139 results on '"Leung, H.Y."'
Search Results
2. Consumer support for a public utilities commission in Hong Kong
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Woo, C.K., Cheng, Y.S., Law, A., Zarnikau, J., Ho, S.T., and Leung, H.Y.
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- 2015
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3. Virtual Bidding, Wind Generation and California's Day-Ahead Electricity Forward Premium
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Woo, C.K., Zarnikau, J., Cutter, E., Ho, S.T., and Leung, H.Y.
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- 2015
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4. Loss of ARID1A drives aggressive prostate cancer through aberrant cell cycle signalling
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Hartley, A., primary, Shaw, R., additional, Galbraith, L., additional, Tibbo, A., additional, Blyth, K., additional, Leung, H.Y., additional, and Ahmad, I., additional
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- 2022
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5. MBTPS2 acts as a regulator of lipogenesis and cholesterol synthesis through SREBP signalling in prostate cancer
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Tibbo, A., primary, Hartley, A., additional, Mui, E., additional, Leung, H.Y., additional, and Ahmad, I., additional
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- 2022
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6. Prostate cancer incidence in patients on 5α-reductase inhibitors for lower urinary tract symptoms: A 14-year retrospective study
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Ahmad, I., Small, D.R., Krishna, N.S., Akhtar, M.N., and Leung, H.Y.
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- 2012
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7. Sorptivity of self-compacting concrete containing fly ash and silica fume
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Leung, H.Y., Kim, J., Nadeem, A., Jaganathan, Jayaprakash, and Anwar, M.P.
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Concrete -- Analysis -- Mechanical properties ,Fly ash -- Analysis -- Mechanical properties ,Business ,Construction and materials industries - Abstract
ABSTRACT This paper presents the surface water absorption of self-compacting concrete (SCC) containing fly ash and silica fume using sorptivity test. Ordinary Portland cement was partially replaced by various combinations [...]
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- 2016
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8. Flexural performance of concrete beam splices with different surrounding concretes
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Leung, H.Y.
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- 2003
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9. Flexural behaviour of concrete beams internally reinforced with GFRP rods and steel rebars
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Leung, H.Y. and Balendran, R.V.
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- 2003
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10. Fibre reinforced polymer materials for prestressed concrete structures
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Leung, H.Y., Balendran, R.V., Maqsood, T., Nadeem, A., Rana, T.M., and Tang, W.C.
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- 2003
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11. Strengthening of RC beams: some experimental findings
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Leung, H.Y.
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- 2002
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12. Flexural strengthening of reinforced lightweight polystyrene aggregate concrete beams with near-surface mounted GFRP bars
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Tang, W.C., Balendran, R.V., Nadeem, A., and Leung, H.Y.
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- 2006
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13. Effectiveness of physiotherapy interventions for improving erectile function and climacturia in men after prostatectomy: a systematic review and meta-analysis of randomized controlled trials
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Garbien E. Agnieszka, Lam Ho, Lam C. Kin, Stanley John Winser, Priya Kannan, Leung H.Y. Jeffrey, and Leung C. Hei
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Male ,medicine.medical_specialty ,medicine.medical_treatment ,030232 urology & nephrology ,Psychological intervention ,Physical Therapy, Sports Therapy and Rehabilitation ,law.invention ,03 medical and health sciences ,0302 clinical medicine ,Randomized controlled trial ,law ,medicine ,Humans ,030212 general & internal medicine ,Physical Therapy Modalities ,Randomized Controlled Trials as Topic ,Prostatectomy ,business.industry ,Rehabilitation ,Biofeedback, Psychology ,Erectile function ,medicine.disease ,Sexual Dysfunction, Physiological ,Erectile dysfunction ,Sexual dysfunction ,Meta-analysis ,Physical therapy ,medicine.symptom ,business - Abstract
Objective: To determine the effectiveness of physiotherapy interventions for postprostatectomy erectile dysfunction and climacturia. Data sources: Multiple databases were searched from database inception to February 2019. Review methods: Randomized controlled trials comparing physiotherapy interventions to control were included. Results: The search yielded 127 potentially relevant articles; seven met the inclusion criteria and were included in the review. Meta-analysis of two studies revealed a statistically significant effect of pelvic floor muscle training (PFMT) plus biofeedback compared to the no treatment control group for erectile function at the12-month follow-up period (risk ratio (RR) = 3.65, 95% confidence interval (CI) = 1.02–13.05; P = 0.05). Data from one small study ( n = 31) identified a greater number of men reporting improved climacturia in the PFMT plus electrical stimulation group compared to the no treatment control group, and the overall effect was significant (RR = 15.60, 95% CI = 0.95–254.91; P = 0.05). Meta-analyses of two studies found no statistically significant differences between groups receiving PFMT and no treatment control for erectile function or climacturia at long-term follow-up. Conclusions: PFMT augmented with biofeedback improves erectile function after prostatectomy. Data from a single study found PFMT combined with electrical stimulation to be beneficial for postprostatectomy climacturia. However, electrical stimulation is recommended for terminally ill people only. The effect of PFMT alone on postprostatectomy erectile dysfunction and climacturia remains inconclusive. However, this is likely to be affected by the participant adherence and physiotherapy supervision. High-quality trials providing intensive supervision and due consideration of adherence factors are recommended.
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- 2019
14. Analytical behaviour of concrete beams reinforced with steel rebars and FPR rods
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Leung, H.Y., primary, Kitipornchai, S., additional, Balendran, R.V., additional, and Leung, A.Y.T., additional
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- 2002
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15. P25 - MBTPS2 acts as a regulator of lipogenesis and cholesterol synthesis through SREBP signalling in prostate cancer
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Tibbo, A., Hartley, A., Mui, E., Leung, H.Y., and Ahmad, I.
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- 2022
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16. O09 - Loss of ARID1A drives aggressive prostate cancer through aberrant cell cycle signalling
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Hartley, A., Shaw, R., Galbraith, L., Tibbo, A., Blyth, K., Leung, H.Y., and Ahmad, I.
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- 2022
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17. Analysis of FRP-Reinforced Concrete Beam with Aramid Spirals as Compression Confinement
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Leung, H.Y., primary and Burgoyne, C.J., additional
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- 2001
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18. Compressive Behaviour of Concrete Confined by Aramid Fibre Spirals
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Leung, H.Y., primary and Burgoyne, C.J., additional
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- 2001
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19. Nuclear Accumulation of Histone Deacetylase 4 (HDAC4) Coincides with the Loss of Androgen Sensitivity in Hormone Refractory Cancer of the Prostate
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Halkidou, K, Cook, S, Leung, H.Y, Neal, D.E, and Robson, C.N
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- 2004
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20. Androgen receptor signalling in the prostate
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Gnanapragasam, V.J., Robson, C.N., Leung, H.Y., and Neal, D.E.
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- 2000
21. Fibroblast growth factor receptor-2 mutation analysis in human prostate cancer
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Mehta, P, Robson, C.N, Neal, D.E, and Leung, H.Y
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- 2000
22. TCEAL1 loss sensitises prostate cancer cells to docetaxel treatment
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Rushworth, L.K., primary, Harle, V., additional, Repiscak, P., additional, Clark, W., additional, Shaw, R., additional, Patel, R., additional, and Leung, H.Y., additional
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- 2019
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23. Cost-effectiveness of physiotherapy interventions in neurological rehabilitation: a systematic review of economic evaluation
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Winser, S., primary, Lee, S.H., additional, Law, H.S., additional, Leung, H.Y., additional, Bello, U.M., additional, and Kannan, P., additional
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- 2019
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24. The prognostic significance of androgen receptor phosphorylation and the immune infiltrate in prostate cancer
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Gan, H.W.G., primary, McAllister, M., additional, Constancio, V., additional, Payne, S., additional, Underwood, M.A., additional, Leung, H.Y., additional, and Edwards, J., additional
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- 2018
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25. Androgen receptor phosphorylation status at serine 578 predicts poor outcome in prostate cancer patients
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Patek, S.C., Willder, J.M., Heng, J.S., Taylor, B., Horgan, P.G., Leung, H.Y., Underwood, M.A., and Edwards, J.
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Purpose: Prostate cancer growth is dependent upon androgen receptor (AR) activation, regulated via phosphorylation. Protein kinase C (PKC) is one kinase that can mediate AR phosphorylation. This study aimed to establish if AR phosphorylation by PKC is of prognostic significance.\ud Methods: Immunohistochemistry for AR, AR phosphorylated at Ser-81 (pARS81), AR phosphorylated at Ser-578 (pARS578), PKC and phosphorylated PKC (pPKC) was performed on 90 hormone-naïve prostate cancer specimens. Protein expression was quantified using the weighted histoscore method and examined with regard to clinico-pathological factors and outcome measures; time to biochemical relapse, survival from biochemical relapse and disease-specific survival.\ud Results: Nuclear PKC expression strongly correlated with nuclear pARS578 (c.c. 0.469, p=0.001) and cytoplasmic pARS578 (c.c. 0.426 p=0.002). High cytoplasmic and nuclear pARS578 were associated with disease-specific survival (p
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- 2016
26. SERUM KERATINOCYTE GROWTH FACTOR MEASUREMENT IN PATIENTS WITH PROSTATE CANCER
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MEHTA, P.B., ROBSON, C.N., NEAL, D.E., and LEUNG, H.Y.
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- 2000
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27. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
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Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. Atherton, S.S. Atkin, J.D. Attardi, L.D. Auberger, P. Auburger, G. Aurelian, L. Autelli, R. Avagliano, L. Avantaggiati, M.L. Avrahami, L. Azad, N. Awale, S. Bachetti, T. Backer, J.M. Bae, D.-H. Bae, J.-S. Bae, O.-N. Bae, S.H. Baehrecke, E.H. Baek, S.-H. Baghdiguian, S. Bagniewska-Zadworna, A. Bai, H. Bai, J. Bai, X.-Y. Bailly, Y. Balaji, K.N. Balduini, W. Ballabio, A. Balzan, R. Banerjee, R. Bánhegyi, G. Bao, H. Barbeau, B. Barrachina, M.D. Barreiro, E. Bartel, B. Bartolomé, A. Bassham, D.C. Bassi, M.T. Bast, R.C., Jr. Basu, A. Batista, M.T. Batoko, H. Battino, M. Bauckman, K. Baumgarner, B.L. Bayer, K.U. Beale, R. Beaulieu, J.-F. Beck, G.R., Jr. Becker, C. Beckham, J.D. Bédard, P.-A. Bednarski, P.J. Begley, T.J. Behl, C. Behrends, C. Behrens, G.M.N. Behrns, K.E. Bejarano, E. Belaid, A. Belleudi, F. Bénard, G. Berchem, G. Bergamaschi, D. Bergami, M. Berkhout, B. Berliocchi, L. Bernard, A. Bernard, M. Bernassola, F. Bertolotti, A. Bess, A.S. Besteiro, S. Bettuzzi, S. Bhalla, S. Bhattacharyya, S. Bhutia, S.K. Biagosch, C. Bianchi, M.W. Biard-Piechaczyk, M. Billes, V. Bincoletto, C. Bingol, B. Bird, S.W. Bitoun, M. Bjedov, I. Blackstone, C. Blanc, L. Blanco, G.A. Blomhoff, H.K. Boada-Romero, E. Böckler, S. Boes, M. Boesze-Battaglia, K. Boise, L.H. Bolino, A. Boman, A. Bonaldo, P. Bordi, M. Bosch, J. Botana, L.M. Botti, J. Bou, G. Bouché, M. Bouchecareilh, M. Boucher, M.-J. Boulton, M.E. Bouret, S.G. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N. Braga, V.M.M. Brancolini, C. Braus, G.H. Bravo-San-Pedro, J.M. Brennan, L.A. Bresnick, E.H. Brest, P. Bridges, D. Bringer, M.-A. Brini, M. Brito, G.C. Brodin, B. Brookes, P.S. Brown, E.J. Brown, K. Broxmeyer, H.E. Bruhat, A. Brum, P.C. Brumell, J.H. Brunetti-Pierri, N. Bryson-Richardson, R.J. Buch, S. Buchan, A.M. Budak, H. Bulavin, D.V. Bultman, S.J. Bultynck, G. Bumbasirevic, V. Burelle, Y. Burke, R.E. Burmeister, M. Bütikofer, P. Caberlotto, L. Cadwell, K. Cahova, M. Cai, D. Cai, J. Cai, Q. Calatayud, S. Camougrand, N. Campanella, M. Campbell, G.R. Campbell, M. Campello, S. Candau, R. Caniggia, I. Cantoni, L. Cao, L. Caplan, A.B. Caraglia, M. Cardinali, C. Cardoso, S.M. Carew, J.S. Carleton, L.A. Carlin, C.R. Carloni, S. Carlsson, S.R. Carmona-Gutierrez, D. Carneiro, L.A.M. Carnevali, O. Carra, S. Carrier, A. Carroll, B. Casas, C. Casas, J. Cassinelli, G. Castets, P. Castro-Obregon, S. Cavallini, G. Ceccherini, I. Cecconi, F. Cederbaum, A.I. Ceña, V. Cenci, S. Cerella, C. Cervia, D. Cetrullo, S. Chaachouay, H. Chae, H.-J. Chagin, A.S. Chai, C.-Y. Chakrabarti, G. Chamilos, G. Chan, E.Y.W. Chan, M.T.V. Chandra, D. Chandra, P. Chang, C.-P. Chang, R.C.-C. Chang, T.Y. Chatham, J.C. Chatterjee, S. Chauhan, S. Che, Y. Cheetham, M.E. Cheluvappa, R. Chen, C.-J. Chen, G. Chen, G.-C. Chen, G. Chen, H. Chen, J.W. Chen, J.-K. Chen, M. Chen, M. Chen, P. Chen, Q. Chen, Q. Chen, S.-D. Chen, S. Chen, S.S.-L. Chen, W. Chen, W.-J. Chen, W.Q. Chen, W. Chen, X. Chen, Y.-H. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Y.-Q. Chen, Y. Chen, Z. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, H. Cheong, H. Cherry, S. Chesney, J. Cheung, C.H.A. Chevet, E. Chi, H.C. Chi, S.-G. Chiacchiera, F. Chiang, H.-L. Chiarelli, R. Chiariello, M. Chieppa, M. Chin, L.-S. Chiong, M. Chiu, G.N.C. Cho, D.-H. Cho, S.-G. Cho, W.C. Cho, Y.-Y. Cho, Y.-S. Choi, A.M.K. Choi, E.-J. Choi, E.-K. Choi, J. Choi, M.E. Choi, S.-I. Chou, T.-F. Chouaib, S. Choubey, D. Choubey, V. Chow, K.-C. Chowdhury, K. Chu, C.T. Chuang, T.-H. Chun, T. Chung, H. Chung, T. Chung, Y.-L. Chwae, Y.-J. Cianfanelli, V. Ciarcia, R. Ciechomska, I.A. Ciriolo, M.R. Cirone, M. Claerhout, S. Clague, M.J. Cl� ria, J. Clarke, P.G.H. Clarke, R. Clementi, E. Cleyrat, C. Cnop, M. Coccia, E.M. Cocco, T. Codogno, P. Coers, J. Cohen, E.E.W. Colecchia, D. Coletto, L. Coll, N.S. Colucci-Guyon, E. Comincini, S. Condello, M. Cook, K.L. Coombs, G.H. Cooper, C.D. Cooper, J.M. Coppens, I. Corasaniti, M.T. Corazzari, M. Corbalan, R. Corcelle-Termeau, E. Cordero, M.D. Corral-Ramos, C. Corti, O. Cossarizza, A. Costelli, P. Costes, S. Cotman, S.L. Coto-Montes, A. Cottet, S. Couve, E. Covey, L.R. Cowart, L.A. Cox, J.S. Coxon, F.P. Coyne, C.B. Cragg, M.S. Craven, R.J. Crepaldi, T. Crespo, J.L. Criollo, A. Crippa, V. Cruz, M.T. Cuervo, A.M. Cuezva, J.M. Cui, T. Cutillas, P.R. Czaja, M.J. Czyzyk-Krzeska, M.F. Dagda, R.K. Dahmen, U. Dai, C. Dai, W. Dai, Y. Dalby, K.N. Valle, L.D. Dalmasso, G. D'amelio, M. Damme, M. Darfeuille-Michaud, A. Dargemont, C. Darley-Usmar, V.M. Dasarathy, S. Dasgupta, B. Dash, S. Dass, C.R. Davey, H.M. Davids, L.M. Dávila, D. Davis, R.J. Dawson, T.M. Dawson, V.L. Daza, P. de Belleroche, J. de Figueiredo, P. de Figueiredo, R.C.B.Q. de la Fuente, J. De Martino, L. De Matteis, A. De Meyer, G.R.Y. De Milito, A. De Santi, M. de Souza, W. De Tata, V. De Zio, D. Debnath, J. Dechant, R. Decuypere, J.-P. Deegan, S. Dehay, B. Del Bello, B. Del Re, D.P. Delage-Mourroux, R. Delbridge, L.M.D. Deldicque, L. Delorme-Axford, E. Deng, Y. Dengjel, J. Denizot, M. Dent, P. Der, C.J. Deretic, V. Derrien, B. Deutsch, E. Devarenne, T.P. Devenish, R.J. Di Bartolomeo, S. Di Daniele, N. Di Domenico, F. Di Nardo, A. Di Paola, S. Di Pietro, A. Di Renzo, L. Di Antonio, A. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dickey, C.A. Dickson, R.C. Diederich, M. Digard, P. Dikic, I. Dinesh-Kumar, S.P. Ding, C. Ding, W.-X. Ding, Z. Dini, L. Distler, J.H.W. Diwan, A. Djavaheri-Mergny, M. Dmytruk, K. Dobson, R.C.J. Doetsch, V. Dokladny, K. Dokudovskaya, S. Donadelli, M. Dong, X.C. Dong, X. Dong, Z. Donohue, T.M., Jr. Donohue-Jr, T.M. Doran, K.S. D'orazi, G. Dorn, G.W., II Dosenko, V. Dridi, S. Drucker, L. Du, J. Du, L.-L. Du, L. du Toit, A. Dua, P. Duan, L. Duann, P. Dubey, V.K. Duchen, M.R. Duchosal, M.A. Duez, H. Dugail, I. Dumit, V.I. Duncan, M.C. Dunlop, E.A. Dunn, W.A., Jr. Dupont, N. Dupuis, L. Durán, R.V. Durcan, T.M. Duvezin-Caubet, S. Duvvuri, U. Eapen, V. Ebrahimi-Fakhari, D. Echard, A. Eckhart, L. Edelstein, C.L. Edinger, A.L. Eichinger, L. Eisenberg, T. Eisenberg-Lerner, A. Eissa, N.T. El-Deiry, W.S. El-Khoury, V. Elazar, Z. Eldar-Finkelman, H. Elliott, C.J.H. Emanuele, E. Emmenegger, U. Engedal, N. Engelbrecht, A.-M. Engelender, S. Enserink, J.M. Erdmann, R. Erenpreisa, J. Eri, R. Eriksen, J.L. Erman, A. Escalante, R. Eskelinen, E.-L. Espert, L. Esteban-Martínez, L. Evans, T.J. Fabri, M. Fabrias, G. Fabrizi, C. Facchiano, A. Færgeman, N.J. Faggioni, A. Fairlie, W.D. Fan, C. Fan, D. Fan, J. Fang, S. Fanto, M. Fanzani, A. Farkas, T. Faure, M. Favier, F.B. Fearnhead, H. Federici, M. Fei, E. Felizardo, T.C. Feng, H. Feng, Y. Feng, Y. Ferguson, T.A. Fernández, Á.F. Fernandez-Barrena, M.G. Fernandez-Checa, J.C. Fernández-López, A. Fernandez-Zapico, M.E. Feron, O. Ferraro, E. Ferreira-Halder, C.V. Fesus, L. Feuer, R. Fiesel, F.C. Filippi-Chiela, E.C. Filomeni, G. Fimia, G.M. Fingert, J.H. Finkbeiner, S. Finkel, T. Fiorito, F. Fisher, P.B. Flajolet, M. Flamigni, F. Florey, O. Florio, S. Floto, R.A. Folini, M. Follo, C. Fon, E.A. Fornai, F. Fortunato, F. Fraldi, A. Franco, R. Francois, A. François, A. Frankel, L.B. Fraser, I.D.C. Frey, N. Freyssenet, D.G. Frezza, C. Friedman, S.L. Frigo, D.E. Fu, D. Fuentes, J.M. Fueyo, J. Fujitani, Y. Fujiwara, Y. Fujiya, M. Fukuda, M. Fulda, S. Fusco, C. Gabryel, B. Gaestel, M. Gailly, P. Gajewska, M. Galadari, S. Galili, G. Galindo, I. Galindo, M.F. Galliciotti, G. Galluzzi, L. Galluzzi, L. Galy, V. Gammoh, N. Gandy, S. Ganesan, A.K. Ganesan, S. Ganley, I.G. Gannagé, M. Gao, F.-B. Gao, F. Gao, J.-X. Nannig, L.G. Véscovi, E.G. Garcia-Macía, M. Garcia-Ruiz, C. Garg, A.D. Garg, P.K. Gargini, R. Gassen, N.C. Gatica, D. Gatti, E. Gavard, J. Gavathiotis, E. Ge, L. Ge, P. Ge, S. Gean, P.-W. Gelmetti, V. Genazzani, A.A. Geng, J. Genschik, P. Gerner, L. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghigo, E. Ghosh, D. Giammarioli, A.M. Giampieri, F. Giampietri, C. Giatromanolaki, A. Gibbings, D.J. Gibellini, L. Gibson, S.B. Ginet, V. Giordano, A. Giorgini, F. Giovannetti, E. Girardin, S.E. Gispert, S. Giuliano, S. Gladson, C.L. Glavic, A. Gleave, M. Godefroy, N. Gogal, R.M., Jr. Gokulan, K. Goldman, G.H. Goletti, D. Goligorsky, M.S. Gomes, A.V. Gomes, L.C. Gomez, H. Gomez-Manzano, C. Gómez-Sánchez, R. Gonçalves, D.A.P. Goncu, E. Gong, Q. Gongora, C. Gonzalez, C.B. Gonzalez-Alegre, P. Gonzalez-Cabo, P. González-Polo, R.A. Goping, I.S. Gorbea, C. Gorbunov, N.V. Goring, D.R. Gorman, A.M. Gorski, S.M. Goruppi, S. Goto-Yamada, S. Gotor, C. Gottlieb, R.A. Gozes, I. Gozuacik, D. Graba, Y. Graef, M. Granato, G.E. Grant, G.D. Grant, S. Gravina, G.L. Green, D.R. Greenhough, A. Greenwood, M.T. Grimaldi, B. Gros, F. Grose, C. Groulx, J.-F. Gruber, F. Grumati, P. Grune, T. Guan, J.-L. Guan, K.-L. Guerra, B. Guillen, C. Gulshan, K. Gunst, J. Guo, C. Guo, L. Guo, M. Guo, W. Guo, X.-G. Gust, A.A. Gustafsson, Å.B. Gutierrez, E. Gutierrez, M.G. Gwak, H.-S. Haas, A. Haber, J.E. Hadano, S. Hagedorn, M. Hahn, D.R. Halayko, A.J. 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- Published
- 2016
28. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
- Author
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Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. 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Pozuelo-Rubio, M. Prak, K. Prange, R. Prescott, M. Priault, M. Prince, S. Proia, R.L. Proikas-Cezanne, T. Prokisch, H. Promponas, V.J. Przyklenk, K. Puertollano, R. Pugazhenthi, S. Puglielli, L. Pujol, A. Puyal, J. Pyeon, D. Qi, X. Qian, W.-B. Qin, Z.-H. Qiu, Y. Qu, Z. Quadrilatero, J. Quinn, F. Raben, N. Rabinowich, H. Radogna, F. Ragusa, M.J. Rahmani, M. Raina, K. Ramanadham, S. Ramesh, R. Rami, A. Randall-Demllo, S. Randow, F. Rao, H. Rao, V.A. Rasmussen, B.B. Rasse, T.M. Ratovitski, E.A. Rautou, P.-E. Ray, S.K. Razani, B. Reed, B.H. Reggiori, F. Rehm, M. Reichert, A.S. Rein, T. Reiner, D.J. Reits, E. Ren, J. Ren, X. Renna, M. Reusch, J.E.B. Revuelta, J.L. Reyes, L. Rezaie, A.R. Richards, R.I. Richardson, R. Richetta, C. Riehle, M.A. Rihn, B.H. Rikihisa, Y. Riley, B.E. Rimbach, G. Rippo, M.R. Ritis, K. Rizzi, F. Rizzo, E. Roach, P.J. Robbins, J. Roberge, M. Roca, G. Roccheri, M.C. Rocha, S. Rodrigues, C.M.P. Rodríguez, C.I. de Cordoba, S.R. Rodriguez-Muela, N. Roelofs, J. Rogov, V.V. Rohn, T.T. Rohrer, B. Romanelli, D. Romani, L. Romano, P.S. Roncero, M.I.G. Rosa, J.L. Rosello, A. Rosen, K.V. Rosenstiel, P. Rost-Roszkowska, M. Roth, K.A. Roué, G. Rouis, M. Rouschop, K.M. Ruan, D.T. Ruano, D. Rubinsztein, D.C. Rucker, E.B., III Rudich, A. Rudolf, E. Rudolf, R. Ruegg, M.A. Ruiz-Roldan, C. Ruparelia, A.A. Rusmini, P. Russ, D.W. Russo, G.L. Russo, G. Russo, R. Rusten, T.E. Ryabovol, V. Ryan, K.M. Ryter, S.W. Sabatini, D.M. Sacher, M. Sachse, C. Sack, M.N. Sadoshima, J. Saftig, P. Sagi-Eisenberg, R. Sahni, S. Saikumar, P. Saito, T. Saitoh, T. Sakakura, K. Sakoh-Nakatogawa, M. Sakuraba, Y. Salazar-Roa, M. Salomoni, P. Saluja, A.K. Salvaterra, P.M. Salvioli, R. Samali, A. Sanchez, A.M.J. Sánchez-Alcázar, J.A. Sanchez-Prieto, R. Sandri, M. Sanjuan, M.A. Santaguida, S. Santambrogio, L. Santoni, G. Dos Santos, C.N. Saran, S. Sardiello, M. Sargent, G. Sarkar, P. Sarkar, S. Sarrias, M.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. Schönenberger, M.J. Schönthal, A.H. Schorderet, D.F. Schröder, 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. Seguí-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.-K.J. Shen, C.-C. Shen, H.-M. Shen, S. Shen, W. Sheng, R. Sheng, X. Sheng, Z.-H. Shepherd, T.G. Shi, J. Shi, Q. Shi, Q. Shi, Y. Shibutani, S. Shibuya, K. Shidoji, Y. Shieh, J.-J. Shih, C.-M. 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.-W. 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.-U. 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.N. Sittler, A. Siu, P.M. Sivridis, E. Skwarska, A. Slack, R. Slaninová, I. Slavov, N. Smaili, S.S. Smalley, K.S.M. 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.-X. 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. Clair, D.S. 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. Ström, A.-L. Stromhaug, P. Stulik, J. Su, Y.-X. Su, Z. Subauste, C.S. Subramaniam, S. Sue, C.M. Suh, S.W. Sui, X. Sukseree, S. Sulzer, D. Sun, F.-L. Sun, J. Sun, J. Sun, S.-Y. 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. Swärd, 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.G. Takacs-Vellai, K. Takahashi, Y. Takáts, S. Takemura, G. Takigawa, N. Talbot, N.J. Tamagno, E. Tamburini, J. Tan, C.-P. Tan, L. Tan, M.L. Tan, M. Tan, Y.-J. 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.-B. Teng, R.-J. Terro, F. Tettamanti, G. Theiss, A.L. Theron, A.E. Thomas, K.J. Thomé, M.P. Thomes, P.G. Thorburn, A. Thorner, J. Thum, T. Thumm, M. Thurston, T.L.M. Tian, L. Till, A. Ting, J.P.-Y. Ting, J.P.Y. 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.-J. Tschan, M.P. Tseng, Y.-H. Tsukuba, T. Tsung, A. Tsvetkov, A.S. Tu, S. Tuan, H.-Y. Tucci, M. Tumbarello, D.A. Turk, B. Turk, V. Turner, R.F.B. 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. Uzcátegui, N.L. Vaccari, T. Vaccaro, M.I. Váchová, 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.W. van Doorn, W.G. van Egmond, M. van Golen, K.L. Van Kaer, L. Campagne, M.L. 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.T. Verdier, M. Vertessy, B.G. Viale, A. Vidal, M. Vieira, H.L.A. 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.-Y. Wang, C. Wang, C. Wang, C. Wang, D. Wang, F. Wang, F. Wang, G. Wang, H.-J. Wang, H. Wang, H.-G. Wang, H. Wang, H.-D. Wang, J. Wang, J. Wang, M. Wang, M.-Q. Wang, P.-Y. Wang, P. Wang, R.C. Wang, S. Wang, T.-F. Wang, X. Wang, X.-J. Wang, X.-W. Wang, X. Wang, X. Wang, Y. Wang, Y. Wang, Y. Wang, Y.-J. Wang, Y. Wang, Y. Wang, Y.T. Wang, Y. Wang, Z.-N. Wappner, P. Ward, C. Ward, D.M.V. 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.W. 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.K. Wu, Y. Wu, Z. Xavier, C.P.R. Xavier, R.J. Xia, G.-X. Xia, T. Xia, W. Xia, Y. Xiao, H. Xiao, J. Xiao, S. Xiao, W. Xie, C.-M. 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.-X. 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.-S. Yang, J.-M. Yang, L. Yang, M. Yang, P.-M. Yang, P. Yang, Q. Yang, W. Yang, W.Y. Yang, X. Yang, Y. Yang, Y. Yang, Z. Yang, Z. Yao, M.-C. 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.-M. Yip, C.K. Yoo, Y.-M. Yoo, Y.H. Yoon, S.-Y. Yoshida, K.-I. Yoshimori, T. Young, K.H. Yu, H. Yu, J.J. Yu, J.-T. Yu, J. Yu, L. Yu, W.H. Yu, X.-F. Yu, Z. Yuan, J. Yuan, Z.-M. Yue, B.Y.J.T. 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.-C. Zhang, H. Zhang, H. Zhang, H. Zhang, J. Zhang, J. Zhang, J. Zhang, J.-P. Zhang, L. Zhang, L. Zhang, L. Zhang, M.-Y. Zhang, X. Zhang, X.D. Zhang, Y. Zhang, Y. Zhang, Y. Zhang, Y. Zhang, Y. Zhao, M. Zhao, W.-L. Zhao, X. Zhao, Y.G. Zhao, Y. Zhao, Y. Zhao, Y.-X. Zhao, Z. Zhao, Z.J. Zheng, D. Zheng, X.-L. Zheng, X. Zhivotovsky, B. Zhong, Q. Zhou, G.-Z. Zhou, G. Zhou, H. Zhou, S.-F. Zhou, X.-J. Zhu, H. Zhu, H. Zhu, W.-G. Zhu, W. Zhu, X.-F. Zhu, Y. Zhuang, S.-M. Zhuang, X. Ziparo, E. Zois, C.E. Zoladek, T. Zong, W.-X. Zorzano, A. Zughaier, S.M.
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- 2016
29. Identification of a candidate prognostic gene signature by transcriptome analysis of matched pre-and post-treatment prostatic biopsies from patients with advanced prostate cancer
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Rajan, P., Stockley, J., Sudbery, I.M., Fleming, J.T., Hedley, A., Kalna, G., Sims, D., Ponting, C.P., Heger, A., Robson, C.N., McMenemin, R.M., Pedley, I.D., and Leung, H.Y.
- Abstract
Background: Although chemotherapy for prostate cancer (PCa) can improve patient survival, some tumours are\ud chemo-resistant. Tumour molecular profiles may help identify the mechanisms of drug action and identify potential\ud prognostic biomarkers. We performed in vivo transcriptome profiling of pre- and post-treatment prostatic biopsies\ud from patients with advanced hormone-naive prostate cancer treated with docetaxel chemotherapy and androgen\ud deprivation therapy (ADT) with an aim to identify the mechanisms of drug action and identify prognostic biomarkers.\ud \ud Methods: RNA sequencing (RNA-Seq) was performed on biopsies from four patients before and ~22 weeks after\ud docetaxel and ADT initiation. Gene fusion products and differentially-regulated genes between treatment pairs were\ud identified using TopHat and pathway enrichment analyses undertaken. Publically available datasets were interrogated\ud to perform survival analyses on the gene signatures identified using cBioportal.\ud \ud Results: A number of genomic rearrangements were identified including the TMPRSS2/ERG fusion and 3 novel gene\ud fusions involving the ETS family of transcription factors in patients, both pre and post chemotherapy. In total, gene\ud expression analyses showed differential expression of at least 2 fold in 575 genes in post-chemotherapy biopsies. Of\ud these, pathway analyses identified a panel of 7 genes (ADAM7, FAM72B, BUB1B, CCNB1, CCNB2, TTK, CDK1), including\ud a cell cycle-related geneset, that were differentially-regulated following treatment with docetaxel and ADT. Using\ud cBioportal to interrogate the MSKCC-Prostate Oncogenome Project dataset we observed a statistically-significant\ud reduction in disease-free survival of patients with tumours exhibiting alterations in gene expression of the above\ud panel of 7 genes (p = 0.015).\ud \ud Conclusions: Here we report on the first “real-time” in vivo RNA-Seq-based transcriptome analysis of clinical PCa from\ud pre- and post-treatment TRUSS-guided biopsies of patients treated with docetaxel chemotherapy plus ADT. We identify\ud a chemotherapy-driven PCa transcriptome profile which includes the down-regulation of important positive regulators\ud of cell cycle progression. A 7 gene signature biomarker panel has also been identified in high-risk prostate cancer\ud patients to be of prognostic value. Future prospective study is warranted to evaluate the clinical value of this panel.
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- 2014
30. P67 - TCEAL1 loss sensitises prostate cancer cells to docetaxel treatment
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Rushworth, L.K., Harle, V., Repiscak, P., Clark, W., Shaw, R., Patel, R., and Leung, H.Y.
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- 2019
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31. 17P - The prognostic significance of androgen receptor phosphorylation and the immune infiltrate in prostate cancer
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Gan, H.W.G., McAllister, M., Constancio, V., Payne, S., Underwood, M.A., Leung, H.Y., and Edwards, J.
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- 2018
- Full Text
- View/download PDF
32. Sprouty2, PTEN, and PP2A interact to regulate prostate cancer progression
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Patel, R., Gao, M, Ahmad, I., Fleming, J., Singh, L.B., Rai, T.S., McKie, A.B., Seywright, M., Barnetson, R.J., Edwards, J., Sansom, O.J., and Leung, H.Y.
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endocrine system - Abstract
Concurrent activation of RAS/ERK and PI3K/AKT pathways is implicated in prostate cancer progression. The negative regulators of these pathways, including sprouty2 (SPRY2), protein phosphatase 2A (PP2A), and phosphatase and tensin homolog (PTEN), are commonly inactivated in prostate cancer. The molecular basis of cooperation between these genetic alterations is unknown. Here, we show that SPRY2 deficiency alone triggers activation of AKT and ERK, but this is insufficient to drive tumorigenesis. In addition to AKT and ERK activation, SPRY2 loss also activates a PP2A-dependent tumor suppressor checkpoint. Mechanistically, the PP2A-mediated growth arrest depends on GSK3β and is ultimately mediated by nuclear PTEN. In murine prostate cancer models, Pten haploinsufficiency synergized with Spry2 deficiency to drive tumorigenesis, including metastasis. Together, these results show that loss of Pten cooperates with Spry2 deficiency by bypassing a novel tumor suppressor checkpoint. Furthermore, loss of SPRY2 expression correlates strongly with loss of PTEN and/or PP2A subunits in human prostate cancer. This underlines the cooperation between SPRY2 deficiency and PTEN or PP2A inactivation in promoting tumorigenesis. Overall, we propose SPRY2, PTEN, and PP2A status as an important determinant of prostate cancer progression. Characterization of this trio may facilitate patient stratification for targeted therapies and chemopreventive interventions.
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- 2013
33. Targeting the DNA double strand break repair machinery in prostate cancer
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Shaheen, F.S., Znojek, P., Fisher, A., Webster, M., Plummer, R., Gaughan, L., Smith, G.C. M., Leung, H.Y., Curtin, N.J., and Robson, C.N.
- Abstract
Regardless of the achievable remissions with first line hormone therapy in patients with prostate cancer (CaP), the disease escapes the hormone dependent stage to a more aggressive status where chemotherapy is the only effective treatment and no treatment is curative. This makes it very important to identify new targets that can improve the outcome of treatment. ATM and DNA-PK are the two kinases responsible for signalling and repairing double strand breaks (DSB). Thus, both kinases are pertinent targets in CaP treatment to enhance the activity of the numerous DNA DSB inducing agents used in CaP treatment such as ionizing radiation (IR). Colony formation assay was used to assess the sensitivity of hormone dependent, p53 wt (LNCaP) and hormone independent p53 mutant (PC3) CaP cell lines to the cytotoxic effect of IR and Doxorubicin in the presence or absence of Ku55933 and NU7441 which are small molecule inhibitors of ATM and DNA-PK, respectively. Flow cytometry based methods were used to assess the effect of the two inhibitors on cell cycle, apoptosis and H2AX foci formation. Neutral comet assay was used to assess the induction of DNA DSBs. Ku55933 or NU7441 alone increased the sensitivity of CaP cell lines to the DNA damaging agents, however combining both inhibitors together resulted in further enhancement of sensitivity. The cell cycle profile of both cell lines was altered with increased cell death, DNA DSBs and H2AX foci formation. This study justifies further evaluation of the ATM and DNA-PK inhibitors for clinical application in CaP patients. Additionally, the augmented effect resulting from combining both inhibitors may have a significant implication for the treatment of CaP patients who have a defect in one of the two DSB repair pathways
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- 2011
34. Identification of novel androgen-regulated pathways and mRNA isoforms through genome-wide exon-specific profiling of the LNCaP transcriptome
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Chan, F.L., Rajan, P., Dalgliesh, C., Carling, P.J., Buist, T., Zhang, C., Grellscheid, S.N., Armstrong, K., Stockley, J., Simillion, C., Gaughan, L., Kalna, G., Zhang, M.Q., Robson, C.N., Leung, H.Y., and Elliott, D.J.
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urologic and male genital diseases - Abstract
Androgens drive the onset and progression of prostate cancer (PCa) by modulating androgen receptor (AR) transcriptional activity. Although several microarray-based studies have identified androgen-regulated genes, here we identify in-parallel global androgen-dependent changes in both gene and alternative mRNA isoform expression by exon-level analyses of the LNCaP transcriptome. While genome-wide gene expression changes correlated well with previously-published studies, we additionally uncovered a subset of 226 novel androgen-regulated genes. Gene expression pathway analysis of this subset revealed gene clusters associated with, and including the tyrosine kinase LYN, as well as components of the mTOR (mammalian target of rapamycin) pathway, which is commonly dysregulated in cancer. We also identified 1279 putative androgen-regulated alternative events, of which 325 (similar to 25%) mapped to known alternative splicing events or alternative first/last exons. We selected 30 androgen-dependent alternative events for RT-PCR validation, including mRNAs derived from genes encoding tumour suppressors and cell cycle regulators. Of seven positively-validating events (similar to 23%), five events involved transcripts derived from alternative promoters of known AR gene targets. In particular, we found a novel androgen-dependent mRNA isoform derived from an alternative internal promoter within the TSC2 tumour suppressor gene, which is predicted to encode a protein lacking an interaction domain required for mTOR inhibition. We confirmed that expression of this alternative TSC2 mRNA isoform was directly regulated by androgens, and chromatin immunoprecipitation indicated recruitment of AR to the alternative promoter region at early timepoints following androgen stimulation, which correlated with expression of alternative transcripts. Together, our data suggest that alternative mRNA isoform expression might mediate the cellular response to androgens, and may have roles in clinical PCa
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- 2011
35. Src family kinase activity is up-regulated in hormone refractory prostate cancer
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Tatarov, O., Mitchell, T.J., Seywright, M., Leung, H.Y., Brunton, V.G., and Edwards, J.
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RC0254 - Abstract
Purpose: Although Src family kinase (SFK) inhibitors are now in clinical trials for the treatment of androgen-independent prostate cancer (AIPC), there are no studies relating SFK activation to patient survival. This study was designed to determine if SFK activation was up-regulated with the development of AIPC and if patients could be selected who were more likely to respond to therapy.\ud \ud Experimental Design: A unique cohort of matched prostate tumor samples, taken before hormone deprivation therapy and following hormone relapse, was used to determine by immunohistochemistry on an individual patient basis if SFK activity changed with progression to AIPC and whether this related to patient outcome measures. Using matched, hormone-sensitive and hormone-refractory cell lines, we determined if hormone status affected the way prostate cancer cells respond to suppression of SFK activity by the small-molecule inhibitor dasatinib.\ud \ud Results: In the current study, 28% of patients with AIPC exhibited an increase in SFK activity in prostate cancer tissue, these patients had significantly shorter overall survival (PConclusion: Appropriate patient selection may allow better targeting of prostate cancer patients who are likely to respond to the treatment with SFK inhibitors at the same time improving the outcome of clinical trials.
- Published
- 2009
36. Aberrant expression of extracellular signal-regulated kinase 5 in human prostate cancer
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McCracken, S.R.C., Ramsay, A., Heer, R., Mathers, M.E., Jenkins, B.L., Edwards, J., Robson, C.N., Marquez, R., Cohen, P., and Leung, H.Y.
- Subjects
RC0254 - Abstract
Abnormal intracellular signaling contributes to carcinogenesis and may represent novel therapeutic targets. mitogen/extracellular signal-regulated kinase kinase-5 (MEK5) overexpression is associated with aggressive prostate cancer. In this study, we examined the role of extracellular signal-regulated kinase (ERK5, an MAPK and specific substrate for MEK5) in prostate cancer. ERK5 immunoreactivity was significantly upregulated in high-grade prostate cancer when compared to benign prostatic hyperplasia (PPP=0.0044) and locally advanced disease at diagnosis (P=0.0023), with a weak association with shorter disease-specific survival (P=0.036). A subgroup of patients showed strong nuclear ERK5 localization, which correlated with poor disease-specific survival and, on multivariant analysis, was an independent prognostic factor (PP=0.0078). Similarly, ERK5 protein expression was increased in an androgen-independent LNCaP subline. We obtained the following in vitro and in vivo evidence to support the above expression data: (1) cotransfection of ERK5wt and MEK5D constructs in PC3 cells results in predominant ERK5 nuclear localization, similar to that observed in aggressive clinical disease; (2) ERK5-overexpressing PC3 cells have enhanced proliferative, migrative and invasive capabilities in vitro (Pin vivo (P
- Published
- 2008
37. Editorial comment on: increased expression of tumor-associated trypsin inhibitor, TATI, in prostate cancer and in androgen-independent 22Rv1 cells
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Edwards, J. and Leung, H.Y.
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RC0254 - Abstract
No abstract available.
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- 2007
38. Effective Allocation of Database Buffers by Mining Users' Access Histories
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Feng, L., Li, Q, Leung, H.Y., and Databases (Former)
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DB-DM: DATA MINING ,EWI-6963 - Abstract
The problem of database buffer management has extensively been studied for nearly three decades. In this paper, we explore the use of newly emerging data mining technology to tackle the traditional buffer management issue. In particular, we address the buffer size setting problem for distributed database systems. The main goal is to minimize physical I/O while achieving better buffer utilization at the same time. Different from the traditional buffer management strategies where limited knowledge of user access patterns is analyzed and used, our buffer allocation mechanism extracts knowledge from historical reference streams, and then determines the optimal buffer space based on the discovered knowledge. Simulation experiments show that the proposed method can achieve an optimal buffer allocation solution for distributed database systems.
- Published
- 2002
39. Adaptive reversible data hiding based on block median preservation and modification of prediction errors
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Leung, H.Y., primary, Cheng, L.M., additional, Liu, F., additional, and Fu, Q.K., additional
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- 2013
- Full Text
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40. Field measurements of natural periods of vibration and structural damping of wind-excited tall residential buildings
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Campbell, S., Kwok, K.C.S., Hitchcock, P.A., Tse, K.T., Leung, H.Y., Campbell, S., Kwok, K.C.S., Hitchcock, P.A., Tse, K.T., and Leung, H.Y.
- Abstract
Field measurements of the wind-induced response of two residential reinforced concrete buildings, among the tallest in the world, have been performed during two typhoons. Natural periods and damping values have been deter-mined and compared with other field measurements and empirical predictors. Suitable and common empirical predictors of natural period and structural damping have been obtained that describe the trend of tall, reinforced concrete buildings whose structural vibrations have been measured in the collection of studies in Hong Kong compiled by the authors. This data is especially important as the amount of information known about the dynamic parameters of buildings of these heights is limited. Effects of the variation of the natural period and damping values on the alongwind response of a tall building for serviceability-level wind conditions have been profiled using the gust response factor approach. When using this approach on these two buildings, the often overestimated natural periods and structural damping values suggested by empirical predictors tended to offset each other. Gust response factors calculated using the natural periods and structural damping values measured in the field were smaller than if calculated using design-stage values.
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- 2007
41. Mitogenic growth signalling, DNA replication licensing, and survival are linked in prostate cancer
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Dudderidge, Tim, McCracken, S.R., Loddo, Marco, Fanshawe, Thomas, Kelly, J.D., Neal, D.E., Leung, H.Y., Williams, Gareth, Stoeber, Kai, Dudderidge, Tim, McCracken, S.R., Loddo, Marco, Fanshawe, Thomas, Kelly, J.D., Neal, D.E., Leung, H.Y., Williams, Gareth, and Stoeber, Kai
- Abstract
Activation of mitogen/extracellular-signal-regulated kinase kinase 5/extracellular signal-regulated kinase-5 (MEK5/ERK5) growth signalling is coupled to increased cell proliferation in prostate cancer (PCa). Dysregulation of the DNA replication licensing pathway, a critical step in growth control downstream of transduction signalling pathways, is associated with development of PCa. In this study we have investigated linkages between the MEK5/ERK5 pathway and DNA replication licensing during prostate carcinogenesis. The effects of increased MEK5/ERK5 signalling on the expression of replication licensing factors Mcm2 and geminin and the proliferation marker Ki67 were studied in an ecdysone-inducible system expressing a constitutively activated mutant of MEK5 in EcR293 cells and in stable ERK5 over-expressing PC3 clones. In parallel, expression of these biomarkers in PCa biopsy specimens (n=58) was studied and compared to clinicopathological parameters. In both in vitro systems induction of MEK5 expression resulted in increased levels of phosphorylated ERK5 and Mcm2, geminin and Ki67 proteins. In PCa specimens average Mcm2 expression was greater than Ki67 and geminin expression (median labelling index (LI) 36.7, 18.1, and 3.4% respectively), consistent with their differential expression according to growth status (P<0.0001). Mcm2, geminin and Ki67 expression were significantly associated with Gleason grade (P=0.0002, P=0.0003, P=0.004); however there was no link with T or M stage. There was a significant relationship between increasing ERK5 expression and increasing Mcm2 (P=0.003) and Ki67 (P=0.009) expression, with non-significant trends seen with increasing MEK5 expression. There were significant associations between Gleason grade and the number of cells traversing G1 phase (Ki67LI-gemininLI; (P=0.001)), with high ERK5 levels associated with both an increase in replication licensed but non-cycling cells (Mcm2LI-Ki67LI; (P=0
- Published
- 2007
42. 760 Phosphorylation of the Androgen Receptor by Cdk1 Predicts Outcome in Prostate Cancer Patients with PSA ⩽ 20 ng/ml
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Willder, J.M., primary, Heng, S.J., additional, Tannahill, C., additional, McCall, P., additional, Orange, C., additional, Fyffe, G., additional, Seywright, M., additional, Leung, H.Y., additional, Underwood, M.A., additional, and Edwards, J., additional
- Published
- 2012
- Full Text
- View/download PDF
43. 646 HER2 overcomes PTEN (loss) induced senescence to cause aggressive prostate cancer
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Ahmad, I., primary, Patel, R., additional, Sansom, O.J., additional, and Leung, H.Y., additional
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- 2012
- Full Text
- View/download PDF
44. 662 Activation of the Wnt signalling pathway synergises with either PI3K or MAPK activation to lead to urothelial cell carcinomas (UCC) with differing treatment requirements
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Ahmad, I., primary, Leung, H.Y., additional, and Sansom, O.J., additional
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- 2012
- Full Text
- View/download PDF
45. Sustainability - a new business vision and strategy for a century-old international energy enterprise
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Yee, T.C., primary, Tsang, Y.M., additional, and Leung, H.Y., additional
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- 2012
- Full Text
- View/download PDF
46. Measurements of Dynamic Properties of Tall Buildings
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Kwok, K.C.S., Campbell, S., Tse, K.T., Hitchcock, P.A., Leung, H.Y., Kwok, K.C.S., Campbell, S., Tse, K.T., Hitchcock, P.A., and Leung, H.Y.
- Published
- 2004
47. 543 RNA Polymerase III transcription deregulation in cancer: study of Brf1 expression in prostate cancer
- Author
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Nam, N.A., primary, Ahmad, I., additional, Edwards, J., additional, Leung, H.Y., additional, and White, R.J., additional
- Published
- 2010
- Full Text
- View/download PDF
48. The New BAUS Section of Academic Urology: A Survey of the Urological Community
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Nelson, A.W., primary, Ahmad, I., additional, Pickard, R.S., additional, and Leung, H.Y., additional
- Published
- 2009
- Full Text
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49. The role of androgen in determining differentiation and regulation of androgen receptor expression in the human prostatic epithelium transient amplifying population
- Author
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Heer, R., primary, Robson, C.N., additional, Shenton, B.K., additional, and Leung, H.Y., additional
- Published
- 2008
- Full Text
- View/download PDF
50. Hardware Realization of Steganographic Techniques
- Author
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Leung, H.Y., primary, Cheng, L.M., additional, Cheng, L.L., additional, and Chan, Chi-Kwong, additional
- Published
- 2007
- Full Text
- View/download PDF
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