Author: "Cohen JC" - Searchworks@Jio Institute Digital Library Search Results

323 results on '"Cohen JC"'

1. TRIPS, the Doha Declaration and increasing access to medicines: policy options for Ghana

Author: Torpey K, Gyansa-Lutterodt M, Cohen JC, Esmail LC, and Kurokawa G
Subjects: Public aspects of medicine, RA1-1270
Abstract: Abstract There are acute disparities in pharmaceutical access between developing and industrialized countries. Developing countries make up approximately 80% of the world's population but only represent approximately 20% of global pharmaceutical consumption. Among the many barriers to drug access are the potential consequences of the Trade Related Aspects of Intellectual Property Rights (TRIPS) Agreement. Many developing countries have recently modified their patent laws to conform to the TRIPS standards, given the 2005 deadline for developing countries. Safeguards to protect public health have been incorporated into the TRIPS Agreement; however, in practice governments may be reluctant to exercise such rights given concern about the international trade and political ramifications. The Doha Declaration and the recent Decision on the Implementation of Paragraph 6 of the Doha Declaration on the TRIPS Agreement and Public Health may provide more freedom for developing countries in using these safeguards. This paper focuses on Ghana, a developing country that recently changed its patent laws to conform to TRIPS standards. We examine Ghana's patent law changes in the context of the Doha Declaration and assess their meaning for access to drugs of its population. We discuss new and existing barriers, as well as possible solutions, to provide policy-makers with lessons learned from the Ghanaian experience.
Published: 2005
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2. Lung sound amplitude measured by vibration response imaging is influenced by the presence of secretions

Author: Lev, S, Stern-Cohen, AS, Shapiro, MS, Cohen, JC, Glickman, YG, and Singer, PS
Published: 2011
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3. Precision electroweak measurements on the Z resonance

Author: Schael, S, Barate, R, Bruneliere, R, Buskulic, D, Bonis, De, Decamp, I, Ghez, D, Goy, P, Jezequel, C, Lees, S, Lucotte, Jp, Martin, A, Merle, F, Minard, E, Nief, Mn, Odier, Jy, Pietrzyk, P, Trocme, B, Bravo, B, Casado, S, Chmeissani, Mp, Comas, M, Crespo, P, Fernandez, Jm, E, Fernandez, Bosman, Garrido, M, Grauges, L, Juste, E, Martinez, A, Merino, M, Miquel, G, Mir, R, Orteu, Lm, Pacheco, S, Park, A, Perlas, Ic, Riu, J, Ruiz, I, Sanchez, H, Colaleo, F, Creanza, A, D, Filippis, De, N, Palma, De, Iaselli, M, Maggi, G, Nuzzo, M, Ranieri, S, Raso, A, Ruggieri, G, Selvaggi, F, Silvestris, G, Tempesta, L, Tricomi, P, Zito, A, Huang, G, Lin, X, Ouyang, J, Wang, Q, Xie, T, Xu, Y, Xue, R, Zhang, S, Zhang, J, Zhao, L, Abbaneo, W, Bazarko, D, Becker, A, Boix, U, Bird, G, Blucher, F, Bonvicini, E, B, Bright, Thomas, Barklow, P, Buchmuller, T, Cattaneo, O, Cerutti, M, Ciulli, F, Clerbaux, V, Drevermann, B, Forty, H, Frank, Rw, Greening, M, Hagelberg, Tc, Halley, R, Gianotti, Aw, Girone, F, Hansen, M, Harvey, Jb, Jacobsen, J, Hutchcroft, R, Janot, De, Jost, R, Knobloch, B, Kado, J, Lehraus, M, Lazeyras, I, Maley, P, Mato, R, May, P, Moutussi, J, A, Pepe, Altarelli, Ranjard, M, Rolandi, F, Schlatter, L, Schmitt, D, Schneider, B, Tejessy, O, Teubert, W, Tomalin, F, Tournefier, Ir, Veenhof, E, Valassi, R, Wiedenmann, A, Wright, W, Ajaltouni, Ae, Badaud, Z, Chazelle, F, Deschamps, G, Dessagne, O, Falvard, S, Ferdi, A, Fayolle, C, Gay, D, Guicheney, P, Henrard, C, Jousset, P, Michel, J, Monteil, B, Montret, S, Pallin, Jc, Pascolo, D, Perret, Jm, Podlyski, P, Bertelsen, F, Fernley, H, Hansen, T, Hansen, Jd, Hansen, Jr, Kraan, Ph, Lindahl, Ac, Mollerud, A, Nilsson, R, Rensch, Bs, Waananen, B, Daskalakis, A, Kyriakis, G, Markou, A, Simopoulou, C, Siotis, E, Vayaki, I, Zachariadou, A, Blondel, K, Bonneaud, A, Brient, G, Machefert, Jc, Rouge, E, Rumpf, A, Swynghedauw, M, Tanaka, M, Verderi, R, Videau, M, Focardi, H, Parrini, E, Corden, G, Georgiopoulos, M, Antonelli, C, Antonelli, A, Bencivenni, M, Bologna, G, Bossi, G, Campana, F, Capon, P, Chiarella, G, Felici, V, Laurelli, G, Mannocchi, P, Murtas, G, Passalacqua, Gp, Picchi, L, Colrain, P, P, Ten, Have, Hughes, I, Kennedy, Is, Knowles, J, Lynch, Ig, Morton, Jg, Negus, Wt, Oshea, P., Raine, V, Reeves, C, Scarr, P, Smith, Jm, Thompson, K., Turnbull, As, Wasserbaech, Rm, Cavanaugh, S, Dhamotharan, R, Geweniger, S, Hanke, C, Hansper, P, Hepp, G, Kluge, V, Putzer, Ee, Sommer, A, Stenzel, J, Tittel, H, Werner, K, Wunsch, W, Beuselinck, M, Binnie, R, Cameron, Dm, Davies, W, Dornan, G, Goodsir, Pj, Marinelli, S, Martin, N, Nash, Eb, Nowell, J, Rutherford, J, Sedgbeer, Sa, Thompson, Jk, White, Jc, Williams, R, Ghete, Md, Girtler, Vm, Kneringer, P, Kuhn, E, Rudolph, D, G, Bouhova, Thacker, Bowdery, E, Buck, Ck, Clarke, Pg, Ellis, Dp, Finch, G, Foster, Aj, Hughes, F, Jones, G, Rwl, Keemer, Pearson, Nr, Robertson, Mr, Sloan, Na, Smizanska, T, Snow, M, Williams, Sw, van der Aa, Delaere, O, Leibenguth, C, Lemaitre, G, Bauerdick, V, Lat, Blumenschein, U, Van, Gemmeren, Giehl, P, Holldorfer, I, Jakobs, F, Kasemann, K, Kayser, M, Kleinknecht, F, Muller, K, Quast, As, Renk, G, Rohne, B, Sander, E, Schmeling, Hg, Wachsmuth, S, Wanke, H, Zeitnitz, R, Ziegler, C, Aubert, T, Benchouk, Jj, Bonissent, C, Carr, A, Coyle, J, Curtil, P, Ealet, C, Etienne, A, Fouchez, F, Motsch, D, Payre, F, Rousseau, P, Tilquin, D, Talby, A, Thulasides, M, Aleppo, M, Ragusa, M, Buscher, F, David, V, Dietl, A, Ganis, H, Huttmann, G, Lutjens, K, Mannert, G, Manner, C, Moser, W, Settles, Hg, Seywerd, R, Villegas, H, Wolf, M, Azzurri, G, Boucrot, P, Callot, J, Chen, O, Cordier, S, Davier, A, Duflot, M, Grivaz, L, Heusse, Jf, Jacholkowska, P, Diberder, Le, Lefrancois, F, Mutz, J, Schune, Am, Serin, Mh, Veillet, L, Videau, Jj, Zerwas, I, Bagliesi, D, Bettarini, G, Boccali, S, Bozzi, T, Calderini, C, Dellorso, G, Fantechi, R, Ferrante, R, Fidecaro, I, Foa, F, Giammanco, L, Giassi, A, Gregorio, A, Ligabue, A, Lusiani, F, Marrocchesi, PIER SIMONE, Messineo, Ps, Palla, A, Rizzo, F, Sanguinetti, G, Sciaba, G, Sguazzoni, A, Spagnolo, G, Steinberger, P, Tenchini, J, Venturi, R, Vannini, A, Verdini, C, Awunor, Pg, Blair, O, Cowan, Ga, Garcia, Bellido, Green, A, Medcalf, Mg, Misiejuk, T, Strong, A, Teixeira, Dias, Botterill, P, Clifft, Dr, Edgecock, Rw, Edwards, Tr, Haywood, M, Norton, Sj, Ward, Pr, Bloch, Devaux, Boumediene, B, Colas, D, Emery, P, Fabbro, S, Kozanecki, B, Lancon, W, Lemaire, E, Locci, Mc, Perez, E, Rander, P, Renardy, J, Roussarie, Jf, Schuller, A, Schwindling, Jp, Tuchming, J, Vallage, B, Black, B, Dann, Sn, Kim, Jh, Konstantinidis, Hy, Litke, N, Mcneil, Am, Taylor, Ma, Booth, G, Cartwright, Cn, Combley, S, Hodgson, F, Lehto, Pn, Thompson, M, Affholderbach, Lf, Barberio, K, Bohrer, E, Brandt, A, Burkhardt, S, Feigl, H, Grupen, E, Hess, C, Lutters, J, Meinhard, G, H, Minguet, Rodriguez, Mirabito, J, Neugebauer, L, Ngac, E, Prange, A, Rivera, G, Saraiva, F, Schafer, P, Sieler, U, Smolik, U, Stephan, L, Trier, F, Apollonio, H, Borean, M, Bosisio, C, L, Della, Marina, Giannini, R, Gobbo, G, Musolino, B, Pitis, G, He, L, Kim, H, Putz, H, Rothberg, J, Armstrong, J, Bellantoni, Sr, Berkelman, L, Cinabro, K, Conway, D, Cranmer, Js, Elmer, K, Feng, P, Ferguson, Z, Dps, Gao, Gonzalez, Y, Grahl, S, Harton, J, Hayes, Jl, Hu, Oj, Jin, H, Johnson, S, Kile, Rp, Mcnamara, J, Nielsen, Pa, Orejudos, J, Pan, W, Saadi, Y, Scott, Y, Sharma, Ij, Walsh, V, Walsh, Am, Wear, J, J, von Wimmersperg Toeller, Wu, Jh, Wu, J, Wu, Sl, Yamartino, X, Zobernig, Jm, Dissertori, G, Abdallah, G, Abreu, J, Adam, P, Adye, W, Adzic, T, Ajinenko, P, Albrecht, I, Alderweireld, T, Alekseev, T, Alemany, Fernandez, Allmendinger, R, Allport, T, Almehed, Pp, Amaldi, S, Amapane, U, Amato, N, Anashkin, S, Anassontzis, E, Andersson, Eg, Andreazza, P, Andringa, A, Anjos, S, Antilous, N, Apel, P, Arnoud, Wd, Ask, Y, Asman, S, Augustin, B, Augustinus, Je, Baillon, A, Ballestrero, P, Bambade, A, Barao, P, Barbiellini, F, Barbier, G, Bardin, R, Barker, D, Baroncelli, G, Battaglia, A, Baubillier, M, Becks, M, Begalli, Kh, Behrmann, M, Beilliere, A, Belokopytov, P, Belous, Y, K, Ben, Haim, Benekos, E, Benvenuti, N, Berat, A, Berggren, C, Berntzon, M, Bertini, L, Bertrand, D, Besancon, D, Besson, M, Bianchi, N, Bigi, F, Bilenky, M, Bizouard, Ms, Bloch, Ma, Blom, D, Bluj, M, Bonesini, M, Bonivento, M, Boonekamp, W, Booth, M, Psl, Borgland, Borisov, Aw, Bosio, G, Botner, C, Boudinov, O, Bouquet, E, Bourdarios, B, Bowcock, C, Tjv, Boyko, Bozovic, I, Bozzo, I, Bracko, M, Branchini, M, Brenke, P, Brenner, T, Brodet, R, Bruckman, E, Brunet, P, Bugge, Jm, Buran, L, Burgsmueller, T, Buschbeck, T, Buschmann, B, Cabrera, P, Caccia, S, Calvi, M, Rozas, M, Ajc, Camporesi, Canale, T, Canepa, V, Carena, M, Carroll, F, Caso, L, Gimenez, C, Mvc, Castro, Cattai, N, Cavallo, A, Cerruti, F, Chabaud, C, Chapkin, V, Charpentier, M, Chaussard, P, Checchia, L, Chelkov, P, Chen, Ga, Chierici, M, Chliapnikov, R, Chochula, R, Chorowicz, P, Chudoba, V, Chung, J, Cieslik, Su, Collins, K, Colomer, P, Contri, M, Cortina, R, Cosme, E, Cossuti, G, Costa, F, Cowell, Mj, Crawley, Jh, Crennell, Hb, Crepe, D, Crosetti, S, Cuevas, G, Czellar, J, Dhondt, S, Dalmagne, J, Dalmau, B, Damgaard, J, Davenport, G, M, Silva, Da, T, Deghorain, W, Della, Ricca, Delpierre, G, Demaria, P, Angelis, De, Boer, De, W, Brabandere, De, S, Clercq, De, C, Lotto, De, Maria, De, Min, De, Paula, De, Dijkstra, L, Ciaccio, Di, Diodato, Di, Simone, Di, Djannati, A, Dolbeau, A, Doroba, J, Dracos, K, Drees, M, Drees, J, Dris, Ka, Duperrin, M, Durand, A, Ehret, Jd, Eigen, R, Ekelof, G, Ekspong, T, Ellert, G, Elsing, M, Engel, M, Erzen, Jp, Santo, B, Mce, Falk, Fanourakis, E, Fassouliotis, G, Fayot, D, Feindt, J, Fenyuk, M, Fernandez, A, Ferrari, J, Ferrer, P, Ferrer, Ribas, Ferro, E, Fichet, F, Firestone, S, Fischer, A, Flagmeyer, Pa, Foeth, U, Fokitis, H, Fontanelli, E, Franek, F, Frodesen, B, Fruhwirth, Ag, R, Fulda, Quenzer, Fuster, F, Galloni, J, Gamba, A, Gamblin, D, Gandelman, S, Garcia, M, Garcia, C, Gaspar, J, Gaspar, C, Gasparini, M, Gavillet, U, Gazis, P, Gele, E, Gerber, D, Gerdyukov, Jp, Ghodbane, L, Gil, N, Glege, I, Gokieli, F, Golob, R, Gomez, Ceballos, Goncalves, G, Caballero, P, Gopal, Ig, Gorn, G, Gorski, L, Gouz, M, Gracco, Y, Graziani, V, Green, E, Grefrath, C, Grimm, A, Gris, Hj, Grosdidier, P, Grzelak, G, Gunther, K, Guy, M, Haag, J, Hahn, C, Hahn, F, Hallgren, S, Hamacher, A, Hamilton, K, Hansen, K, Harris, J, Haug, Fj, Hauler, S, Hedberg, F, Heising, V, Hennecke, S, Henriques, M, Hernandez, R, Herquet, Jj, Herr, P, Hessing, H, Heuser, Tl, Higon, Jm, Hoffman, E, Holmgren, J, Holt, So, Holthuizen, Pj, Hoorelbeke, D, Houlden, S, Hrubec, Ma, Huber, J, Huet, M, Hughes, K, Hultqvist, Gj, Jackson, K, Jacobsson, Jn, Jalocha, R, Janik, P, Jarlskog, R, Jarlskog, C, Jarry, G, Jean, Marie, Jeans, B, Johansson, D, Johansson, Ek, Jonsson, Pd, Joram, P, Juillot, C, Jungermann, P, Kapusta, L, Karafasoulis, F, Katsanevas, K, 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Garcia, F, Smi, Masik, Mastroyiannopoulos, J, Matorras, N, Matteuzzi, F, Matthiae, C, Mazik, G, Mazzucato, J, Mazzucato, F, Mccubbin, M, Mckay, M, Mcnulty, R, Meroni, R, Meyer, C, Miagkov, Wt, Migliore, A, Mitaroff, E, Mjoernmark, W, Moa, U, Moch, T, Moeller, M, Moenig, R, Monge, K, Montenegro, R, Moraes, J, Moreau, D, Moreno, X, Morettini, S, Morton, P, Mueller, G, Muenich, U, Mulders, K, Mulet, Marquis, Mundim, C, Muresan, L, Murray, R, Muryn, W, Myatt, B, Myklebust, G, Naraghi, T, Nassiakou, F, Navarria, M, Navas, F, Nawrocki, S, Negri, K, Neufeld, P, Neumann, N, Neumeister, W, Nicolaidou, N, Nielsen, R, Nieuwenhuizen, Bs, Niezurawski, M, Nikolaenko, P, Nikolenko, V, Nomokonov, M, Normand, V, Nygren, A, Oblakowska, Mucha, Obraztsov, A, Olshevski, V, Onofre, A, Orava, A, Orazi, R, Osterberg, G, Ouraou, K, Oyanguren, A, Paganini, A, Paganoni, P, Paiano, M, Pain, S, Paiva, R, Palacios, R, Palka, Jp, Papadopoulou, H, Papageorgiou, Td, Pape, K, Parkes, L, Parodi, C., Parzefall, F, Passeri, U, Passon, A, Pavel, O, Pegoraro, T, Peralta, M, Perepelitsa, L, Pernicka, V, Perrotta, M, Petridou, A, Petrolini, C, Philips, A, Piana, Ht, Piedra, G, Pieri, J, Pierre, L, Pimenta, F, Piotto, M, Podobnik, E, Poireau, T, Pol, V, Polok, Me, Polycarpo, G, Poropat, E, Pozdniakov, P, Privitera, V, Pukhaeva, R, Pullia, N, Radojicic, A, Ragazzi, D, Rahmani, S, Rakoczy, H, Rames, D, Ramler, J, Ratoff, L, Read, Pn, Rebecchi, A, Redaelli, P, Regler, Ng, Rehn, M, Reid, J, Reinhardt, D, Renton, R, Resvanis, P, Richard, Lk, Ridky, F, Rinaudo, J, Ripp, Baudot, Rivero, I, Rodriguez, M, Rohne, D, Romero, O, Ronchese, A, Rosenberg, P, Rosinsky, Ei, Roudeau, P, Rovelli, R, Royon, T, Ruhlmann, Kleider, Ruiz, V, Ryabtchikov, A, Saarikko, D, Sacquin, H, Sadovsky, Y, Sajot, A, Salmi, G, Salt, L, Sampsonidis, J, Sannino, D, Savoy, Navarro, Scheidle, A, Schneider, T, Schwemling, H, Schwering, P, Schwickerath, B, Schyns, U, Mae, Scuri, Seager, F, Sedykh, P, Segar, Y, Seibert, A, Sekulin, N, Shellard, R, Sheridan, Rc, Siebel, A, Silvestre, M, Simard, R, Simonetto, L, Sisakian, F, Skaali, A, Smadja, Tb, Smirnov, G, Smirnova, N, Smith, O, Sokolov, Gr, Sopczak, A, Sosnowski, A, Spassov, R, Spiriti, T, Sponholz, E, Squarcia, P, Stampfer, S, Stanescu, D, Stanic, C, Stanitzki, S, Stapnes, M, Stevenson, S, Stocchi, K, Strauss, A, Strub, J, Stugu, R, Szczekowski, B, Szeptycka, M, Szumlak, M, Tabarelli, T, Taffard, T, Tegenfeldt, Ac, Terranova, F, Thomas, F, Timmermans, J, Tinti, J, Tkatchev, N, Tobin, L, Todorov, M, Todorovova, T, Toet, S, Tomaradze, Dz, Tome, A, Tonazzo, B, Tortora, A, Tortosa, L, Transtromer, P, Travnicek, G, Treille, P, Tristram, D, Trochimczuk, G, Trombini, M, Troncon, A, Tsirou, C, Turluer, A, Tyapkin, Ml, Tyapkin, Ia, Tzamarias, P, Ullaland, S, Uvarov, O, Valenti, V, Vallazza, G, Vander, Velde, Van, Apeldoorn, Van, Dam, Van den Boeck, Van, Doninck, Van, Eldik, Van, Lysebetten, Van, Remortel, Van, Vulpen, Vassilopoulos, I, Vegni, N, Velos, G, Ventura, F, Venus, L, Verbeure, W, Verdier, F, Verlato, P, Vertogradov, M, Verzi, Ls, Vilanova, V, Vitale, D, Vlasov, L, Vodopyanov, E, Vollmer, As, Voulgaris, C, Vrba, G, Wahlen, V, Walck, H, Washbrook, C, Weiser, Aj, Wetherell, C, Wicke, Am, Wickens, D, Wilkinson, J, Winter, G, Witek, M, Wlodek, M, Yi, T, Yushchenko, J, Zaitsev, O, Zalewska, A, Zalewski, A, Zavrtanik, P, Zevgolatakos, D, Zhuravlov, E, Zimin, V, Zintchenko, Ni, Zoller, A, Zucchelli, P, Zumerle, Gc, Zupan, G, Acciarri, M, Achard, M, Adriani, P, O, Aguilar, Benitez, Alcaraz, M, Alemanni, J, Allaby, G, Aloisio, J, Alviggi, A, Ambrosi, Mg, Anderhub, G, Andreev, H, Angelescu, Vp, Anselmo, T, Arefiev, F, Azemoon, A, Aziz, T, Bagnaia, T, Bajo, P, Baksay, A, Baksay, G, Balandras, L, Baldew, A, Ball, Sv, Banerjee, Rc, Barczyk, S, Barillere, A, Barone, R, Bartalini, L, Basile, P, Batalova, M, Battiston, N, Bay, R, Becattini, A, Behner, F, Bellucci, F, Berbeco, L, Berdugo, R, Berges, J, Bertucci, P, Betev, B, Bhattacharya, Bl, Biasini, S, Biglietti, 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Thaler, Fe, Thom, Jj, Trandafir, J, Turk, Ai, Usher, Jd, Vavra, T, Vella, J, Venuti, E, Verdier, Jp, Wagner, R, Waite, Sr, Walston, Ap, Wang, S, Watts, J, Weidemann, Sj, Weiss, Aw, Whitaker, Er, White, Js, Wickens, Sl, Williams, Fj, Williams, Da, Williams, Dc, Willocq, Sh, Wilson, S, Wisniewski, Rj, Wittlin, Wj, Woods, Jl, Word, M, Wright, Gb, Wyss, Tr, Yamamoto, J, Yang, Rk, Yashima, Xq, Yellin, J, Young, Sj, Yuta, Cc, Zapalac, H, Zdarko, G, Zeitlin, Rw, Zhou, C, Blondel, Alain, Schael, S, Barate, R, Bruneliere, R, Spagnolo, Stefania Antonia, S., Schael, Aloisio, Alberto, Alviggi, Mariagrazia, Canale, Vincenzo, Chiefari, Giovanni, DELLA VOLPE, Domenico, Merola, Leonardo, Napolitano, Marco, Patricelli, Sergio, Sciacca, Crisostomo, Lista, Luca, Laboratoire d'Annecy de Physique des Particules (LAPP), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Corpusculaire - Clermont-Ferrand (LPC), Université Blaise Pascal - Clermont-Ferrand 2 (UBP)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Théorique et Astroparticules (LPTA), Université Montpellier 2 - Sciences et Techniques (UM2)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire Leprince-Ringuet (LLR), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-École polytechnique (X)-Centre National de la Recherche Scientifique (CNRS), Centre de Physique des Particules de Marseille (CPPM), Aix Marseille Université (AMU)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de l'Accélérateur Linéaire (LAL), Université Paris-Sud - Paris 11 (UP11)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Nucléaire et de Hautes Énergies (LPNHE), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Subatomique et de Cosmologie (LPSC), Université Joseph Fourier - Grenoble 1 (UJF)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP )-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Institut Polytechnique de Grenoble - Grenoble Institute of Technology-Centre National de la Recherche Scientifique (CNRS), Institut de Physique Nucléaire de Lyon (IPNL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Institut de Recherches Subatomiques (IReS), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Cancéropôle du Grand Est-Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), Physique Corpusculaire et Cosmologie - Collège de France (PCC), Collège de France (CdF (institution))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), ALEPH, DELPHI, L3, OPAL, SLD, BARBIELLINI AMIDEI, Guido, Bosisio, Luciano, DELLA RICCA, Giuseppe, Giannini, Gianrossano, Gregorio, Anna, Lanceri, Livio, Poropat, Paolo, Vitale, Lorenzo, Buskulic, D, De Bonis, I, Decamp, D, Ghez, P, Goy, C, Jezequel, S, Lees, J, Lucotte, A, Martin, F, Merle, E, Minard, M, Nief, J, Odier, P, Pietrzyk, B, Trocme, B, Bravo, S, Casado, M, Chmeissani, M, Comas, P, Crespo, J, Fernandez, E, Fernandez Bosman, M, Garrido, L, Grauges, E, Juste, A, Martinez, M, Merino, G, Miquel, R, Mir, L, Orteu, S, Pacheco, A, Park, I, Perlas, J, Riu, I, Ruiz, H, Sanchez, F, Colaleo, A, Creanza, D, De Filippis, N, De Palma, M, Iaselli, G, Maggi, G, Maggi, M, Nuzzo, S, Ranieri, A, Raso, G, Ruggieri, F, Selvaggi, G, Silvestris, L, Tempesta, P, Tricomi, A, Zito, G, Huang, X, Lin, J, Ouyang, Q, Wang, T, Xie, Y, Xu, R, Xue, S, Zhang, J, Zhang, L, Zhao, W, Abbaneo, D, Bazarko, A, Becker, U, Boix, G, Bird, F, Blucher, E, Bonvicini, B, Bright Thomas, P, Barklow, T, Buchmuller, O, Cattaneo, M, Cerutti, F, Ciulli, V, Clerbaux, B, Drevermann, H, Forty, R, Frank, M, Greening, T, Hagelberg, R, Halley, A, Gianotti, F, Girone, M, Hansen, J, Harvey, J, Jacobsen, R, Hutchcroft, D, Janot, R, Jost, B, Knobloch, J, Kado, M, Lehraus, I, Lazeyras, P, Maley, R, Mato, P, May, J, Moutussi, A, Pepe Altarelli, M, Ranjard, F, Rolandi, L, Schlatter, D, Schmitt, B, Schneider, O, Tejessy, W, Teubert, F, Tomalin, I, Tournefier, E, Veenhof, R, Valassi, A, Wiedenmann, W, Wright, A, Ajaltouni, Z, Badaud, F, Chazelle, G, Deschamps, O, Dessagne, S, Falvard, A, Ferdi, C, Fayolle, D, Gay, P, Guicheney, C, Henrard, P, Jousset, J, Michel, B, Monteil, S, Montret, J, Pallin, D, Pascolo, J, Perret, P, Podlyski, F, Bertelsen, H, Fernley, T, Hansen, P, Kraan, A, Lindahl, A, Mollerud, R, Nilsson, B, Rensch, B, Waananen, A, Daskalakis, G, Kyriakis, A, Markou, C, Simopoulou, E, Siotis, I, Vayaki, A, Zachariadou, K, Blondel, A, Bonneaud, G, Brient, J, Machefert, E, Rouge, A, Rumpf, M, Swynghedauw, M, Tanaka, R, Verderi, M, Videau, H, Focardi, E, Parrini, G, Corden, M, Georgiopoulos, C, Antonelli, A, Antonelli, M, Bencivenni, G, Bologna, G, Bossi, F, Campana, P, Capon, G, Chiarella, V, Felici, G, Laurelli, P, Mannocchi, G, Murtas, G, Passalacqua, L, Picchi, P, Colrain, P, Ten Have, I, Hughes, I, Kennedy, J, Knowles, I, Lynch, J, Morton, W, Negus, P, O'Shea, V, Raine, C, Reeves, P, Scarr, J, Smith, K, Thompson, A, Turnbull, R, Wasserbaech, S, Cavanaugh, R, Dhamotharan, S, Geweniger, C, Hanke, P, Hansper, G, Hepp, V, Kluge, E, Putzer, A, Sommer, J, Stenzel, H, Tittel, K, Werner, W, Wunsch, M, Beuselinck, R, Binnie, D, Cameron, W, Davies, G, Dornan, P, Goodsir, S, Marinelli, N, Martin, E, Nash, J, Nowell, J, Rutherford, S, Sedgbeer, J, Thompson, J, White, R, Williams, M, Ghete, V, Girtler, P, Kneringer, E, Kuhn, D, Rudolph, G, Bouhova Thacker, E, Bowdery, C, Buck, P, Clarke, D, Ellis, G, Finch, A, Foster, F, Hughes, G, Jones, R, Keemer, N, Pearson, M, Robertson, N, Sloan, T, Smizanska, M, Snow, S, Van Der Aa, O, Delaere, C, Leibenguth, G, Lemaitre, V, Bauerdick, L, Blumenschein, U, Van Gemmeren, P, Giehl, I, Holldorfer, F, Jakobs, K, Kasemann, M, Kayser, F, Kleinknecht, K, Muller, A, Quast, G, Renk, B, Rohne, E, Sander, H, Schmeling, S, Wachsmuth, H, Wanke, R, Zeitnitz, C, Ziegler, T, Aubert, J, Benchouk, C, Bonissent, A, Carr, J, 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MCGOWAN, A.K. MCKEMEY, B.T. MEADOWS, R. MESSNER, P.M. MOCKETT, K.C. MOFFEIT, T.B. MOORE, M. MORII, B. MOURS, D. MULLER, G. MUELLER, V. MURZIN, T. NAGAMINE, S. NARITA, U. NAUENBERG, H. NEAL, G. NESOM, M. NUSSBAUM, Y. OHNISHI, N. OISHI, D. ONOPRIENKO, L.S. OSBORNE, R.S. PANVINI, C.H.PARK, H. PARK, T.J. PAVEL, I. PERUZZI, L. PESCARA, M. PICCOLO, L. PIEMONTESE, E. PIERONI, K.T. PITTS, R.J. PLANO, R. PREPOST, C.Y. PRESCOTT, G. PUNKAR, J. QUIGLEY, B.N. RATCLIFF, K. REEVES, T.W. REEVES, J. REIDY, P.L. REINERTSEN, P.E. RENSING, L.S. ROCHESTER, J.E. ROTHBERG, P.C. ROWSON, J.J. RUSSELL, O.H. SAXTON, T. SCHALK, R.H. SCHINDLER, U. SCHNEEKLOTH, B.A. SCHUMM, J. SCHWIENING, A. SEIDEN, S. SEN, V.V. SERBO, L. SERVOLI, M.H. SHAEVITZ, J.T. SHANK, G. SHAPIRO, D.J. SHERDEN, K.D. SHMAKOV, C. SIMOPOULOS, N.B. SINEV, S.R. SMITH, M.B. SMY, J.A. SNYDER, M.D. SOKOLOFF, H. STAENGLE, A. STAHL, P. STAMER, H. STEINER, R. STEINER, M.G. STRAUSS, D. SU, F. SUEKANE, A. SUGIYAMA, A. SUZUKI, S. SUZUKI, M. SWARTZ, A. SZUMILO, T. TAKAHASHI, F.E. TAYLOR, J.J. THALER, J. THOM, E. TORRENCE, A.I. TRANDAFIR, J.D. TURK, T. USHER, J. VA VRA, C. VANNINI, E. VELLA, J.P. VENUTI, R. VERDIER, P.G. VERDINI, D.L. WAGNER, S.R. WAGNER, A.P. WAITE, S. WALSTON, J. WANG, S.J. WATTS, A.W. WEIDEMANN, E.R. WEISS, J.S. WHITAKER, S.L. WHITE, F.J. WICKENS, D.A. WILLIAMS, D.C. WILLIAMS, S.H. WILLIAMS, S. WILLOCQ, R.J. WILSON, W.J. WISNIEWSKI, J.L. WITTLIN, M. WOODS, G.B. WORD, T.R. WRIGHT, J. WYSS, R.K. YAMAMOTO, J.M. YAMARTINO, X.Q. YANG, J. YASHIMA, S.J. YELLIN, C.C.YOUNG, H.YUTA, G. ZAPALAC, R.W. ZDARKO, C. ZEITLIN, J. ZHOU, Centre National de la Recherche Scientifique (CNRS)-École polytechnique (X)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Paris-Sud - Paris 11 (UP11), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP )-Institut Polytechnique de Grenoble - Grenoble Institute of Technology-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Joseph Fourier - Grenoble 1 (UJF)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Laboratoire d'Annecy de Physique des Particules (LAPP/Laboratoire d'Annecy-le-Vieux de Physique des Particules), Centre National de la Recherche Scientifique (CNRS)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Aix Marseille Université (AMU), Université Joseph Fourier - Grenoble 1 (UJF)-Institut polytechnique de Grenoble - Grenoble Institute of Technology (Grenoble INP)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Institut Polytechnique de Grenoble - Grenoble Institute of Technology-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA), Collège de France (CdF)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), GRUNEVALD M, NEWALD M, SCHAEL S, BARATE R, BRUNELIE, RE R, BUSKULIC D, DE BONIS I, DECAMP D, GHEZ P, GOY C, JE, ZE, QUEL S, LEES J, LUCOTTE A, MARTIN M, MERLE E, MINARD M, NIEF J, ODIER P, PIETRZYK B, TROCME, BRAVO S, CASADO MP, CHMEISSANI M, COMAS P, CRESPO JM, FERNANDEZ E, FERNANDEZ-BOSMAN M, GARRIDO L, GRAUGES E, JUSTE A, MARTINEZ M, MERINO G, MIQUEL R, MIR LM, ORTEU S, PACHECO A, PARK IC, PERLAS J, RIU I, RUIZ H, SANCHEZ F, COLALEO A, CREANZA D, DE FILIPPIS N, DE PALMA M, IASELLI G, MAGGI G, MAGGI M, NUZZO S, RANIERI, A, RASO, G, RUGGIERI F, SELVAGGI, G, SILVESTRIS L, TEMPESTA P, TRICOMI A, ZITO G, HUANG X, LIN J, OUYANG Q, WANG T, XIE Y, XU R, XUE S, ZHANG J, ZHANG L, ZHAO W, ABBANEO D, BAZARKO A, BECKER U, BOIX G, BIRD F, BLUCHER E, BONVICINI B, BRIGHT-THOMAS P, BARKLOW T, BUCHMU, LLER O, CATTANEO M, CERUTTI F, CIULLI V, CLERBAUX B, DREVERMANN H, FORTY RW, FRANK M, GREENING TC, HAGELBERG R, HALLEY AW, GIANOTTI F, GIRONE M, HANSEN JB, HARVEY J, JACOBSEN J, HUTCHCROFT DE, JANOT P, JOST B, KNOBLOCH J, KADO M, LEHRAUS I, LAZEYRAS P, and MALEY P
Subjects: Top quark, FORWARD-BACKWARD ASYMMETRY, PARTICLE PHYSICS, LARGE ELECTRON POSITRON COLLIDER, ALEPH, DELPHI, L3, OPAL, General Physics and Astronomy, 01 natural sciences, 7. Clean energy, High Energy Physics - Experiment, Settore FIS/04 - Fisica Nucleare e Subnucleare, High Energy Physics - Experiment (hep-ex), High Energy Physics - Phenomenology (hep-ph), electron-positron physics, [PHYS.HEXP]Physics [physics]/High Energy Physics - Experiment [hep-ex], Electroweak interaction, Physics, Quantum chromodynamics, Electron–positron physics, Electroweak interactions, Decays of heavy intermediate gauge bosons, Fermion–antifermion production, Precision measurements at the Z resonance, Tests of the Standard Model, Radiative corrections, Effective coupling constants, Neutral weak current, Z boson, W boson, Higgs boson, Particle physics - Experiment, Settore FIS/01 - Fisica Sperimentale, FERMION-PAIR PRODUCTION, HADRONIC-Z-DECAYS, TOP-QUARK MASS, ANGLE BHABHA SCATTERING, W-BOSON MASS, CROSS-SECTION ASYMMETRY, Z-LINE-SHAPE, SEMILEPTONIC BRANCHING RATIOS, CARLO EVENT GENERATOR, decays of heavy intermediate gauge bosons, effective coupling constants, electroweak interactions, fermion-antifermion production, higgs boson, neutral weak current, precision measurements at the z resonance, radiative corrections, tests of the standard model, top quark, w boson, z boson, Radiative correction, High Energy Physics - Phenomenology, FIS/01 - FISICA SPERIMENTALE, Física nuclear, Neutrino, Particle physics, FOS: Physical sciences, ddc:500.2, Elementary particle physics, LEP, electroweak, Decays of heavy intermediate gauge boson, Effective coupling constant, Partícules (Física nuclear), Standard Model, electroweak theory, Z boson, DELPHI, ALEPH, OPAL, L3, 0103 physical sciences, 010306 general physics, Coupling constant, 010308 nuclear & particles physics, High Energy Physics::Phenomenology, Fermion, FORWARD-BACKWARD ASYMMETRY, FERMION-PAIR PRODUCTION, HADRONIC-Z-DECAYS, TOP-QUARK MASS, ANGLE BHABHA SCATTERING, W-BOSON MASS, CROSS-SECTION ASYMMETRY, Z-LINE-SHAPE, SEMILEPTONIC BRANCHING RATIOS, CARLO EVENT GENERATOR, [PHYS.HPHE]Physics [physics]/High Energy Physics - Phenomenology [hep-ph], Experimental High Energy Physics, Electron–positron physic, High Energy Physics::Experiment, FIS/04 - FISICA NUCLEARE E SUBNUCLEARE
Abstract: We report on the final electroweak measurements performed with data taken at the Z resonance by the experiments operating at the electron-positron colliders SLC and LEP. The data consist of 17 million Z decays accumulated by the ALEPH, DELPHI, L3 and OPAL experiments at LEP, and 600 thousand Z decays by the SLD experiment using a polarised beam at SLC. The measurements include cross-sections, forward-backward asymmetries and polarised asymmetries. The mass and width of the Z boson, $\MZ$ and $\GZ$, and its couplings to fermions, for example the $\rho$ parameter and the effective electroweak mixing angle, are precisely measured. The number of light neutrino species is determined to be 2.9840+/-0.0082. The results are compared to the predictions of the Standard Model. Electroweak radiative corrections beyond the running of the QED and QCD coupling constants are observed with a significance of five standard deviations, and in agreement with the Standard Model. Of the many Z-pole measurements, the forward-backward asymmetry in b-quark production shows the largest difference with respect to its Standard Model expectation, at the level of 2.8 standard deviations. Through radiative corrections evaluated in the framework of the Standard Model, the masses of the top quark and the W Boson are predicted. These indirect constraints are compared to the direct measurements, providing a stringent test of the Standard Model. Using in addition the direct measurements of $\Mt$ and $\MW$, the mass of the as yet unobserved Standard Model Higgs boson is predicted., Comment: 302 pages, v2: minor corrections and updates of references. Accepted for publication by Physics Reports, v3: further small corrections and journal version
Published: 2006
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4. 100% Hyperoxia at Birth Results in Increased Levels of Heat Shock Protein 27 (HSP27) and Decreased Levels of Tumor Necrosis Factor Alpha (TNF-alpha), Toll-Like Receptor 4 (TLR-4), Thyroid Transcription Factor (TTF-1), and Interleukins 6 and 10 (IL-6,10) in the Lungs of Adult Sprague-Dawley Rats.

Author: Stenson, E, primary, Killeen, E, additional, Cohen, JC, additional, and Shah, SI, additional
Published: 2009
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5. Administration of Nebulized Albuterol Prior to Surfactant Administration Results in Improved Airway Resistance but Decreased Small Airway Compliance in Neonatal Sprague Dawley Rats.

Author: Shah, SI, primary, Hudak, J, additional, Dylag, A, additional, and Cohen, JC, additional
Published: 2009
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6. Birth Hyperoxia Alters Pro-Inflammatory Cytokine Expression and Downregulates Toll-Like Receptors (TLR) 2 and 4 in the Lungs of Sprague-Dawley Rats.

Author: Shah, S, primary, Stenson, E, additional, Killeen, E, additional, and Cohen, JC, additional
Published: 2009
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7. Long Term Respiratory Function after Birth Hyperoxia in Sprague-Dawley Rats with Equivalent Cumulative Oxygen Exposure.

Author: Stenson, E, primary, Cohen, JC, additional, and Shah, SI, additional
Published: 2009
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8. Correlation between lung sound distribution and functional residual capacity: preliminary findings

Author: Lev, S, primary, Glickman, YG, additional, Kagan, IK, additional, Cohen, JC, additional, and Singer, PS, additional
Published: 2009
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9. TRIPS, the Doha Declaration and increasing access to medicines: policy options for Ghana

Author: Cohen, JC, primary, Gyansa-Lutterodt, M, additional, Torpey, K, additional, Esmail, LC, additional, and Kurokawa, G, additional
Published: 2005
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10. Pulmonary Function in the Cystic Fibrosis Knockout Mouse

Author: Larson, JE, primary and Cohen, JC, additional
Published: 2001
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11. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease.

Author: Cohen JC, Boerwinkle E, Mosley TH Jr., Hobbs HH, Cohen, Jonathan C, Boerwinkle, Eric, Mosley, Thomas H Jr, and Hobbs, Helen H
Abstract: Background: A low plasma level of low-density lipoprotein (LDL) cholesterol is associated with reduced risk of coronary heart disease (CHD), but the effect of lifelong reductions in plasma LDL cholesterol is not known. We examined the effect of DNA-sequence variations that reduce plasma levels of LDL cholesterol on the incidence of coronary events in a large population.Methods: We compared the incidence of CHD (myocardial infarction, fatal CHD, or coronary revascularization) over a 15-year interval in the Atherosclerosis Risk in Communities study according to the presence or absence of sequence variants in the proprotein convertase subtilisin/kexin type 9 serine protease gene (PCSK9) that are associated with reduced plasma levels of LDL cholesterol.Results: Of the 3363 black subjects examined, 2.6 percent had nonsense mutations in PCSK9; these mutations were associated with a 28 percent reduction in mean LDL cholesterol and an 88 percent reduction in the risk of CHD (P=0.008 for the reduction; hazard ratio, 0.11; 95 percent confidence interval, 0.02 to 0.81; P=0.03). Of the 9524 white subjects examined, 3.2 percent had a sequence variation in PCSK9 that was associated with a 15 percent reduction in LDL cholesterol and a 47 percent reduction in the risk of CHD (hazard ratio, 0.50; 95 percent confidence interval, 0.32 to 0.79; P=0.003).Conclusions: These data indicate that moderate lifelong reduction in the plasma level of LDL cholesterol is associated with a substantial reduction in the incidence of coronary events, even in populations with a high prevalence of non-lipid-related cardiovascular risk factors. [ABSTRACT FROM AUTHOR]
Published: 2006

12. Effects of glucose ingestion on postprandial lipemia and triglyceride clearance in humans.

Author: Cohen, JC, primary and Berger, GM, additional
Published: 1990
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13. Lipoprotein(a) and apolipoprotein(a) isoforms: no association with coronary artery calcification in the Dallas Heart Study.

Author: Guerra R, Yu Z, Marcovina S, Peshock R, Cohen JC, and Hobbs HH
Published: 2005

14. Mammary preneoplasia and tumorigenesis in the BALB/c mouse: structure and modification of mouse mammary tumor virus DNA sequences

Author: Gama-Sosa Ma, Breznik T, Janet S. Butel, Daniel Medina, and Cohen Jc
Subjects: Cancer Research, Genes, Viral, BALB/c Mouse, 9,10-Dimethyl-1,2-benzanthracene, viruses, Virus Replication, medicine.disease_cause, Methylation, Virus, Cytosine, Mice, Mammary Glands, Animal, Virology, medicine, Animals, Virus Integration, Recombination, Genetic, Mice, Inbred BALB C, biology, Mouse mammary tumor virus, Mammary Neoplasms, Experimental, DNA Restriction Enzymes, Provirus, biology.organism_classification, Molecular biology, Cell Transformation, Neoplastic, Infectious Diseases, Mammary Tumor Virus, Mouse, DNA, Viral, 5-Methylcytosine, Female, Carcinogenesis, Precancerous Conditions, Oncovirus
Abstract: Mouse mammary tumor virus (MMTV) DNA sequences were examined in mammary tissues from BALB/c mice, including both preneoplastic hyperplastic alveolar nodule (HAN) outgrowth lines, tumors derived from those preneoplastic tissues, and DMBA-induced mammary tumors. Over 60 different HAN and tumors samples were analyzed. The D2 HAN line contained one additional provirus, whereas Cv-2 and Cv-4 HAN lines that are infected with exogenous virus exhibited multiple virus integration events. D2 tumors showed the same provirus pattern as D2 HANs, whereas Cv-2 and Cv-4 tumors exhibited a subset of the acquired proviruses found in the parental HAN populations. Differential methylation patterns of virus-specific sequences were observed that resembled those described for other tissues in which viral DNA replication and integration has occurred, i.e., acquired proviruses were hypomethylated and endogenous proviruses were methylated. In tumors that arose from HAN lines and exhibited only endogenous proviruses, demethylation of the subgenomic Mtv -6 locus was observed. Demethylation of Mtv -6 was not detected in any of the preneoplastic tissues. Altered methylation of Mtv-8 and −9 was observed in both Cv-2 and Cv-4 tumors. Finally, mammary tumors induced by DMBA carried no acquired proviruses and demethylation of endogenous MMTV proviruses was demonstrated.
Published: 1987
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15. Targeted integration of baboon endogenous virus in the BEVI locus on human chromosome 6

Author: Cohen Jc and Michael Murphey-Corb
Subjects: Genetics, Chromosomes, Human, 6-12 and X, Multidisciplinary, Hybridomas, Base Sequence, viruses, Locus (genetics), Provirus, Biology, Molecular biology, DNA sequencing, Virus, Restriction enzyme, chemistry.chemical_compound, Viral replication, chemistry, Cricetinae, DNA, Viral, Viruses, Animals, Humans, Human genome, Lysogeny, DNA, Papio
Abstract: The infection of cultured human cells with baboon endogenous virus (BEV) frequently leads to an association of viral DNA with a specific genetic locus (termed BEVI, for baboon endogenous virus infection) on chromosome 6. Restriction endonuclease digestion of DNA from BEV-infected human cells and their derived somatic cell clones frequently revealed a common cellular DNA sequence in the proximity of one of the junctions between cellular DNA and the integrated virus. We propose that a short cellular DNA sequence, repeated on chromosome 6 and separated by unique DNA sequences, presents a high-affinity target for the integration of BEV in human cells.
Published: 1983

16. Hypotheses for testing deviations from random integration: evidence for nonrandom retroviral integration

Author: Wilson Af and Cohen Jc
Subjects: Genetics, Recombination, Genetic, Proviral integration, Biometry, Models, Statistical, Basis (linear algebra), Models, Genetic, Computational biology, DNA, Biology, chemistry.chemical_compound, chemistry, Complementary DNA, A-DNA, Cluster analysis, Null hypothesis, Sequence (medicine)
Abstract: The use of a recently developed in vitro model for retroviral integration provides a means of statistically testing hypotheses concerning the distribution of integration sites and hypotheses about the sequence of proviral orientations. In this study, three null hypotheses are formulated and applied to previously published data. Statistical analyses of these data suggest that the distribution of integration sites may not be uniform, and the sequence of proviral orientations is not random. On the basis of these results and the observed clustering of orientations, it was postulated that if a DNA sequence was involved in nonrandom proviral integration, that sequence would be found in the regions where the orientations change direction with respect to the target DNA (“I” regions). Computer analyses for homologous and complementary DNA sequences were performed on all possible pairs of indentiflable “I” regions. A common sequence (at least 8 bp in size) was found in three out of four regions and that sequence was absent elsewhere in the target DNA. A model, with features of recombination reminiscent of chi sequences in bacteria, is proposed that may account for these results.
Published: 1988

17. Serum triglyceride responses to fatty meals: effects of meal fat content

Author: Cohen, JC, primary, Noakes, TD, additional, and Benade, AJ, additional
Published: 1988
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18. Simulated transport alters surfactant homeostasis and causes dose-dependent changes in respiratory function in neonatal Sprague-Dawley rats.

Author: Shah S, Hudak J III, Gad A, Cohen JC, and Chander A
Published: 2010

19. [Commentary on] A common allele on chromosome 9 associated with coronary heart disease.

Author: Jaffe RB, Boerwinklle E, Hobbs HH, and Cohen JC
Published: 2007

20. Adult onset lung disease following transient disruption of fetal stretch-induced differentiation.

Author: Hudak JJ, Killeen E, Chandran A, Cohen JC, Larson JE, Hudak, Joseph J, Killeen, Erin, Chandran, Ashok, Cohen, J Craig, and Larson, Janet E
Abstract: One of the mechanisms by which adult disease can arise from a fetal origin is by in utero disruption of organogenesis. These studies were designed to examine respiratory function changes in aging rats following transient disruption of lung growth at 16 days gestation. Fetuses were treated in utero with a replication deficient adenovirus containing the cystic fibrosis conductance transmembrane regulator (CFTR) gene fragment cloned in the anti-sense direction. The in utero-treated rats demonstrated abnormal lung function beginning as early as 30 days of age and the pathology progressed as the animals aged. The pulmonary function abnormalities included decreased static compliance as well as increased conducting airway resistance, tissue damping, and elastance. Pressure volume (PV) curves demonstrated a slower early rise to volume and air trapping at end-expiration. The alterations of pulmonary function correlated with lung structural changes determined by morphometric analysis. These studies demonstrate how transient disruption of lung organogensis by single gene interference can result in progressive change in lung function and structure. They illustrate how an adult onset disease can arise from subtle changes in gene expression during fetal development. [ABSTRACT FROM AUTHOR]
Published: 2009
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21. PNPLA3(148M) is a gain-of-function mutation that promotes hepatic steatosis by inhibiting ATGL-mediated triglyceride hydrolysis.

Author: Wang Y, Hong S, Hudson H, Kory N, Kinch LN, Kozlitina J, Cohen JC, and Hobbs HH
Abstract: Background & Aims: PNPLA3(148M) (patatin-like phospholipase domain-containing protein 3) is the most impactful genetic risk factor for steatotic liver disease (SLD). A key unresolved issue is whether PNPLA3(148M) confers a loss- or gain-of-function. Here we test the hypothesis that PNPLA3 causes steatosis by sequestering ABHD5 (α/β hydrolase domain containing protein 5), the cofactor of ATGL (adipose TG lipase), thus limiting mobilization of hepatic triglyceride (TG)., Methods: We quantified and compared the physical interactions between ABHD5 and PNPLA3/ATGL in cultured hepatocytes using NanoBiT complementation assays and immunocytochemistry. Recombinant proteins purified from human cells were used to compare TG hydrolytic activities of PNPLA3 and ATGL in the presence or absence of ABHD5. Adenoviruses and adeno-associated viruses were used to express PNPLA3 in liver-specific Atgl -/- mice and to express ABHD5 in livers of Pnpla3 M/M mice, respectively., Results: ABHD5 interacted preferentially with PNPLA3 relative to ATGL in cultured hepatocytes. No differences were seen in the strength of the interactions between ABHD5 with PNPLA3(WT) and PNPLA3(148M). In contrast to prior findings, we found that PNPLA3, like ATGL, is activated by ABHD5 in in vitro assays using purified proteins. PNPLA3(148M)-associated inhibition of TG hydrolysis required that ATGL be expressed and that PNPLA3 be located on LDs. Finally, overexpression of ABHD5 reversed the hepatic steatosis in Pnpla3 M/M mice., Conclusions: These findings support the premise that PNPLA3(148M) is a gain-of-function mutation that promotes hepatic steatosis by accumulating on LDs and inhibiting ATGL-mediated lipolysis in an ABHD5-dependent manner. Our results predict that reducing, rather that increasing, PNPLA3 expression will be the best strategy to treat PNPLA3(148M)-associated SLD., Impact and Implications: Steatotic liver disease (SLD) is a common complex disorder associated with both environmental and genetic risk factors. PNPLA3(148M) is the most impactful genetic risk factor for SLD and yet its pathogenic mechanism remains controversial. Here we provide evidence that PNPLA3(148M) promotes triglyceride (TG) accumulation by sequestering ABHD5, thus limiting its availability to activate ATGL. Although the substitution of methionine for isoleucine reduces the TG hydrolase activity of PNPLA3, the loss of enzymatic function is not directly related to the steatotic effect of the variant. It is the resulting accumulation of PNPLA3 on LDs that confers a gain-of-function by interfering with ATGL-mediated TG hydrolysis. These findings have implications for the design of potential PNPLA3(148M)-based therapies. Reducing, rather than increasing, PNPLA3 levels is predicted to reverse steatosis in susceptible individuals., Competing Interests: Declaration of Competing Interest Helen Hobbs is on the Corporate Board of Pfizer, Inc., (Copyright © 2024. Published by Elsevier B.V.)
Published: 2024
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22. Disintegration at the Syntax-Semantics Interface in Prodromal Alzheimer's Disease: New Evidence from Complex Sentence Anaphora in Amnestic Mild Cognitive Impairment (aMCI).

Author: Lust B, Flynn S, Henderson C, Gair J, and Sherman JC
Abstract: Although diverse language deficits have been widely observed in prodromal Alzheimer's disease (AD), the underlying nature of such deficits and their explanation remains opaque. Consequently, both clinical applications and brain-language models are not well-defined. In this paper we report results from two experiments which test language production in a group of individuals with amnestic Mild Cognitive Impairment (aMCI) in contrast to healthy aging and healthy young. The experiments apply factorial designs informed by linguistic analysis to test two forms of complex sentences involving anaphora (relations between pronouns and their antecedents). Results show that aMCI individuals differentiate forms of anaphora depending on sentence structure, with selective impairment of sentences which involve construal with reference to context (anaphoric coreference). We argue that aMCI individuals maintain core structural knowledge while evidencing deficiency in syntax-semantics integration, thus locating the source of the deficit in the language-thought interface of the Language Faculty., Competing Interests: Declaration of Competing Interests All co-authors declare no conflict of interest.
Published: 2024
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23. The ubiquitin E3 ligase BFAR promotes degradation of PNPLA3.

Author: Das A, Cheng H, Wang Y, Kinch LN, Liang G, Hong S, Hobbs HH, and Cohen JC
Subjects: Animals, Mice, Acyltransferases, Hepatocytes metabolism, Phospholipases A2, Calcium-Independent genetics, Ubiquitin, Ubiquitin-Protein Ligases genetics, Humans, Cell Line, Tumor, Non-alcoholic Fatty Liver Disease metabolism, Membrane Proteins metabolism, Adaptor Proteins, Signal Transducing metabolism, Apoptosis Regulatory Proteins metabolism
Abstract: A missense variant in patatin-like phospholipase domain-containing protein 3 [PNPLA3(I148M)] is the most impactful genetic risk factor for fatty liver disease (FLD). We previously showed that PNPLA3 is ubiquitylated and subsequently degraded by proteasomes and autophagosomes and that the PNPLA3(148M) variant interferes with this process. To define the machinery responsible for PNPLA3 turnover, we used small interfering (si)RNAs to inactivate components of the ubiquitin proteasome system. Inactivation of bifunctional apoptosis regulator (BFAR), a membrane-bound E3 ubiquitin ligase, reproducibly increased PNPLA3 levels in two lines of cultured hepatocytes. Conversely, overexpression of BFAR decreased levels of endogenous PNPLA3 in HuH7 cells. BFAR and PNPLA3 co-immunoprecipitated when co-expressed in cells. BFAR promoted ubiquitylation of PNPLA3 in vitro in a reconstitution assay using purified, epitope-tagged recombinant proteins. To confirm that BFAR targets PNPLA3, we inactivated Bfar in mice. Levels of PNPLA3 protein were increased twofold in hepatic lipid droplets of Bfar -/- mice with no associated increase in PNPLA3 mRNA levels. Taken together these data are consistent with a model in which BFAR plays a role in the post-translational degradation of PNPLA3. The identification of BFAR provides a potential target to enhance PNPLA3 turnover and prevent FLD., Competing Interests: Competing interests statement:The authors declare no competing interest.
Published: 2024
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24. PCSK9: From Nature's Loss to Patient's Gain.

Author: Hobbs HH, Cohen JC, and Horton JD
Subjects: Humans, Cholesterol, LDL, Receptors, LDL, Proprotein Convertase 9 genetics, Serine Endopeptidases
Abstract: Competing Interests: Disclosures Dr Horton is a consultant for Merck, Pfizer, and Regeneron. Drs Hobbs and Cohen report no conflicts.
Published: 2024
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25. Effect of donor HSD17B13 genotype on patient survival after liver transplant: a retrospective cohort study.

Author: Kozlitina J, Cohen NM, Sturtevant D, Cohen JC, Murphey-Half C, Saltarrelli JG, Jindra P, Askar M, Hwang CS, Vagefi PA, Lacelle C, Hobbs HH, and MacConmara MP
Abstract: Background: Several genetic variants are associated with chronic liver disease. The role of these variants in outcomes after liver transplantation (LT) is uncertain. The aim of this study was to determine if donor genotype at risk-associated variants in PNPLA3 (rs738409 C>G, p.I148M) and HSD17B13 (rs72613567 T>TA; rs80182459, p.A192Lfs∗8) influences post-LT survival., Methods: In this retrospective cohort study, data on 2346 adults who underwent first-time LT between January 1, 1999 and June 30, 2020 and who had donor DNA samples available at five large Transplant Immunology Laboratories in Texas, USA, were obtained from the United Network for Organ Sharing (UNOS). Duplicates, patients with insufficient donor DNA for genotyping, those who were <18 years of age at the time of transplant, had had a previous transplant or had missing genotype data were excluded. The primary outcomes were patient and graft survival after LT. The association between donor genotype and post-LT survival was examined using Kaplan-Meier method and multivariable-adjusted Cox proportional hazards models., Findings: Median age of LT recipients was 57 [interquartile range (IQR), 50-62] years; 837 (35.7%) were women; 1362 (58.1%) White, 713 (30.4%) Hispanic, 182 (7.8%) Black/African-American. Median follow-up time was 3.95 years. Post-LT survival was not affected by donor PNPLA3 genotype but was significantly reduced among recipients of livers with two HSD17B13 loss-of-function (LoF) variants compared to those receiving livers with no HSD17B13 LoF alleles (unadjusted one-year survival: 82.6% vs 93.9%, P < 0.0001; five-year survival: 73.1% vs 82.9%, P = 0.0017; adjusted hazard ratio [HR], 2.25; 95% CI, 1.61-3.15 after adjustment for recipient age, sex, and self-reported ethnicity). Excess mortality was restricted to those receiving steroid induction immunosuppression (crude 90-day post-LT mortality, 9.3% [95% CI, 1.9%-16.1%] vs 1.9% [95% CI, 0.9%-2.9%] in recipients of livers with two vs no HSD17B13 LoF alleles, P = 0.0012; age, sex, and ethnicity-adjusted HR, 2.85; 95% CI, 1.72-4.71, P < 0.0001). No reduction was seen among patients who did not receive steroid induction (90-day mortality 3.1% [95% CI, 0%-7.3%] vs 2% [95% CI, 0.9%-3.1%], P = 0.65; adjusted HR, 1.17; 95% CI, 0.66-2.08, P = 0.60)., Interpretation: Donor HSD17B13 genotype adversely affects post-LT survival in patients receiving steroid induction. Additional studies are required to confirm this association., Funding: The National Institutes of Health and American Society of Transplant Surgeons Collaborative Scientist Grant., Competing Interests: All authors declare no competing interests., (© 2023 The Authors.)
Published: 2023
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26. Separate circuit nasal cannulae for end-tidal CO 2 monitoring may lead to hypoxia in patients with unilateral nasal airway obstruction.

Author: Cohen JC, Ho AM, O'Reilly HD, and Mizubuti GB
Subjects: Humans, Carbon Dioxide, Cannula, Intubation, Hypoxia etiology, Nasal Obstruction, Airway Obstruction
Abstract: Competing Interests: Conflicts of interest The authors declare no conflicts of interest.
Published: 2023
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27. Gait analysis of leprosy patients with foot drop using principal component analysis.

Author: Cohen JC, de Souza Muniz AM, Carvalho Junior RB, de Oliveira HLC, Miranda ST, Gomes MK, da Cunha AJLA, and Menegaldo LL
Subjects: Humans, Gait Analysis, Principal Component Analysis, Gait physiology, Walking physiology, Muscle Weakness, Ankle Joint, Biomechanical Phenomena, Peroneal Neuropathies, Foot Orthoses
Abstract: Background: Peripheral nerve injury caused by leprosy can lead to foot drop, resulting in an altered gait pattern that has not been previously described using 3D gait analysis., Methods: Gait kinematics and dynamics were analyzed in 12 patients with unilateral foot drop caused by leprosy and in 15 healthy controls. Biomechanical data from patients' affected and unaffected limbs were compared with controls using inferential statistics and a standard distance, based on principal components analysis (PCA)., Findings: Patients walked slower than controls (0.8 ± 0.2 vs. 1.1 ± 0.2 m/s, p = 0.003), with a reduced stance and increased swing percentage. The affected limb increased (p < 0.05) plantar flexion at the initial contact (-16.8 o ± 8.3), terminal stance (-29.1 o ± 11.5), and swing (-12.4 o ± 6.2) in the affected limb compared to unaffected (-6.6 o ± 10.3; -14.6 o ± 11.6; 2.4 o ± 7.6) and controls (-5.4 o ± 2.5; -18.8 o ± 5.8; -1.4 o ± 3.9). Increased pelvic tilt and knee adduction/abduction range, with lower hip adduction, were observed. The second peak of ground reaction force (98.6 ± 5.2 %BW), ankle torque (0.99 ± 0.33 Nm/kg), and net ankle work in stance (-0.03 ± 5.4 J/Kg) decreased in the affected limb compared to controls (104.1 ± 5.5 %BW; 1.24 ± 0.4 Nm/kg; -4.58 ± 5.19 J/kg; p < 0.05). There were decreasing multivariate standard distances in the affected limb compared with the unaffected and controls. PCA loading factors highlighted the major differences between groups., Interpretation: Leprosy patients with foot drop presented altered gait patterns in affected and unaffected limbs. There were remarkable differences in ankle kinematics and dynamics. Rehabilitation devices, such as ankle foot orthosis or tendon transfer surgeries to increase ankle dorsiflexion, could benefit these patients and reduce deviations from normal gait., Competing Interests: Declaration of Competing Interest None., (Copyright © 2023 Elsevier Ltd. All rights reserved.)
Published: 2023
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28. Contribution of a genetic risk score to ethnic differences in fatty liver disease.

Author: Kubiliun MJ, Cohen JC, Hobbs HH, and Kozlitina J
Subjects: Alleles, Case-Control Studies, Ethnicity genetics, Genetic Predisposition to Disease, Humans, Polymorphism, Single Nucleotide, Risk Factors, Liver Diseases genetics, Non-alcoholic Fatty Liver Disease genetics
Abstract: Background and Aims: Susceptibility to fatty liver disease (FLD) varies among individuals and between racial/ethnic groups. Several genetic variants influence FLD risk, but whether these variants explain racial/ethnic differences in FLD prevalence is unclear. We examined the contribution of genetic risk factors to racial/ethnic-specific differences in FLD., Methods: A case-control study comparing FLD patients (n = 1194) and population-based controls (n = 3120) was performed. Patient characteristics, FLD risk variants (PNPLA3-rs738409 + rs6006460, TM6SF2-rs58542926, HSD17B13-rs80182459 + rs72613567, MBOAT7/TMC4-rs641738, and GCKR-rs1260326) and a multi-locus genetic risk score (GRS) were examined. The odds of FLD for individuals with different risk factor burdens were determined., Results: Hispanics and Whites were over-represented (56% vs. 38% and 36% vs. 29% respectively) and Blacks under-represented (5% vs. 23%) among FLD patients, compared to the population from which controls were selected (p < .001). Among cases and controls, Blacks had a lower and Hispanics a greater, net number of risk alleles than Whites (p < .001). GRS was associated with increased odds of FLD (OR Q5vsQ1 = 8.72 [95% CI = 5.97-13.0], p = 9.8 × 10 -28 ), with the association being stronger in Hispanics (OR Q5vsQ1 = 14.8 [8.3-27.1]) than Blacks (OR Q5vsQ1 = 3.7 [1.5-11.5], P-interaction = 0.002). After accounting for GRS, the odds of FLD between Hispanics and Whites did not differ significantly (OR = 1.06 [0.87-1.28], p = .58), whereas Blacks retained much lower odds of FLD (OR = 0.21, [0.15-0.30], p < .001)., Conclusions: Blacks had a lower and Hispanics a greater FLD risk allele burden than Whites. These differences contributed to, but did not fully explain, racial/ethnic differences in FLD prevalence. Identification of additional factors protecting Blacks from FLD may provide new targets for prevention and treatment of FLD., (© 2022 The Authors. Liver International published by John Wiley & Sons Ltd.)
Published: 2022
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29. CORRELATION BETWEEN QUALITY OF LIFE AND THE CLINICAL RESULTS OF PATIENTS WITH LEPROSY WITH DROP FOOT AFTER TENDON TRANSFER.

Author: Cohen JC, Rodrigues NC, Cabral EF, de Miranda ST, da Cunha AJLA, and Gomes MK
Abstract: Objective: To evaluate the functional results of surgically correcting drop foot in patients with leprosy and compare their SALSA, Social Participation, and AOFAS score., Methods: Overall, 22 patients were subjected to posterior tibial tendon transfer via the subcutaneous route to the foot dorsum with an average follow-up of 56 months (min 12, max 70). In our sample, 15 of the enrolled patients were men and seven, women, aged between 20 and 73 years old who were operated on from January 2014 to December 2017. The Pearson's correlation test (r) was used to measure the correlation among those scales. A p < 0.05 was considered significant between the pre- and pos-operative AOFAS scale scores., Results: Pre-operative average AOFAS score was 59.6 (min 35, max 74) and 77.2 postoperative (min 36, max 97) (p < 0.0001), postoperative Salsa and Social Participation scale, 30.6 and 22.5, respectively. Statistical analysis suggests a strong positive correlation between AOFAS and Salsa scales (r = -0.83) and AOFAS and social participation (r = -0.78). Average dorsiflexion was 5.4 degrees., Conclusion: The surgical correction of drop foot positively affects the quality of life and social participation of patients with leprosy. Level of Evidence III, Retrospective Study. , Competing Interests: All authors declare no potential conflict of interest related to this article.
Published: 2022
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30. Sharpening, focusing, and developing: A study of change in nonsymbolic number comparison skills and math achievement in 1st grade.

Author: Wilkey ED, Shanley L, Sabb F, Ansari D, Cohen JC, Men V, Heller NA, and Clarke B
Subjects: Child, Humans, Inhibition, Psychological, Mathematics, Achievement, Executive Function
Abstract: Children's ability to discriminate nonsymbolic number (e.g., the number of items in a set) is a commonly studied predictor of later math skills. Number discrimination improves throughout development, but what drives this improvement is unclear. Competing theories suggest that it may be due to a sharpening numerical representation or an improved ability to pay attention to number and filter out non-numerical information. We investigate this issue by studying change in children's performance (N = 65) on a nonsymbolic number comparison task, where children decide which of two dot arrays has more dots, from the middle to the end of 1st grade (mean age at time 1 = 6.85 years old). In this task, visual properties of the dot arrays such as surface area are either congruent (the more numerous array has more surface area) or incongruent. Children rely more on executive functions during incongruent trials, so improvements in each congruency condition provide information about the underlying cognitive mechanisms. We found that accuracy rates increased similarly for both conditions, indicating a sharpening sense of numerical magnitude, not simply improved attention to the numerical task dimension. Symbolic number skills predicted change in congruent trials, but executive function did not predict change in either condition. No factor predicted change in math achievement. Together, these findings suggest that nonsymbolic number processing undergoes development related to existing symbolic number skills, development that appears not to be driving math gains during this period. Children's ability to discriminate nonsymbolic number improves throughout development. Competing theories suggest improvement due to sharpening magnitude representations or changes in attention and inhibition. The current study investigates change in nonsymbolic number comparison performance during first grade and whether symbolic number skills, math skills, or executive function predict change. Children's performance increased across visual control conditions (i.e., congruent or incongruent with number) suggesting an overall sharpening of number processing. Symbolic number skills predicted change in nonsymbolic number comparison performance., (© 2021 John Wiley & Sons Ltd.)
Published: 2022
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31. Hepatic TM6SF2 Is Required for Lipidation of VLDL in a Pre-Golgi Compartment in Mice and Rats.

Author: Luo F, Smagris E, Martin SA, Vale G, McDonald JG, Fletcher JA, Burgess SC, Hobbs HH, and Cohen JC
Subjects: Animals, Mice, Rats, Membrane Proteins metabolism, Non-alcoholic Fatty Liver Disease metabolism
Abstract: Background & Aims: Substitution of lysine for glutamic acid at residu 167 in Transmembrane 6 superfamily member 2 (TM6SF2) is associated with fatty liver disease and reduced plasma lipid levels. Tm6sf2 -/- mice replicate the human phenotype but were not suitable for detailed mechanistic studies. As an alternative model, we generated Tm6sf2 -/- rats to determine the subcellular location and function of TM6SF2., Methods: Two lines of Tm6sf2 -/- rats were established using gene editing. Lipids from tissues and from newly secreted very low density lipoproteins (VLDLs) were quantified using enzymatic assays and mass spectrometry. Neutral lipids were visualized in tissue sections using Oil Red O staining. The rate of dietary triglyceride (TG) absorption and hepatic VLDL-TG secretion were compared in Tm6sf2 -/- mice and in their wild-type littermates. The intracellular location of TM6SF2 was determined by cell fractionation. Finally, TM6SF2 was immunoprecipitated from liver and enterocytes to identify interacting proteins., Results: Tm6sf2 -/- rats had a 6-fold higher mean hepatic TG content (56.1 ± 28.9 9 vs 9.8 ± 3.9 mg/g; P < .0001) and lower plasma cholesterol levels (99.0 ± 10.5 vs 110.6 ± 14.0 mg/dL; P = .0294) than their wild-type littermates. Rates of appearance of dietary and hepatic TG into blood were reduced significantly in Tm6sf2 -/- rats (P < .001 and P < .01, respectively). Lipid content of newly secreted VLDLs isolated from perfused livers was reduced by 53% (TG) and 62% (cholesterol) (P = .005 and P = .01, respectively) in Tm6sf2 -/- mice. TM6SF2 was present predominantly in the smooth endoplasmic reticulum and endoplasmic reticulum-Golgi intermediate compartments, but not in Golgi. Both apolipoprotein B-48 and acyl-CoA synthetase long chain family member 5 physically interacted with TM6SF2., Conclusions: TM6SF2 acts in the smooth endoplasmic reticulum to promote bulk lipidation of apolipoprotein B-containing lipoproteins, thus preventing fatty liver disease., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)
Published: 2022
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32. Language Decline Characterizes Amnestic Mild Cognitive Impairment Independent of Cognitive Decline.

Author: Sherman JC, Henderson CR Jr, Flynn S, Gair JW, and Lust B
Subjects: Humans, Language, Memory, Short-Term, Neuropsychological Tests, Alzheimer Disease, Cognitive Dysfunction
Abstract: Purpose This research investigated the nature of cognitive decline in prodromal Alzheimer's disease (AD), particularly in mild cognitive impairment, amnestic type (aMCI). We assessed language in aMCI as compared with healthy aging (HA) and healthy young (HY) with new psycholinguistic assessment of complex sentences, and we tested the degree to which deficits on this language measure relate to performance in other general cognitive domains such as memory. Method Sixty-one individuals with aMCI were compared with 24 HA and 10 HY adults on a psycholinguistic measure of complex sentence production (relative clauses). In addition, HA, HY, and a subset of the aMCI participants ( n = 22) were also tested on a multidomain cognitive screen, the Addenbrooke's Cognitive Examination-Revised (ACE-R), and on a verbal working memory Brown-Peterson (BP) test. General and generalized linear mixed models were used to test psycholinguistic results and to test whether ACE-R and BP performance predicted performance on the psycholinguistic test similarly in the aMCI and HA groups. Results On the psycholinguistic measure, sentence imitation was significantly deficited in aMCI in comparison with that in HA and HY. Experimental factorial designs revealed that individuals with aMCI had particular difficulty repeating sentences that especially challenged syntax-semantics integration. As expected, the aMCI group also performed significantly below the HY and HA groups on the ACE-R. Neither the ACE-R Memory subtest nor the BP total scores predicted performance on the psycholinguistic task for either the aMCI or the HA group. However, the ACE-R total score significantly predicted psycholinguistic task performance, with increased ACE-R performance predicting increased psycholinguistic task performance only for the HA group, not for the aMCI group. Conclusions Results suggest a selective deterioration in language in aMCI, specifically a weakening of syntax-semantics integration in complex sentence processing, and a general independence of this language deficit and memory decline. Results cohere with previous assessments of the nature of difficulty in complex sentence formation in aMCI. We argue that clinical screening for prodromal AD can be strengthened by supplementary testing of language, as well as memory, and extended evaluation of strength of their relation.
Published: 2021
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33. Missense variant in insulin receptor (Y1355H) segregates in family with fatty liver disease.

Author: Luo F, Xing C, Asrani SK, Li S, Liang G, Hobbs HH, and Cohen JC
Subjects: Adolescent, Adult, Aged, Animals, Antigens, CD blood, Antigens, CD metabolism, Female, Humans, Male, Mice, Mice, Inbred C57BL, Middle Aged, Mutation, Missense, Non-alcoholic Fatty Liver Disease blood, Non-alcoholic Fatty Liver Disease metabolism, Receptor, Insulin blood, Receptor, Insulin metabolism, Young Adult, Antigens, CD genetics, Non-alcoholic Fatty Liver Disease genetics, Receptor, Insulin genetics
Abstract: A missense variant in the cytoplasmic domain of the insulin receptor (INSR) was identified by exome sequencing in affected members of a four-generation family with fatty liver disease (FLD). The variant (rs766457461, c.4063T>C, p.Y1355H) results in the substitution of histidine for a tyrosine that undergoes autophosphorylation in response to insulin stimulation in vitro. Because insulin promotes lipogenesis in hepatocytes, we hypothesized that the variant was causally linked to FLD in the family. To test this hypothesis, we used CRISPR/Cas9 technology to replace the corresponding tyrosine in mouse INSR with histidine (Y1345H). No significant differences were found in hepatic insulin signaling, as assessed by phosphorylation of INSR or AKT levels or in activation of the insulin-responsive transcription factor SREBP-1c. Glucose tolerance and hepatic triglyceride (TG) content in Insr 1345H/H mice fed a chow diet or diets rich in fat, sucrose or fructose did not differ significantly from WT littermates. Thus, our studies in mice failed to support the notion that INSR (Y1355H) is causally related to FLD in the family or that phosphorylation of this residue alters hepatic TG metabolism., (Copyright © 2021 The Authors. Published by Elsevier GmbH.. All rights reserved.)
Published: 2021
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34. Molecular basis of cholesterol efflux via ABCG subfamily transporters.

Author: Sun Y, Wang J, Long T, Qi X, Donnelly L, Elghobashi-Meinhardt N, Esparza L, Cohen JC, Xie XS, Hobbs HH, and Li X
Subjects: ATP Binding Cassette Transporter, Subfamily G, Member 1 chemistry, ATP Binding Cassette Transporter, Subfamily G, Member 1 genetics, ATP Binding Cassette Transporter, Subfamily G, Member 8 chemistry, ATP Binding Cassette Transporter, Subfamily G, Member 8 genetics, Binding Sites, Biological Transport, Cryoelectron Microscopy, Humans, Protein Conformation, ATP Binding Cassette Transporter, Subfamily G, Member 1 metabolism, ATP Binding Cassette Transporter, Subfamily G, Member 8 metabolism, Adenosine Triphosphate metabolism, Cholesterol metabolism
Abstract: The ABCG1 homodimer (G1) and ABCG5-ABCG8 heterodimer (G5G8), two members of the adenosine triphosphate (ATP)-binding cassette (ABC) transporter G family, are required for maintenance of cellular cholesterol levels. G5G8 mediates secretion of neutral sterols into bile and the gut lumen, whereas G1 transports cholesterol from macrophages to high-density lipoproteins (HDLs). The mechanisms used by G5G8 and G1 to recognize and export sterols remain unclear. Here, we report cryoelectron microscopy (cryo-EM) structures of human G5G8 in sterol-bound and human G1 in cholesterol- and ATP-bound states. Both transporters have a sterol-binding site that is accessible from the cytosolic leaflet. A second site is present midway through the transmembrane domains of G5G8. The Walker A motif of G8 adopts a unique conformation that accounts for the marked asymmetry in ATPase activities between the two nucleotide-binding sites of G5G8. These structures, along with functional validation studies, provide a mechanistic framework for understanding cholesterol efflux via ABC transporters., Competing Interests: The authors declare no competing interest., (Copyright © 2021 the Author(s). Published by PNAS.)
Published: 2021
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35. Genetic and Metabolic Determinants of Plasma Levels of ANGPTL8.

Author: Oldoni F, Bass K, Kozlitina J, Hudson H, Shihanian LM, Gusarova V, Cohen JC, and Hobbs HH
Subjects: Adolescent, Adult, Aged, Aged, 80 and over, Angiopoietin-Like Protein 8, Angiopoietin-like Proteins genetics, Cohort Studies, Energy Metabolism genetics, Ethnicity genetics, Ethnicity statistics & numerical data, Female, Glucose metabolism, Humans, Male, Middle Aged, Obesity ethnology, Obesity genetics, Obesity metabolism, Peptide Hormones genetics, Texas epidemiology, Triglycerides metabolism, Young Adult, Angiopoietin-like Proteins blood, Energy Metabolism physiology, Genetic Background, Peptide Hormones blood
Abstract: Context: ANGPTL8 (A8) plays a key role in determining the tissue fate of circulating triglycerides (TGs). Plasma A8 levels are associated with several parameters of glucose and TG metabolism, but the causality of these relationships and the contribution of genetic variants to differences in A8 levels have not been explored., Objective: To characterize the frequency distribution of plasma A8 levels in a diverse population using a newly-developed enzyme-linked immunosorbent assay (ELISA) and to identify genetic factors contributing to differences in plasma A8 levels., Methods: We studied a population-based sample of Dallas County, comprising individuals in the Dallas Heart Study (DHS-1, n = 3538; DHS-2, n = 3283), including 2131 individuals with repeated measurements 7 to 9 years apart (age 18-85 years; >55% female; 52% Black; 29% White; 17% Hispanic; and 2% other). The main outcome measures were associations of A8 levels with body mass index (BMI), plasma levels of glucose, insulin, lipids, and hepatic TGs, as well as DNA variants identified by exome-wide sequencing., Results: A8 levels varied over a 150-fold range (2.1-318 ng/mL; median, 13.3 ng/mL) and differed between racial/ethnic groups (Blacks > Hispanics > Whites). A8 levels correlated with BMI, fasting glucose, insulin, and TG levels. A variant in A8, R59W, accounted for 17% of the interindividual variation in A8 levels but was not associated with the metabolic parameters correlated with plasma A8 concentrations., Conclusions: A8 levels were strongly associated with indices of glucose and TG metabolism, but the lack of association of genetic variants at the A8 locus that impact A8 levels with these parameters indicates that differences in A8 levels are not causally related to the associated metabolic phenotypes., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society.)
Published: 2021
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36. Effects of Intravenous Tranexamic Acid During Rhytidectomy: A Randomized, Controlled, Double-Blind Pilot Study.

Author: Cohen JC, Glasgold RA, Alloju LM, and Glasgold MJ
Subjects: Blood Loss, Surgical prevention & control, Double-Blind Method, Humans, Pilot Projects, Postoperative Hemorrhage etiology, Postoperative Hemorrhage prevention & control, Prospective Studies, Rhytidoplasty adverse effects, Tranexamic Acid adverse effects
Abstract: Background: Tranexamic acid (TXA) is an antifibrinolytic agent shown to decrease intraoperative bleeding, reduce transfusions, and improve outcomes across multiple specialties. Within plastic surgery, initial reports are encouraging but formal studies are lacking., Objectives: The aim of this study was to determine whether intravenous (IV) TXA has any effect on intraoperative bleeding or postoperative sequelae in patients undergoing a deep-plane facelift., Methods: This is a prospective, randomized, double-blind, case series in a private practice surgery center. The participants were 44 patients undergoing rhytidectomy with the senior authors (R.A.G. or M.J.G). The treatment group received a 1-g dose of IV TXA prior to skin incision and the same dose 4 hours later (vs saline). Bleeding was rated mild, moderate, or severe. Postoperative ecchymosis and edema were subjectively evaluated by patient and surgeon and scores were aggregated for analysis., Results: The TXA group showed decreased intraoperative bleeding but this difference did not reach statistical significance. Postoperative ecchymosis/edema ratings were lower for patients who received TXA, including a statistically significant decrease in surgeon-rated bruising. TXA resulted in a statistically significant decrease in postoperative collections in this study and no major complications occurred., Conclusions: TXA is a safe, low-cost addition to any existing surgical protocol and may lead to fewer surgical sequelae and improved satisfaction. Although we did not observe a dramatically different intraoperative experience, postoperative bruising and collections were significantly reduced. TXA acid may have great value in the management of patients undergoing rhytidectomy and its use warrants further study., (© 2020 The Aesthetic Society. Reprints and permission: journals.permissions@oup.com.)
Published: 2021
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37. ANGPTL8 has both endocrine and autocrine effects on substrate utilization.

Author: Oldoni F, Cheng H, Banfi S, Gusarova V, Cohen JC, and Hobbs HH
Subjects: Adipose Tissue cytology, Angiopoietin-Like Protein 8, Animals, Female, Liver cytology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Paracrine Communication, Adipose Tissue metabolism, Angiopoietin-like Proteins physiology, Autocrine Communication, Dietary Fats metabolism, Lipoprotein Lipase metabolism, Liver metabolism, Triglycerides metabolism
Abstract: The angiopoietin-like protein ANGPTL8 (A8) is one of 3 ANGPTLs (A8, A3, A4) that coordinate changes in triglyceride (TG) delivery to tissues by inhibiting lipoprotein lipase (LPL), an enzyme that hydrolyzes TG. Previously we showed that A8, which is expressed in liver and adipose tissue, is required to redirect dietary TG from oxidative to storage tissues following food intake. Here we show that A8 from liver and adipose tissue have different roles in this process. Mice lacking hepatic A8 have no circulating A8, high intravascular LPL activity, low plasma TG levels, and evidence of decreased delivery of dietary lipids to adipose tissue. In contrast, mice lacking A8 in adipose tissue have higher postprandial TG levels and similar intravascular LPL activity and plasma A8 levels and higher levels of plasma TG. Expression of A8, together with A4, in cultured cells reduced A4 secretion and A4-mediated LPL inhibition. Thus, hepatic A8 (with A3) acts in an endocrine fashion to inhibit intravascular LPL in oxidative tissues, whereas A8 in adipose tissue enhances LPL activity by autocrine/paracrine inhibition of A4. These combined actions of A8 ensure that TG stores are rapidly replenished and sufficient energy is available until the next meal.
Published: 2020
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38. Prevalence and intensity of persistent post-surgical pain following breast cancer surgery: a systematic review and meta-analysis of observational studies.

Author: Wang L, Cohen JC, Devasenapathy N, Hong BY, Kheyson S, Lu D, Oparin Y, Kennedy SA, Romerosa B, Arora N, Kwon HY, Jackson K, Prasad M, Jayasekera D, Li A, Guarna G, Natalwalla S, Couban RJ, Reid S, Khan JS, McGillion M, and Busse JW
Subjects: Breast Neoplasms epidemiology, Female, Humans, Prevalence, Severity of Illness Index, Breast Neoplasms surgery, Chronic Pain epidemiology, Observational Studies as Topic, Pain, Postoperative epidemiology
Abstract: Background: The prevalence and intensity of persistent post-surgical pain (PPSP) after breast cancer surgery are uncertain. We conducted a systematic review and meta-analysis to further elucidate this issue., Methods: We searched MEDLINE, Embase, CINAHL, and PsycINFO, from inception to November 2018, for observational studies reporting persistent pain (≥3 months) after breast cancer surgery. We used random-effects meta-analysis and the Grading of Recommendations, Assessment, Development and Evaluations approach to rate quality of evidence., Results: We included 187 observational studies with 297 612 breast cancer patients. The prevalence of PPSP ranged from 2% to 78%, median 37% (inter-quartile range: 22-48%); the pooled prevalence was 35% (95% confidence interval [CI]: 32-39%). The pooled pain intensity was 3.9 cm on a 10 cm visual analogue scale (95% CI: 3.6-4.2 cm). Moderate-quality evidence supported the subgroup effects of PPSP prevalence for localized pain vs any pain (29% vs 44%), moderate or greater vs any pain (26% vs 44%), clinician-assessed vs patient-reported pain (23% vs 36%), and whether patients underwent sentinel lymph node biopsy vs axillary lymph node dissection (26% vs 43%). The adjusted analysis found that the prevalence of patient-reported PPSP (any severity/location) was 46% (95% CI: 36-56%), and the prevalence of patient-reported moderate-to-severe PPSP at any location was 27% (95% CI: 10-43%)., Conclusions: Moderate-quality evidence suggests that almost half of all women undergoing breast cancer surgery develop persistent post-surgical pain, and about one in four develop moderate-to-severe persistent post-surgical pain; the higher prevalence was associated with axillary lymph node dissection. Future studies should explore whether nerve sparing for axillary procedures reduces persistent post-surgical pain after breast cancer surgery., (Copyright © 2020 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.)
Published: 2020
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39. Angiopoietin-like protein 3 governs LDL-cholesterol levels through endothelial lipase-dependent VLDL clearance.

Author: Adam RC, Mintah IJ, Alexa-Braun CA, Shihanian LM, Lee JS, Banerjee P, Hamon SC, Kim HI, Cohen JC, Hobbs HH, Van Hout C, Gromada J, Murphy AJ, Yancopoulos GD, Sleeman MW, and Gusarova V
Subjects: Humans, Animals, Mice, Lipoproteins, VLDL metabolism, Lipoproteins, VLDL blood, Male, Receptors, LDL metabolism, Female, Angiopoietin-Like Protein 3, Cholesterol, LDL metabolism, Cholesterol, LDL blood, Lipase metabolism, Angiopoietin-like Proteins metabolism
Abstract: Angiopoietin-like protein (ANGPTL)3 regulates plasma lipids by inhibiting LPL and endothelial lipase (EL). ANGPTL3 inactivation lowers LDL-C independently of the classical LDLR-mediated pathway and represents a promising therapeutic approach for individuals with homozygous familial hypercholesterolemia due to LDLR mutations. Yet, how ANGPTL3 regulates LDL-C levels is unknown. Here, we demonstrate in hyperlipidemic humans and mice that ANGPTL3 controls VLDL catabolism upstream of LDL. Using kinetic, lipidomic, and biophysical studies, we show that ANGPTL3 inhibition reduces VLDL-lipid content and size, generating remnant particles that are efficiently removed from the circulation. This suggests that ANGPTL3 inhibition lowers LDL-C by limiting LDL particle production. Mechanistically, we discovered that EL is a key mediator of ANGPTL3's novel pathway. Our experiments revealed that, although dispensable in the presence of LDLR, EL-mediated processing of VLDL becomes critical for LDLR-independent particle clearance. In the absence of EL and LDLR, ANGPTL3 inhibition perturbed VLDL catabolism, promoted accumulation of atypical remnants, and failed to reduce LDL-C. Taken together, we uncover ANGPTL3 at the helm of a novel EL-dependent pathway that lowers LDL-C in the absence of LDLR., Competing Interests: Conflict of interest—R.C.A., I.J.M., C.A.A-B., L.M.S., J.S.L., P.B., S.C.H., H.I.K., C.V.H., G.D.Y., A.J.M., J.G., M.W.S. and V.G. are or were employees and stockholders at Regeneron Pharmaceuticals while engaged in this study. All other authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2020 Adam et al. Published by The American Society for Biochemistry and Molecular Biology, Inc.)
Published: 2020
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40. Rituximab for chronic inflammatory demyelinating polyneuropathy-A potential therapeutic option.

Author: Cohen JC and Lewis RA
Subjects: Humans, Rituximab, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating
Published: 2020
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41. Orthopedic Surgical Foot Management in Hansen Disease.

Author: Cohen JC and de Miranda ST
Subjects: Foot Diseases diagnosis, Foot Diseases drug therapy, Foot Diseases microbiology, Humans, Leprosy diagnosis, Leprosy drug therapy, Leprosy microbiology, Nerve Transfer, Peripheral Nervous System Diseases diagnosis, Peripheral Nervous System Diseases drug therapy, Peripheral Nervous System Diseases etiology, Foot Diseases surgery, Leprosy surgery, Peripheral Nervous System Diseases surgery
Abstract: Hansen disease remains a common problem worldwide with 750,000 new cases diagnosed each year. Nerve injury is a central feature of the pathogenesis because of the unique tendency of Mycobacterium leprae to invade Schwann cells and the peripheral nervous system, that can be permanent and develop into disabilities. The orthopedic surgeon has an important role in the management of neuropathy, performing surgical release of the tibial and common peroneal nerves in potentially constricting areas, thus providing a better environment for nerve function. In cases of permanent loss of nerve function with drop foot, specific tendon transfers can be used., Competing Interests: Disclosure The author has nothing to disclose., (Copyright © 2020 Elsevier Inc. All rights reserved.)
Published: 2020
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42. Sugammadex in Ontario hospitals: Access and institutional policies.

Author: Cohen JC and Latchford KJ
Subjects: Child, Hospitals, Humans, Ontario, Organizational Policy, Sugammadex, Neuromuscular Blockade, Neuromuscular Nondepolarizing Agents, gamma-Cyclodextrins
Abstract: Rationale and Aims: Sugammadex is a novel neuromuscular blockade reversal agent which rapidly reverses the effects of rocuronium and vecuronium. Compared with the first-generation neuromuscular blockade reversal agent, neostigmine, sugammadex has a number of superior properties; however, sugammadex is significantly more expensive per dose compared with neostigmine (~CAD$95 vs $4). Given the high cost of sugammadex, many Ontario hospitals either do not stock the drug or have specific policies on when the drug can be administered. This study was designed to determine access to sugammadex in Ontario hospitals, as well as the prevalence and content of institutional policies on its use., Methods: We designed a survey assessing the availability of sugammadex and institutional policies on its use. We identified 60 Ontario hospitals with surgical services and obtained contact information for 45 of the anaesthesia departments. Surveys were sent to each department chief, and results were collected from July to October 2018., Results: Thirty-four (75.6%) hospitals responded to the survey. Twenty-seven (79.4%) of the 34 respondent hospitals had sugammadex. Of the seven hospitals that did not have sugammadex, six were group B hospitals, and one was a paediatric hospital. Of the 27 hospitals with sugammadex, 16 (59.3%) hospitals had specific policies on when sugammadex may be used. Based on policies, sugammadex was most frequently allowed to be used in emergency situations, especially failed intubations or "can't intubate, can't ventilate" situations where 100% of policies allowed its use. Policies on specific patient populations for sugammadex use were uncommon, with 43.8% of existing hospital policies not specifying any patient populations., Conclusions: Though most hospitals have sugammadex available, there is a marked heterogeneity in hospital policies on its use. Given the high cost of sugammadex use, it is worthwhile to have evidence-based policies on its use. Judicious use of sugammadex may also have secondary cost-saving benefits, through improved operating room efficiency and decreased complication rates., (© 2019 John Wiley & Sons, Ltd.)
Published: 2020
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43. Secularity: Guiding Questions for Inclusive Yoga in Schools.

Author: Cook-Cottone C, Childress T, and Harper JC
Subjects: Humans, Meditation, Recreation, Schools, Spirituality, Yoga
Abstract: This commentary explores the legal and ethical obligations of yoga programs and teachers to uphold both the principles and the spirit of secularism when teaching yoga in schools. Arguing that secularity is essential both to comply with legal mandates and to maximize inclusivity and access, each facet of a secular approach to yoga in schools is explored through an inquiry-based model meant to help the reader gain clarity and make informed choices when developing school-based yoga programming. This article does not address the use of nonsecular yoga for children outside the school setting. It instead speaks to the complexities of topics such as spirituality, personal transformation, secular ethics, and the use of cultural and historical artifacts within school programs. While inviting continued reflection on the nuances of the topic, the article concludes that given both the legal imperatives and potential risk of exclusion, failure to offer school-based yoga using a secular approach threatens to undermine the success of the field and hinder access to practices that have positive effects on young people.
Published: 2019
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44. [Rubber granules on synthetic turf pitches: safe or not safe for children?]

Author: van den Berg M, de Bruin A, Tervaert JC, and Sauer PJJ
Subjects: Carcinogens, Environmental standards, Child, Child Welfare, Environmental Exposure adverse effects, Environmental Pollutants adverse effects, Europe, Humans, Risk Assessment, Rubber adverse effects, Sports, Environmental Exposure standards, Environmental Pollutants standards, Hazardous Substances standards, Play and Playthings, Rubber standards
Abstract: Rubber granules from old car tyres used in synthetic turf pitches contain a significant number of carcinogenic and endocrine-disrupting chemicals. In 2017 the Dutch National Institute for Public Health and the Environment (RIVM) and the European Chemical Agency (ECHA) concluded that the risks for children are negligible. However, their reports contain some scientific inaccuracies and omissions which may have led them to underestimate the risks for children. It is therefore premature to conclude that it is safe for children to play on synthetic turf pitches with rubber granules. It is now primarily up to the parents to decide whether or not playing sports is acceptable in these circumstances. The Dutch government should, in accordance with ECHA recommendations, advise parents that their children ought to avoid hand-and-mouth contact with these granules as much as possible.
Published: 2019

45. PNPLA3, CGI-58, and Inhibition of Hepatic Triglyceride Hydrolysis in Mice.

Author: Wang Y, Kory N, BasuRay S, Cohen JC, and Hobbs HH
Subjects: Animals, Cells, Cultured, Disease Models, Animal, Disease Progression, Humans, Hydrolysis, Lipid Metabolism genetics, Mice, Mice, Inbred Strains, Mice, Knockout, Random Allocation, Reference Values, Fatty Liver genetics, Fatty Liver pathology, Phospholipases A2, Calcium-Independent genetics, Triglycerides metabolism
Abstract: A variant (148M) in patatin-like phospholipase domain-containing protein 3 (PNPLA3) is a major risk factor for fatty liver disease. Despite its clinical importance, the pathogenic mechanism linking the variant to liver disease remains poorly defined. Previously, we showed that PNPLA3(148M) accumulates to high levels on hepatic lipid droplets (LDs). Here we examined the effect of that accumulation on triglyceride (TG) hydrolysis by adipose triglyceride lipase (ATGL), the major lipase in the liver. As expected, overexpression of ATGL in cultured hepatoma (HuH-7) cells depleted the cells of LDs, but unexpectedly, co-expression of PNPLA3(wild type [WT] or 148M) with ATGL inhibited that depletion. The inhibitory effect of PNPLA3 was not caused by the displacement of ATGL from LDs. We tested the hypothesis that PNPLA3 interferes with ATGL activity by interacting with its cofactor, comparative gene identification-58 (CGI-58). Evidence supporting such an interaction came from two findings. First, co-expression of PNPLA3 and CGI-58 resulted in LD depletion in cultured cells, but expression of PNPLA3 alone did not. Second, PNPLA3 failed to localize to hepatic LDs in liver-specific Cgi-58 knockout (KO) mice. Moreover, overexpression of PNPLA3(148M) increased hepatic TG levels in WT, but not in Cgi-58 KO mice. Thus, the pro-steatotic effects of PNPLA3 required the presence of CGI-58. Co-immunoprecipitation and pulldown experiments in livers of mice and in vitro using purified proteins provided evidence that PNPLA3 and CGI-58 can interact directly. Conclusion: Taken together, these findings are consistent with a model in which PNPLA3(148M) promotes steatosis by CGI-58-dependent inhibition of ATGL on LDs., (© 2019 The Authors. Hepatology published by Wiley Periodicals, Inc. on behalf of American Association for the Study of Liver Diseases.)
Published: 2019
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46. Accumulation of PNPLA3 on lipid droplets is the basis of associated hepatic steatosis.

Author: BasuRay S, Wang Y, Smagris E, Cohen JC, and Hobbs HH
Subjects: Animals, Fatty Liver chemically induced, Fatty Liver genetics, Fatty Liver pathology, Lipid Droplets pathology, Liver pathology, Mice, Mice, Transgenic, Phospholipases A2, Calcium-Independent genetics, Sucrose adverse effects, Sucrose pharmacology, Triglycerides genetics, Ubiquitination drug effects, Ubiquitination genetics, Fatty Liver metabolism, Lipid Droplets metabolism, Liver metabolism, Phospholipases A2, Calcium-Independent metabolism, Triglycerides metabolism
Abstract: Fatty liver disease (FLD) is a disorder in which accumulation of triglycerides (TGs) in the liver can lead to inflammation, fibrosis, and cirrhosis. Previously, we identified a variant (I148M) in patatin-like phospholipase domain-containing protein 3 (PNPLA3) that is strongly associated with FLD, but the mechanistic basis for the association remains elusive. Although PNPLA3 has TG hydrolase activity in vitro, inactivation or overexpression of the WT protein in mice does not cause steatosis. In contrast, expression of two catalytically defective forms of PNPLA3 (I148M or S47A) in sucrose-fed mice causes accumulation of both PNPLA3 and TGs on hepatic lipid droplets (LDs). To determine if amassing PNPLA3 on LDs is a cause or consequence of steatosis, we engineered a synthetic isoform of PNPLA3 that uncouples protein accumulation from loss of enzymatic activity. Expression of a ubiquitylation-resistant form of PNPLA3 in mice caused accumulation of PNPLA3 on hepatic LDs and development of FLD. Lowering PNPLA3 levels by either shRNA knockdown or proteolysis-targeting chimera (PROTAC)-mediated degradation reduced liver TG content in mice overexpressing PNPLA3(148M). Taken together, our results show that the steatosis associated with PNPLA3(148M) is caused by accumulation of PNPLA3 on LDs., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2019 the Author(s). Published by PNAS.)
Published: 2019
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47. Lateral Sesamoid Position Relative to the Second Metatarsal in Feet with and without Hallux Valgus.

Author: Machado DG, Gondim EDS, Cohen JC, and Amorim LEC
Abstract: Objective To determine if the sesamoids migrate laterally in the feet with hallux valgus or if they only appear to move, maintaining their relationship with the other forefoot structures. Methods Anteroposterior radiographs of 80 patients (94 feet, all weight-bearing), from the period between 2015 and 2016, were evaluated. Forty-eight had a valgus hallux angle greater than 15° (hallux valgus group) and 46 presented a hallux valgus angle lower than 15° (control group). The distances from the first metatarsus head and the lateral sesamoid bone to the second metatarsus axis were measured. Subsequently, the coefficients of these distances were determined by the length of the second metatarsus to adjust it for different foot sizes. Results Both the absolute and the relative measures from the first metatarsus head to the second metatarsus axis were significantly different between the groups, with a positive correlation with hallux valgus and intermetatarsal angles. However, neither the absolute nor the relative distance of the lateral sesamoid bone to the second metatarsus was different between the groups, as they did not correlate with hallux valgus or intermetatarsal angles. Conclusion Despite the medial deviation of the first metatarsus in hallux valgus, the sesamoid bone maintains its relationship with the second metatarsus in the transverse plane. This apparent lateral displacement may lead to misinterpretation of these radiographs. This fact is of paramount importance in the pre-, intra-, and postoperative period of patients with hallux valgus.
Published: 2019
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48. HSD17B13 and Chronic Liver Disease in Blacks and Hispanics.

Author: Kozlitina J, Stender S, Hobbs HH, and Cohen JC
Subjects: Adult, Child, Chronic Disease, Frameshift Mutation, Genetic Predisposition to Disease, Hispanic or Latino, Humans, Liver chemistry, Triglycerides analysis, 17-Hydroxysteroid Dehydrogenases genetics, Black or African American, Liver Diseases ethnology, Liver Diseases genetics, Loss of Function Mutation
Published: 2018
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49. Patatin-like phospholipase domain-containing protein 3 promotes transfer of essential fatty acids from triglycerides to phospholipids in hepatic lipid droplets.

Author: Mitsche MA, Hobbs HH, and Cohen JC
Published: 2018
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50. Relationship between genetic variation at PPP1R3B and levels of liver glycogen and triglyceride.

Author: Stender S, Smagris E, Lauridsen BK, Kofoed KF, Nordestgaard BG, Tybjaerg-Hansen A, Pennacchio LA, Dickel DE, Cohen JC, and Hobbs HH
Subjects: Adult, Aged, Animals, Female, Genetic Variation, Humans, Male, Mice, Middle Aged, Liver chemistry, Liver Glycogen analysis, Protein Phosphatase 1 genetics, Triglycerides analysis
Abstract: Genetic variation at rs4240624 on chromosome 8 is associated with an attenuated signal on hepatic computerized tomography, which has been attributed to changes in hepatic fat. The closest coding gene to rs4240624, PPP1R3B, encodes a protein that promotes hepatic glycogen synthesis. Here, we performed studies to determine whether the x-ray attenuation associated with rs4240624 is due to differences in hepatic glycogen or hepatic triglyceride content (HTGC). A sequence variant in complete linkage disequilibrium with rs4240624, rs4841132, was genotyped in the Dallas Heart Study (DHS), the Dallas Liver Study, and the Copenhagen Cohort (n = 112,428) of whom 1,539 had nonviral liver disease. The minor A-allele of rs4841132 was associated with increased hepatic x-ray attenuation (n = 1,572; P = 4 × 10 -5 ), but not with HTGC (n = 2,674; P = 0.58). Rs4841132-A was associated with modest, but significant, elevations in serum alanine aminotransferase (ALT) in the Copenhagen Cohort (P = 3 × 10 -4 ) and the DHS (P = 0.004), and with odds ratios for liver disease of 1.13 (95% CI, 0.97-1.31) and 1.23 (1.01-1.51), respectively. Mice lacking protein phosphatase 1 regulatory subunit 3B (PPP1R3B) were deficient in hepatic glycogen, whereas HTGC was unchanged. Hepatic overexpression of PPP1R3B caused accumulation of hepatic glycogen and elevated plasma levels of ALT, but did not change HTGC., Conclusion: These observations are consistent with the notion that the minor allele of rs4841132 promotes a mild form of hepatic glycogenosis that is associated with hepatic injury. (Hepatology 2018;67:2182-2195)., (© 2017 by the American Association for the Study of Liver Diseases.)
Published: 2018
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