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  • Breast and Cervical Cancer Screening Literacy Among Korean American Women: A Community Health Worker-Led Intervention. American journal of public health Han, H., Song, Y., Kim, M., Hedlin, H. K., Kim, K., Ben Lee, H., Roter, D. 2017; 107 (1): 159-165

    Abstract

    To test a community health worker (CHW)-led health literacy intervention on mammogram and Papanicolaou test screening among Korean American women.We conducted a cluster-randomized trial at 23 ethnic churches in the Baltimore, Maryland-Washington, DC, metropolitan area between 2010 and 2014. Trained CHWs enrolled 560 women. The intervention group received an individually tailored cancer-screening brochure followed by CHW-led health literacy training and monthly telephone counseling with navigation assistance. Study outcomes included receipt of an age-appropriate cancer screening test, health literacy, cancer knowledge, and perceptions about cancer screening at 6 months.The odds of having received a mammogram were 18.5 (95% confidence interval [CI] = 9.2, 37.4) times higher in the intervention than in the control group, adjusting for covariates. The odds of receiving a Papanicolaou test were 13.3 (95% CI = 7.9, 22.3) times higher; the odds of receiving both tests were 17.4 (95% CI = 7.5, 40.3) times higher. Intervention effects also included increases in health literacy and positive perceptions about cancer screening.A health literacy-focused CHW intervention successfully promoted cancer-screening behaviors and related cognitive and attitudinal outcomes in Korean American women.

    View details for PubMedID 27854539

  • LOCALIZATION AND BROADBAND FOLLOW-UP OF THE GRAVITATIONAL-WAVE TRANSIENT GW 150914 ASTROPHYSICAL JOURNAL LETTERS Abbott, B. P., Abbott, R., Abbott, T. D., ABERNATHY, M. R., Acernese, F., Ackley, K., Adams, C., Adams, T., Addesso, P., Adhikari, R. X., Adya, V. B., Affeldt, C., Agathos, M., Agatsuma, K., Aggarwal, N., Aguiar, O. D., Aiello, L., Ain, A., Ajith, P., Allen, B., ALLOCCA, A., Altin, P. A., Anderson, S. B., Anderson, W. G., Arai, K., Araya, M. C., Arceneaux, C. C., Areeda, J. S., Arnaud, N., Arun, K. G., Ascenzi, S., Ashton, G., Ast, M., Aston, S. M., Astone, P., Aufmuth, P., Aulbert, C., Babak, S., Bacon, P., Bader, M. K., Baker, P. T., Baldaccini, F., Ballardin, G., Ballmer, S. W., Barayoga, J. C., Barclay, S. E., Barish, B. C., Barker, D., Barone, F., Barr, B., Barsotti, L., Barsuglia, M., BARTA, D., Barthelmy, S., Bartlett, J., Bartos, I., BASSIRI, R., Basti, A., Batch, J. C., Baune, C., Bavigadda, V., Bazzan, M., Behnke, B., Bejger, M., Bell, A. S., Bell, C. J., Berger, B. K., Bergman, J., Bergmann, G., Berry, C. P., Bersanetti, D., Bertolini, A., Betzwieser, J., Bhagwat, S., Bhandare, R., Bilenko, I. A., Billingsley, G., Birch, J., BIRNEY, R., Biscans, S., BISHT, A., Bitossi, M., Bitossi, M., Bizouard, M. A., Blackburn, J. K., Blair, C. D., Blair, D. G., Blair, R. M., Bloemen, S., Bock, O., Bodiya, T. P., Boer, M., Bogaert, G., Bogan, C., Bohe, A., Bojtos, P., Bond, C., Bondu, F., Bonnand, R., Boom, B. A., Bork, R., Boschi, V., Bose, S., Bouffanais, Y., Bozzi, A., Bradaschia, C., Brady, P. R., Braginsky, V. B., Branchesi, M., Brau, J. E., Briant, T., Brillet, A., Brinkmann, M., Brisson, V., Brockill, P., Brooks, A. F., Brown, D. A., Brown, D. D., Brown, N. M., BUCHANAN, C. C., Buikema, A., Bulik, T., Bulten, H. J., Buonanno, A., Buskulic, D., Buy, C., Byer, R. L., Cadonati, L., Cagnoli, G., Cahillane, C., Bustillo, J. C., Callister, T., Calloni, E., Camp, J. B., Cannon, K. C., Cao, J., Capano, C. D., Capocasa, E., Carbognani, F., Caride, S., Diaz, J. C., Casentini, C., Caudill, S., Cavaglia, M., Cavalier, F., Cavalieri, R., Cella, G., Cepeda, C. B., Baiardi, L. C., Cerretani, G., Cesarini, E., Chakraborty, R., Chalermsongsak, T., Chamberlin, S. J., Chan, M., Chao, S., Charlton, P., Chassande-Mottin, E., Chen, H. Y., Chen, Y., Cheng, C., Chincarini, A., Chiummo, A., Cho, H. S., Cho, M., Chow, J. H., Christensen, N., Chu, Q., Chua, S., Chung, S., Ciani, G., CLARA, F., Clark, J. A., Clark, J. A., Coccia, E., Cohadon, P., Colla, A., Collette, C. G., Cominsky, L., Constancio, M., Conte, A., Conti, L., Cook, D., Corbitt, T. R., Cornish, N., Corsi, A., Cortese, S., Costa, C. A., Coughlin, M. W., Coughlin, S. B., Coulon, J., Countryman, S. T., Couvares, P., Cowan, E. E., Coward, D. M., Cowart, M. J., COYNE, D. C., Coyne, R., Craig, K., Creighton, J. D., Cripe, J., Crowder, S. G., Cumming, A., Cunningham, L., Cuoco, E., Dal Canton, T., Danilishin, S. 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C., Ferrini, F., Fidecaro, F., Fiori, I., Fiorucci, D., Fisher, R. P., Flaminio, R., Fletcher, M., Fournier, J., Franco, S., Frasca, S., Frasconi, F., Frei, Z., Freise, A., Frey, R., Frey, V., Fricke, T. T., Fritschel, P., Frolov, V. V., Fulda, P., Fyffe, M., Gabbard, H. A., Gair, J. R., Gammaitoni, L., Gaonkar, S. G., Garufi, F., Gatto, A., Gaur, G., Gehrels, N., Gemme, G., Gendre, B., Genin, E., Gennai, A., George, J., GERGELY, L., Germain, V., Ghosh, A., Ghosh, S., Giaime, J. A., Giardina, K. D., Giazotto, A., Gill, K., Glaefke, A., Goetz, E., Goetz, R., Gondan, L., Gonzalez, G., Castro, J. M., Gopakumar, A., Gordon, N. A., Gorodetsky, M. L., Gossan, S. E., Gosselin, M., Gouaty, R., Graef, C., Graff, P. B., Granata, M., Grant, A., Gras, S., Gray, C., Greco, G., Green, A. C., Groot, P., GROTE, H., Grunewald, S., Guidi, G. M., Guo, X., Gupta, A., Gupta, M. K., Gushwa, K. E., Gustafson, E. K., Gustafson, R., HACKER, J. J., Hall, B. R., Hall, E. D., Hammond, G., Haney, M., HANKE, M. M., Hanks, J., Hanna, C., Hannam, M. D., Hanson, J., Hardwick, T., Haris, K., Harms, J., Harry, G. M., Harry, I. W., Hart, M. J., HARTMAN, M. T., Haster, C., Haughian, K., Heidmann, A., Heintze, M. C., Heitmann, H., Hello, P., Hemming, G., Hendry, M., Heng, I. S., Hennig, J., Heptonstall, A. W., Heurs, M., Hild, S., Hoak, D., HODGE, K. A., Hofman, D., Hollitt, S. E., Holt, K., Holz, D. E., Hopkins, P., Hosken, D. J., Hough, J., Houston, E. A., Howell, E. J., Hu, Y. M., Huang, S., Huerta, E. A., Huet, D., Hughey, B., Husa, S., Huttner, S. H., Huynh-Dinh, T., Idrisy, A., Indik, N., Ingram, D. R., Inta, R., Isa, H. N., Isac, J., Isi, M., Islas, G., Isogai, T., Iyer, B. R., Izumi, K., Jacqmin, T., Jang, H., Jani, K., Jaranowski, P., Jawahar, S., Jimenez-Forteza, F., Johnson, W. W., Jones, D. I., Jones, R., Jonker, R. J., Ju, L., Kalaghatgi, C. V., Kalogera, V., Kandhasamy, S., Kang, G., Kanner, J. B., Karki, S., Kasprzack, M., Katsavounidis, E., Katzman, W., Kaufer, S., Kaur, T., Kawabe, K., Kawazoe, F., Kefelian, F., Kehl, M. S., Keitel, D., Kelley, D. B., Kells, W., Kennedy, R., Key, J. S., Khalaidovski, A., Khalili, F. Y., Khan, I., Khan, S., Khan, Z., Khazanov, E. A., Kijbunchoo, N., Kim, C., Kim, J., Kim, K., Kim, N., Kim, N., Kim, Y., King, E. J., King, P. J., KINZEL, D. L., Kissel, J. S., Kleybolte, L., Klimenko, S., Koehlenbeck, S. M., Kokeyama, K., Koley, S., Kondrashov, V., Kontos, A., Korobko, M., Korth, W. Z., Kowalska, I., Kozak, D. B., Kringel, V., Krolak, A., Krueger, C., Kuehn, G., Kumar, P., Kuo, L., Kuo, L., Lackey, B. D., Landry, M., Lange, J., Lantz, B., Lasky, P. D., Lazzarini, A., Lazzaro, C., Leaci, P., Leavey, S., LeBigot, E. O., Lee, C. H., Lee, H. K., Lee, H. M., Lee, K., Lenon, A., Leonardi, M., Leong, J. R., Leroy, N., Letendre, N., Levin, Y., Levine, B. M., Li, T. G., Libson, A., Littenberg, T. B., Lockerbie, N. A., Logue, J., Lombardi, A. L., Lord, J. E., Lorenzini, M., Loriette, V., Lormand, M., Losurdo, G., Losurdo, G., Lueck, H., Lundgren, A. P., Luo, J., Lynch, R., Ma, Y., MacDonald, T., Machenschalk, B., MacInnis, M., Macleod, D. M., Magana-Sandoval, F., Magee, R. M., Mageswaran, M., Majorana, E., Maksimovic, I., Malvezzi, V., Man, N., Mandel, I., Mandic, V., Mangano, V., Mansell, G. L., Manske, M., Mantovani, M., Marchesoni, F., Marion, F., Marka, S., Marka, Z., Markosyan, A. S., Maros, E., Martelli, F., Martellini, L., MARTIN, I. W., Martin, R. M., Martynov, D. V., Marx, J. N., Mason, K., Masserot, A., Massinger, T. J., Masso-Reid, M., Matichard, F., Matone, L., Mavalvala, N., Mazumder, N., Mazzolo, G., McCarthy, R., McClelland, D. E., McCormick, S., McGuire, S. C., McIntyre, G., McIver, J., McManus, D. J., McWilliams, S. T., Meacher, D., Meadors, G. D., MEIDAM, J., Melatos, A., Mendell, G., Mendoza-Gandara, D., Mercer, R. A., Merilh, E., MERZOUGUI, M., Meshkov, S., Messenger, C., Messick, C., Meyers, P. 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A., Konig, S., RENDON, F., Mateo Sanguino, T. d., Fernandez-Munoz, R., Yock, P. C., Rattenbury, N., Allen, W. H., QUEREL, R., Jeong, S., Park, I. H., Bai, J., Cui, C., Fan, Y., Wang, C., Hiriart, D., Lee, W. H., Claret, A., Sanchez-Ramirez, R., Pandey, S. B., Mediavilla, T., Sabau-Graziati, L., Abbott, T. M., Abdalla, F. B., Allam, S., Annis, J., Armstrong, R., Benoit-Levy, A., Berger, E., Bernstein, R. A., Bertin, E., BROUT, D., Buckley-Geer, E., Burke, D. L., Capozzi, D., Carretero, J., Castander, F. J., Chornock, R., Cowperthwaite, P. S., Cowperthwaite, P. S., Cunha, C. E., D'Andrea, C. B., da Costa, L. N., Desai, S., Diehl, H. T., Dietrich, J. P., Doctor, Z., Drlica-Wagner, A., Drout, M. R., Eifler, T. F., Estrada, J., Evrard, A. E., Fernandez, E., Finley, D. A., Flaugher, B., Fong, W., Fosalba, P., Fox, D. B., Frieman, J., Fryer, C. L., Gaztanaga, E., Gerdes, D. W., Goldstein, D. A., Gruen, D., Gruendl, R. A., Gutierrez, G., Herner, K., Honscheid, K., James, D. J., Johnson, M. 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  • Plasma-Enhanced Atomic Layer Deposition of SiN-AIN Composites for Ultra Low Wet Etch Rates in Hydrofluoric Acid ACS APPLIED MATERIALS & INTERFACES Kim, Y., Provine, J., Waich, S. P., Park, J., Phuthong, W., Dadlani, A. L., Kim, H., Schindier, P., Kim, K., Prinz, F. B. 2016; 8 (27): 17599-17605

    Abstract

    The continued scaling in transistors and memory elements has necessitated the development of atomic layer deposited (ALD) of hydrofluoric acid (HF) etch resistant and electrically insulating films for sidewall spacer processing. Silicon nitride (SiN) has been the prototypical material for this need and extensive work has been conducted into realizing sufficiently lower wet etch rates (WERs) as well as leakage currents to meet industry needs. In this work, we report on the development of plasma-enhanced atomic layer deposition (PEALD) composites of SiN and AlN to minimize WER and leakage current density. In particular, the role of aluminum and the optimum amount of Al contained in the composite structures have been explored. Films with near zero WER in dilute HF and leakage currents density similar to pure PEALD SiN films could be simultaneously realized through composites which incorporate ≥13 at. % Al, with a maximum thermal budget of 350 °C.

    View details for DOI 10.1021/acsami.6b03194

    View details for Web of Science ID 000379794100069

    View details for PubMedID 27295338

  • Correlation of film density and wet etch rate in hydrofluoric acid of plasma enhanced atomic layer deposited silicon nitride AIP ADVANCES Provine, J., Schindler, P., Kim, Y., Walch, S. P., Kim, H. J., Kim, K., Prinz, F. B. 2016; 6 (6)

    View details for DOI 10.1063/1.4954238

    View details for Web of Science ID 000379041400012

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R., Sarwal, M. M., Sasakawa, C., Sasaki, M., Sass, M., Sato, K., Sato, M., Satriano, J., Savaraj, N., Saveljeva, S., Schaefer, L., Schaible, U. E., Scharl, M., Schatzl, H. M., Schekman, R., Scheper, W., Schiavi, A., Schipper, H. M., Schmeisser, H., Schmidt, J., Schmitz, I., Schneider, B. E., Schneider, E. M., Schneider, J. L., Schon, E. A., Schoenenberger, M. J., Schoenthal, A. H., Schorderet, D. F., Schroeder, B., Schuck, S., Schulze, R. J., Schwarten, M., Schwarz, T. L., Sciarretta, S., Scotto, K., Scovassi, A. I., Screaton, R. A., Screen, M., Seca, H., Sedej, S., Segatori, L., Segev, N., Seglen, P. O., Segui-Simarro, J. M., Segura-Aguilar, J., Seiliez, I., Seki, E., Sell, C., Semenkovich, C. F., Semenza, G. L., Sen, U., Serra, A. L., Serrano-Puebla, A., Sesaki, H., Setoguchi, T., Settembre, C., Shacka, J. J., Shajahan-Haq, A. N., Shapiro, I. M., Sharma, S., She, H., Shen, C. J., Shen, C., Shen, H., Shen, S., Shen, W., Sheng, R., Sheng, X., Sheng, Z., Shepherd, T. G., Shi, J., Shi, Q., Shi, Q., Shi, Y., Shibutani, S., Shibuya, K., Shidoji, Y., Shieh, J., Shih, C., Shimada, Y., Shimizu, S., Shin, D. W., Shinohara, M. L., Shintani, M., Shintani, T., Shioi, T., Shirabe, K., Shiri-Sverdlov, R., Shirihai, O., Shore, G. C., Shu, C., Shukla, D., Sibirny, A. A., Sica, V., Sigurdson, C. J., Sigurdsson, E. M., Sijwali, P. S., Sikorska, B., Silveira, W. A., Silvente-Poirot, S., Silverman, G. A., Simak, J., Simmet, T., Simon, A. K., Simon, H., Simone, C., Simons, M., Simonsen, A., Singh, R., Singh, S. V., Singh, S. K., Sinha, D., Sinha, S., Sinicrope, F. A., Sirko, A., Sirohi, K., Sishi, B. J., Sittler, A., Siu, P. M., Sivridis, E., Skwarska, A., Slack, R., Slaninova, I., Slavov, N., Smaili, S. S., Smalley, K. S., Smith, D. R., Soenen, S. J., Soleimanpour, S. A., Solhaug, A., Somasundaram, K., Son, J. H., Sonawane, A., Song, C., Song, F., Song, H. K., Song, J., Song, W., Soo, K. Y., Sood, A. K., Soong, T. W., Soontornniyomkij, V., Sorice, M., Sotgia, F., Soto-Pantoja, D. R., Sotthibundhu, A., Sousa, M. J., Spaink, H. P., Span, P. N., Spang, A., Sparks, J. D., Speck, P. G., Spector, S. A., Spies, C. D., Springer, W., St Clair, D., Stacchiotti, A., Staels, B., Stang, M. T., Starczynowski, D. T., Starokadomskyy, P., Steegborn, C., Steele, J. W., Stefanis, L., Steffan, J., Stellrecht, C. M., Stenmark, H., Stepkowski, T. M., Stern, S. T., Stevens, C., Stockwell, B. R., Stoka, V., Storchova, Z., Stork, B., Stratoulias, V., Stravopodis, D. J., Strnad, P., Strohecker, A. M., Stroem, A., Stromhaug, P., Stulik, J., Su, Y., Su, Z., Subauste, C. S., Subramaniam, S., Sue, C. M., Suh, S. W., Sui, X., Sukseree, S., Sulzer, D., Sun, F., Sun, J., Sun, J., Sun, S., Sun, Y., Sun, Y., Sun, Y., Sundaramoorthy, V., Sung, J., Suzuki, H., Suzuki, K., Suzuki, N., Suzuki, T., Suzuki, Y. J., Swanson, M. S., Swanton, C., Swaerd, K., Swarup, G., Sweeney, S. T., Sylvester, P. W., Szatmari, Z., Szegezdi, E., Szlosarek, P. W., Taegtmeyer, H., Tafani, M., Taillebourg, E., Tait, S. W., Takacs-Vellai, K., Takahashi, Y., Takats, S., Takemura, G., Takigawa, N., Talbot, N. J., Tamagno, E., Tamburini, J., Tan, C., Tan, L., Tan, M. L., Tan, M., Tan, Y., Tanaka, K., Tanaka, M., Tang, D., Tang, D., Tang, G., Tanida, I., Tanji, K., Tannous, B. A., Tapia, J. A., Tasset-Cuevas, I., Tatar, M., Tavassoly, I., Tavernarakis, N., Taylor, A., Taylor, G. S., Taylor, G. A., Taylor, J. P., Taylor, M. J., Tchetina, E. V., Tee, A. R., Teixeira-Clerc, F., Telang, S., Tencomnao, T., Teng, B., Teng, R., Terro, F., Tettamanti, G., Theiss, A. L., Theron, A. E., Thomas, K. J., Thome, M. P., Thomes, P. G., Thorburn, A., Thorner, J., Thum, T., Thumm, M., Thurston, T. L., Tian, L., Till, A., Ting, J. P., Titorenko, V. I., Toker, L., Toldo, S., Tooze, S. A., Topisirovic, I., Torgersen, M. L., Torosantucci, L., Torriglia, A., Torrisi, M. R., Tournier, C., Towns, R., Trajkovic, V., Travassos, L. H., Triola, G., Tripathi, D. N., Trisciuoglio, D., Troncoso, R., Trougakos, I. P., Truttmann, A. C., Tsai, K., Tschan, M. P., Tseng, Y., Tsukuba, T., Tsung, A., Tsvetkov, A. S., Tu, S., Tuan, H., Tucci, M., Tumbarello, D. A., Turk, B., Turk, V., Turner, R. F., Tveita, A. A., Tyagi, S. C., Ubukata, M., Uchiyama, Y., Udelnow, A., Ueno, T., Umekawa, M., Umemiya-Shirafuji, R., Underwood, B. R., Ungermann, C., Ureshino, R. P., Ushioda, R., Uversky, V. N., Uzcategui, N. L., Vaccari, T., Vaccaro, M. I., Vachova, L., Vakifahmetoglu-Norberg, H., Valdor, R., Valente, E. M., Vallette, F., Valverde, A. M., Van den Berghe, G., Van Den Bosch, L., van den Brink, G. R., van der Goot, F. G., van der Klei, I. J., van der Laan, L. J., van Doorn, W. G., van Egmond, M., van Golen, K. L., Van Kaer, L., Campagne, M. v., Vandenabeele, P., Vandenberghe, W., Vanhorebeek, I., Varela-Nieto, I., Vasconcelos, M. H., Vasko, R., Vavvas, D. G., Vega-Naredo, I., Velasco, G., Velentzas, A. D., Velentzas, P. D., Vellai, T., Vellenga, E., Vendelbo, M. H., Venkatachalam, K., Ventura, N., Ventura, S., Veras, P. S., Verdier, M., Vertessy, B. G., Viale, A., Vidal, M., Vieira, H. L., Vierstra, R. D., Vigneswaran, N., Vij, N., Vila, M., Villar, M., Villar, V. H., Villarroya, J., Vindis, C., Viola, G., Viscomi, M. T., Vitale, G., Vogl, D. T., Voitsekhovskaja, O. V., von Haefen, C., von Schwarzenberg, K., Voth, D. E., Vouret-Craviari, V., Vuori, K., Vyas, J. M., Waeber, C., Walker, C. L., Walker, M. J., Walter, J., Wan, L., Wan, X., Wang, B., Wang, C., Wang, C., Wang, C., Wang, C., Wang, C., Wang, D., Wang, F., Wang, F., Wang, G., Wang, H., Wang, H., Wang, H., Wang, H., Wang, H., Wang, J., Wang, J., Wang, M., Wang, M., Wang, P., Wang, P., Wang, R. C., Wang, S., Wang, T., Wang, X., Wang, X., Wang, X., Wang, X., Wang, X., Wang, Y., Wang, Y., Wang, Y., Wang, Y., Wang, Y., Wang, Y., Wang, Y. T., Wang, Y., Wang, Z., Wappner, P., Ward, C., Ward, D. M., Warnes, G., Watada, H., Watanabe, Y., Watase, K., Weaver, T. E., Weekes, C. D., Wei, J., Weide, T., Weihl, C. C., Weindl, G., Weis, S. N., Wen, L., Wen, X., Wen, Y., Westermann, B., Weyand, C. M., White, A. R., White, E., Whitton, J. L., Whitworth, A. J., Wiels, J., Wild, F., Wildenberg, M. E., Wileman, T., Wilkinson, D. S., Wilkinson, S., Willbold, D., Williams, C., Williams, K., Williamson, P. R., Winklhofer, K. F., Witkin, S. S., Wohlgemuth, S. E., Wollert, T., Wolvetang, E. J., Wong, E., Wong, G. W., Wong, R. W., Wong, V. K., Woodcock, E. A., Wright, K. L., Wu, C., Wu, D., Wu, G. S., Wu, J., Wu, J., Wu, M., Wu, M., Wu, S., Wu, W. K., Wu, Y., Wu, Z., Xavier, C. P., Xavier, R. J., Xia, G., Xia, T., Xia, W., Xia, Y., Xiao, H., Xiao, J., Xiao, S., Xiao, W., Xie, C., Xie, Z., Xie, Z., Xilouri, M., Xiong, Y., Xu, C., Xu, C., Xu, F., Xu, H., Xu, H., Xu, J., Xu, J., Xu, J., Xu, L., Xu, X., Xu, Y., Xu, Y., Xu, Z., Xu, Z., Xue, Y., Yamada, T., Yamamoto, A., Yamanaka, K., Yamashina, S., Yamashiro, S., Yan, B., Yan, B., Yan, X., Yan, Z., Yanagi, Y., Yang, D., Yang, J., Yang, L., Yang, M., Yang, P., Yang, P., Yang, Q., Yang, W., Yang, W. Y., Yang, X., Yang, Y., Yang, Y., Yang, Z., Yang, Z., Yao, M., Yao, P. J., Yao, X., Yao, Z., Yao, Z., Yasui, L. S., Ye, M., Yedvobnick, B., Yeganeh, B., Yeh, E. S., Yeyati, P. L., Yi, F., Yi, L., Yin, X., Yip, C. K., Yoo, Y., Yoo, Y. H., Yoon, S., Yoshida, K., Yoshimori, T., Young, K. H., Yu, H., Yu, J. J., Yu, J., Yu, J., Yu, L., Yu, W. H., Yu, X., Yu, Z., Yuan, J., Yuan, Z., Yue, B. Y., Yue, J., Yue, Z., Zacks, D. N., Zacksenhaus, E., Zaffaroni, N., Zaglia, T., Zakeri, Z., Zecchini, V., Zeng, J., Zeng, M., Zeng, Q., Zervos, A. S., Zhang, D. D., Zhang, F., Zhang, G., Zhang, G., Zhang, H., Zhang, H., Zhang, H., Zhang, H., Zhang, J., Zhang, J., Zhang, J., Zhang, J., Zhang, J., Zhang, L., Zhang, L., Zhang, L., Zhang, L., Zhang, M., Zhang, X., Zhang, X. D., Zhang, Y., Zhang, Y., Zhang, Y., Zhang, Y., Zhang, Y., Zhao, M., Zhao, W., Zhao, X., Zhao, Y. G., Zhao, Y., Zhao, Y., Zhao, Y., Zhao, Z., Zhao, Z. J., Zheng, D., Zheng, X., Zheng, X., Zhivotovsky, B., Zhong, Q., Zhou, G., Zhou, G., Zhou, H., Zhou, S., Zhou, X., Zhu, H., Zhu, H., Zhu, W., Zhu, W., Zhu, X., Zhu, Y., Zhuang, S., Zhuang, X., Ziparo, E., Zois, C. E., Zoladek, T., Zong, W., Zorzano, A., Zughaier, S. M. 2016; 12 (1): 1-222

    View details for DOI 10.1080/15548627.2015.1100356

    View details for PubMedID 26799652

  • Body Fat Distribution and Risk of Incident and Regressed Nonalcoholic Fatty Liver Disease CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Kim, D., Chung, G. E., Kwak, M., Seo, H. B., Kang, J. H., Kim, W., Kim, Y. J., Yoon, J., Lee, H., Kim, C. Y. 2016; 14 (1): 132-?

    Abstract

    Some studies have examined correlations between visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) with nonalcoholic fatty liver disease (NAFLD) or between VAT and NAFLD. We investigated the longitudinal association between body fat distribution (VAT vs SAT) and incidence and regression of NAFLD, adjusting for risk factors, in a large population-based cohort.We collected data from adults who underwent abdominal ultrasonography (to identify liver fat), abdominal fat computed tomography scan, and blood tests from March 2007 through December 2008. Each patient underwent an anthropometric assessment and completed a questionnaire about their medical history, physical activity, and diet. Our final analysis involved 2017 subjects from the initial cohort who participated in a voluntary follow-up health screen performed in 2011 and 2013. The median follow-up time was 4.43 years.We found 288 incident cases of NAFLD; 159 patients had NAFLD regression during the follow-up period. An increasing area of VAT was associated with higher incidence of NAFLD in the multivariable analysis (highest quintile vs lowest quintile of VAT hazard ratio [HR], 2.23; 95% confidence interval [CI], 1.28-3.89; P for trend = .002; HR, 1.36 [per 1 standard deviation]; 95% CI, 1.16-1.59). An increased area of SAT was significantly associated with regression of NAFLD (highest quintile vs lowest quintile of SAT HR, 2.30; 95% CI, 1.28-4.12; P for trend = .002; HR, 1.36 [per 1 standard deviation]; 95% CI, 1.08-1.72).In a large cohort study, larger areas of VAT were longitudinally associated with higher risk of incident NAFLD (during a period of approximately 4 years). In contrast, larger areas of SAT were longitudinally associated with regression of NAFLD. These data indicate that certain types of body fat are risk factors for NAFLD, whereas other types could reduce risk for NAFLD.

    View details for DOI 10.1016/j.cgh.2015.07.024

    View details for PubMedID 26226099

  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE Sampson, J. N., Wheeler, W. A., Yeager, M., Panagiotou, O., Wang, Z., Berndt, S. I., Lan, Q., Abnet, C. C., Amundadottir, L. T., Figueroa, J. D., Landi, M. T., Mirabello, L., Savage, S. A., Taylor, P. R., De Vivo, I., McGlynn, K. A., Purdue, M. P., Rajaraman, P., Adami, H., Ahlbom, A., Albanes, D., Amary, M. F., An, S., Andersson, U., Andriole, G., Andrulis, I. L., Angelucci, E., Ansell, S. M., Arici, C., Armstrong, B. K., Arslan, A. A., Austin, M. A., Baris, D., Barkauskas, D. A., Bassig, B. A., Becker, N., Benavente, Y., Benhamou, S., Berg, C., Van Den Berg, D., Bernstein, L., Bertrand, K. A., Birmann, B. M., Black, A., Boeing, H., Boffetta, P., Boutron-Ruault, M., Bracci, P. M., Brinton, L., Brooks-Wilson, A. R., Bueno-de-Mesquita, H. B., Burdett, L., Buring, J., Butler, M. A., Cai, Q., Cancel-Tassin, G., Canzian, F., Carrato, A., Carreon, T., Carta, A., Chan, J. K., Chang, E. T., Chang, G., Chang, I., Chang, J., Chang-Claude, J., Chen, C., Chen, C., Chen, C., Chen, C., Chen, C., Chen, H., Chen, K., Chen, K., Chen, K., Chen, Y., Chen, Y., Chen, Y., Chen, Y., Chien, L., Chirlaque, M., Choi, J. E., Choi, Y. Y., Chow, W., Chung, C. C., Clavel, J., Clavel-Chapelon, F., Cocco, P., Colt, J. S., Comperat, E., Conde, L., Connors, J. M., Conti, D., Cortessis, V. K., Cotterchio, M., Cozen, W., Crouch, S., Crous-Bou, M., Cussenot, O., Davis, F. G., Ding, T., Diver, W. R., Dorronsoro, M., Dossus, L., Duell, E. J., Ennas, M. G., Erickson, R. L., Feychting, M., Flanagan, A. M., Foretova, L., Fraumeni, J. F., Freedman, N. D., Freeman, L. E., Fuchs, C., Gago-Dominguez, M., Gallinger, S., Gao, Y., Gapstur, S. M., Garcia-Closas, M., Garcia-Closas, R., Gascoyne, R. D., Gastier-Foster, J., Gaudet, M. M., Gaziano, J. M., Giffen, C., Giles, G. G., Giovannucci, E., Glimelius, B., Goggins, M., Gokgoz, N., Goldstein, A. M., Gorlick, R., Gross, M., Grubb, R., Gu, J., Guan, P., Gunter, M., Guo, H., Habermann, T. M., Haiman, C. A., Halai, D., Hallmans, G., Hassan, M., Hattinger, C., He, Q., He, X., Helzlsouer, K., Henderson, B., Henriksson, R., Hjalgrim, H., Hoffman-Bolton, J., Hohensee, C., Holford, T. R., Holly, E. A., Hong, Y., Hoover, R. N., Horn-Ross, P. L., Hosain, G. M., Hosgood, H. D., Hsiao, C., Hu, N., Hu, W., Hu, Z., Huang, M., Huerta, J., Hung, J., Hutchinson, A., Inskip, P. D., Jackson, R. D., Jacobs, E. J., Jenab, M., Jeon, H., Ji, B., Jin, G., Jin, L., Johansen, C., Johnson, A., Jung, Y. J., Kaaks, R., Kamineni, A., Kane, E., Kang, C. H., Karagas, M. R., Kelly, R. S., Khaw, K., Kim, C., Kim, H. N., Kim, J. H., Kim, J. S., Kim, Y. H., Kim, Y. T., Kim, Y., Kitahara, C. M., Klein, A. P., Klein, R. J., Kogevinas, M., Kohno, T., Kolonel, L. N., Kooperberg, C., Kricker, A., Krogh, V., Kunitoh, H., Kurtz, R. C., Kweon, S., LaCroix, A., Lawrence, C., Lecanda, F., Lee, V. H., Li, D., Li, H., Li, J., Li, Y., Li, Y., Liao, L. M., Liebow, M., Lightfoot, T., Lim, W., Lin, C., Lin, D., Lindstrom, S., Linet, M. S., Link, B. K., Liu, C., Liu, J., Liu, L., Ljungberg, B., Lloreta, J., di Lollo, S., Lu, D., Lund, E., Malats, N., Mannisto, S., Le Marchand, L., Marina, N., Masala, G., Mastrangelo, G., Matsuo, K., Maynadie, M., McKay, J., McKean-Cowdin, R., Melbye, M., Melin, B. S., Michaud, D. S., Mitsudomi, T., Monnereau, A., Montalvan, R., Moore, L. E., Mortensen, L. M., Nieters, A., North, K. E., Novak, A. J., Oberg, A. L., Offit, K., Oh, I., Olson, S. H., Palli, D., Pao, W., Park, I. K., Park, J. Y., Park, K. H., Patino-Garcia, A., Pavanello, S., Peeters, P. H., Perng, R., Peters, U., Petersen, G. M., Picci, P., Pike, M. C., Porru, S., Prescott, J., Prokunina-Olsson, L., Qian, B., Qiao, Y., Rais, M., Riboli, E., Riby, J., Risch, H. A., Rizzato, C., Rodabough, R., Roman, E., Roupret, M., Ruder, A. M., de Sanjose, S., Scelo, G., Schned, A., Schumacher, F., Schwartz, K., Schwenn, M., Scotlandi, K., Seow, A., Serra, C., Serra, M., Sesso, H. D., Setiawan, V. W., Severi, G., Severson, R. K., Shanafelt, T. D., Shen, H., Shen, W., Shin, M., Shiraishi, K., Shu, X., Siddiq, A., Sierrasesumaga, L., Sihoe, A. D., Skibola, C. F., Smith, A., Smith, M. T., Southey, M. C., Spinelli, J. J., Staines, A., Stampfer, M., Stern, M. C., Stevens, V. L., Stolzenberg-Solomon, R. S., Su, J., Su, W., Sund, M., Sung, J. S., Sung, S. W., Tan, W., Tang, W., Tardon, A., Thomas, D., Thompson, C. A., Tinker, L. F., Tirabosco, R., Tjonneland, A., Travis, R. C., Trichopoulos, D., Tsai, F., Tsai, Y., Tucker, M., Turner, J., Vajdic, C. M., Vermeulen, R. C., Villano, D. J., Vineis, P., Virtamo, J., Visvanathan, K., Wactawski-Wende, J., Wang, C., Wang, C., Wang, J., Wang, J., Wei, F., Weiderpass, E., Weiner, G. J., Weinstein, S., Wentzensen, N., White, E., Witzig, T. E., Wolpin, B. M., Wong, M. P., Wu, C., Wu, G., Wu, J., Wu, T., Wu, W., Wu, X., Wu, Y., Wunder, J. S., Xiang, Y., Xu, J., Xu, P., Yang, P., Yang, T., Ye, Y., Yin, Z., Yokota, J., Yoon, H., Yu, C., Yu, H., Yu, K., Yuan, J., Zelenetz, A., Zeleniuch-Jacquotte, A., Zhang, X., Zhang, Y., Zhao, X., Zhao, Z., Zheng, H., Zheng, T., Zheng, W., Zhou, B., Zhu, M., Zucca, M., Boca, S. M., Cerhan, J. R., Ferri, G. M., Hartge, P., Hsiung, C. A., Magnani, C., Miligi, L., Morton, L. M., Smedby, K. E., Teras, L. R., Vijai, J., Wang, S. S., Brennan, P., Caporaso, N. E., Hunter, D. J., Kraft, P., Rothman, N., Silverman, D. T., Slager, S. L., Chanock, S. J., Chatterjee, N. 2015; 107 (12)

    Abstract

    Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.

    View details for DOI 10.1093/jnci/djv279

    View details for Web of Science ID 000366970900015

    View details for PubMedID 26464424

    View details for PubMedCentralID PMC4806328

  • Visceral Obesity Predicts Significant Fibrosis in Patients With Nonalcoholic Fatty Liver Disease. Medicine Yu, S. J., Kim, W., Kim, D., Yoon, J., Lee, K., Kim, J. H., Cho, E. J., Lee, J., Kim, H. Y., Kim, Y. J., Kim, C. Y. 2015; 94 (48)

    Abstract

    Nonalcoholic fatty liver disease (NAFLD) is associated with visceral obesity. However, the association between visceral adipose tissue (VAT) area and fibrosis in NAFLD patients has not been completely established. This study was aimed to determine the relationship between the computed tomography-measured VAT area and significant fibrosis in NAFLD patients. A total of 324 NAFLD patients and 132 controls were evaluated by liver biopsy. NAFLD was diagnosed based on histological examinations and alcohol consumption <20 g/day. The NAFLD patients showed a higher age and gender-adjusted VAT area than the control group (86.1 ± 2.3 vs 56.7 ± 3.7, P < 0.001). The VAT area increased across the control, NAFLD without significant fibrosis, and NAFLD with significant fibrosis groups (54.9 ± 3.5, 80.6 ± 2.4, and 123.4 ± 6.4, P < 0.001). This association persisted after adjusting for multiple confounders (P for trend = 0.028). A multivariate regression analysis demonstrated the VAT area was independently associated with NAFLD with significant fibrosis (F2-F4) (odds ratio [OR] 1.21 95% confidence interval [CI] 1.07-1.37 per 10 cm(2) increase of VAT area; OR 2.62 [per 1 - standard deviation (SD)] 95% CI 1.41-4.86). Moreover, a multivariate logistic regression analysis revealed the VAT area was independently associated with nonalcoholic steatohepatitis (NASH) in NAFLD (OR 1.17 95% CI 1.05-1.32 per 10 cm increase of VAT area; OR 2.21 [per 1 - SD] 95% CI 1.25-3.89). Increased VAT area is independently associated with NASH or significant fibrosis and VAT might be a central target for lifestyle modifications in NAFLD patients.

    View details for DOI 10.1097/MD.0000000000002159

    View details for PubMedID 26632897

    View details for PubMedCentralID PMC4674200

  • First Observation of CP Violation in (B)over-bar(0) -> D(CP)((*))h(0) Decays by a Combined Time-Dependent Analysis of BABAR and Belle Data PHYSICAL REVIEW LETTERS Abdesselam, A., Adachi, I., Adametz, A., Adye, T., Ahmed, H., Aihara, H., Akar, S., Alam, M. S., Albert, J., Al Said, S., Andreassen, R., Angelini, C., Anulli, F., Arinstein, K., Arnaud, N., Asner, D. M., Aston, D., Aulchenko, V., Aushev, T., Ayad, R., Babu, V., Badhrees, I., Bahinipati, S., Bakich, A. M., Band, H. R., Banerjee, S., Barberio, E., Bard, D. J., Barlow, R. J., Batignani, G., Beaulieu, A., Bellis, M., Ben-Haim, E., Bernard, D., Bernlochner, F. U., Bettarini, S., Bettoni, D., Bevan, A. J., Bhardwaj, V., Bhuyan, B., Bianchi, F., Biasini, M., BISWAL, J., Blinov, V. E., Bloom, P. C., Bobrov, A., Bomben, M., Bondar, A., Bonneaud, G. R., Bonvicini, G., Bozek, A., Bozzi, C., Bracko, M., Briand, H., Browder, T. E., Brown, D. N., Brown, D. N., Buenger, C., Burchat, P. R., Buzykaev, A. 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M., Roodman, A., Rossi, A., Rostomyan, A., Rotondo, M., Roudeau, P., Sacco, R., Sakai, Y., Sandilya, S., Santelj, L., Santoro, V., Sanuki, T., Sato, Y., Savinov, V., Schindler, R. H., Schneider, O., Schnell, G., Schroeder, T., Schubert, K. R., Schumm, B. A., Schwanda, C., Schwartz, A. J., Schwitters, R. F., Sciacca, C., Seiden, A., Sekula, S. J., Senyo, K., Seon, O., Serednyakov, S. I., Sevior, M. E., Shapkin, M., Shebalin, V., Shen, C. P., Shibata, T., Shiu, J., Simard, M., Simi, G., Simon, F., Simonetto, F., Skovpen, Y. I., Smith, A. J., Smith, J. G., Snyder, A., So, R. Y., Sobie, R. J., Soffer, A., Sohn, Y., Sokoloff, M. D., Sokolov, A., Solodov, E. P., Solovieva, E., Spaan, B., Spanier, S. M., Staric, M., Stocchi, A., Stroili, R., Stugu, B., Su, D., Sullivan, M. K., Sumihama, M., Sumisawa, K., Sumiyoshi, T., Summers, D. J., Sun, L., Tamponi, U., Taras, P., Tasneem, N., Teramoto, Y., Tisserand, V., Todyshev, K. Y., Toki, W. H., Touramanis, C., Trabelsi, K., Tsuboyama, T., Uchida, M., Uglov, T., Unno, Y., Uno, S., Usov, Y., Uwer, U., Vahsen, S. E., van Hulse, C., Vanhoefer, P., Varner, G., Vasseur, G., Va'vra, J., Verderi, M., Vinokurova, A., Vitale, L., Vorobyev, V., Voss, C., Wagner, M. N., Wagner, S. R., Waldi, R., Walsh, J. J., Wang, C. H., Wang, M., Wang, P., Watanabe, Y., West, C. A., Williams, K. M., Wilson, F. F., Wilson, J. R., Wisniewski, W. J., Won, E., Wormser, G., Wright, D. M., Wu, S. L., Wulsin, H. W., Yamamoto, H., Yamaoka, J., Yashchenko, S., Yuan, C. Z., Yusa, Y., Zallo, A., Zhang, C. C., Zhang, Z. P., Zhilich, V., Zhulanov, V., Zupanc, A. 2015; 115 (12)

    Abstract

    We report a measurement of the time-dependent CP asymmetry of B[over ¯]^{0}→D_{CP}^{(*)}h^{0} decays, where the light neutral hadron h^{0} is a π^{0}, η, or ω meson, and the neutral D meson is reconstructed in the CP eigenstates K^{+}K^{-}, K_{S}^{0}π^{0}, or K_{S}^{0}ω. The measurement is performed combining the final data samples collected at the ϒ(4S) resonance by the BABAR and Belle experiments at the asymmetric-energy B factories PEP-II at SLAC and KEKB at KEK, respectively. The data samples contain (471±3)×10^{6} BB[over ¯] pairs recorded by the BABAR detector and (772±11)×10^{6} BB[over ¯] pairs recorded by the Belle detector. We measure the CP asymmetry parameters -η_{f}S=+0.66±0.10(stat)±0.06(syst) and C=-0.02±0.07(stat)±0.03(syst). These results correspond to the first observation of CP violation in B[over ¯]^{0}→D_{CP}^{(*)}h^{0} decays. The hypothesis of no mixing-induced CP violation is excluded in these decays at the level of 5.4 standard deviations.

    View details for DOI 10.1103/PhysRevLett.115.121604

    View details for Web of Science ID 000361316500005

    View details for PubMedID 26430984

  • In situ surface cleaning on a Ge substrate using TMA and MgCp2 for HfO2-based gate oxides JOURNAL OF MATERIALS CHEMISTRY C Oh, I., Kim, K., Lee, Z., Song, J., Lee, C. W., Thompson, D., Lee, H., Kim, W., Maeng, W. J., Kim, H. 2015; 3 (19): 4852-4858

    View details for DOI 10.1039/c4tc02686a

    View details for Web of Science ID 000354209500003

  • The Physics of the B Factories EUROPEAN PHYSICAL JOURNAL C Bevan, A. J., Golob, B., Mannel, T., Prell, S., Yabsley, B. D., Abe, K., Aihara, H., Anulli, F., Arnaud, N., Aushev, T., Beneke, M., Beringer, J., Bianchi, F., Bigi, I. I., Bona, M., Brambilla, N., Brodzicka, J., Chang, P., Charles, M. J., Cheng, C. H., Cheng, H., Chistov, R., Colangelo, P., Coleman, J. P., Drutskoy, A., Druzhinin, V. P., Eidelman, S., Eigen, G., Eisner, A. M., Faccini, R., Flood, K. T., Gambino, P., Gaz, A., Gradl, W., Hayashii, H., Higuchi, T., Hulsbergen, W. D., Hurth, T., Iijima, T., Itoh, R., Jackson, P. D., Kass, R., Kolomensky, Y. G., Kou, E., Krizan, P., Kronfeld, A., Kumano, S., Kwon, Y. J., Latham, T. E., Leith, D. W., Uth, V. L., Martinez-Vidal, F., Meadows, B. T., Mussa, R., Nakao, M., Nishida, S., Ocariz, J., Olsen, S. L., Pakhlov, P., Pakhlova, G., Palano, A., Pich, A., Playfer, S., Poluektov, A., Porter, F. C., Robertson, S. H., Roney, J. 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P., Treadwell, E., Triggiani, G., Trincaz-Duvoid, S., Trischuk, W., Troost, D., Trunov, A., Tsai, K. L., Tsai, Y. T., Tsujita, Y., Tsukada, K., Tsukamoto, T., Tuggle, J. M., Tumanov, A., Tung, Y. W., Turnbull, L., Turner, J., Turri, M., Uchida, K., Uchida, M., Uchida, Y., Ueki, M., Ueno, K., Ueno, K., Ujiie, N., Ulmer, K. A., Unno, Y., Urquijo, P., Ushiroda, Y., Usov, Y., Usseglio, M., Usuki, Y., Uwer, U., Va'vra, J., Vahsen, S. E., Vaitsas, G., Valassi, A., Vallazza, E., Vallereau, A., Vanhoefer, P., van Hoek, W. C., van Hulse, C., Van Winkle, D., Varner, G., Varnes, E. W., Varvell, K. E., Vasileiadis, G., Velikzhanin, Y. S., Verderi, M., Versille, S., Vervink, K., Viaud, B., Vidal, P. B., Villa, S., Villanueva-Perez, P., Vinograd, E. L., Vitale, L., Vitug, G. M., Voss, C., Voci, C., Voena, C., Volk, A., von Wimmersperg-Toeller, J. H., Vorobyev, V., Vossen, A., Vuagnin, G., Vuosalo, C. O., Wacker, K., Wagner, A. P., Wagner, D. L., Wagner, G., Wagner, M. N., Wagner, S. R., Wagoner, D. E., Walker, D., Walkowiak, W., Wallom, D., Wang, C. C., Wang, C. H., Wang, J., Wang, J. G., Wang, K., Wang, L., Wang, L. L., Wang, P., Wang, P., Wang, T. J., Wang, W. F., Wang, X. L., Wang, Y. F., Wappler, F. R., Watanabe, M., Watson, A. T., Watson, J. E., Watson, N. K., Watt, M., Weatherall, J. H., Weaver, M., Weber, T., Wedd, R., Wei, J. T., Weidemann, A. W., Weinstein, A. J., Wenzel, W. A., West, C. A., West, C. G., West, T. J., White, E., White, R. M., Wicht, J., Widhalm, L., Wiechczynski, J., Wienands, U., Wilden, L., Wilder, M., Williams, D. C., Williams, G., Williams, J. C., Williams, K. M., Williams, M. I., Willocq, S. Y., Wilson, J. R., Wilson, M. G., Wilson, R. J., Winklmeier, F., Winstrom, L. O., Winter, M. A., Wisniewski, W. J., Wittgen, M., Wittlin, J., WITTMER, W., Wixted, R., Woch, A., Wogsland, B. J., Won, E., Wong, Q. K., Wray, B. C., Wren, A. C., Wright, D. M., Wu, C. H., Wu, J., Wu, S. L., Wulsin, H. W., Xella, S. M., Xie, Q. L., Xie, Y., Xie, Y., Xu, Z. Z., Yeche, C., Yamada, Y., Yamaga, M., Yamaguchi, A., Yamaguchi, H., Yamaki, T., Yamamoto, H., Yamamoto, N., Yamamoto, R. K., Yamamoto, S., Yamanaka, T., Yamaoka, H., Yamaoka, J., Yamaoka, Y., Yamashita, Y., Yamauchi, M., Yan, D. S., Yan, Y., Yanai, H., Yanaka, S., Yang, H., Yang, R., Yang, S., Yarritu, A. K., Yashchenko, S., Yashima, J., Yasin, Z., Yasu, Y., Ye, S. W., Yeh, P., Yi, J. I., Yi, K., Yi, M., Yin, Z. W., Ying, J., Yocky, G., Yokoyama, K., Yokoyama, M., Yokoyama, T., Yoshida, K., Yoshida, M., Yoshimura, Y., Young, C. C., Yu, C. X., Yu, Z., Yuan, C. Z., Yuan, Y., Yumiceva, F. X., Yusa, Y., Yushkov, A. N., Yuta, H., Zacek, V., Zain, S. B., Zallo, A., Zambito, S., Zander, D., Zang, S. L., Zanin, D., Zaslavsky, B. G., Zeng, Q. L., Zghiche, A., Zhang, B., Zhang, J., Zhang, J., Zhang, L., Zhang, L. M., Zhang, S. Q., Zhang, Z. P., Zhao, H. W., Zhao, H. W., Zhao, M., Zhao, Z. G., Zheng, Y., Zheng, Y. H., Zheng, Z. P., Zhilich, V., Zhou, P., Zhu, R. Y., Zhu, Y. S., Zhu, Z. M., Zhulanov, V., Ziegler, T., Ziegler, V., Zioulas, G., Zisman, M., Zito, M., Zuercher, D., Zwahlen, N., Zyukova, O., Zivko, T., Zontar, D. 2014; 74 (11): I-898
  • Quantitative analysis of computed tomography images and early detection of cerebral edema for pediatric traumatic brain injury patients: retrospective study BMC MEDICINE Kim, H., Kim, G., Yoon, B. C., Kim, K., Kim, B., Choi, Y. H., Czosnyka, M., Oh, B., Kim, D. 2014; 12

    Abstract

    The purpose of this study was to identify whether the distribution of Hounsfield Unit (HU) values across the intracranial area in computed tomography (CT) images can be used as an effective diagnostic tool for determining the severity of cerebral edema in pediatric traumatic brain injury (TBI) patients.CT images, medical records and radiology reports on 70 pediatric patients were collected. Based on radiology reports and the Marshall classification, the patients were grouped as mild edema patients (n=37) or severe edema patients (n=33). Automated quantitative analysis using unenhanced CT images was applied to eliminate artifacts and identify the difference in HU value distribution across the intracranial area between these groups.The proportion of pixels with HU=17 to 24 was highly correlated with the existence of severe cerebral edema (P<0.01). This proportion was also able to differentiate patients who developed delayed cerebral edema from mild TBI patients. A significant difference between deceased patients and surviving patients in terms of the HU distribution came from the proportion of pixels with HU=19 to HU=23 (P<0.01).The proportion of pixels with an HU value of 17 to 24 in the entire cerebral area of a non-enhanced CT image can be an effective basis for evaluating the severity of cerebral edema. Based on this result, we propose a novel approach for the early detection of severe cerebral edema.

    View details for DOI 10.1186/s12916-014-0186-2

    View details for Web of Science ID 000344893100001

    View details for PubMedCentralID PMC4219082

  • Transcriptional activation of hypoxia-inducible factor-1 (HIF-1) in myeloid cells promotes angiogenesis through VEGF and S100A8 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Ahn, G., Seita, J., Hong, B., Kim, Y., Bok, S., Lee, C., Kim, K. S., Lee, J. C., Leeper, N. J., Cooke, J. P., Kim, H. J., Kim, I. H., Weissman, I. L., Brown, J. M. 2014; 111 (7): 2698-2703

    Abstract

    Emerging evidence indicates that myeloid cells are essential for promoting new blood vessel formation by secreting various angiogenic factors. Given that hypoxia-inducible factor (HIF) is a critical regulator for angiogenesis, we questioned whether HIF in myeloid cells also plays a role in promoting angiogenesis. To address this question, we generated a unique strain of myeloid-specific knockout mice targeting HIF pathways using human S100A8 as a myeloid-specific promoter. We observed that mutant mice where HIF-1 is transcriptionally activated in myeloid cells (by deletion of the von Hippel-Lindau gene) resulted in erythema, enhanced neovascularization in matrigel plugs, and increased production of vascular endothelial growth factor (VEGF) in the bone marrow, all of which were completely abrogated by either genetic or pharmacological inactivation of HIF-1. We further found that monocytes were the major effector producing VEGF and S100A8 proteins driving neovascularization in matrigel. Moreover, by using a mouse model of hindlimb ischemia we observed significantly improved blood flow in mice intramuscularly injected with HIF-1-activated monocytes. This study therefore demonstrates that HIF-1 activation in myeloid cells promotes angiogenesis through VEGF and S100A8 and that this may become an attractive therapeutic strategy to treat diseases with vascular defects.

    View details for DOI 10.1073/pnas.1320243111

    View details for Web of Science ID 000331396500062

    View details for PubMedID 24497508

    View details for PubMedCentralID PMC3932909

  • Transarterial chemoembolization in Barcelona Clinic Liver Cancer Stage 0/A hepatocellular carcinoma WORLD JOURNAL OF GASTROENTEROLOGY Kim, H. C., Suk, K. T., Kim, D. J., Yoon, J. H., Kim, Y. S., Baik, G. H., Kim, J. B., Kim, C. H., Sung, H., Choi, J. Y., Han, K. H., Park, S. H. 2014; 20 (3): 745-754

    Abstract

    To evaluate the clinical characteristics of patients with Barcelona Clinic Liver Cancer (BCLC) stage 0 and A hepatocellular carcinoma (HCC) after transarterial chemoembolization (TACE).Between January 2001 and September 2011, 129 patients with BCLC stage 0 and stage A HCC who underwent TACE were retrospectively enrolled. Patient characteristics, routine computed tomography and TACE findings, survival time and 1-, 5-, and 10-year survival rates, risk factors for mortality, and survival rates according to the number of risk factors were assessed.The mean size of HCC tumors was 2.4 ± 1.1 cm, and the mean number of TACE procedures performed was 2.5 ± 2.1. The mean overall survival time and 1-, 5-, and 10-year survival rates were 80.6 ± 4.9 mo and 91%, 63% and 49%, respectively. In the Cox regression analysis, a Child-Pugh score > 5 (P = 0.005, OR = 3.86), presence of arterio-venous shunt (P = 0.032, OR = 4.41), amount of lipiodol used (> 7 mL; P = 0.013, OR = 3.51), and female gender (P = 0.008, OR = 3.47) were risk factors for mortality. The 1-, 5-, and 10-year survival rates according to the number of risk factors present were 96%, 87% and 87% (no risk factors), 89%, 65%, and 35% (1 risk factor), 96%, 48% and unavailable (2 risk factors), and 63%, 17%, and 0% (3 risk factors), respectively (P < 0.001).TACE may be used as curative-intent therapy in patients with BCLC stage 0 and stage A HCC. The Child-Pugh score, arterio-venous shunt, amount of lipiodol used, and gender were related to mortality after TACE.

    View details for DOI 10.3748/wjg.v20.i3.745

    View details for Web of Science ID 000330856400014

    View details for PubMedID 24574748

    View details for PubMedCentralID PMC3921484

  • Diagnostic accuracy of hepatic venous pressure gradient measurement in the prediction of stage 1 compensated liver cirrhosis in patients with chronic hepatitis B. European journal of gastroenterology & hepatology Suk, K. T., Kim, H. C., Namkung, S., Han, S. H., Choi, K. C., Park, S. H., Sung, H. T., Kim, C. H., Kim, S. H., Ham, Y. L., Kang, H. M., Kim, D. J. 2013; 25 (10): 1170-1176

    Abstract

    Hepatic venous pressure gradient (HVPG) of 6-10 mmHg has been accepted as a hemodynamic parameter of stage 1 compensated liver cirrhosis (LC). The diagnostic accuracy of HVPG in the prediction of stage 1 compensated LC has been investigated in patients with chronic hepatitis B (CHB).A total of 219 patients with CHB who underwent HVPG and liver biopsy were enrolled. The diagnostic accuracy of two methods was compared. Risk factors associated with the diagnosis of stage 1 compensated LC on the basis of the findings of HVPG, biopsy, and both HVPG and biopsy were evaluated.The HVPG score was correlated positively with the stage of biopsy (r=0.439). The sensitivity/specificity of HVPG for predicting stage 1 compensated LC were 78/81% in 6 mmHg, respectively. A total of 57 (26%), 28 (13%), and 20 (9%) patients were diagnosed with stage 1 compensated LC on the basis of the findings of HVPG, biopsy, and both HVPG and biopsy (P>0.05), respectively. Platelet/age (-0.77-0.01×platelet+0.03×age), albumin/platelet (5.05-1.19×albumin-0.01×platelet), and platelet (0.24-0.01×platelet) were found to be risk factors (logit model) for the diagnosis of stage 1 compensated LC on the basis of the findings of HVPG, biopsy, and both HVPG and biopsy.HVPG showed a positive correlation with biopsy, and platelet was found to be a common risk factor for the diagnosis of stage 1 compensated LC in patients with CHB.

    View details for DOI 10.1097/MEG.0b013e3283613139

    View details for PubMedID 23603784

  • Anti-oxidant and natural killer cell activity of Korean red ginseng (Panax ginseng) and urushiol (Rhus vernicifera Stokes) on non-alcoholic fatty liver disease of rat FOOD AND CHEMICAL TOXICOLOGY Hong, S. H., Suk, K. T., Choi, S. H., Lee, J. W., Sung, H. T., Kim, C. H., Kim, E. J., Kim, M. J., Han, S. H., Kim, M. Y., Baik, S. K., Kim, D. J., Lee, G., Lee, S., Park, S. H., Ryu, O. H. 2013; 55: 586-591

    Abstract

    Anti-oxidative and immunologic effects of the Korea red ginseng (KRG; Panax ginseng) and urushiol (Rhus vernicifera Stokes) on non-alcoholic fatty liver disease (NAFLD) were evaluated. Forty-five rats (five Long-Evans Tokushima Otsuka and 40 Otsuka Long-Evans Tokushima Fatty [OLETF] rats) received chew diets for 10months; after this period. The OLETF rats were divided into the following four groups according to diet for 2months: NAFLD (chew), KRG (chew+KRG [200mg/kg/day]), urushiol (chew+urushiol [0.5mg/kg/day]), and ursodeoxycholic acid (UDCA) (chew+UDCA [15mg/kg/day]) groups. Liver function, lipid profiles and anti-oxidant activity of liver and serum, natural killer (NK) cell activity, and pathology were compared. In KRG and urushiol groups, the level of serum triglyceride ([302.0±70.4 and 275.2±63.8] vs. 527.7±153.3mg/dL) were lower compared with that of NAFLD group (p<0.05). The levels of HDL-cholesterol (liver tissue: [4.8±0.2 and 4.8±0.5] vs. 4.2±0.2mg/g) and NK cell activity ([3485±910 and 3559±910] vs. 2486±619 counts) were significantly higher than those of the NAFLD group (p<0.001). Inflammation with neutrophil infiltration was observed in only two rats in the NAFLD group. These results suggest that 2months of oral KRG or urushiol administration improves lipid profiles and stimulates NK cell activity, while inhibiting steatohepatitis in OLEFT rats.

    View details for DOI 10.1016/j.fct.2013.01.022

    View details for Web of Science ID 000317536900073

    View details for PubMedID 23369934

  • Comparison of Hepatic Venous Pressure Gradient and Two Models of End-stage Liver Disease for Predicting the Survival in Patients With Decompensated Liver Cirrhosis JOURNAL OF CLINICAL GASTROENTEROLOGY Suk, K. T., Kim, C. H., Park, S. H., Sung, H. T., Choi, J. Y., Han, K. H., Hong, S. H., Kim, D. Y., Yoon, J. H., Kim, Y. S., Baik, G. H., Kim, J. B., Kim, D. J. 2012; 46 (10): 880-886

    Abstract

    We evaluated the efficacy of initial and follow-up hepatic venous pressure gradient (HVPG), models of end-stage liver disease (MELD), and MELD-Na for predicting the survival of patients with decompensated liver cirrhosis (LC).MELD with/without Na score and HVPG have been important predictors of mortality in patients with LC.Between January 2006 and 2011, a total of 57 patients with decompensated LC, all of whom underwent >2 HVPG measurements for the confirmation of propranolol dosing, were enrolled. MELD and MELD-Na scores were calculated on the day of HVPG measurement. The prognostic accuracy of the initial and follow-up HVPG, MELD, and MELD-Na were analyzed, and independent factors for mortality were evaluated.Ten patients (17.5%) died from LC. Initial HVPG (0.883), initial MELD-Na (0.877), follow-up HVPG (0.829), and follow-up MELD-Na (0.802) showed good area under the receiver operating characteristic curve scores in predicting 1-year mortality. In predicting 2-year mortality, only follow-up HVPG (0.821, cut-off value 18 mm Hg) showed good score. Overall area under the receiver operating characteristic curves (initial and follow-up) were 0.843 and 0.864 in HVPG, 0.721 and 0.674 in MELD, and 0.762 and 0.715 in MELD-Na, respectively. In the Cox regression analysis, only follow-up HVPG (P=0.02; odds ratio, 1.11) was associated with mortality.The efficacy of HVPG for predicting mortality is excellent compared with that of MELD or MELD-Na. Therefore, aside from the confirmation of adequate propranolol dosing, HVPG may be needed for predicting the survival of patients with decompensated LC.

    View details for DOI 10.1097/MCG.0b013e31825f2622

    View details for Web of Science ID 000312953400020

    View details for PubMedID 22810110

  • Oxygen-content-dependent electronic structures of electron-doped cuprates PHYSICAL REVIEW B Song, D., Park, S. R., Kim, C., Kim, Y., Leem, C., Choi, S., Jung, W., Koh, Y., Han, G., Yoshida, Y., Eisaki, H., Lu, D. H., Shen, Z., Kim, C. 2012; 86 (14)
  • Diagnostic accuracy of biomarkers measured in the hepatic vein and peripheral vein in the prediction of advanced fibrosis in patients with chronic viral hepatitis CLINICAL BIOCHEMISTRY Suk, K. T., Kim, D. J., Kim, C. H., Park, S. H., Cheong, J. y., Cho, S. W., Choi, J. Y., Han, K. H., Sung, H. T., Hong, S. H., Kim, D. Y., Yoon, J. H., Kim, Y. S., Baik, G. H., Kim, J. B. 2012; 45 (13-14): 1075-1080

    Abstract

    The accuracies of biomarkers checked in the hepatic vein (HV) and peripheral vein (PV) were compared in the prediction of advanced fibrosis (AF) of liver.Patients with chronic viral hepatitis (n=101) who underwent hepatic venous pressure gradient, liver biopsy, and paired HV-PV samples (6 biomarkers: hyaluronic acid [HA], haptoglobin, matrix metalloproteinase-2 [MMP2], tissue inhibitor of metalloproteinases-1 [TIMP1], procollagen III N-terminal peptide [PIIINP], and apolipoprotein-A1 [Apo-A1]) were enrolled.Differences were displayed between the HV and PV in the predictive logit-models for predicting AF (-3.13+0.017×MMP2-0.019×haptoglobin and -0.270+0.007×HA-0.018×haptoglobin, respectively). In the area under the receiver operating characteristic curves, PIIINP (0.74/0.68, p=0.03), MMP2 (0.72/0.63, p=0.04), HA (0.79/0.76, p=0.94), Apo-A1 (0.56/0.48, p=0.73), and predictive logit-model (0.81/0.78, p=0.68) showed higher diagnostic value in the HV sample.While most biomarkers were correlated better with hepatic fibrosis in HV than in PV, individually and in predictive logit-models, they were inadequate to determine the degree of advanced fibrosis.

    View details for DOI 10.1016/j.clinbiochem.2012.04.031

    View details for Web of Science ID 000308899400015

    View details for PubMedID 22579966

  • A Prospective Nationwide Study of Drug-Induced Liver Injury in Korea AMERICAN JOURNAL OF GASTROENTEROLOGY Suk, K. T., Kim, D. J., Kim, C. H., Park, S. H., Yoon, J. H., Kim, Y. S., Baik, G. H., Kim, J. B., Kweon, Y. o., Kim, B. I., Kim, S. H., Kim, I. h., Kim, J. H., Nam, S. W., Paik, Y. H., Suh, J. I., Sohn, J. H., Ahn, B. M., Um, S. H., Lee, H. J., Cho, M., Jang, M. K., Choi, S. K., Hwang, S. G., Sung, H. T., Choi, J. Y., Han, K. H. 2012; 107 (9): 1380-1387

    Abstract

    To address a growing concern about drug-induced liver injury (DILI), a nationwide study was performed to investigate the significance of DILI in Korea.From May 2005 to May 2007, cases of DILI (alanine transferase > 3 × upper normal limit or total bilirubin > 2 × upper normal limit) from 17 referral university hospitals were prospectively enrolled. Adjudication by the seven review boards was considered for the confirmation of causality and the Roussel Uclaf Causality Assessment Method (RUCAM) scale was used.A total of 371 cases were diagnosed with DILI. The extrapolated incidence of hospitalization at university hospital in Korea was 12/100,000 persons/year. The causes included "herbal medications" (102, 27.5%), "prescription or non-prescription medications" (101, 27.3%), "health foods or dietary supplements" (51, 13.7%), "medicinal herbs or plants" (35, 9.4%), "folk remedies" (32, 8.6%), "combined" (30, 8.2%), "herbal preparations" (12, 3.2%), and others (8, 2.2%). Nine cases were linked to acetaminophen. The frequencies of hepatocellular, mixed, and cholestatic types were 76.3, 14.8, and 8.9%, respectively. A total of 234 cases met the criteria for Hy's law. Five patients died or underwent transplantation. Twenty-five cases (21 herbs and 4 medications) did not meet the time-to-onset criteria of the RUCAM.DILI appears to be a highly relevant health problem in Korea. "Herbal medications" are the principal cause of DILI. A more objective and reproducible causality assessment tool is strongly desired as the RUCAM scale frequently undercounts the cases caused by herbs owing to a lack of previous information and incompatible time criteria.

    View details for DOI 10.1038/ajg.2012.138

    View details for Web of Science ID 000308689200015

    View details for PubMedID 22733303

  • Function of COP9 Signalosome in Regulation of Mouse Oocytes Meiosis by Regulating MPF Activity and Securing Degradation PLOS ONE Kim, E., Yoon, S., Kim, E., Kim, Y., Lee, H., Kim, K., Lee, K. 2011; 6 (10)

    Abstract

    The COP9 (constitutive photomorphogenic) signalosome (CSN), composed of eight subunits, is a highly conserved protein complex that regulates processes such as cell cycle progression and kinase signalling. Previously, we found the expression of the COP9 constitutive photomorphogenic homolog subunit 3 (CSN3) and subunit 5 (CSN5) changes as oocytes mature for the first time, and there is no report regarding roles of COP9 in the mammalian oocytes. Therefore, in the present study, we examined the effects of RNA interference (RNAi)-mediated transient knockdown of each subunit on the meiotic cell cycle in mice oocytes. Following knockdown of either CSN3 or CSN5, oocytes failed to complete meiosis I. These arrested oocytes exhibited a disrupted meiotic spindle and misarranged chromosomes. Moreover, down-regulation of each subunit disrupted the activity of maturation-promoting factor (MPF) and concurrently reduced degradation of the anaphase-promoting complex/cyclosome (APC/C) substrates Cyclin B1 and Securin. Our data suggest that the CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C.

    View details for DOI 10.1371/journal.pone.0025870

    View details for Web of Science ID 000295943000088

    View details for PubMedID 21991377

    View details for PubMedCentralID PMC3185060

  • Revealing the dual nature of magnetism in iron pnictides and iron chalcogenides using x-ray emission spectroscopy PHYSICAL REVIEW B Gretarsson, H., Lupascu, A., Kim, J., Casa, D., Gog, T., Wu, W., Julian, S. R., Xu, Z. J., Wen, J. S., Gu, G. D., Yuan, R. H., Chen, Z. G., Wang, N., Khim, S., Kim, K. H., Ishikado, M., Jarrige, I., Shamoto, S., Chu, J., Fisher, I. R., Kim, Y. 2011; 84 (10)
  • Molecular Inflammation as an Underlying Mechanism of the Aging Process and Age-related Diseases JOURNAL OF DENTAL RESEARCH Chung, H. Y., Lee, E. K., Choi, Y. J., Kim, J. M., Kim, D. H., Zou, Y., Kim, C. H., Lee, J., Kim, H. S., Kim, N. D., Jung, J. H., Yu, B. P. 2011; 90 (7): 830-840

    Abstract

    Aging is a biological process characterized by time-dependent functional declines that are influenced by changes in redox status and by oxidative stress-induced inflammatory reactions. An organism's pro-inflammatory status may underlie the aging process and age-related diseases. In this review, we explore the molecular basis of low-grade, unresolved, subclinical inflammation as a major risk factor for exacerbating the aging process and age-related diseases. We focus on the redox-sensitive transcription factors, NF-κB and FOXO, which play essential roles in the expression of pro-inflammatory mediators and anti-oxidant enzymes, respectively. Major players in molecular inflammation are discussed with respect to the age-related up-regulation of pro-inflammatory cytokines and adhesion molecules, cyclo-oxygenase-2, lipoxygenase, and inducible nitric oxide synthase. The molecular inflammation hypothesis proposed by our laboratory is briefly described to give further molecular insights into the intricate interplay among redox balance, pro-inflammatory gene activation, and chronic age-related inflammatory diseases. The final section discusses calorie restriction as an aging-retarding intervention that also exhibits extraordinarily effective anti-inflammatory activity by modulating GSH redox, NF-κB, SIRT1, PPARs, and FOXOs.

    View details for DOI 10.1177/0022034510387794

    View details for Web of Science ID 000291696900004

    View details for PubMedID 21447699

  • Fractional Flow Reserve Versus Angiography in Left Circumflex Ostial Intervention After Left Main Crossover Stenting KOREAN CIRCULATION JOURNAL Nam, C., Hur, S., Koo, B., Doh, J. H., Cho, Y., Park, H., Yoon, H., Kim, H., Chung, I., Kim, Y., Fearon, W. F., Tahk, S., Kim, K. 2011; 41 (6): 304-307

    Abstract

    Discrepancy between angiographic percent (%) diameter stenosis and fractional flow reserve (FFR) exists in non-left main bifurcation lesions. The aim of this study was to compare angiographic stenosis severity and FFR in jailed ostial left circumflex artery (LCX) lesions after left main (LM)-to-left anterior descending artery (LAD) crossover stenting.Twenty-nine (n=29) patients with distal LM or ostial LAD lesions treated by LM-to-LAD crossover stenting were consecutively enrolled. After successful stenting, FFR was measured at the jailed LCX. Additional intervention was performed in lesions with FFR <0.8.The mean reference diameter of LCX was 3.1±0.4 mm, and percent diameter stenosis after crossover stenting was 56±21%. Angiographically significant stenosis (>50%) at the ostial LCX occurred in 59% (17/29) of cases. Among them, only five (29%) lesions had functional significance, and underwent additional procedure. During follow-up, three patients in the deferral group and two patients in the additional intervention group had target lesion revascularization.There was a discrepancy between angiographic percent diameter stenosis and FFR in jailed LCX lesions after LM crossover stenting.

    View details for DOI 10.4070/kcj.2011.41.6.304

    View details for Web of Science ID 000209078700004

    View details for PubMedCentralID PMC3132691

  • Photoemission studies on electron doped cuprate Pr0.85LaCe0.15CuO4: Revisiting the chemical pressure effect International Conference on Spectroscopies in Novel Superconductors (SNS2010) Song, D. J., Kyung, W. S., Park, S. R., Leem, C. S., Kim, C., Kim, Y. K., Choi, S. K., Jung, W. S., Koh, Y. Y., Choi, H. Y., Han, G., Yoshida, Y., Eisaki, H., Lu, D. H., Shen, Z., Kim, C. PERGAMON-ELSEVIER SCIENCE LTD. 2011: 533–35
  • Self-energy analysis of multiple-bosonic mode coupling in Sr2RuO4 International Conference on Spectroscopies in Novel Superconductors (SNS2010) Kim, C., Kyung, W. S., Park, S. R., Leem, C. S., Song, D. J., Kim, Y. K., Choi, S. K., Jung, W. S., Koh, Y. Y., Choi, H. Y., Yoshida, Y., Moore, R. G., Shen, Z., Kim, C. PERGAMON-ELSEVIER SCIENCE LTD. 2011: 556–58
  • O-free polyacrylonitrile doping to improve the J(c)(B) and H-c2 of MgB2 wires 22nd International Symposium on Superconductivity (ISS 2009) Hwang, S. M., Sung, K., Choi, J. H., Kim, W., Joo, J., Lim, J. H., Kim, C., Park, Y. S., Kim, D. H. ELSEVIER SCIENCE BV. 2010: 1430–34
  • Negative Regulation of Hypoxic Responses via Induced Reptin Methylation MOLECULAR CELL Lee, J. S., Kim, Y., Kim, I. S., Kim, B., Choi, H. J., Lee, J. M., Shin, H. R., Kim, J. H., Kim, J., Seo, S., Lee, H., Binda, O., Gozani, O., Semenza, G. L., Kim, M., Il Kim, K., Hwang, D., Baek, S. H. 2010; 39 (1): 71-85

    Abstract

    Lysine methylation within histones is crucial for transcriptional regulation and thus links chromatin states to biological outcomes. Although recent studies have extended lysine methylation to nonhistone proteins, underlying molecular mechanisms such as the upstream signaling cascade that induces lysine methylation and downstream target genes modulated by this modification have not been elucidated. Here, we show that Reptin, a chromatin-remodeling factor, is methylated at lysine 67 in hypoxic conditions by the methyltransferase G9a. Methylated Reptin binds to the promoters of a subset of hypoxia-responsive genes and negatively regulates transcription of these genes to modulate cellular responses to hypoxia.

    View details for DOI 10.1016/j.molcel.2010.06.008

    View details for Web of Science ID 000280139200009

    View details for PubMedID 20603076

    View details for PubMedCentralID PMC4651011

  • Numerical simulation of friction stir spot welding process for aluminum alloys METALS AND MATERIALS INTERNATIONAL Kim, D., Badarinarayan, H., Ryu, I., Kim, J. H., Kim, C., Okamoto, K., Wagoner, R. H., Chung, K. 2010; 16 (2): 323-332
  • Regulated RalBP1 Binding to RalA and PSD-95 Controls AMPA Receptor Endocytosis and LTD PLOS BIOLOGY Han, K., Kim, M., Seeburg, D., Seo, J., Verpelli, C., Han, S., Chung, H. S., Ko, J., Lee, H. W., Kim, K., Heo, W. D., Meyer, T., Kim, H., Sala, C., Choi, S., Sheng, M., Kim, E. 2009; 7 (9)

    Abstract

    Long-term depression (LTD) is a long-lasting activity-dependent decrease in synaptic strength. NMDA receptor (NMDAR)-dependent LTD, an extensively studied form of LTD, involves the endocytosis of AMPA receptors (AMPARs) via protein dephosphorylation, but the underlying mechanism has remained unclear. We show here that a regulated interaction of the endocytic adaptor RalBP1 with two synaptic proteins, the small GTPase RalA and the postsynaptic scaffolding protein PSD-95, controls NMDAR-dependent AMPAR endocytosis during LTD. NMDAR activation stimulates RalA, which binds and translocates widespread RalBP1 to synapses. In addition, NMDAR activation dephosphorylates RalBP1, promoting the interaction of RalBP1 with PSD-95. These two regulated interactions are required for NMDAR-dependent AMPAR endocytosis and LTD and are sufficient to induce AMPAR endocytosis in the absence of NMDAR activation. RalA in the basal state, however, maintains surface AMPARs. We propose that NMDAR activation brings RalBP1 close to PSD-95 to promote the interaction of RalBP1-associated endocytic proteins with PSD-95-associated AMPARs. This suggests that scaffolding proteins at specialized cellular junctions can switch their function from maintenance to endocytosis of interacting membrane proteins in a regulated manner.

    View details for DOI 10.1371/journal.pbio.1000187

    View details for Web of Science ID 000270820800002

    View details for PubMedID 19823667

    View details for PubMedCentralID PMC2730530

  • High-resolution angle-resolved photoemission studies of quasiparticle dynamics in graphite PHYSICAL REVIEW B Leem, C. S., Kim, C., Park, S. R., Kim, M., Choi, H. J., Kim, C., Kim, B. J., Johnston, S., DEVEREAUX, T., Ohta, T., Bostwick, A., Rotenberg, E. 2009; 79 (12)
  • Rare earth ion effects on the pseudo-gap in electron-doped superconductors and possible nodeless d-wave gap 61st Yamada Conference on Spectroscopies in Novel Superconductors Park, S. R., Leem, C. S., Roh, Y. S., Choi, K. J., Kim, J. H., Kim, B. J., Koh, H., Eisaki, H., Lu, D. H., Shen, Z., Armitage, N. P., Kim, C. PERGAMON-ELSEVIER SCIENCE LTD. 2008: 2939–43
  • Phospholipase D activity regulates integrin-mediated cell spreading and migration by inducing GTP-Rac translocation to the plasma membrane MOLECULAR BIOLOGY OF THE CELL Chae, Y. C., Kim, J. H., Kim, K. L., Kim, H. W., Lee, H. Y., Do Heo, W., Meyer, T., Suh, P., Ryu, S. H. 2008; 19 (7): 3111-3123

    Abstract

    Small GTPase Rac is a crucial regulator of actin cytoskeletal rearrangement, and it plays an important role in cell spreading, migration, mitogenesis, phagocytosis, superoxide generation, and axonal growth. It is generally accepted that Rac activity is regulated by the guanosine triphosphate (GTP)/guanosine diphosphate (GDP) cycle. But, it is suggested that in addition to Rac-GTP loading, membrane localization is required for the initiation of downstream effector signaling. However, the molecular mechanisms that control the targeting of GTP-Rac to the plasma membrane remain largely unknown. Here, we have uncovered a signaling pathway linking phospholipase D (PLD) to the localized functions of Rac1. We show that PLD product phosphatidic acid (PA) acts as a membrane anchor of Rac1. The C-terminal polybasic motif of Rac1 is responsible for direct interaction with PA, and Rac1 mutated in this region is incapable of translocating to the plasma membrane and of activating downstream target p21-activated kinase upon integrin activation. Finally, we show that PA induces dissociation of Rho-guanine nucleotide dissociation inhibitor from Rac1 and that PA-mediated Rac1 localization is important for integrin-mediated lamellipodia formation, cell spreading, and migration. These results provide a novel molecular mechanism for the GTP-Rac1 localization through the elevating PLD activity, and they suggest a general mechanism for diverse cellular functions that is required localized Rac activation.

    View details for DOI 10.1091/mbc.E07-04-0337

    View details for Web of Science ID 000259158200037

    View details for PubMedID 18480413

    View details for PubMedCentralID PMC2441685

  • Negative differential transconductance characteristics and inter-band tunneling mechanism of fabricated FITETs 13th Korean Conference on Semiconductors Song, S., Kim, J. H., Kang, S., Lee, J. D., Park, B., Kim, K. R., Kang, K. C. KOREAN PHYSICAL SOC. 2006: S790–S794
  • Spin-charge separation in 1D Mott-insulators and related systems JOURNAL OF ELECTRON SPECTROSCOPY AND RELATED PHENOMENA Kim, C. 2001; 117: 503-515
  • ARPES features of the AF insulators Sr2CuO2Cl2 and Ca2CuO2Cl2 close to the AF zone boundary International Conference on Materials and Mechanisms of Superconductivity High Temperature Superconductors VI Ronning, F., Kim, C., Damascelli, A., Armitage, N. P., Lu, D. H., Shen, K. M., MILLER, L. L., Kim, Y. J., Kastner, M. A., Birgeneau, R. J., Shen, Z. X. ELSEVIER SCIENCE BV. 2000: 2087–2090
  • Systematics of the photoemission spectral function of cuprates: Insulators and hole- and electron-doped superconductors PHYSICAL REVIEW LETTERS Kim, C., White, P. J., Shen, Z. X., Tohyama, T., Shibata, Y., Maekawa, S., Wells, B. O., Kim, Y. J., Birgeneau, R. J., Kastner, M. A. 1998; 80 (19): 4245-4248
  • MONOSUBSTITUTED GUANIDINES FROM PRIMARY AMINES AND AMINOIMINOMETHANESULFONIC ACID TETRAHEDRON LETTERS Kim, K. Y., Lin, Y. T., Mosher, H. S. 1988; 29 (26): 3183-3186
  • SYNTHESIS, CHARACTERIZATION, AND ELECTROCHEMISTRY OF NOVEL DIRUTHENIUM COFACIAL PORPHYRIN DIMERS INORGANIC CHEMISTRY Collman, J. P., Kim, K., LEIDNER, C. R. 1987; 26 (7): 1152-1157
  • INSITU HIGH-RESOLUTION ELECTRON-MICROSCOPY REACTIONS IN SEMICONDUCTORS ULTRAMICROSCOPY Sinclair, R., Parker, M. A., Kim, K. B. 1987; 23 (3-4): 383-395
  • COFACIAL PORPHYRIN DIMERS CONTAINING INTRAMOLECULAR METAL METAL BONDS JOURNAL OF THE CHEMICAL SOCIETY-CHEMICAL COMMUNICATIONS Collman, J. P., Kim, K., Garner, J. M. 1986: 1711-1713
  • A MULTI-DIRECTOR FORMULATION FOR NONLINEAR ELASTIC VISCOELASTIC LAYERED SHELLS COMPUTERS & STRUCTURES PINSKY, P. M., Kim, K. O. 1986; 24 (6): 901-913
  • MAGNETIC DIPOLE AND ELECTRIC QUADRUPOLE-MOMENTS OF W+/- MESON PHYSICAL REVIEW D Kim, K. J., Tsai, Y. S. 1973; 7 (12): 3710-3721
  • RENORMALIZED SIGMA MODEL ANNALS OF PHYSICS Kim, K. J. 1973; 79 (2): 287-337
  • ASYMPTOTIC CONSERVATION OF HELICITY FOR VERTEX FUNCTIONS INVOLVING ARBITRARY SPIN PHYSICAL REVIEW D Kim, K. J. 1973; 8 (2): 555-559