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PubMed Central Canada to be taken offline in February 2018

On February 23, 2018, PubMed Central Canada (PMC Canada) will be taken offline permanently. No author manuscripts will be deleted, and the approximately 2,900 manuscripts authored by Canadian Institutes of Health Research (CIHR)-funded researchers currently in the archive will be copied to the National Research Council’s (NRC) Digital Repository over the coming months. These manuscripts along with all other content will also remain publicly searchable on PubMed Central (US) and Europe PubMed Central, meaning such manuscripts will continue to be compliant with the Tri-Agency Open Access Policy on Publications.

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1.  Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) 
Klionsky, Daniel J | Abdelmohsen, Kotb | Abe, Akihisa | Abedin, Md Joynal | Abeliovich, Hagai | Acevedo Arozena, Abraham | Adachi, Hiroaki | Adams, Christopher M | Adams, Peter D | Adeli, Khosrow | Adhihetty, Peter J | Adler, Sharon G | Agam, Galila | Agarwal, Rajesh | Aghi, Manish K | Agnello, Maria | Agostinis, Patrizia | Aguilar, Patricia V | Aguirre-Ghiso, Julio | Airoldi, Edoardo M | Ait-Si-Ali, Slimane | Akematsu, Takahiko | Akporiaye, Emmanuel T | Al-Rubeai, Mohamed | Albaiceta, Guillermo M | Albanese, Chris | Albani, Diego | Albert, Matthew L | Aldudo, Jesus | Algül, Hana | Alirezaei, Mehrdad | Alloza, Iraide | Almasan, Alexandru | Almonte-Beceril, Maylin | Alnemri, Emad S | Alonso, Covadonga | Altan-Bonnet, Nihal | Altieri, Dario C | Alvarez, Silvia | Alvarez-Erviti, Lydia | Alves, Sandro | Amadoro, Giuseppina | Amano, Atsuo | Amantini, Consuelo | Ambrosio, Santiago | Amelio, Ivano | Amer, Amal O | Amessou, Mohamed | Amon, Angelika | An, Zhenyi | Anania, Frank A | Andersen, Stig U | Andley, Usha P | Andreadi, Catherine K | Andrieu-Abadie, Nathalie | Anel, Alberto | Ann, David K | Anoopkumar-Dukie, Shailendra | Antonioli, Manuela | Aoki, Hiroshi | Apostolova, Nadezda | Aquila, Saveria | Aquilano, Katia | Araki, Koichi | Arama, Eli | Aranda, Agustin | Araya, Jun | Arcaro, Alexandre | Arias, Esperanza | Arimoto, Hirokazu | Ariosa, Aileen R | Armstrong, Jane L | Arnould, Thierry | Arsov, Ivica | Asanuma, Katsuhiko | Askanas, Valerie | Asselin, Eric | Atarashi, Ryuichiro | Atherton, Sally S | Atkin, Julie D | Attardi, Laura D | Auberger, Patrick | Auburger, Georg | Aurelian, Laure | Autelli, Riccardo | Avagliano, Laura | Avantaggiati, Maria Laura | Avrahami, Limor | Awale, Suresh | Azad, Neelam | Bachetti, Tiziana | Backer, Jonathan M | Bae, Dong-Hun | Bae, Jae-sung | Bae, Ok-Nam | Bae, Soo Han | Baehrecke, Eric H | Baek, Seung-Hoon | Baghdiguian, Stephen | Bagniewska-Zadworna, Agnieszka | Bai, Hua | Bai, Jie | Bai, Xue-Yuan | Bailly, Yannick | Balaji, Kithiganahalli Narayanaswamy | Balduini, Walter | Ballabio, Andrea | Balzan, Rena | Banerjee, Rajkumar | Bánhegyi, Gábor | Bao, Haijun | Barbeau, Benoit | Barrachina, Maria D | Barreiro, Esther | Bartel, Bonnie | Bartolomé, Alberto | Bassham, Diane C | Bassi, Maria Teresa | Bast, Robert C | Basu, Alakananda | Batista, Maria Teresa | Batoko, Henri | Battino, Maurizio | Bauckman, Kyle | Baumgarner, Bradley L | Bayer, K Ulrich | Beale, Rupert | Beaulieu, Jean-François | Beck, George R. | Becker, Christoph | Beckham, J David | Bédard, Pierre-André | Bednarski, Patrick J | Begley, Thomas J | Behl, Christian | Behrends, Christian | Behrens, Georg MN | Behrns, Kevin E | Bejarano, Eloy | Belaid, Amine | Belleudi, Francesca | Bénard, Giovanni | Berchem, Guy | Bergamaschi, Daniele | Bergami, Matteo | Berkhout, Ben | Berliocchi, Laura | Bernard, Amélie | Bernard, Monique | Bernassola, Francesca | Bertolotti, Anne | Bess, Amanda S | Besteiro, Sébastien | Bettuzzi, Saverio | Bhalla, Savita | Bhattacharyya, Shalmoli | Bhutia, Sujit K | Biagosch, Caroline | Bianchi, Michele Wolfe | Biard-Piechaczyk, Martine | Billes, Viktor | Bincoletto, Claudia | Bingol, Baris | Bird, Sara W | Bitoun, Marc | Bjedov, Ivana | Blackstone, Craig | Blanc, Lionel | Blanco, Guillermo A | Blomhoff, Heidi Kiil | Boada-Romero, Emilio | Böckler, Stefan | Boes, Marianne | Boesze-Battaglia, Kathleen | Boise, Lawrence H | Bolino, Alessandra | Boman, Andrea | Bonaldo, Paolo | Bordi, Matteo | Bosch, Jürgen | Botana, Luis M | Botti, Joelle | Bou, German | Bouché, Marina | Bouchecareilh, Marion | Boucher, Marie-Josée | Boulton, Michael E | Bouret, Sebastien G | Boya, Patricia | Boyer-Guittaut, Michaël | Bozhkov, Peter V | Brady, Nathan | Braga, Vania MM | Brancolini, Claudio | Braus, Gerhard H | Bravo-San Pedro, José M | Brennan, Lisa A | Bresnick, Emery H | Brest, Patrick | Bridges, Dave | Bringer, Marie-Agnès | Brini, Marisa | Brito, Glauber C | Brodin, Bertha | Brookes, Paul S | Brown, Eric J | Brown, Karen | Broxmeyer, Hal E | Bruhat, Alain | Brum, Patricia Chakur | Brumell, John H | Brunetti-Pierri, Nicola | Bryson-Richardson, Robert J | Buch, Shilpa | Buchan, Alastair M | Budak, Hikmet | Bulavin, Dmitry V | Bultman, Scott J | Bultynck, Geert | Bumbasirevic, Vladimir | Burelle, Yan | Burke, Robert E | Burmeister, Margit | Bütikofer, Peter | Caberlotto, Laura | Cadwell, Ken | Cahova, Monika | Cai, Dongsheng | Cai, Jingjing | Cai, Qian | Calatayud, Sara | Camougrand, Nadine | Campanella, Michelangelo | Campbell, Grant R | Campbell, Matthew | Campello, Silvia | Candau, Robin | Caniggia, Isabella | Cantoni, Lavinia | Cao, Lizhi | Caplan, Allan B | Caraglia, Michele | Cardinali, Claudio | Cardoso, Sandra Morais | Carew, Jennifer S | Carleton, Laura A | Carlin, Cathleen R | Carloni, Silvia | Carlsson, Sven R | Carmona-Gutierrez, Didac | Carneiro, Leticia AM | Carnevali, Oliana | Carra, Serena | Carrier, Alice | Carroll, Bernadette | Casas, Caty | Casas, Josefina | Cassinelli, Giuliana | Castets, Perrine | Castro-Obregon, Susana | Cavallini, Gabriella | Ceccherini, Isabella | Cecconi, Francesco | Cederbaum, Arthur I | Ceña, Valentín | Cenci, Simone | Cerella, Claudia | Cervia, Davide | Cetrullo, Silvia | Chaachouay, Hassan | Chae, Han-Jung | Chagin, Andrei S | Chai, Chee-Yin | Chakrabarti, Gopal | Chamilos, Georgios | Chan, Edmond YW | Chan, Matthew TV | Chandra, Dhyan | Chandra, Pallavi | Chang, Chih-Peng | Chang, Raymond Chuen-Chung | Chang, Ta Yuan | Chatham, John C | Chatterjee, Saurabh | Chauhan, Santosh | Che, Yongsheng | Cheetham, Michael E | Cheluvappa, Rajkumar | Chen, Chun-Jung | Chen, Gang | Chen, Guang-Chao | Chen, Guoqiang | Chen, Hongzhuan | Chen, Jeff W | Chen, Jian-Kang | Chen, Min | Chen, Mingzhou | Chen, Peiwen | Chen, Qi | Chen, Quan | Chen, Shang-Der | Chen, Si | Chen, Steve S-L | Chen, Wei | Chen, Wei-Jung | Chen, Wen Qiang | Chen, Wenli | Chen, Xiangmei | Chen, Yau-Hung | Chen, Ye-Guang | Chen, Yin | Chen, Yingyu | Chen, Yongshun | Chen, Yu-Jen | Chen, Yue-Qin | Chen, Yujie | Chen, Zhen | Chen, Zhong | Cheng, Alan | Cheng, Christopher HK | Cheng, Hua | Cheong, Heesun | Cherry, Sara | Chesney, Jason | Cheung, Chun Hei Antonio | Chevet, Eric | Chi, Hsiang Cheng | Chi, Sung-Gil | Chiacchiera, Fulvio | Chiang, Hui-Ling | Chiarelli, Roberto | Chiariello, Mario | Chieppa, Marcello | Chin, Lih-Shen | Chiong, Mario | Chiu, Gigi NC | Cho, Dong-Hyung | Cho, Ssang-Goo | Cho, William C | Cho, Yong-Yeon | Cho, Young-Seok | Choi, Augustine MK | Choi, Eui-Ju | Choi, Eun-Kyoung | Choi, Jayoung | Choi, Mary E | Choi, Seung-Il | Chou, Tsui-Fen | Chouaib, Salem | Choubey, Divaker | Choubey, Vinay | Chow, Kuan-Chih | Chowdhury, Kamal | Chu, Charleen T | Chuang, Tsung-Hsien | Chun, Taehoon | Chung, Hyewon | Chung, Taijoon | Chung, Yuen-Li | Chwae, Yong-Joon | Cianfanelli, Valentina | Ciarcia, Roberto | Ciechomska, Iwona A | Ciriolo, Maria Rosa | Cirone, Mara | Claerhout, Sofie | Clague, Michael J | Clària, Joan | Clarke, Peter GH | Clarke, Robert | Clementi, Emilio | Cleyrat, Cédric | Cnop, Miriam | Coccia, Eliana M | Cocco, Tiziana | Codogno, Patrice | Coers, Jörn | Cohen, Ezra EW | Colecchia, David | Coletto, Luisa | Coll, Núria S | Colucci-Guyon, Emma | Comincini, Sergio | Condello, Maria | Cook, Katherine L | Coombs, Graham H | Cooper, Cynthia D | Cooper, J Mark | Coppens, Isabelle | Corasaniti, Maria Tiziana | Corazzari, Marco | Corbalan, Ramon | Corcelle-Termeau, Elisabeth | Cordero, Mario D | Corral-Ramos, Cristina | Corti, Olga | Cossarizza, Andrea | Costelli, Paola | Costes, Safia | Cotman, Susan L | Coto-Montes, Ana | Cottet, Sandra | Couve, Eduardo | Covey, Lori R | Cowart, L Ashley | Cox, Jeffery S | Coxon, Fraser P | Coyne, Carolyn B | Cragg, Mark S | Craven, Rolf J | Crepaldi, Tiziana | Crespo, Jose L | Criollo, Alfredo | Crippa, Valeria | Cruz, Maria Teresa | Cuervo, Ana Maria | Cuezva, Jose M | Cui, Taixing | Cutillas, Pedro R | Czaja, Mark J | Czyzyk-Krzeska, Maria F | Dagda, Ruben K | Dahmen, Uta | Dai, Chunsun | Dai, Wenjie | Dai, Yun | Dalby, Kevin N | Dalla Valle, Luisa | Dalmasso, Guillaume | D'Amelio, Marcello | Damme, Markus | Darfeuille-Michaud, Arlette | Dargemont, Catherine | Darley-Usmar, Victor M | Dasarathy, Srinivasan | Dasgupta, Biplab | Dash, Srikanta | Dass, Crispin R | Davey, Hazel Marie | Davids, Lester M | Dávila, David | Davis, Roger J | Dawson, Ted M | Dawson, Valina L | Daza, Paula | de Belleroche, Jackie | de Figueiredo, Paul | de Figueiredo, Regina Celia Bressan Queiroz | de la Fuente, José | De Martino, Luisa | De Matteis, Antonella | De Meyer, Guido RY | De Milito, Angelo | De Santi, Mauro | de Souza, Wanderley | De Tata, Vincenzo | De Zio, Daniela | Debnath, Jayanta | Dechant, Reinhard | Decuypere, Jean-Paul | Deegan, Shane | Dehay, Benjamin | Del Bello, Barbara | Del Re, Dominic P | Delage-Mourroux, Régis | Delbridge, Lea MD | Deldicque, Louise | Delorme-Axford, Elizabeth | Deng, Yizhen | Dengjel, Joern | Denizot, Melanie | Dent, Paul | Der, Channing J | Deretic, Vojo | Derrien, Benoît | Deutsch, Eric | Devarenne, Timothy P | Devenish, Rodney J | Di Bartolomeo, Sabrina | Di Daniele, Nicola | Di Domenico, Fabio | Di Nardo, Alessia | Di Paola, Simone | Di Pietro, Antonio | Di Renzo, Livia | DiAntonio, Aaron | Díaz-Araya, Guillermo | Díaz-Laviada, Ines | Diaz-Meco, Maria T | Diaz-Nido, Javier | Dickey, Chad A | Dickson, Robert C | Diederich, Marc | Digard, Paul | Dikic, Ivan | Dinesh-Kumar, Savithrama P | Ding, Chan | Ding, Wen-Xing | Ding, Zufeng | Dini, Luciana | Distler, Jörg HW | Diwan, Abhinav | Djavaheri-Mergny, Mojgan | Dmytruk, Kostyantyn | Dobson, Renwick CJ | Doetsch, Volker | Dokladny, Karol | Dokudovskaya, Svetlana | Donadelli, Massimo | Dong, X Charlie | Dong, Xiaonan | Dong, Zheng | Donohue, Terrence M | Doran, Kelly S | D'Orazi, Gabriella | Dorn, Gerald W | Dosenko, Victor | Dridi, Sami | Drucker, Liat | Du, Jie | Du, Li-Lin | Du, Lihuan | du Toit, André | Dua, Priyamvada | Duan, Lei | Duann, Pu | Dubey, Vikash Kumar | Duchen, Michael R | Duchosal, Michel A | Duez, Helene | Dugail, Isabelle | Dumit, Verónica I | Duncan, Mara C | Dunlop, Elaine A | Dunn, William A | Dupont, Nicolas | Dupuis, Luc | Durán, Raúl V | Durcan, Thomas M | Duvezin-Caubet, Stéphane | Duvvuri, Umamaheswar | Eapen, Vinay | Ebrahimi-Fakhari, Darius | Echard, Arnaud | Eckhart, Leopold | Edelstein, Charles L | Edinger, Aimee L | Eichinger, Ludwig | Eisenberg, Tobias | Eisenberg-Lerner, Avital | Eissa, N Tony | El-Deiry, Wafik S | El-Khoury, Victoria | Elazar, Zvulun | Eldar-Finkelman, Hagit | Elliott, Chris JH | Emanuele, Enzo | Emmenegger, Urban | Engedal, Nikolai | Engelbrecht, Anna-Mart | Engelender, Simone | Enserink, Jorrit M | Erdmann, Ralf | Erenpreisa, Jekaterina | Eri, Rajaraman | Eriksen, Jason L | Erman, Andreja | Escalante, Ricardo | Eskelinen, Eeva-Liisa | Espert, Lucile | Esteban-Martínez, Lorena | Evans, Thomas J | Fabri, Mario | Fabrias, Gemma | Fabrizi, Cinzia | Facchiano, Antonio | Færgeman, Nils J | Faggioni, Alberto | Fairlie, W Douglas | Fan, Chunhai | Fan, Daping | Fan, Jie | Fang, Shengyun | Fanto, Manolis | Fanzani, Alessandro | Farkas, Thomas | Faure, Mathias | Favier, Francois B | Fearnhead, Howard | Federici, Massimo | Fei, Erkang | Felizardo, Tania C | Feng, Hua | Feng, Yibin | Feng, Yuchen | Ferguson, Thomas A | Fernández, Álvaro F | Fernandez-Barrena, Maite G | Fernandez-Checa, Jose C | Fernández-López, Arsenio | Fernandez-Zapico, Martin E | Feron, Olivier | Ferraro, Elisabetta | Ferreira-Halder, Carmen Veríssima | Fesus, Laszlo | Feuer, Ralph | Fiesel, Fabienne C | Filippi-Chiela, Eduardo C | Filomeni, Giuseppe | Fimia, Gian Maria | Fingert, John H | Finkbeiner, Steven | Finkel, Toren | Fiorito, Filomena | Fisher, Paul B | Flajolet, Marc | Flamigni, Flavio | Florey, Oliver | Florio, Salvatore | Floto, R Andres | Folini, Marco | Follo, Carlo | Fon, Edward A | Fornai, Francesco | Fortunato, Franco | Fraldi, Alessandro | Franco, Rodrigo | Francois, Arnaud | François, Aurélie | Frankel, Lisa B | Fraser, Iain DC | Frey, Norbert | Freyssenet, Damien G | Frezza, Christian | Friedman, Scott L | Frigo, Daniel E | Fu, Dongxu | Fuentes, José M | Fueyo, Juan | Fujitani, Yoshio | Fujiwara, Yuuki | Fujiya, Mikihiro | Fukuda, Mitsunori | Fulda, Simone | Fusco, Carmela | Gabryel, Bozena | Gaestel, Matthias | Gailly, Philippe | Gajewska, Malgorzata | Galadari, Sehamuddin | Galili, Gad | Galindo, Inmaculada | Galindo, Maria F | Galliciotti, Giovanna | Galluzzi, Lorenzo | Galluzzi, Luca | Galy, Vincent | Gammoh, Noor | Gandy, Sam | Ganesan, Anand K | Ganesan, Swamynathan | Ganley, Ian G | Gannagé, Monique | Gao, Fen-Biao | Gao, Feng | Gao, Jian-Xin | García Nannig, Lorena | García Véscovi, Eleonora | Garcia-Macía, Marina | Garcia-Ruiz, Carmen | Garg, Abhishek D | Garg, Pramod Kumar | Gargini, Ricardo | Gassen, Nils Christian | Gatica, Damián | Gatti, Evelina | Gavard, Julie | Gavathiotis, Evripidis | Ge, Liang | Ge, Pengfei | Ge, Shengfang | Gean, Po-Wu | Gelmetti, Vania | Genazzani, Armando A | Geng, Jiefei | Genschik, Pascal | Gerner, Lisa | Gestwicki, Jason E | Gewirtz, David A | Ghavami, Saeid | Ghigo, Eric | Ghosh, Debabrata | Giammarioli, Anna Maria | Giampieri, Francesca | Giampietri, Claudia | Giatromanolaki, Alexandra | Gibbings, Derrick J | Gibellini, Lara | Gibson, Spencer B | Ginet, Vanessa | Giordano, Antonio | Giorgini, Flaviano | Giovannetti, Elisa | Girardin, Stephen E | Gispert, Suzana | Giuliano, Sandy | Gladson, Candece L | Glavic, Alvaro | Gleave, Martin | Godefroy, Nelly | Gogal, Robert M | Gokulan, Kuppan | Goldman, Gustavo H | Goletti, Delia | Goligorsky, Michael S | Gomes, Aldrin V | Gomes, Ligia C | Gomez, Hernando | Gomez-Manzano, Candelaria | Gómez-Sánchez, Rubén | Gonçalves, Dawit AP | Goncu, Ebru | Gong, Qingqiu | Gongora, Céline | Gonzalez, Carlos B | Gonzalez-Alegre, Pedro | Gonzalez-Cabo, Pilar | González-Polo, Rosa Ana | Goping, Ing Swie | Gorbea, Carlos | Gorbunov, Nikolai V | Goring, Daphne R | Gorman, Adrienne M | Gorski, Sharon M | Goruppi, Sandro | Goto-Yamada, Shino | Gotor, Cecilia | Gottlieb, Roberta A | Gozes, Illana | Gozuacik, Devrim | Graba, Yacine | Graef, Martin | Granato, Giovanna E | Grant, Gary Dean | Grant, Steven | Gravina, Giovanni Luca | Green, Douglas R | Greenhough, Alexander | Greenwood, Michael T | Grimaldi, Benedetto | Gros, Frédéric | Grose, Charles | Groulx, Jean-Francois | Gruber, Florian | Grumati, Paolo | Grune, Tilman | Guan, Jun-Lin | Guan, Kun-Liang | Guerra, Barbara | Guillen, Carlos | Gulshan, Kailash | Gunst, Jan | Guo, Chuanyong | Guo, Lei | Guo, Ming | Guo, Wenjie | Guo, Xu-Guang | Gust, Andrea A | Gustafsson, Åsa B | Gutierrez, Elaine | Gutierrez, Maximiliano G | Gwak, Ho-Shin | Haas, Albert | Haber, James E | Hadano, Shinji | Hagedorn, Monica | Hahn, David R | Halayko, Andrew J | Hamacher-Brady, Anne | Hamada, Kozo | Hamai, Ahmed | Hamann, Andrea | Hamasaki, Maho | Hamer, Isabelle | Hamid, Qutayba | Hammond, Ester M | Han, Feng | Han, Weidong | Handa, James T | Hanover, John A | Hansen, Malene | Harada, Masaru | Harhaji-Trajkovic, Ljubica | Harper, J Wade | Harrath, Abdel Halim | Harris, Adrian L | Harris, James | Hasler, Udo | Hasselblatt, Peter | Hasui, Kazuhisa | Hawley, Robert G | Hawley, Teresa S | He, Congcong | He, Cynthia Y | He, Fengtian | He, Gu | He, Rong-Rong | He, Xian-Hui | He, You-Wen | He, Yu-Ying | Heath, Joan K | Hébert, Marie-Josée | Heinzen, Robert A | Helgason, Gudmundur Vignir | Hensel, Michael | Henske, Elizabeth P | Her, Chengtao | Herman, Paul K | Hernández, Agustín | Hernandez, Carlos | Hernández-Tiedra, Sonia | Hetz, Claudio | Hiesinger, P Robin | Higaki, Katsumi | Hilfiker, Sabine | Hill, Bradford G | Hill, Joseph A | Hill, William D | Hino, Keisuke | Hofius, Daniel | Hofman, Paul | Höglinger, Günter U | Höhfeld, Jörg | Holz, Marina K | Hong, Yonggeun | Hood, David A | Hoozemans, Jeroen JM | Hoppe, Thorsten | Hsu, Chin | Hsu, Chin-Yuan | Hsu, Li-Chung | Hu, Dong | Hu, Guochang | Hu, Hong-Ming | Hu, Hongbo | Hu, Ming Chang | Hu, Yu-Chen | Hu, Zhuo-Wei | Hua, Fang | Hua, Ya | Huang, Canhua | Huang, Huey-Lan | Huang, Kuo-How | Huang, Kuo-Yang | Huang, Shile | Huang, Shiqian | Huang, Wei-Pang | Huang, Yi-Ran | Huang, Yong | Huang, Yunfei | Huber, Tobias B | Huebbe, Patricia | Huh, Won-Ki | Hulmi, Juha J | Hur, Gang Min | Hurley, James H | Husak, Zvenyslava | Hussain, Sabah NA | Hussain, Salik | Hwang, Jung Jin | Hwang, Seungmin | Hwang, Thomas IS | Ichihara, Atsuhiro | Imai, Yuzuru | Imbriano, Carol | Inomata, Megumi | Into, Takeshi | Iovane, Valentina | Iovanna, Juan L | Iozzo, Renato V | Ip, Nancy Y | Irazoqui, Javier E | Iribarren, Pablo | Isaka, Yoshitaka | Isakovic, Aleksandra J | Ischiropoulos, Harry | Isenberg, Jeffrey S | Ishaq, Mohammad | Ishida, Hiroyuki | Ishii, Isao | Ishmael, Jane E | Isidoro, Ciro | Isobe, Ken-ichi | Isono, Erika | Issazadeh-Navikas, Shohreh | Itahana, Koji | Itakura, Eisuke | Ivanov, Andrei I | Iyer, Anand Krishnan V | Izquierdo, José M | Izumi, Yotaro | Izzo, Valentina | Jäättelä, Marja | Jaber, Nadia | Jackson, Daniel John | Jackson, William T | Jacob, Tony George | Jacques, Thomas S | Jagannath, Chinnaswamy | Jain, Ashish | Jana, Nihar Ranjan | Jang, Byoung Kuk | Jani, Alkesh | Janji, Bassam | Jannig, Paulo Roberto | Jansson, Patric J | Jean, Steve | Jendrach, Marina | Jeon, Ju-Hong | Jessen, Niels | Jeung, Eui-Bae | Jia, Kailiang | Jia, Lijun | Jiang, Hong | Jiang, Hongchi | Jiang, Liwen | Jiang, Teng | Jiang, Xiaoyan | Jiang, Xuejun | Jiang, Xuejun | Jiang, Ying | Jiang, Yongjun | Jiménez, Alberto | Jin, Cheng | Jin, Hongchuan | Jin, Lei | Jin, Meiyan | Jin, Shengkan | Jinwal, Umesh Kumar | Jo, Eun-Kyeong | Johansen, Terje | Johnson, Daniel E | Johnson, Gail VW | Johnson, James D | Jonasch, Eric | Jones, Chris | Joosten, Leo AB | Jordan, Joaquin | Joseph, Anna-Maria | Joseph, Bertrand | Joubert, Annie M | Ju, Dianwen | Ju, Jingfang | Juan, Hsueh-Fen | Juenemann, Katrin | Juhász, Gábor | Jung, Hye Seung | Jung, Jae U | Jung, Yong-Keun | Jungbluth, Heinz | Justice, Matthew J | Jutten, Barry | Kaakoush, Nadeem O | Kaarniranta, Kai | Kaasik, Allen | Kabuta, Tomohiro | Kaeffer, Bertrand | Kågedal, Katarina | Kahana, Alon | Kajimura, Shingo | Kakhlon, Or | Kalia, Manjula | Kalvakolanu, Dhan V | Kamada, Yoshiaki | Kambas, Konstantinos | Kaminskyy, Vitaliy O | Kampinga, Harm H | Kandouz, Mustapha | Kang, Chanhee | Kang, Rui | Kang, Tae-Cheon | Kanki, Tomotake | Kanneganti, Thirumala-Devi | Kanno, Haruo | Kanthasamy, Anumantha G | Kantorow, Marc | Kaparakis-Liaskos, Maria | Kapuy, Orsolya | Karantza, Vassiliki | Karim, Md Razaul | Karmakar, Parimal | Kaser, Arthur | Kaushik, Susmita | Kawula, Thomas | Kaynar, A Murat | Ke, Po-Yuan | Ke, Zun-Ji | Kehrl, John H | Keller, Kate E | Kemper, Jongsook Kim
Autophagy  2016;12(1):1-222.
doi:10.1080/15548627.2015.1100356
PMCID: PMC4835977  PMID: 26799652
autolysosome; autophagosome; chaperone-mediated autophagy; flux; LC3; lysosome; macroautophagy; phagophore; stress; vacuole
2.  Variations in the AURKA Gene: Biomarkers for the Development and Progression of Hepatocellular Carcinoma 
Hepatocellular carcinoma (HCC) is a liver malignancy and a major cause of cancer mortality worldwide. AURKA (aurora kinase A) is a mitotic serine/threonine kinase that functions as an oncogene and plays a critical role in hepatocarcinogenesis. We report on the association between 4 single nucleotide polymorphisms (SNPs) of the AURKA gene (rs1047972, rs2273535, rs2064836, and rs6024836) and HCC susceptibility as well as clinical outcomes in 312 patients with HCC and in 624 cancer-free controls. We found that carriers of the TT allele of the variant rs1047972 were at greater risk of HCC compared with wild-type (CC) carriers. Moreover, carriers of at least one A allele in rs2273535 were less likely to progress to stage III/IV disease, develop large tumors or be classified into Child-Pugh class B or C. Individuals with at least one G allele at AURKA SNP rs2064863 were at lower risk of developing large tumors or progressing to Child-Pugh grade B or C. Our results indicate that genetic variations in the AURKA gene may serve as an important predictor of early-stage HCC and be a reliable biomarker for the development of HCC.
doi:10.7150/ijms.22513
PMCID: PMC5765730
AURKA polymorphisms; Hepatocellular carcinoma; Single nucleotide polymorphism; Susceptibility.
3.  Deep Sea Water Improves Abnormalities in Lipid Metabolism through Lipolysis and Fatty Acid Oxidation in High-Fat Diet-Induced Obese Rats 
Marine Drugs  2017;15(12):386.
Deep sea water (DSW) is a natural marine resource that has been utilized for food, agriculture, cosmetics, and medicine. The aim of this study was to investigate whether DSW has beneficial lipid metabolic effects in an animal model. Our previous in vitro study indicated that DSW significantly decreased the intracellular triglyceride and glycerol-3-phosphate dehydrogenase activity in 3T3-L1 adipocytes. DSW also inhibited the gene levels of adipocyte differentiation, lipogenesis, and adipocytokines, and up-regulated gene levels of lipolysis and fatty acid oxidation. In the present study, the results showed that body weight, liver, adipose tissue, hepatic triglycerides and cholesterol, and serum parameters in the high-fat diet (HFD) + DSW groups were significantly lower compared to the HFD group. Moreover, the fecal output of total lipids, triglycerides, and cholesterol in the HFD + DSW groups was significantly higher than that of the HFD group. Regarding gene expression, DSW significantly increased the gene levels of lipolysis and fatty acid oxidation, and decreased the gene levels of adipocytokine in the adipose tissue of rats with HFD-induced obesity. These results indicate a potential molecular mechanism by which DSW can suppress obesity in rats with HFD-induced obesity through lipolysis and fatty acid oxidation.
doi:10.3390/md15120386
PMCID: PMC5742846  PMID: 29232925
deep sea water; high fat-diet; Wistar rat; gene expression
4.  Association between malignancies and Marfan syndrome: a population-based, nested case–control study in Taiwan 
BMJ Open  2017;7(10):e017243.
Objective
Marfan syndrome (MFS) involves a deficiency of the structural extracellular matrix component fibrillin-1 and overactivation of the transforming growth factor-β (TGF-β) signalling pathway. The TGF-β signalling pathway also actively participates in malignant transformation. Although anecdotal case reports have suggested associations between MFS/MFS-like conditions and several haematological and solid malignancies, such associations have not been thoroughly evaluated in large-scale studies. We sought to use a nationwide healthcare insurance claim database to evaluate whether patients with MFS are at increased risk of malignancy.
Patients and methods
We conducted a nested case–control analysis using a database extracted from Taiwan’s National Health Insurance Research Database. All medical conditions for each case and control were categorised using the International Classification of Diseases, 9th Revision classifications. ORs and 95% CIs for associations between MFS and malignancies were estimated using conditional logistic regression and adjusted for comorbidities.
Results
Our analyses included 1 153 137 cancer cases and 1 153 137 propensity score-matched controls. Relative to other subjects, patients with MFS had a significantly higher risk of having a malignancy (adjusted OR 3.991) and hypertension (adjusted OR 1.964) and were significantly more likely to be men. Malignancies originating from the head and neck and the urinary tract were significantly more frequent among patients with MFS than among subjects without MFS.
Conclusion
Patients with MFS are at increased risk of developing various malignancies. Healthcare professionals should be aware of this risk when treating such patients, and increased cancer surveillance may be necessary for these patients.
doi:10.1136/bmjopen-2017-017243
PMCID: PMC5652471  PMID: 29042385
marfan syndrome; malignancy; fibrillin; transforming growth factor-β
5.  Manipulating the adhesion of electroless nickel-phosphorus film on silicon wafers by silane compound modification and rapid thermal annealing 
Scientific Reports  2017;7:9656.
In this study, the effect of 3-2-(2-aminoethylamino) ethylamino propyl trimethoxysilane (ETAS) modification and post rapid thermal annealing (RTA) treatment on the adhesion of electroless plated nickel-phosphorus (ELP Ni-P) film on polyvinyl alcohol-capped palladium nanoclusters (PVA-Pd) catalyzed silicon wafers is systematically investigated. Characterized by pull-off adhesion, atomic force microscopy, X-ray spectroscopy and water contact angle, a time-dependent, three-staged ETAS grafting mechanism including islandish grafting, a self-assembly monolayer (SAM) and multi-layer grafting is proposed and this mechanism is well correlated to the pull-off adhesion of ELP Ni-P film. In the absence of RTA, the highest ELP Ni-P film adhesion occurs when ETAS modification approaches SAM, where insufficient or multi-layer ETAS grafting fails to provide satisfactory results. On the other hand, if RTA is applied, the best ELP Ni-P film adhesion happens when ETAS modification is islandish owing to the formation of nickel silicide, where SAM or multi-layer ETAS modification cannot provide satisfactory adhesion because the interaction between ETAS and PVA-Pd has been sabotaged during RTA. Evidenced by microstructural images, we also confirmed that ETAS can act as an efficient barrier layer for nickel diffusion to bulk silicon.
doi:10.1038/s41598-017-08639-x
PMCID: PMC5574985  PMID: 28851883
6.  Association of time-serial changes in ambient particulate matters (PMs) with respiratory emergency cases in Taipei's Wenshan District 
PLoS ONE  2017;12(7):e0181106.
Ambient air pollution poses a significant risk for a group of common and often debilitating respiratory diseases, but its direct impact on cause-specific respiratory diseases using emergency room visit (ERV) as an indicator remains to be fully explored. In this study, we conducted a time-series study of ambient PM2.5, NO2, SO2 and their association with ERV for asthma, COPD and pneumonia in a four-year time span. Relative risks for ERV as per log increase in the level of ambient pollutants with time lags of up to 10 days were calculated, using a generalized additive model of Poisson regression. Daily 24-h average concentrations of PM2.5 and pollutant gases were obtained from a local Gutting air quality monitoring station. Results showed that the ERVs for pneumonia and asthma were associated with the level of PM2.5. The effects of PM2.5 on the risk of ERV for asthma were found to be significant at lag days 1 and 2 with increasing risk of 4.34% [RR: 1.091; CI: 1.020–1.166 (95%)] and 3.58% [RR: 1.074; CI: 1.007–1.146 (95%)], respectively. The ERV for pneumonia was associated with the level of PM2.5 at lag days 5, 6 and 7, with increasing risk of 1.92% [RR: 1.039; CI: 1.009–1.070 (95%)], 2.03% [RR: 1.041; CI: 1.009–1.075 (95%)], and 1.82% [RR: 1.037; CI: 1.001–1.075 (95%)], respectively. Further, PM2.5, but not NO2 and SO2, posed a significant risk of ERV for asthma during spring at lag days 0, 1 and 2 (17.12%, RR: 1.408, CI: 1.075–1.238; 15.30%, RR: 1.358 CI: 1.158–1.166; 11.94%, RR: 1.165, CI: 1.004–1.121), which was particularly evident for those who were younger than 75 years of age. In contrast, only PM2.5 was a significant risk of ERV for COPD, which was primarily for those who were younger than 75 years of age during summer season at lag days 3, 4 and 5. (26.66%, RR: 1.704, CI: 1.104–2.632; 26.99%; RR: 1.716, CI: 1.151–2.557; 24.09%; RR: 1.619, CI: 1.111–2.360). Collectively, these results suggested significant seasonal variation and differential time lag effects of PM2.5 on ERV for asthma, COPD and pneumonia.
doi:10.1371/journal.pone.0181106
PMCID: PMC5521777  PMID: 28732014
7.  Glycated hemoglobin A1c-based adjusted glycemic variables in patients with diabetes presenting with acute exacerbation of chronic obstructive pulmonary disease 
Acute hyperglycemia is a common finding in patients presenting to emergency departments (EDs) with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Several studies have argued against the association between hyperglycemia at admission and adverse outcomes in patients with diabetes and an acute illness. Recent studies have shown that glucose-related variables (eg, glycemic gaps and stress hyperglycemia ratios) that are adjusted for glycated hemoglobin levels can indicate the severity of a variety of diseases. The objective of this study was to assess whether these hemoglobin A1c (HbA1c)-based adjusted average glycemic variables were associated with unfavorable outcomes in patients admitted to a hospital with AECOPD. We found that 1) pulmonary infection is a major risk factor for AECOPD; 2) a higher glycemic gap and modified stress hyperglycemia ratio were associated with the development of acute respiratory failure (ARF) in patients with diabetes admitted to an ED because of AECOPD; and 3) the glycemic gap and modified stress hyperglycemia ratio had superior discriminative power over acute hyperglycemia and HbA1c for predicting the development of ARF, although the HbA1c-adjusted glycemic variables alone were not independent risk factors for ARF.
doi:10.2147/COPD.S131232
PMCID: PMC5505159
chronic obstructive pulmonary disease; diabetes mellitus; acute respiratory failure; glycated hemoglobin; hyperglycemia; glycemic gap; stress hyperglycemia ratio
8.  Difference in Striae Periodicity of Heilongjiang and Singaporean Chinese Teeth 
Striae periodicity refers to the number of cross-striations between successive lines of Retzius in tooth enamel. A regular time dependency of striae periodicity, known as the circaseptan interval, has been proposed. Previous studies on striae periodicity have been carried out on both modern and early humans given its potential applications in forensic age estimations and anthropology. Nevertheless, research comparing striae periodicities across gender groups and populations in different geographical locations, particularly in Asia, is lacking. In this study, we compared the striae periodicities of Heilongjiang and Singaporean Chinese, as well as that of Singaporean Chinese males and females. Results showed that while the median striae periodicity counts of Heilongjiang Chinese and Singaporean Chinese teeth are both 7, Heilongjiang Chinese tend to have lower striae periodicity counts than Singaporean Chinese (p < 0.01). No significant gender difference was observed between the median striae periodicity of Singaporean Chinese Female and Singaporean Chinese Male teeth (p = 0.511). We concluded that the median striae periodicity may statistically differ with geographical location, but not gender, provided that ethnicity and geographical location are held constant. Further studies are required to examine the causes for variation in striae periodicities between geographical locations, as well as to verify the other bio-environmental determinants of striae periodicity.
doi:10.3389/fphys.2017.00442
PMCID: PMC5489628  PMID: 28706489
striae periodicity; striae of Retzius; cross-striations; circaseptan interval; enamel
9.  Intra-abdominal bleeding with hemorrhagic shock: a case of adrenal myelolipoma and review of literature 
BMC Surgery  2017;17:74.
doi:10.1186/s12893-017-0270-6
PMCID: PMC5485648  PMID: 28651560
Adrenal myelolipoma; Hemorrhagic shock; Fat-content mass; Retroperitoneum
10.  Glycated hemoglobin level is an independent predictor of major adverse cardiac events after nonfatal acute myocardial infarction in nondiabetic patients 
Medicine  2017;96(18):e6743.
Abstract
The effect of glycemic control on the prognosis of nondiabetic patients after acute myocardial infarction (AMI) remains uncertain. We investigated whether glycated hemoglobin (HbA1c) is associated with adverse outcomes after AMI in nondiabetic patients. In this observational study, we enrolled nondiabetic patients with AMI in the emergency department of 2 medical centers from January 2011 to September 2014. All patients received primary percutaneous coronary intervention and were divided into 4 groups according to the interquartile range of average HbA1c level (Group I, ≤5.6%; Group II, 5.6%–5.8%; Group III, 5.8%–6.0%; and Group IV, >6.0%). Multivariate logistic analysis was performed to estimate the correlation of HbA1c with major adverse cardiac events (MACEs) after AMI. In total, 267 eligible patients were enrolled; 48 patients (18%) developed MACEs within a median follow-up of 178 days. Univariate analysis showed HbA1c > 6.0%, with a higher risk of MACEs in Group IV than in Group I (odds ratio [OR]: 2.733; 95% confidence interval [CI]: 1.123–6.651 vs OR: 1.511; 95% CI: 0.595–3.835). Multivariate analysis revealed an approximately 3.8 times higher risk of MACEs in Group IV than in Group I (OR: 3.769; 95% CI: 1.30–10.86). The HbA1 level is a significant predictor of MACEs after AMI in nondiabetic patients.
doi:10.1097/MD.0000000000006743
PMCID: PMC5419913  PMID: 28471967
acute myocardial infarction; glycated hemoglobin; MACEs; nondiabetic
11.  YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells 
YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis.
doi:10.3390/ijms18050920
PMCID: PMC5454833  PMID: 28448439
YKL-40; IL-18; osteoblasts; angiogenesis; rheumatoid arthritis
13.  Enhancement of CCL2 expression and monocyte migration by CCN1 in osteoblasts through inhibiting miR-518a-5p: implication of rheumatoid arthritis therapy 
Scientific Reports  2017;7:421.
Cysteine-rich 61 (Cyr61 or CCN1), a secreted protein from the CCN family, is an important proinflammatory cytokine. Migration and infiltration of mononuclear cells to inflammatory sites play a critical role in the pathogenesis of rheumatoid arthritis (RA). Monocyte chemoattractant protein-1 (MCP-1/CCL2) is the key chemokine that regulates migration and infiltration of monocytes. Here, we examined the role of CCN1 in monocyte migration, and CCL2 expression in osteoblasts. We found higher levels of CCN1 and CCL2 in synovial fluid from RA patients compared with levels from non-RA controls. We also found that the CCN1-induced increase in CCL2 expression is mediated by the MAPK signaling pathway and that miR-518a-5p expression was negatively regulated by CCN1 via the MAPK cascade. In contrast, inhibition of CCN1 expression with lentiviral vectors expressing short hairpin RNA ameliorated articular swelling, cartilage erosion, and infiltration of monocytes in the ankle joints of mice with collagen-induced arthritis. Our study describes how CCN1 promotes monocyte migration by upregulating CCL2 expression in osteoblasts in RA disease. CCN1 could serve as a potential target for RA treatment.
doi:10.1038/s41598-017-00513-0
PMCID: PMC5428676  PMID: 28341837
14.  Human parvovirus B19 VP1u Protein as inflammatory mediators induces liver injury in naïve mice 
Virulence  2015;7(2):110-118.
Human parvovirus B19 (B19V) is a human pathogen known to be associated with many non-erythroid diseases, including hepatitis. Although B19V VP1-unique region (B19-VP1u) has crucial roles in the pathogenesis of B19V infection, the influence of B19-VP1u proteins on hepatic injury is still obscure. This study investigated the effect and possible inflammatory signaling of B19-VP1u in livers from BALB/c mice that were subcutaneously inoculated with VP1u-expressing COS-7 cells. The in vivo effects of B19-VP1u were analyzed by using live animal imaging system (IVIS), Haematoxylin-Eosin staining, gel zymography, and immunoblotting after inoculation. Markedly hepatocyte disarray and lymphocyte infiltration, enhanced matrix metalloproteinase (MMP)-9 activity and increased phosphorylation of p38, ERK, IKK-α, IκB and NF-κB (p-p65) proteins were observed in livers from BALB/c mice receiving COS-7 cells expressing B19-VP1u as well as the significantly increased CRP, IL-1β and IL-6. Notably, IFN-γ and phosphorylated STAT1, but not STAT3, were also significantly increased in the livers of BALB/c mice that were subcutaneously inoculated with VP1u-expressing COS-7 cells. These findings revealed the effects of B19-VP1u on liver injury and suggested that B19-VP1u may have a role as mediators of inflammation in B19V infection.
doi:10.1080/21505594.2015.1122165
PMCID: PMC4994834  PMID: 26632342
Human parvovirus B19 (B19V); inflammation; liver injury; VP1-unique region (VP1u)
15.  Evaluating the Primary Prevention of Ischemic Stroke of Oral Antithrombotic Therapy in Head and Neck Cancer Patients with Radiation Therapy 
BioMed Research International  2016;2016:6205158.
Although previous studies demonstrated the risk of ischemic stroke (IS) in patients with head and neck cancer (HNC), the impact of oral antithrombotic therapy (OAT) on this risk has not yet been assessed. We aimed to evaluate the effectiveness and safety of OAT in patients with HNC treated with RT. This retrospective cohort study was performed using the National Health Insurance Research Database of Taiwan. A total of 37,638 patients diagnosed with HNC included in the study were classified as users and nonusers of OAT. Primary outcome was IS or transient ischemic attack (TIA), and secondary outcomes were death and major bleeding. The Cox proportional hazards model was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). There was no significant difference in the risk of IS or TIA between patients on continuous OAT and nonusers (adjusted HR, 0.812; 95% CI, 0.199–3.309). The risk of major bleeding was not significantly different between the groups. From a national population database, we did not find an association between OAT and decreasing risk of ischemic stroke/TIA or increasing hazard of major bleeding.
doi:10.1155/2016/6205158
PMCID: PMC5136628  PMID: 27990433
16.  Electronegative low density lipoprotein induces renal apoptosis and fibrosis: STRA6 signaling involved[S] 
Journal of Lipid Research  2016;57(8):1435-1446.
Dyslipidemia has been proven to capably develop and aggravate chronic kidney disease. We also report that electronegative LDL (L5) is the most atherogenic LDL. On the other hand, retinoic acid (RA) and RA receptor (RAR) agonist are reported to be beneficial in some kidney diseases. “Stimulated by retinoic acid 6” (STRA6), one retinol-binding protein 4 receptor, was recently identified to regulate retinoid homeostasis. Here, we observed that L5 suppressed STRA6 cascades [STRA6, cellular retinol-binding protein 1 (CRBP1), RARs, retinoid X receptor α, and retinol, RA], but L5 simultaneously induced apoptosis and fibrosis (TGFβ1, Smad2, collagen 1, hydroxyproline, and trichrome) in kidneys of L5-injected mice and L5-treated renal tubular cells. These L5-induced changes of STRA6 cascades, renal apoptosis, and fibrosis were reversed in kidneys of LOX1−/− mice. LOX1 RNA silencing and inhibitor of c-Jun N-terminal kinase and p38MAPK rescued the suppression of STRA6 cascades and apoptosis and fibrosis in L5-treated renal tubular cells. Furthermore, crbp1 gene transfection reversed downregulation of STRA6 cascades, apoptosis, and fibrosis in L5-treated renal tubular cells. For mimicking STRA6 deficiency, efficient silencing of STRA6 RNA was performed and was found to repress STRA6 cascades and caused apoptosis and fibrosis in L1-treated renal tubular cells. In summary, this study reveals that electronegative L5 can cause kidney apoptosis and fibrosis via the suppression of STRA6 cascades, and implicates that STRA6 signaling may be involved in dyslipidemia-mediated kidney disease.
doi:10.1194/jlr.M067215
PMCID: PMC4959859  PMID: 27256691
lectin-like oxidized LDL receptor-1; stimulated by retinoic acid 6; renal tubular cells
17.  An Elevated Glycemic Gap is Associated with Adverse Outcomes in Diabetic Patients with Acute Myocardial Infarction 
Scientific Reports  2016;6:27770.
Acute hyperglycemia is a frequent finding in patients presenting to the emergency department (ED) with acute myocardial infarction (AMI). The prognostic role of hyperglycemia in diabetic patients with AMI remains controversial. We retrospectively reviewed patients’ medical records to obtain demographic data, clinical presentation, major adverse cardiac events (MACEs), several clinical scores and laboratory data, including the plasma glucose level at initial presentation and HbA1c levels. The glycemic gap, which represents changes in serum glucose levels during the index event, was calculated from the glucose level upon ED admission minus the HbA1c-derived average glucose (ADAG). We enrolled 331 patients after the review of medical records. An elevated glycemic gap between admission serum glucose levels and ADAG were associated with an increased risk of mortality in patients. The glycemic gap showed superior discriminative power regarding the development of MACEs when compared with the admission glucose level. The calculation of the glycemic gap may increase the discriminative powers of established clinical scoring systems in diabetic patients presenting to the ED with AMI. In conclusion, the glycemic gap could be used as an adjunct parameter to assess the severity and prognosis of diabetic patients presenting with AMI. However, the usefulness of the glycemic gap should be further explored in prospective longitudinal studies.
doi:10.1038/srep27770
PMCID: PMC4904212  PMID: 27291987
18.  Knockout of ho-1 protects the striatum from ferrous iron-induced injury in a male-specific manner in mice 
Scientific Reports  2016;6:26358.
Men have worse survival than premenopausal women after intracerebral hemorrhage (ICH). After ICH, overproduction of iron associated with induction of heme oxygenase-1 (HO-1) in brain was observed. Rodent ICH model using ferrous citrate (FC)-infusion into the striatum to simulate iron overload, showed a higher degree of injury severity in males than in females. However, the participation of HO-1 in sex-differences of iron-induced brain injury remains unknown. The present results showed a higher level of HO-1 expression associated with more severe injury in males compared with females after FC-infusion. Estradiol (E2) contributed to lower levels of FC-induced HO-1 expression in females compared with males. Heterozygote ho-1 KO decreased the levels of FC-induced injury severity, histological lesions, behavioral deficits, autophagy and autophagic cell death in the striatum of males but not in females. Moreover, ho-1 deficiency enhanced the neuroprotection by E2 only in males. These results suggested that over induction of HO-1 plays a harmful role in FC-induced brain injury in a male-specific manner. Suppression of HO-1 combined with E2 exhibits a synergistic effect on neuroprotection against FC-induced striatal injury in males. These findings open up the prospect for male-specific neuroprotection targeting HO-1 suppression for patients suffering from striatal iron overload.
doi:10.1038/srep26358
PMCID: PMC4873828  PMID: 27198537
19.  Ambient temperature reduction extends lifespan via activating cellular degradation activity in an annual fish (Nothobranchius rachovii) 
Age  2015;37(2):33.
Ambient temperature reduction (ATR) can extend the lifespan of organisms, but the underlying mechanism is poorly understood. In this study, cellular degradation activity was evaluated in the muscle of an annual fish (Nothobranchius rachovii) reared under high (30 °C), moderate (25 °C), and low (20 °C) ambient temperatures. The results showed the following: (i) the activity of the 20S proteasome and the expression of polyubiquitin aggregates increased with ATR, whereas 20S proteasome expression did not change; (ii) the expression of microtubule-associated protein 1 light chain 3-II (LC3-II) increased with ATR; (iii) the expression of lysosome-associated membrane protein type 2a (Lamp 2a) increased with ATR, whereas the expression of the 70-kD heat shock cognate protein (Hsc 70) decreased with ATR; (iv) lysosome activity increased with ATR, whereas the expression of lysosome-associated membrane protein type 1 (Lamp 1) did not change with ATR; and (v) the expression of molecular target of rapamycin (mTOR) and phosphorylated mTOR (p-mTOR) as well as the p-mTOR/mTOR ratio did not change with ATR. These findings indicate that ATR activates cellular degradation activity, constituting part of the mechanism underlying the longevity-promoting effects of ATR in N. rachovii.
doi:10.1007/s11357-015-9775-z
PMCID: PMC4393827  PMID: 25864186
Aging; Temperature; Degradation; Autophagy; Fish
20.  Adiponectin Induces Oncostatin M Expression in Osteoblasts through the PI3K/Akt Signaling Pathway 
Rheumatoid arthritis (RA), a common autoimmune disorder, is associated with a chronic inflammatory response and unbalanced bone metabolism within the articular microenvironment. Adiponectin, an adipokine secreted by adipocytes, is involved in multiple functions, including lipid metabolism and pro-inflammatory activity. However, the mechanism of adiponectin performance within arthritic inflammation remains unclear. In this study, we observed the effect of adiponectin on the expression of oncostatin M (OSM), a pro-inflammatory cytokine, in human osteoblastic cells. Pretreatment of cells with inhibitors of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor (NF)-κB reduced the adiponectin-induced OSM expression in osteoblasts. Stimulation of the cells with adiponectin increased phosphorylation of PI3K, Akt, and p65. Adiponectin treatment of osteoblasts increased OSM-luciferase activity and p65 binding to NF-κB on the OSM promoter. Our results indicate that adiponectin increased OSM expression via the PI3K, Akt, and NF-κB signaling pathways in osteoblastic cells, suggesting that adiponectin is a novel target for arthritis treatment.
doi:10.3390/ijms17010029
PMCID: PMC4730275  PMID: 26712749
rheumatoid arthritis; adiponectin; oncostatin M; osteoblasts
21.  Successful treatment of a pancreatic pseudocyst accompanied by massive hemothorax: a case report 
Background
It is rare to encounter massive hemothorax as a complication of pancreatic pseudocyst. In addition, as no obvious hypotension and abdominal discomfort were noted, it was difficult to consider gastrointestinal lesion a possibility.
Case presentation
A 54-year-old Taiwanese man had tightness on the left side of his chest and shortness of breath for 3 days. He had a history of acute pancreatitis 3 months ago. After history taking and a series of examinations including thoracocentesis and computed tomography of his abdomen and chest, the diagnosis was finally confirmed based on the high amylase levels in his pleural fluid.
Conclusions
Treatment with distal pancreatectomy and splenectomy was subsequently successfully performed. Based on our experience, we briefly discuss the currently available treatment options for pancreatic pseudocyst.
doi:10.1186/s13256-015-0791-5
PMCID: PMC4696274  PMID: 26714770
Distal pancreatectomy; Hemothorax; Pancreatic pseudocyst
22.  Novel Investigations of Flavonoids as Chemopreventive Agents for Hepatocellular Carcinoma 
BioMed Research International  2015;2015:840542.
We would like to highlight the application of natural products to hepatocellular carcinoma (HCC). We will focus on the natural products known as flavonoids, which target this disease at different stages of hepatocarcinogenesis. In spite of the use of chemotherapy and radiotherapy in treating HCC, patients with HCC still face poor prognosis because of the nature of multidrug resistance and toxicity derived from chemotherapy and radiotherapy. Flavonoids can be found in many vegetables, fruits, and herbal medicines that exert their different anticancer effects via different intracellular signaling pathways and serve as antioxidants. In this review, we will discuss seven common flavonoids that exert different biological effects against HCC via different pathways.
doi:10.1155/2015/840542
PMCID: PMC4695650  PMID: 26858957
24.  Particulate Matter Exposure in a Police Station Located near a Highway 
People living or working near roadways have experienced an increase in cardiovascular or respiratory diseases due to vehicle emissions. Very few studies have focused on the PM exposure of highway police officers, particularly for the number concentration and size distribution of ultrafine particles (UFP). This study evaluated exposure concentrations of particulate matter (PM) in the Sinying police station near a highway located in Tainan, Taiwan, under different traffic volumes, traffic types, and shift times. We focused on periods when the wind blew from the highway toward the police station and when the wind speed was greater than or equal to 0.5 m/s. PM2.5, UFP, and PM-PAHs concentrations in the police station and an upwind reference station were measured. Results indicate that PM2.5, UFP, and PM-PAHs concentrations in the police station can be on average 1.13, 2.17, and 5.81 times more than the upwind reference station concentrations, respectively. The highest exposure level for PM2.5 and UFP was observed during the 12:00 PM–4:00 PM shift while the highest PAHs concentration was found in the 4:00 AM–8:00 AM shift. Thus, special attention needs to be given to protect police officers from exposure to high PM concentration.
doi:10.3390/ijerph121114541
PMCID: PMC4661666  PMID: 26580641
particulate matter; ultrafine particles; police station; highway
25.  Usefulness of Glycemic Gap to Predict ICU Mortality in Critically Ill Patients With Diabetes 
Medicine  2015;94(36):e1525.
Abstract
Stress-induced hyperglycemia (SIH) has been independently associated with an increased risk of mortality in critically ill patients without diabetes. However, it is also necessary to consider preexisting hyperglycemia when investigating the relationship between SIH and mortality in patients with diabetes. We therefore assessed whether the gap between admission glucose and A1C-derived average glucose (ADAG) levels could be a predictor of mortality in critically ill patients with diabetes.
We retrospectively reviewed the Acute Physiology and Chronic Health Evaluation II (APACHE-II) scores and clinical outcomes of patients with diabetes admitted to our medical intensive care unit (ICU) between 2011 and 2014. The glycosylated hemoglobin (HbA1c) levels were converted to the ADAG by the equation, ADAG = [(28.7 × HbA1c) − 46.7]. We also used receiver operating characteristic (ROC) curves to determine the optimal cut-off value for the glycemic gap when predicting ICU mortality and used the net reclassification improvement (NRI) to measure the improvement in prediction performance gained by adding the glycemic gap to the APACHE-II score.
We enrolled 518 patients, of which 87 (17.0%) died during their ICU stay. Nonsurvivors had significantly higher APACHE-II scores and glycemic gaps than survivors (P < 0.001). Critically ill patients with diabetes and a glycemic gap ≥80 mg/dL had significantly higher ICU mortality and adverse outcomes than those with a glycemic gap <80 mg/dL (P < 0.001). Incorporation of the glycemic gap into the APACHE-II score increased the discriminative performance for predicting ICU mortality by increasing the area under the ROC curve from 0.755 to 0.794 (NRI = 13.6%, P = 0.0013).
The glycemic gap can be used to assess the severity and prognosis of critically ill patients with diabetes. The addition of the glycemic gap to the APACHE-II score significantly improved its ability to predict ICU mortality.
doi:10.1097/MD.0000000000001525
PMCID: PMC4616648  PMID: 26356728

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