resource is a standardized reference library of mouse models with defined genetic backgrounds that enables the analysis of gene-disease associations in mice of different genetic makeup and should therefore have a major impact on biomedical research., Competing Interests: Conflict of interest: EMS, and the University of British Columbia have filed for US patent protection on a subset of the MiniPs used in cre-driver strains developed by Pleiades/CanEuCre.
- Published
- 2016
- Full Text
- View/download PDF
11. Regenerative medicine: the challenge of translation. Editorial.
- Author
-
Rosenthal N and Grounds MD
- Subjects
- Animals, Humans, Recovery of Function, Regenerative Medicine trends, Translational Research, Biomedical trends, Wound Healing, Wounds and Injuries physiopathology, Wounds and Injuries therapy, Regenerative Medicine methods, Translational Research, Biomedical methods
- Published
- 2014
- Full Text
- View/download PDF
12. Extracellular matrix considerations for scar-free repair and regeneration: insights from regenerative diversity among vertebrates.
- Author
-
Godwin J, Kuraitis D, and Rosenthal N
- Subjects
- Animals, Extracellular Matrix metabolism, Extracellular Matrix Proteins metabolism, Extracellular Matrix Proteins physiology, Models, Biological, Neovascularization, Physiologic physiology, Vertebrates physiology, Cicatrix physiopathology, Extracellular Matrix physiology, Regeneration physiology, Wound Healing physiology
- Abstract
The extracellular matrix (ECM) is an essential feature of development, tissue homeostasis and recovery from injury. How the ECM responds dynamically to cellular and soluble components to support the faithful repair of damaged tissues in some animals but leads to the formation of acellular fibrotic scar tissue in others has important clinical implications. Studies in highly regenerative organisms such as the zebrafish and the salamander have revealed a specialist formulation of ECM components that support repair and regeneration, while avoiding scar tissue formation. By comparing a range of different contexts that feature scar-less healing and full regeneration vs. scarring through fibrotic repair, regenerative therapies that incorporate ECM components could be significantly enhanced to improve both regenerative potential and functional outcomes. This article is part of a directed issue entitled: Regenerative Medicine: the challenge of translation., (Copyright © 2014 Elsevier Ltd. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
13. A tribute to Sir John Gurdon.
- Author
-
Rosenthal N and Zernicka-Goetz M
- Subjects
- History, 21st Century, Nobel Prize, Stem Cells cytology, Cell Differentiation
- Published
- 2014
- Full Text
- View/download PDF
14. Scar-free wound healing and regeneration in amphibians: immunological influences on regenerative success.
- Author
-
Godwin JW and Rosenthal N
- Subjects
- Animals, Anura immunology, Cicatrix immunology, Cicatrix pathology, Extracellular Matrix immunology, Humans, Skin immunology, Urodela immunology, Anura growth & development, Regeneration immunology, Urodela growth & development, Wound Healing immunology
- Abstract
Salamanders and frogs are distinct orders of Amphibians with very different immune systems during adult life, exhibiting varying potential for scar free repair and regeneration. While salamanders can regenerate a range of body parts throughout all stages of life, regeneration is restricted to early stages of frog development. Comparison of these two closely related amphibian orders provides insights into the immunological influences on wound repair, and the different strategies that have evolved either to limit infection or to facilitate efficient regeneration. After injury, cells of the immune system are responsible for the removal of damaged cells and providing a cohort of important growth factors and signaling molecules. Immune cells not only regulate new vessel growth important for supplying essential nutrients to damaged tissue but, modulate the extracellular matrix environment by regulating fibroblasts and the scarring response. The profile of immune cell infiltration and their interaction with local tissue immune cells directly influences many aspects of the wound healing outcomes and can facilitate or prevent regeneration. Evidence is emerging that the transition from wound healing to regeneration is reliant on immune cell engagement and that the success of regeneration in amphibians may depend on complex interactions between stem cell progenitors and immune cell subsets. The potential immunological barriers to mammalian regeneration are discussed with implications for the successful delivery of stem cell therapeutic strategies in patients., (Copyright © 2014 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
15. PCR amplification and high throughput sequencing of immunoglobulin heavy chain genes from formalin-fixed paraffin-embedded human biopsies.
- Author
-
Tabibian-Keissar H, Schibby G, Michaeli M, Rakovsky-Shapira A, Azogui-Rosenthal N, Dunn-Walters DK, Rosenblatt K, Mehr R, and Barshack I
- Subjects
- Adult, Aged, Female, Formaldehyde, Genetic Variation, Humans, Male, Middle Aged, Paraffin Embedding, Polymerase Chain Reaction, Receptors, Antigen, B-Cell genetics, Tissue Fixation, Genes, Immunoglobulin Heavy Chain, High-Throughput Nucleotide Sequencing, Immunoglobulin Heavy Chains genetics, Sequence Analysis, DNA
- Abstract
The use of high throughput sequencing (HTS) technologies in biomedicine is expanding in a variety of fields in recent years. The 454 system is an HTS platform that is ideally suited to characterize B cell receptor (BCR) repertoires by sequencing of immunoglobulin (Ig) genes, as it is able to sequence stretches of several hundred nucleotides. Most studies that used this platform for antibody repertoire analyses have started from fresh or frozen tissues or peripheral blood samples, and rely on starting with optimal quality DNA. In this paper we demonstrate that BCR repertoire analysis can be done using DNA from formalin-fixed paraffin-embedded (FFPE) human tissue samples. The heterogeneity of BCR repertoires we obtained confirms the plausibility of HTS of DNA from FFPE specimens. The establishment of experimental protocols and computational tools that enable sequence data analysis from the low quality DNA of FFPE tissues is important for enabling research, as it would enable the use of the rich source of preserved samples in clinical biobanks and biopsy archives., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
16. In search of a wide-angle perspective.
- Author
-
Rosenthal N and Stewart C
- Subjects
- Humans, Periodicals as Topic, Cell Differentiation
- Published
- 2012
- Full Text
- View/download PDF
17. Proximal tubule overexpression of a locally acting IGF isoform, Igf-1Ea, increases inflammation after ischemic injury.
- Author
-
Rae FK, Suhaimi N, Li J, Nastasi T, Slonimsky E, Rosenthal N, and Little MH
- Subjects
- Animals, Inflammation metabolism, Insulin-Like Growth Factor I genetics, Mice, Mice, Transgenic, Protein Isoforms genetics, Protein Isoforms metabolism, Insulin-Like Growth Factor I metabolism, Kidney blood supply, Kidney Tubules, Proximal metabolism, Reperfusion Injury metabolism
- Abstract
Objective: IGF-1 is an important regulator of postnatal growth in mammals. In mice, a non-circulating, locally acting isoform of IGF-1, IGF-1Ea, has been documented as a central regulator of muscle regeneration and has been shown to improve repair in the heart and skin. In this study, we examine whether local production of IGF1-Ea protein improves tubular repair after renal ischemia reperfusion injury., Design: Transgenic mice in which the proximal-tubule specific promoter Sglt2 was driving the expression of an Igf-1Ea transgene. These animals were treated with an ischemic-reperfusion injury and the response at 24h and 5days compared with wildtype littermates., Results: Transgenic mice demonstrated rapid and enhanced renal injury in comparison to wild type mice. Five days after injury the wild type and low expressing Igf-1Ea transgenic mice showed significant tubular recovery, while high expressing Igf-1Ea transgenic mice displayed significant tubular damage. This marked injury was accompanied by a two-fold increase in the number of F4/80 positive macrophages and a three-fold increase in the number of Gr1-positive neutrophils in the kidney. At the molecular level, Igf-1Ea expression resulted in significant up-regulation of proinflammatory cytokines such as TNF-α and Ccl2. Expression of Nfatc1 was also delayed, suggesting reduced tubular proliferation after kidney injury., Conclusions: These data indicate that, unlike the muscle, heart and skin, elevated levels of IGF-1Ea in the proximal tubules exacerbates ischemia reperfusion injury resulting in increased recruitment of macrophages and neutrophils and delays repair in a renal setting., (Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2012
- Full Text
- View/download PDF
18. Increased cardiogenesis in P19-GFP teratocarcinoma cells expressing the propeptide IGF-1Ea.
- Author
-
Poudel B, Bilbao D, Sarathchandra P, Germack R, Rosenthal N, and Santini MP
- Subjects
- Animals, Cell Cycle, Cell Line, Tumor, Cell Survival, Insulin-Like Growth Factor I genetics, Mesoderm embryology, Mice, Peptides genetics, Protein Serine-Threonine Kinases, Pyruvate Dehydrogenase Acetyl-Transferring Kinase, Cell Differentiation, Heart embryology, Insulin-Like Growth Factor I biosynthesis, Myocytes, Cardiac cytology, Organogenesis, Pluripotent Stem Cells metabolism
- Abstract
The mechanism implicated in differentiation of endogenous cardiac stem cells into cardiomyocytes to regenerate the heart tissue upon an insult remains elusive, limiting the therapeutical goals to exogenous cell injection and/or gene therapy. We have shown previously that cardiac specific overexpression of the insulin-like growth factor 1 propeptide IGF-1Ea induces beneficial myocardial repair after infarct. Although the mechanism is still under investigation, the possibility that this propeptide may be involved in promoting stem cell differentiation into the cardiac lineage has yet to be explored. To investigate whether IGF-1Ea promote cardiogenesis, we initially modified P19 embryonal carcinoma cells to express IGF-1Ea. Taking advantage of their cardiomyogenic nature, we analyzed whether overexpression of this propeptide affected cardiac differentiation program. The data herein presented showed for the first time that constitutively overexpressed IGF-1Ea increased cardiogenic differentiation program in both undifferentiated and DMSO-differentiated cells. In details, IGF-1Ea overexpression promoted localization of alpha-actinin in finely organized sarcomeric structure compared to control cells and upregulated the cardiac mesodermal marker NKX-2.5 and the ventricular structural protein MLC2v. Furthermore, activated IGF-1 signaling promoted cardiac mesodermal induction in undifferentiated cells independently of cell proliferation. This analysis suggests that IGF-1Ea may be a good candidate to improve both in vitro production of cardiomyocytes from pluripotent stem cells and in vivo activation of the differentiation program of cardiac progenitor cells., (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
19. IGF-1Ea induces vessel formation after injury and mediates bone marrow and heart cross-talk through the expression of specific cytokines.
- Author
-
Santini MP, Lexow J, Borsellino G, Slonimski E, Zarrinpashneh E, Poggioli T, and Rosenthal N
- Subjects
- Animals, Antigens, Ly metabolism, Bone Marrow Cells metabolism, Coronary Vessels physiology, Insulin-Like Growth Factor I genetics, Membrane Proteins metabolism, Mice, Mice, Transgenic, Myocardial Infarction metabolism, Myocardial Infarction pathology, Proto-Oncogene Proteins c-kit metabolism, Stem Cells metabolism, Stem Cells physiology, Bone Marrow Cells physiology, Cytokines metabolism, Heart physiology, Insulin-Like Growth Factor I physiology, Myocardial Infarction physiopathology, Neovascularization, Physiologic, Regeneration
- Abstract
The aim of this study was to investigate whether supplemental IGF-1Ea transgene expression induces activation of local cardiac and bone marrow stem cell population to mediate mammalian heart repair. In physiologic conditions, cardiac overexpression of the IGF-1Ea propeptide is associated with an enrichment of c-Kit/Sca-1 positive side population cells in the bone marrow and the occurrence of an endothelial-primed CD34 positive side population in the heart. This cellular profile is shown here to correlate with the expression of cytokines involved in stem cell mobilization and vessel formation. This molecular and cellular interplay favored IGF-1Ea-mediated vessel formation in injured hearts. The physiologic and pathologic connection between cytokines and stem cells in response to IGF-1Ea may represent an important model to understand how to elicit endogenous reparative signaling., (Copyright © 2011 Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
20. Erosion of an Amplatzer septal occluder device into the aortic root.
- Author
-
Kamouh A, Osman MN, Rosenthal N, and Blitz A
- Subjects
- Aorta, Thoracic diagnostic imaging, Balloon Occlusion methods, Cardiac Catheterization methods, Device Removal, Echocardiography, Transesophageal methods, Emergency Treatment methods, Follow-Up Studies, Heart Failure diagnosis, Heart Failure etiology, Heart Septal Defects, Atrial diagnosis, Humans, Male, Middle Aged, Radiography, Reoperation methods, Severity of Illness Index, Treatment Outcome, Vascular Surgical Procedures methods, Aorta, Thoracic surgery, Balloon Occlusion adverse effects, Heart Failure surgery, Heart Septal Defects, Atrial therapy, Prosthesis Failure, Septal Occluder Device adverse effects
- Abstract
Atrial septal defects can be closed surgically or percutaneously. We report a patient who underwent percutaneous closure of an atrial septal defect with an Amplatzer septal occluder device (AGA Medical Corp, Golden Valley, MN). The patient presented 4 months later with congestive heart failure secondary to an erosion of the Amplatzer septal occluder into the aortic root. The device was removed surgically, and the fistula was repaired. Amplatzer septal occluder indications, selection criteria, and complications are discussed., (Copyright © 2011 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
21. High-throughput applicable genomic sex typing of chicken by TaqMan real-time quantitative polymerase chain reaction.
- Author
-
Rosenthal NF, Ellis H, Shioda K, Mahoney C, Coser KR, and Shioda T
- Subjects
- Animals, Chick Embryo, DNA chemistry, DNA genetics, Female, Male, Polymerase Chain Reaction veterinary, Chickens genetics, Sex Chromosomes, Sex Determination Analysis veterinary
- Abstract
Genetic sex typing of vertebrate animals is an essential technique for research on reproductive phenomena such as sex determination of embryonic tissues. Polymerase chain reaction amplification of genomic DNA segments in the Z and W sex chromosomes has been widely used as a standard laboratory method to determine genetic sex of the chicken (Gallus gallus domesticus). However, conventional protocols for PCR determination of avian sex typically involve tedious steps of genomic DNA isolation, which often require relatively large amounts of tissue samples, and the purity of genomic DNA specimens significantly affects PCR efficiency. Moreover, detection of sex chromosome-specific PCR products by gel electrophoresis is prone to misjudgment caused by amplification of contaminating genomic DNA segments derived from tissue or DNA samples as well as previously generated PCR products. Thus, the credibility of genetic sex typing by conventional PCR-based methods that measure the relative amounts of the end product DNA amplicons critically depends on several experimental steps that are potentially vulnerable to errors. Here, we describe an optimized protocol of chicken genetic sex typing by TaqMan real-time quantitative PCR amplification of markers on the sex chromosomes. This TaqMan sex typing method accurately quantifies relative amounts of the Z and W sex chromosome markers directly from only 0.5 to 2 microL of total blood lysate without nucleic acid purification. The real-time amplification curves of the quantitative PCR reaction readily distinguished truly homozygous (ZZ) and heterozygous (ZW) sex chromosomes from contamination of the sex chromosomal DNA, ensuring highly credible sex determination. Thus, the TaqMan typing of chicken genetic sex has several advantageous features for high-throughput operation compared with conventional methods.
- Published
- 2010
- Full Text
- View/download PDF
22. Class 2 IGF-1 isoforms are dispensable for viability, growth and maintenance of IGF-1 serum levels.
- Author
-
Temmerman L, Slonimsky E, and Rosenthal N
- Subjects
- Alleles, Animals, Animals, Newborn, Cells, Cultured, Genotype, Insulin-Like Growth Factor I classification, Insulin-Like Growth Factor I genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, Protein Isoforms classification, Protein Isoforms genetics, Protein Isoforms metabolism, Protein Isoforms physiology, Protein Sorting Signals genetics, Protein Sorting Signals physiology, Rats, Fetal Viability genetics, Growth genetics, Insulin-Like Growth Factor I metabolism, Insulin-Like Growth Factor I physiology, Serum metabolism
- Abstract
Insulin-like growth factor 1 (IGF-1) is a pleiotropic factor involved in growth, cell survival and cellular differentiation. It exerts its functions through endocrine, paracrine or autocrine mechanisms. Circulating IGF-1 is essential for normal fetal and postnatal growth, although the published phenotypes of IGF-1 null animals have been only partially penetrant, presumably due to mixed genetic backgrounds. Molecular dissection of IGF-1 action is complicated by the existence of at least nine different IGF-1 isoforms, generated in both humans and rodents by usage of alternate promoters, differential splicing and different post-translational modifications. Several lines of evidence suggest that the Class 2 IGF-1 isoform is specifically destined for circulation, supporting an endocrine role of IGF-1 in normal growth processes. Using Cre/LoxP conditional gene targeting of exon 2 of the IGF-1 gene, we have generated a Class 2 IGF-1 knockout mouse line in a pure C57/Bl6 genetic background, where the specific removal of exon 2 ablated Class 2 IGF-1 isoform. Class 2 IGF-1 knockout mice exhibited normal development and postnatal growth patterns and had normal IGF-1 circulating levels, due to compensatory upregulation of Class 1 transcripts. In contrast, progeny of a total IGF-1 knockout line lacking exon 3 in the same genetic background were predictably smaller, displayed dramatically reduced IGF-1 receptor phosphorylation and all died perinatally, apparently due to respiratory failure. These results confirm that Class 2 signal peptide is not necessary for systemic circulation of IGF-1, revealing an internal compensation system for maintaining IGF-1 serum concentrations. We also uncover a vital requirement of IGF-1 for perinatal viability, previously obscured by modifiers in heterogeneous genetic backgrounds., (Copyright 2010 Elsevier Ltd. All rights reserved.)
- Published
- 2010
- Full Text
- View/download PDF
23. Overexpression of mIGF-1 in keratinocytes improves wound healing and accelerates hair follicle formation and cycling in mice.
- Author
-
Semenova E, Koegel H, Hasse S, Klatte JE, Slonimsky E, Bilbao D, Paus R, Werner S, and Rosenthal N
- Subjects
- Animals, Cell Differentiation, Cell Movement, Cell Proliferation, Epithelium metabolism, Flow Cytometry, Gene Expression Regulation, Homeostasis, Insulin-Like Growth Factor I genetics, Keratin-14 metabolism, Keratinocytes cytology, Mice, Mice, Transgenic, Morphogenesis, Phenotype, Rats, Skin cytology, Skin growth & development, Stromal Cells cytology, Transgenes, Cell Cycle, Hair Follicle cytology, Hair Follicle growth & development, Insulin-Like Growth Factor I metabolism, Keratinocytes metabolism, Wound Healing
- Abstract
Insulin-like growth factor 1 (IGF-1) is an important regulator of growth, survival, and differentiation in many tissues. It is produced in several isoforms that differ in their N-terminal signal peptide and C-terminal extension peptide. The locally acting isoform of IGF-1 (mIGF-1) was previously shown to enhance the regeneration of both muscle and heart. In this study, we tested the therapeutic potential of mIGF-1 in the skin by generating a transgenic mouse model in which mIGF-1 expression is driven by the keratin 14 promoter. IGF-1 levels were unchanged in the sera of hemizygous K14/mIGF-1 transgenic animals whose growth was unaffected. A skin analysis of young animals revealed normal architecture and thickness as well as proper expression of differentiation and proliferation markers. No malignant tumors were formed. Normal homeostasis of the putative stem cell compartment was also maintained. Healing of full-thickness excisional wounds was accelerated because of increased proliferation and migration of keratinocytes, whereas inflammation, granulation tissue formation, and scarring were not obviously affected. In addition, mIGF-1 promoted late hair follicle morphogenesis and cycling. To our knowledge, this is the first work to characterize the simultaneous, stimulatory effect of IGF-1 delivery to keratinocytes on two types of regeneration processes within a single mouse model. Our analysis supports the use of mIGF-1 for skin and hair regeneration and describes a potential cell type-restricted action.
- Published
- 2008
- Full Text
- View/download PDF
24. Reconciling data from transgenic mice that overexpress IGF-I specifically in skeletal muscle.
- Author
-
Shavlakadze T, Winn N, Rosenthal N, and Grounds MD
- Subjects
- Aging, Alternative Splicing, Animals, Base Sequence, Disease Models, Animal, Exons, Humans, Introns, Mice, Molecular Sequence Data, Promoter Regions, Genetic, Protein Isoforms, Protein Structure, Tertiary, RNA, Messenger metabolism, Rats, Transgenes, Insulin-Like Growth Factor I biosynthesis, Insulin-Like Growth Factor I genetics, Mice, Transgenic, Muscle, Skeletal metabolism
- Abstract
Transgenic mice that overexpress insulin-like growth factor-1 (IGF-I) specifically in skeletal muscle have generated much information about the role of this factor for muscle growth and remodelling and provide insight for therapeutic applications of IGF-I for different pathological states and ageing. However, difficulties arise when attempting to critically compare the significance of data obtained in vivo by using different genetically engineered mouse lines and various experimental models. Complications arise due to complexity of the IGF-I system, since multiple transcripts of the IGF-I gene encode different isoforms generated by alternate promoter usage, differential splicing and post-translational modification, and how IGF-I gene expression relates to its diverse autocrine, paracrine and endocrine modes of action in vivo has still to be elucidated. In addition, there are problems related to specification of the exact IGF-I isoform used, expression patterns of the promoters, and availability of the transgene product under different experimental conditions. This review discusses the factors that must be considered when reconciling data from cumulative studies on IGF-I in striated muscle growth and differentiation using genetically modified mice. Critical evaluation of the literature focuses specifically on: (1) the importance of detailed information about the IGF-I isoforms and their mode of action (local, systemic or both); (2) expression pattern and strength of the promoters used to drive transgenic IGF-I in skeletal muscle cells (mono and multi-nucleated); (3) local compared with systemic action of the transgene product and possible indirect effects of transgenic IGF-I due to upregulation of other genes within skeletal muscle; (4) re-interpretation of these results in light of the most recent approaches to the dissection of IGF-I function. Full understanding of these complex in vivo issues is essential, not only for skeletal muscle but for many other tissues, in order to effectively extend observations derived from transgenic studies into potential clinical situations.
- Published
- 2005
- Full Text
- View/download PDF
25. Human hepatocytes in mice receiving pre-immune injection with human cord blood cells.
- Author
-
Turrini P, Monego G, Gonzalez J, Cicuzza S, Bonanno G, Zelano G, Rosenthal N, Paonessa G, Laufer R, and Padron J
- Subjects
- Animals, Cell Differentiation physiology, Cell Proliferation, Female, Humans, Immunocompetence physiology, Injections methods, Liver cytology, Liver physiology, Mice, Mice, SCID, Pregnancy, Cord Blood Stem Cell Transplantation methods, Hepatocytes cytology, Hepatocytes physiology, Liver embryology, Stem Cells cytology, Transplantation, Heterologous methods
- Abstract
It is well established that certain subpopulations of human adult stem cells can generate hepatocyte-like cells when transplanted into adult immunosuppressed mice. In the present study, we wanted to explore whether xeno-transplantation of human cord blood CD34(+) (hCBCD34(+)) cells during pre-immune stages of development in immunocompetent mice might also lead to human-mouse liver chimerism. Freshly isolated hCBCD34(+) cells were xeno-transplanted into non-immunosuppressed mice by both intra-blastocyst and intra-fetal injections. One and four weeks after birth, immunostaining for different human-specific hepatocyte markers: human hepatocyte-specific antigen, human serum albumin, and human alpha-1-antitrypsin indicated the presence of human hepatocyte-like cells in the livers of transplanted animals. Detection of human albumin mRNA further corroborated the development of pre-immune human-mouse chimeras. The current report, besides providing new evidence of the potential of hCBCD34(+) cells to generate human hepatocyte-like cells, suggests novel strategies for generating immunocompetent mice harboring humanized liver.
- Published
- 2005
- Full Text
- View/download PDF
26. Gene therapy for cardiac cachexia?
- Author
-
Rosenthal N and Musarò A
- Subjects
- Animals, Biomarkers blood, Cachexia etiology, Disease Progression, Heart Failure complications, Humans, Insulin-Like Growth Factor I genetics, Insulin-Like Growth Factor I metabolism, Muscle, Skeletal blood supply, Muscle, Skeletal metabolism, Cachexia therapy, Genetic Therapy, Heart Failure therapy
- Abstract
The prevention or attenuation of disease-related skeletal muscle degeneration has been a common goal in the treatment of cardiac cachexia. Cell-based therapies are complicated by insufficient numbers of autologous myoblasts and by ineffective incorporation into host muscle. Pharmacological administration of growth hormone in a variety of clinical conditions characterized by an increase in catabolic rate have been associated with increases in mortality and morbidity, resulting in a decrease in the clinical use of growth hormone and its downstream effector, insulin-like growth factor-1 and a decline in general research into anabolic treatment strategies. In mouse models, however, the selective expression of a muscle-specific transgene encoding a locally acting IGF-1 isoform induces muscle hypertrophy, prevents age- or disease-related atrophy, by increasing stem cell recruitment to injured or degenerating tissue. This gene-based approach avoids hypertrophic effects on distal organs such as the heart, and eliminates risk of possible neoplasms induced by inappropriate high expression levels of circulating IGF-1. The potential therapeutic role of locally expressed IGF-1 is discussed in the context of current strategies for the attenuation of cardiac cachexia.
- Published
- 2002
- Full Text
- View/download PDF
27. Targeted deletion of the MLC1f/3f downstream enhancer results in precocious MLC expression and mesoderm ablation.
- Author
-
Jiang P, Song J, Gu G, Slonimsky E, Li E, and Rosenthal N
- Subjects
- Animals, Blastocyst, Chimera, Congenital Abnormalities embryology, Congenital Abnormalities genetics, Embryonic and Fetal Development genetics, Fetal Proteins genetics, Gene Targeting, Genes, Lethal, Gestational Age, Heterozygote, In Situ Hybridization, Mice, Mice, Knockout, Myosin Light Chains genetics, Reverse Transcriptase Polymerase Chain Reaction, Sequence Deletion, Stem Cells metabolism, Enhancer Elements, Genetic genetics, Enhancer Elements, Genetic physiology, Fetal Proteins physiology, Gene Expression Regulation, Developmental genetics, Mesoderm metabolism, Myosin Light Chains physiology
- Abstract
The expression of skeletal muscle contractile proteins is tightly regulated during embryonic development. In the mouse, the myosin light chain (MLC) 1f/3f gene locus is not activated until E9.5, exclusively in skeletal muscle precursor cells. A potent enhancer downstream of the MLC1f/3f locus confers correct temporal and spatial activation of linked reporter gene in transgenic mouse embryos. To examine roles of the MLC downstream enhancer (MLCE) in its native context of the MLC1f/3f gene locus, we eliminated a 1.5-kb DNA segment containing the enhancer from the mouse genome by targeted deletion, leaving no exogenous sequences at the deletion site. Mouse embryos homozygous for the MLCE deletion were smaller and developmentally delayed, formed no mesoderm by E7.5, and were resorbed almost completely at E8.5. In situ hybridization and RT-PCR analyses of affected mutant embryos at E7.5 revealed ectopic MLC transcripts, whose products would be predicted to interfere with a variety of nonmuscle cell functions determining differentiation of mesoderm. These results suggest that the MLC downstream enhancer and its flanking sequences include negative regulatory elements which block precocious activation of MLC expression in mesodermal precursors during a critical window of development, as well as positive elements which subsequently permit tissue-restricted MLC transcription in differentiating skeletal muscles., ((C)2002 Elsevier Science (USA).)
- Published
- 2002
- Full Text
- View/download PDF
28. Band-specific electroencephalogram and brain cooling abnormalities during NREM sleep in patients with winter depression.
- Author
-
Schwartz PJ, Rosenthal NE, and Wehr TA
- Subjects
- Adult, Alpha Rhythm, Delta Rhythm, Female, Homeostasis physiology, Humans, Male, Middle Aged, Reference Values, Seasonal Affective Disorder diagnosis, Seasonal Affective Disorder psychology, Skin Temperature physiology, Theta Rhythm, Body Temperature Regulation physiology, Brain physiopathology, Electroencephalography, Seasonal Affective Disorder physiopathology, Sleep Stages physiology
- Abstract
Background: We previously reported that delta wave activity and facial skin temperatures, an index of brain cooling activity, were both abnormal during sleep in patients with winter depression (SAD). Because other electroencephalographic (EEG) frequencies may also convey relevant thermal, homeostatic, and circadian information, we sought to spectrally analyze delta, theta, alpha, and sigma frequencies during sleep from 23 patients with SAD and 23 healthy control subjects., Methods: We computed means for delta, theta, alpha, and sigma power during both NREM and REM sleep. We also generated 22 cross-correlation functions for each group by crossing facial and rectal temperature with each other, as well as with delta, theta, alpha, and sigma frequencies., Results: We found that delta, theta, and alpha frequency activities were all increased during NREM, but not REM sleep, in patients with SAD. In addition, there were significant and abnormal cross-correlations between facial temperatures and delta and theta frequencies during NREM sleep in patients with SAD., Conclusions: Patients with winter depression exhibit correlated abnormalities of sleep homeostasis and brain cooling during NREM sleep. Their EEG profiles during NREM sleep resemble the EEG profiles of subjects who have been sleep deprived. Further studies of NREM sleep homeostasis in patients with SAD seem warranted.
- Published
- 2001
- Full Text
- View/download PDF
29. From the bottom of the heart: anteroposterior decisions in cardiac muscle differentiation.
- Author
-
Rosenthal N and Xavier-Neto J
- Subjects
- Aldehyde Oxidoreductases genetics, Aldehyde Oxidoreductases metabolism, Animals, Chick Embryo, Heart drug effects, Mice, Morphogenesis drug effects, Morphogenesis physiology, Myocardium metabolism, Retinal Dehydrogenase, Signal Transduction physiology, Tretinoin metabolism, Tretinoin pharmacology, Body Patterning physiology, Cell Differentiation physiology, Heart embryology, Myocardium cytology
- Abstract
Recently, studies on specification of axes in the developing embryo have focused on the heart, which is the first functional organ to form and probably responds to common cues controlling positional information in surrounding tissues. The early differentiation of heart cells affords an opportunity to link the acquisition of regional identity with the signals underlying terminal differentiation. In the past year, a wealth of information on these signals has emerged, elucidating the general pathways controlling body axes in the context of the developing heart.
- Published
- 2000
- Full Text
- View/download PDF
30. Editorial overview
- Author
-
Rosenthal N and Birchmeier C
- Published
- 2000
- Full Text
- View/download PDF
31. Sequential programs of retinoic acid synthesis in the myocardial and epicardial layers of the developing avian heart.
- Author
-
Xavier-Neto J, Shapiro MD, Houghton L, and Rosenthal N
- Subjects
- Animals, Biological Evolution, Chick Embryo, Gene Expression Regulation, Developmental, Immunohistochemistry, In Situ Hybridization, Myosins genetics, Quail embryology, Retinal Dehydrogenase, Signal Transduction, Transcriptional Activation, Aldehyde Oxidoreductases metabolism, Atrial Myosins, Avian Proteins, Heart embryology, Myocardium metabolism, Myosin Heavy Chains, Pericardium embryology, Pericardium metabolism, Tretinoin metabolism
- Abstract
Endogenous patterns of retinoic acid (RA) signaling in avian cardiac morphogenesis were characterized by localized expression of a key RA-synthetic enzyme, RALDH2, which displayed a biphasic pattern during heart development. RALDH2 immunoreactivity was initially apparent posterior to Hensen's node of stage 5-6 embryos and subsequently in somites and unsegmented paraxial and lateral plate mesoderm overlapping atrial precursors in the cardiogenic plate of stage 9- embryos. Initial RALDH2 synthesis in the posterior myocardium coincided with activation of the AMHC1 gene, a RA-responsive marker of inflow heart segments. A wave of RALDH2 synthesis then swept the myocardium in a posterior-to-anterior direction, reaching the outflow tract by stage 13, then fading from the myocardial layer. The second phase of RALDH2 expression, initiated at stage 18 in the proepicardial organ, persisted in migratory epicardial cells that completely enveloped the heart by stage 24. Early restriction of RALDH2 expression to the posterior cardiogenic plate, overlapping RA-inducible gene activation, provides evidence for commitment of posterior avian heart segments by localized production of RA, whereas subsequent RALDH2 expression exclusively in the migratory epicardium suggests a role for the morphogen in ventricular expansion and morphogenesis of underlying myocardial tissues., (Copyright 2000 Academic Press.)
- Published
- 2000
- Full Text
- View/download PDF
32. An E box comprises a positional sensor for regional differences in skeletal muscle gene expression and methylation.
- Author
-
Ceccarelli E, McGrew MJ, Nguyen T, Grieshammer U, Horgan D, Hughes SH, and Rosenthal N
- Subjects
- Animals, Base Sequence, Binding Sites genetics, Cell Line, Chloramphenicol O-Acetyltransferase genetics, DNA genetics, DNA metabolism, DNA Methylation, Enhancer Elements, Genetic, Genes, Regulator, Genes, Reporter, Humans, Mice, Mice, Transgenic, Molecular Sequence Data, Muscle Development, Muscle, Skeletal embryology, Muscle, Skeletal growth & development, Mutation, MyoD Protein metabolism, Myosin Light Chains genetics, Nuclear Proteins metabolism, Rats, Sequence Homology, Nucleic Acid, Species Specificity, Gene Expression Regulation, Developmental, Muscle, Skeletal metabolism
- Abstract
To dissect the molecular mechanisms conferring positional information in skeletal muscles, we characterized the control elements responsible for the positionally restricted expression patterns of a muscle-specific transgene reporter, driven by regulatory sequences from the MLC1/3 locus. These sequences have previously been shown to generate graded transgene expression in the segmented axial muscles and their myotomal precursors, fortuitously marking their positional address. An evolutionarily conserved E box in the MLC enhancer core, not recognized by MyoD, is a target for a nuclear protein complex, present in a variety of tissues, which includes Hox proteins and Zbu1, a DNA-binding member of the SW12/SNF2 gene family. Mutation of this E box in the MLC enhancer has only a modest positive effect on linked CAT gene expression in transfected muscle cells, but when introduced into transgenic mice the same mutation elevates CAT transgene expression in skeletal muscles, specifically releasing the rostral restriction on MLC-CAT transgene expression in the segmented axial musculature. Increased transgene activity resulting from the E box mutation in the MLC enhancer correlates with reduced DNA methylation of the distal transgenic MLC1 promoter as well as in the enhancer itself. These results identify an E box and the proteins that bind to it as a positional sensor responsible for regional differences in axial skeletal muscle gene expression and accessibility., (Copyright 1999 Academic Press.)
- Published
- 1999
- Full Text
- View/download PDF
33. No coding variant of the tryptophan hydroxylase gene detected in seasonal affective disorder, obsessive-compulsive disorder, anorexia nervosa, and alcoholism.
- Author
-
Han L, Nielsen DA, Rosenthal NE, Jefferson K, Kaye W, Murphy D, Altemus M, Humphries J, Cassano G, Rotondo A, Virkkunen M, Linnoila M, and Goldman D
- Subjects
- Genotype, Humans, Alcoholism genetics, Anorexia Nervosa genetics, Genetic Variation genetics, Obsessive-Compulsive Disorder genetics, Seasonal Affective Disorder genetics, Tryptophan Hydroxylase genetics
- Abstract
Background: The goal of this study was to evaluate the role of genetic variation in the coding sequence of tryptophan hydroxylase (TPH) in the pathogenesis of several psychiatric diseases in which altered serotonin function has been implicated: bipolar affective disorder (BP), obsessive-compulsive disorder (OCD), anorexia nervosa (AN), seasonal affective disorder (SAD), panic disorder (PD), and alcoholism (Alc)., Methods: Ninety-three percent of the TPH coding sequence was screened by polymerase chain reaction single-strand conformation polymorphism (SSCP) for DNA sequence variations in 128 AN, 88 OCD, 72 SAD, 45 PD, and 36 BP patients and 142 normal volunteers. Also included in the screening were 61 Alc randomly selected from a Finnish alcoholic population in which an association of a TPH intron 7 polymorphism with suicidality was previously observed. Polymorphisms detected by SSCP were characterized by DNA sequencing and by allele-specific restriction enzyme digestion. Genotyping was then performed in 34 Finnish alcoholic suicide attempters., Results: A rare silent mutation was identified in exon 10 and is designated T1095C. The C1095 allele was found in 1 OCD and in 2 AN subjects; all 3 individuals were heterozygous (C1095/T1095) for the variant allele. No association was observed between this TPH T1095C variant with either OCD, AN, Alc, or suicidality., Conclusion: These results suggest that the coding sequence of the TPH gene does not contain abundant variants, and may not play a major role in vulnerability to several psychopathologies in which reduced serotonin turnover has been implicated.
- Published
- 1999
- Full Text
- View/download PDF
34. Dynamic patterns of retinoic acid synthesis and response in the developing mammalian heart.
- Author
-
Moss JB, Xavier-Neto J, Shapiro MD, Nayeem SM, McCaffery P, Dräger UC, and Rosenthal N
- Subjects
- Aldehyde Oxidoreductases biosynthesis, Animals, Aorta, Thoracic embryology, Cytochrome P-450 Enzyme System biosynthesis, Endocardium embryology, Heart drug effects, In Vitro Techniques, Isoenzymes biosynthesis, Lac Operon, Mice, Mice, Transgenic, Morphogenesis, Oxygenases biosynthesis, Recombinant Proteins biosynthesis, Regulatory Sequences, Nucleic Acid, Retinal Dehydrogenase, Retinoic Acid 4-Hydroxylase, Teratogens metabolism, Teratogens pharmacology, Tissue Distribution, Tretinoin pharmacology, beta-Galactosidase biosynthesis, Gene Expression Regulation, Developmental, Gene Expression Regulation, Enzymologic, Heart embryology, Tretinoin metabolism
- Abstract
Retinoic acid (RA) has been implicated in cardiac morphogenesis by its teratogenic effects on the heart, although its role in normal cardiogenesis remains unknown. To define the parameters of RA action in cardiac morphogenesis, we analyzed the patterns of ligand synthesis, response, and inactivation in the developing mouse heart. Activation of a lacZ transgene controlled by an RA response element (RARE) was compared to the localization of the retinaldehyde-oxidizing dehydrogenase RALDH2, the earliest RA synthetic enzyme in the mouse embryo, and to the expression of a gene encoding an RA-degrading enzyme (P450RA). We observed that RALDH2 localization and RA response were virtually superimposable throughout heart development. Initially, both RALDH2 and RARE-LacZ activity were restricted to the sinus venosa in unlooped hearts, but were high in the dorsal mesocardium, while P450RA expression was restricted to the endocardium. Later stages were characterized by a sequential, noncontiguous progression of RALDH2 accumulation and RA response, from the sinus venosa to atria, dorsal-medial conotruncus, aortic arches, and the epicardium. This dynamic pattern of RA response was a direct result of localized RALDH2, since hearts of cultured embryos were uniformly competent to respond to an exogenous RA challenge. These observations support a model in which the influence of endogenous RA on heart development depends upon localized presentation of the ligand, with only limited diffusion from the source of its synthesis.
- Published
- 1998
- Full Text
- View/download PDF
35. Case series: pediatric seasonal affective disorder. A follow-up report.
- Author
-
Giedd JN, Swedo SE, Lowe CH, and Rosenthal NE
- Subjects
- Adolescent, Child, Comorbidity, Disease Progression, Female, Follow-Up Studies, Humans, Male, Phototherapy, Seasonal Affective Disorder physiopathology, Seasonal Affective Disorder therapy
- Abstract
Six subjects who as children had received a diagnosis of seasonal affective disorder consented to participate in a 7-year follow-up study. Structured and semistructured interviews were conducted to assess the course of illness, response to treatment, and current clinical state. Seasonal patterns of symptoms and response to light therapy remained relatively stable over a 7-year period. Two subjects were using adjunctive fluoxetine. Seasonal affective disorder can occur in children and adolescents, responds to light therapy, and should be considered in the differential diagnosis of pediatric affective symptoms or cyclic school performance.
- Published
- 1998
- Full Text
- View/download PDF
36. Seasonal variation in core temperature regulation during sleep in patients with winter seasonal affective disorder.
- Author
-
Schwartz PJ, Rosenthal NE, Turner EH, Drake CL, Liberty V, and Wehr TA
- Subjects
- Adult, Circadian Rhythm physiology, Female, Humans, Male, Middle Aged, Phototherapy, Polysomnography, Reference Values, Seasonal Affective Disorder diagnosis, Seasonal Affective Disorder psychology, Body Temperature Regulation physiology, Seasonal Affective Disorder physiopathology, Seasons, Sleep Stages physiology
- Abstract
Nocturnal core temperature during sleep is elevated during depression compared with remission in nonseasonally depressed patients. Similarly, nocturnal core temperature is higher during winter depression compared with remission induced by light treatment in seasonal affective disorder (SAD) patients. We investigated whether nocturnal core temperature in SAD patients naturally becomes lower in summer (during remission) compared with winter (during depression). Twenty-four-hour core temperature profiles were obtained in winter and summer in 22 SAD patients and 22 controls. The nocturnal core temperature minima were lower in summer compared with winter in SAD patients (p < .005), but not controls (p > .4). The seasonal changes in nocturnal core temperatures in SAD patients may reflect a unique physiological responsiveness of SAD patients to the change of seasons, and may be intimately related to the seasonal disturbances of mood and energy that are characteristic of SAD.
- Published
- 1997
- Full Text
- View/download PDF
37. A controlled trial of light therapy for the treatment of pediatric seasonal affective disorder.
- Author
-
Swedo SE, Allen AJ, Glod CA, Clark CH, Teicher MH, Richter D, Hoffman C, Hamburger SD, Dow S, Brown C, and Rosenthal NE
- Subjects
- Adolescent, Child, Cross-Over Studies, Double-Blind Method, Female, Humans, Male, Treatment Outcome, Phototherapy, Seasonal Affective Disorder therapy
- Abstract
Objective: To evaluate the efficacy of light therapy for the treatment of pediatric seasonal affective disorder (SAD)., Method: 28 children (aged 7 to 17 years) at two geographically distinct sites were enrolled in a double-blind, placebo-controlled, crossover trial of bright-light treatment. Subjects initially entered a week-long baseline period during which they wore dark glasses for an hour a day. They were then randomly assigned to receive either active treatment (1 hour of bright-light therapy plus 2 hours of dawn simulation) or placebo (1 hour of clear goggles plus 5 minutes of low-intensity dawn simulation) for 1 week. The treatment phase was followed by a second dark-glasses phase lasting 1 to 2 weeks. After this phase, the children received the alternate treatment. Response was measured using the parent and child versions of the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorders version (SIGH-SAD)., Results: Data were analyzed as change from baseline. SIGH-SAD-P total depression scores were significantly decreased from baseline during light therapy compared with placebo (one-way analysis of variance, rho = .009), and no differences were found between the placebo and control phases. Subscores of atypical and typical depression were also significantly decreased during the active treatment (rho = .004 and .028, respectively). A similar trend was noted with the SIGH-SAD-C, but this did not reach significance. At the end of the study, 78% of the parents questioned and 80% of the children questioned rated light therapy as the phase during which the child "felt best.", Conclusion: Light therapy appears to be an effective treatment for pediatric SAD.
- Published
- 1997
- Full Text
- View/download PDF
38. Developmental regulation of Zbu1, a DNA-binding member of the SWI2/SNF2 family.
- Author
-
Gong X, Kaushal S, Ceccarelli E, Bogdanova N, Neville C, Nguyen T, Clark H, Khatib ZA, Valentine M, Look AT, and Rosenthal N
- Subjects
- Adenosine Triphosphatases metabolism, Adult, Amino Acid Sequence, Animals, Chromosome Mapping, Chromosomes, Human, Pair 3 genetics, Cloning, Molecular, DNA, Complementary genetics, DNA-Binding Proteins metabolism, Enhancer Elements, Genetic genetics, Humans, Mice, Molecular Sequence Data, Muscles cytology, Myosin Light Chains genetics, Organ Specificity, RNA, Messenger analysis, Recombinant Fusion Proteins, Sequence Homology, Amino Acid, Transcription Factors metabolism, DNA Helicases, DNA-Binding Proteins genetics, Gene Expression Regulation, Developmental physiology, Genes, Regulator genetics, Transcription Factors genetics
- Abstract
The SWI2/SNF2 gene family has been implicated in a wide variety of processes, involving regulation of DNA structure and chromatin configuration, mitotic chromosome segregation, and DNA repair. Here we report the characterization of the Zbu1 gene, also known as HIP116, located on human chromosome band 3q25, which encodes a DNA-binding member of this superfamily. Zbu1 was isolated in this study by its affinity for a site in the myosin light chain 1/3 enhancer. The protein has single-stranded DNA-dependent ATPase activity, includes seven helicase motifs, and a RING finger motif that is shared exclusively by the RAD5, spRAD8, and RAD16 family members. During mouse embryogenesis, Zbu1 transcripts are detected relatively late in fetal development and increase in neonatal stages, whereas the protein accumulates asynchronously in heart, skeletal muscle, and brain. In adult human tissues, alternatively spliced Zbu1 transcripts are ubiquitous with highest expression in these tissues. Gene expression is also dramatically induced in human tumor lines and in Li-Fraumeni fibroblast cultures, suggesting that it is aberrantly regulated in malignant cells. The developmental profile of Zbu1 gene expression and the association of the protein with a tissue-specific transcriptional regulatory element distinguish it from other members of the SWI2/SNF2 family and suggest novel roles for the Zbu1 gene product.
- Published
- 1997
- Full Text
- View/download PDF
39. Two naturally occurring amino acid substitutions of the 5-HT2A receptor: similar prevalence in patients with seasonal affective disorder and controls.
- Author
-
Ozaki N, Rosenthal NE, Pesonen U, Lappalainen J, Feldman-Naim S, Schwartz PJ, Turner EH, and Goldman D
- Subjects
- Alleles, Humans, Phenotype, Polymerase Chain Reaction, Polymorphism, Restriction Fragment Length, Polymorphism, Single-Stranded Conformational, Receptors, Serotonin metabolism, Seasonal Affective Disorder metabolism, Amino Acids genetics, Receptors, Serotonin genetics, Seasonal Affective Disorder genetics
- Abstract
We screened the 5-HT2A receptor gene coding region in 50 patients with seasonal affective disorder (SAD) using a single strand conformational polymorphism analysis and estimated the frequencies of two synonymous and two non-synonymous substitutions we detected in 70 Centre d'Etude du Polymorphism Humain (CEPH) population controls and 62 normal controls. Both of the amino acid substitutions: Ala447-Val447 and His452-Tyr452, were located within the cytoplasmic. C-terminal tail of the receptor. Rarer allele frequencies in CEPH were 0.7% and 9.3% for Val447 and Tyr452, respectively. Allele frequencies of all four polymorphisms, including the two amino acid substitutions, were not significantly different in SAD patients as compared to CEPH and normal controls. Lack of association of Val447 and Tyr452 to SAD is consistent with observations showing normal 5-HT2A receptor Ca2+ response in platelets with this disorder, however, the two 5-HT2A amino acid substitutions may lead to differences in behavioral phenotypes.
- Published
- 1996
- Full Text
- View/download PDF
40. Circadian profiles of cortisol, prolactin, and thyrotropin in seasonal affective disorder.
- Author
-
Oren DA, Levendosky AA, Kasper S, Duncan CC, and Rosenthal NE
- Subjects
- Adult, Female, Humans, Male, Middle Aged, Personality Inventory, Phototherapy, Reference Values, Seasonal Affective Disorder diagnosis, Seasonal Affective Disorder psychology, Seasonal Affective Disorder therapy, Circadian Rhythm physiology, Hydrocortisone blood, Prolactin blood, Seasonal Affective Disorder blood, Thyrotropin blood
- Abstract
To determine whether circadian profiles of various plasma hormones are abnormal in patients with winter seasonal affective disorder (SAD), we obtained 24-hour profiles of plasma cortisol, prolactin, and thyrotropin in subsets of a sample of 22 depressed patients with SAD on and off light therapy and in subsets of a sample of 24 normal controls. Cortisol levels did not differ between patients and controls, and levels in patients were not affected by light therapy. Prolactin levels were lower in patients than in controls throughout the day (p < 0.03) but were unaffected by light therapy. Independent of patient vs. control status, prolactin levels were higher in women than in men throughout the day (p < 0.003). Thyrotropin levels were no different in patients and controls, but levels in patients were lower following light therapy (p < 0.05).
- Published
- 1996
- Full Text
- View/download PDF
41. Tryptophan metabolism in chronic inflammatory lung disease.
- Author
-
Meyer KC, Arend RA, Kalayoglu MV, Rosenthal NS, Byrne GI, and Brown RR
- Subjects
- Actins genetics, Adult, Bronchoalveolar Lavage Fluid cytology, Chromatography, High Pressure Liquid, Chronic Disease, Female, Humans, Indoleamine-Pyrrole 2,3,-Dioxygenase, Leukocyte Count, Lung Diseases, Interstitial blood, Lung Diseases, Interstitial immunology, Macrophages enzymology, Male, Middle Aged, RNA, Messenger analysis, Sarcoidosis enzymology, Smoking metabolism, Synovitis metabolism, Tryptophan blood, Tryptophan Oxygenase metabolism, Kynurenine blood, Lung Diseases, Interstitial enzymology, Tryptophan metabolism
- Abstract
Induction of indoleamine 2,3-dioxygenase (IDO), an enzyme expressed by mononuclear phagocytes and some fibroblast cell lines in response to interferon-gamma, leads to enhanced degradation of tryptophan to kynurenine. Because inflammatory lung diseases are generally associated with activation of pulmonary macrophages, we investigated tryptophan metabolism in patients with interstitial lung disease by measuring circulating levels of tryptophan and kynurenine in peripheral blood and by measuring the IDO activity of bronchoalveolar cells. IDO activities were increased for bronchoalveolar lavage (BAL) cells obtained from patients with interstitial lung disease (115.4 +/- 30.4, n = 37) when compared with BAL cells from normal subjects (15.2 +/- 7.4, n = 14; p < 0.05), and messenger RNA for IDO was present in BAL cells from patients with interstitial disease but was not present in BAL cells from normal volunteer subjects. Patients with inflammatory lung disease also had decreased tryptophan and increased kynurenine concentrations in serum. The ratio of serum tryptophan levels to serum kynurenine levels was significantly depressed for patients with idiopathic pulmonary fibrosis (18.4 +/- 1.7, n = 29; p < 0.0001), patients with fibrosing alveolitis associated with collagen vascular disease (13.1 +/- 1.6, n = 18; p < 0.0001), or patients with sarcoidosis (21.0 +/- 1.1, n = 50; p < 0.0001), as compared with the ratio for normal subjects (31.8 +/- 2.3, n = 18). Patients with fibrotic disease had the highest levels of BAL cell IDO activity, and patients with collagen vascular disease associated fibrosing alveolitis had the most depressed levels of serum tryptophan and the greatest elevations in serum kynurenine. Measurement of tryptophan and kynurenine concentrations in serum may provide a useful measure of disease activity in chronic inflammatory parenchymal lung diseases such as sarcoidosis and idiopathic pulmonary fibrosis.
- Published
- 1995
42. Hormonal responses to the administration of m-chlorophenylpiperazine in patients with seasonal affective disorder and controls.
- Author
-
Garcia-Borreguero D, Jacobsen FM, Murphy DL, Joseph-Vanderpool JR, Chiara A, and Rosenthal NE
- Subjects
- Adult, Female, Humans, Male, Personality Inventory, Phototherapy, Seasonal Affective Disorder blood, Seasonal Affective Disorder psychology, Seasonal Affective Disorder therapy, Seasons, Serotonin physiology, Hydrocortisone blood, Piperazines, Prolactin blood, Seasonal Affective Disorder diagnosis, Serotonin Receptor Agonists
- Abstract
We report on the plasma cortisol and prolactin responses to the serotonergic agonist m-CPP (0.1 mg/kg) in 10 patients with winter seasonal affective disorder (SAD) and 10 controls during the winter, in both untreated and bright light-treated conditions; and on 8 other SAD patients and 8 other controls during the summer. Following m-CPP infusion, untreated patients had exaggerated prolactin (p < .05) and cortisol (p < .05) responses compared to controls. Light treatment significantly reduced responses of both hormones to m-CPP (prolactin: p < .01; cortisol: p < .01). When untreated winter subjects and summer subjects were compared, cortisol, but not prolactin responses to m-CPP were found to be higher in patients than in controls during the winter, and lower in patients than in controls during the summer (diagnosis by season: p < .05). These results are consistent with those of our previous report on the behavioral responses to m-CPP in the same patients and suggest an abnormality in serotonergic function in untreated SAD patients in winter, which is normalized following treatment with light therapy and naturally during the summer.
- Published
- 1995
- Full Text
- View/download PDF
43. Platelet [3H]paroxetine binding, 5-HT-stimulated Ca2+ response, and 5-HT content in winter seasonal affective disorder.
- Author
-
Ozaki N, Rosenthal NE, Mazzola P, Chiueh CC, Hardin T, Garcia-Borreguero D, Schwartz PJ, Turner E, Oren DA, and Murphy DL
- Subjects
- Adult, Binding Sites, Female, Humans, Male, Middle Aged, Psychiatric Status Rating Scales, Seasonal Affective Disorder psychology, Blood Platelets metabolism, Calcium metabolism, Paroxetine metabolism, Seasonal Affective Disorder metabolism, Serotonin metabolism
- Abstract
The present study was designed to evaluate cellular serotonergic functions in winter seasonal affective disorder (SAD) using serotonin (5-HT)-stimulated Ca2+ response as an integrated measure of 5-HT2 receptor function in platelets, [3H]paroxetine binding to characterize the platelet 5-HT transporter and 5-HT content as an index of the platelet storage capacity for this neurotransmitter amine. Purified density-dependent subpopulations of platelets in untreated and light-treated SAD patients and matched controls were investigated in order to control for possible variations in platelet turnover. We found no differences between SAD patients and controls on any of the measures, nor between light therapy conditions in SAD patients, although we found a higher Bmax of [3H]paroxetine binding and 5-HT content in heavy platelets compared to light platelets. Although the validity of platelet serotonergic measures as a model for brain serotonergic systems still remains to be elucidated, we found no evidence of platelet serotonergic abnormalities in our sample of SAD patients.
- Published
- 1994
- Full Text
- View/download PDF
44. Seasonal variation in behavioral responses to m-CPP in patients with seasonal affective disorder and controls.
- Author
-
Joseph-Vanderpool JR, Jacobsen FM, Murphy DL, Hill JL, and Rosenthal NE
- Subjects
- Adult, Circadian Rhythm drug effects, Circadian Rhythm physiology, Euphoria drug effects, Euphoria physiology, Female, Humans, Infusions, Intravenous, Male, Middle Aged, Personality Inventory, Piperazines adverse effects, Receptors, Serotonin drug effects, Receptors, Serotonin physiology, Seasonal Affective Disorder physiopathology, Seasonal Affective Disorder psychology, Serotonin physiology, Serotonin Receptor Agonists adverse effects, Synaptic Transmission drug effects, Synaptic Transmission physiology, Piperazines therapeutic use, Seasonal Affective Disorder drug therapy, Seasons, Serotonin Receptor Agonists therapeutic use
- Abstract
This paper reports the behavioral responses to m-chlorophenylpiperazine (m-CPP), a serotonin agonist, in patients with seasonal affective disorder (SAD) and controls during the summer. Results are compared with the responses of SAD patients and controls given m-CPP in the winter. Results of the winter study were reported earlier by our group. Baseline Hamilton depression ratings in SAD patients were significantly lower in the summer than in winter (p < 0.05). Additionally, in both SAD patients and controls, there were seasonal differences on the National Institute of Mental Health (NIMH) self-rating scale items: "depressed affect," "dysphoria," and "functional deficit" at baseline. The behavioral responses to m-CPP across seasons differentiated patients from normals only in the "activation/euphoria" item, on which a far greater response was seen in patients than in controls during the winter. This behavioral response may be a state marker for winter depression, as it was significantly reduced after light treatment of these patients in the winter, and in the summer. SAD patients responded differently from controls on "altered self-awareness" and "dysphoria" independently of seasons, and these responses may be considered as possible trait markers for this condition. These results provide further evidence of a possible deficiency in serotonergic transmission in seasonal affective disorder.
- Published
- 1993
- Full Text
- View/download PDF
45. Extrapulmonary thoracic restriction (hidebound chest) complicating eosinophilic fasciitis.
- Author
-
Chalker RB, Dickey BF, Rosenthal NC, and Simms RW
- Subjects
- Aged, Humans, Male, Radiography, Thoracic, Respiratory Function Tests, Tomography, X-Ray Computed, Eosinophilia complications, Fasciitis complications, Respiration Disorders etiology, Thorax
- Abstract
Eosinophilic fasciitis (EF) is an unusual disorder characterized by diffuse skin thickening and induration due to inflammation within the deep fascia; visceral involvement is generally mild or absent. A patient with biopsy-proved EF developed progressive respiratory limitation. Physical examination revealed marked induration of the thoracic integument with a severely limited chest wall excursion. Total lung capacity was 62 percent of predicted with a normal corrected Dco and maximal inspiratory force; a chest computed tomogram with thin sections showed no evidence of parenchymal lung disease. Extrapulmonary thoracic restriction ("hidebound chest") has not been previously reported to complicate EF.
- Published
- 1991
- Full Text
- View/download PDF
46. Progesterone binding in a clinical isolate of Pseudomonas aeruginosa.
- Author
-
Mosier S, Nakao M, Herman M, Walia SK, Rosenthal N, Hurd C, and Moudgil VK
- Subjects
- Binding Sites, Cytosol metabolism, Humans, Pseudomonas Infections microbiology, Pseudomonas aeruginosa isolation & purification, Urinary Tract Infections microbiology, Progesterone metabolism, Pseudomonas aeruginosa metabolism
- Abstract
We have undertaken the characterization of progestin binding component(s) in the cytosol prepared from Pseudomonas aeruginosa isolated from an immunocompromised patient. Incubation of P. aeruginosa cytosol aliquots at 0 degrees C with 20 nM [3H]R5020 (a synthetic progestin) revealed the presence of saturable binding. The [3H]R5020 binding reached an equilibrium after 1 h at 0 degrees C and showed saturation at 30-50 nM with a Kd value of 7.7 nM. At 0 degrees C, beta-mercaptoethanol increased the [3H]R5020 binding by 20% but sodium molybdate had no effect. The [3H]R5020-macromolecular complex was stable for up to 4 h at 37 degrees C. Steroid binding specificity analysis revealed that [3H]R5020 binding could be eliminated in the presence of 2 microM progesterone, estradiol, or dihydrotestosterone but that the synthetic glucocorticoid, triamcinolone acetonide, did not compete. Postlabeling of the cytosol fractions obtained after 10-30% glycerol gradient analysis demonstrated association of the radioactivity with a molecule that sedimented as a 6-8 S protease-sensitive moiety which was unaltered in the presence of RNase or DNase. When cells were grown in the presence of 100 nM progesterone, a 50% inhibition in the number of resulting colonies was observed. In addition to its evolutionary significance, the presence of this steroid binding molecule suggests a potential in the endocrine manipulation in the treatment of infections caused by P. aeruginosa.
- Published
- 1991
- Full Text
- View/download PDF
47. Core body temperature in patients with seasonal affective disorder and normal controls in summer and winter.
- Author
-
Levendosky AA, Josep-Vanderpool JR, Hardin T, Sorek E, and Rosenthal NE
- Subjects
- Adult, Depressive Disorder diagnosis, Depressive Disorder psychology, Energy Metabolism physiology, Female, Humans, Male, Middle Aged, Psychiatric Status Rating Scales, Thyrotropin blood, Arousal physiology, Body Temperature Regulation physiology, Circadian Rhythm physiology, Depressive Disorder physiopathology, Seasons
- Abstract
The rationale for phototherapy in seasonal affective disorder (SAD) was originally based on the notion that SAD patients were light deprived during the wintertime and needed more light. We previously found normal temperature profiles of untreated SAD patients during the winter, and that phototherapy significantly enhanced the amplitude of the circadian temperature profile in SAD patients during the winter (Rosenthal et al 1990). We hypothesized that summer would act similarly on the temperature rhythm of these patients. In this study we examined the temperature data from SAD patients and normal controls during the summer and compared it to the results of our previous study. We found identical profiles for SAD patients and normal controls during the summer and that summer significantly lowered the overall temperature profiles of both groups and did not alter the amplitudes. These results raise questions about the validity of the current theories of the mechanism of light therapy.
- Published
- 1991
- Full Text
- View/download PDF
48. Effects of bright light on resting metabolic rate in patients with seasonal affective disorder and control subjects.
- Author
-
Gaist PA, Obarzanek E, Skwerer RG, Duncan CC, Shultz PM, and Rosenthal NE
- Subjects
- Adult, Body Weight, Depressive Disorder metabolism, Depressive Disorder psychology, Energy Intake, Female, Follow-Up Studies, Humans, Male, Middle Aged, Personality Tests, Depressive Disorder therapy, Energy Metabolism, Phototherapy, Seasons
- Abstract
Many of the symptoms of seasonal affective disorder (SAD) could be construed as having an energy-conserving function. We predicted that SAD patients would have abnormally low resting metabolic rates (RMR), which would be increased to normal levels by light therapy. To test this hypothesis we measured RMR in 10 patients on and off light treatment and 9 normal controls. Contrary to our prediction we found that SAD patients had significantly higher RMR values compared with the normal population (p less than 0.02) and these values were significantly lowered by light treatment (p less than 0.05). The possible implications of these findings are discussed.
- Published
- 1990
- Full Text
- View/download PDF
49. Effects of light treatment on core body temperature in seasonal affective disorder.
- Author
-
Rosenthal NE, Levendosky AA, Skwerer RG, Joseph-Vanderpool JR, Kelly KA, Hardin T, Kasper S, DellaBella P, and Wehr TA
- Subjects
- Adult, Circadian Rhythm, Depressive Disorder psychology, Female, Humans, Male, Middle Aged, Personality Tests, Body Temperature Regulation, Depressive Disorder therapy, Phototherapy, Seasons
- Abstract
Abnormalities in circadian rhythms of core body temperature have been reported previously in depressed patients. In this study, we compared the temperature rhythms of 10 depressed seasonal affective disorder (SAD) patients with winter depression with those of 12 normal controls and evaluated the effects of bright light on temperature in SAD. Unlike previous studies of depressed patients, the temperature curves of the patients and normal controls during the off-light condition were nearly identical. We found a significant difference in amplitude between the patients in the untreated and light-treated conditions. Although there was no systematic difference in circadian phase across groups or treatment conditions, we present preliminary evidence that suggests that phase-typed subgroups may be present in the population distinguished by their treatment responses.
- Published
- 1990
- Full Text
- View/download PDF
50. Psychobiological effects of carbohydrate- and protein-rich meals in patients with seasonal affective disorder and normal controls.
- Author
-
Rosenthal NE, Genhart MJ, Caballero B, Jacobsen FM, Skwerer RG, Coursey RD, Rogers S, and Spring BJ
- Subjects
- Adult, Amino Acids blood, Arousal physiology, Brain metabolism, Depressive Disorder blood, Female, Humans, Male, Psychological Tests, Depressive Disorder psychology, Dietary Carbohydrates administration & dosage, Dietary Proteins administration & dosage, Food Preferences, Seasons
- Abstract
Patients with seasonal affective disorder (SAD) frequently report carbohydrate craving and note that carbohydrate ingestion energizes them. Bright artificial light has been shown to reverse the symptoms of SAD, including carbohydrate craving. In this study, 16 depressed SAD patients and 16 matched controls were fed two different isocaloric meals, one rich in protein and one rich in carbohydrates, in a crossover design. Although their biochemical response in terms of plasma large neutral amino acid concentrations was identical, SAD patients reported activation following carbohydrate ingestion, whereas normal controls reported sedation. Marked ordering effects on psychological parameters were noted, suggesting that order should be taken into account as a methodological consideration in meal studies.
- Published
- 1989
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.