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2. Peer Effects in Equity Research

Author

Phua, K, Tham, M, Wei, C, Phua, K, Tham, M, and Wei, C

Abstract

We study the importance of peer effects among sell-side analysts who work at the same brokerage house, but cover different firms. By mapping the information network within each brokerage, we identify analysts who occupy central positions in the network. Central analysts incorporate more information from their coworkers and produce better research. Using shocks to network structures around brokerage mergers, we identify the influence of peer effects and the importance of industry expertise on analysts' performance. A portfolio strategy that exploits the forecast revisions of central analysts earns up to 24% per annum.

Published
2023

6. My child's future mental health: Carer's engagement with risk identification in an intervention study for youth with at-risk mental states

Author

Tham, M, Bendall, S, Carlyon-Stewart, T, Polari, A, Hartmann, J, Kerr, M, Amminger, P, McGorry, P, Nelson, B, Ratheesh, A, Tham, M, Bendall, S, Carlyon-Stewart, T, Polari, A, Hartmann, J, Kerr, M, Amminger, P, McGorry, P, Nelson, B, and Ratheesh, A

Abstract

AIM: Prevention and early intervention efforts of serious mental illnesses has yielded promising results. However, alongside benefits, several ethical concerns have been raised, including the effects of being identified as being at-risk. In these debates, the voice of parents or carers is conspicuously absent. This is especially concerning as several at-risk interventions are trialled in under-age youth where parents consent on behalf of young people. Therefore, this study aimed to understand carer's experiences of their teenager being identified as at risk for psychosis. METHODS: Semi-structured interviews were conducted with seven carers who had provided consent for their teenager to participate in a stepped intervention study for youth at-risk for psychosis. Questions explored their experiences regarding having their teenager being identified as at-risk. Transcripts were analysed using thematic analysis. RESULTS: We identified five main themes from seven female carers' experiences of risk identification including: (a) recall of risk information was limited, or variable, (b) goal of risk disclosure was perceived to be positive, (c) negative emotions were associated with knowledge of risk, (d) relief from uncertainty and helplessness and (e) effects of risk disclosure were mediated by individual circumstance. CONCLUSION: Overall, the results demonstrate that carers' experience of risk disclosure varied with factors surrounding their individual circumstances, and the process of disclosure. Whilst participants acknowledged potential adverse effects associated with risk disclosure, many still adopted a positive outlook. Tailoring safe and effective disclosure of risk to suit the needs of youth and carers could outweigh the potential risks.

Published
2022

7. Phytochemical Screening, Antioxidant Activity and α-Glucosidase Inhibitability of Bauhinia × blakeana Dunn Leaf and Flower Extracts from Vietnam.

Author

Tran, Chen V., Vo, Tham M., Bui, Phong T., Duong, Duc N. P., Duong, Lam X. N., Dinh, Diep Q., and Nguyen, Hien T. T.

Subjects
PLANT extracts, PHYTOCHEMICALS, ANTIOXIDANT analysis, GLUCOSIDASES, BAUHINIA
Abstract

Bauhinia × blakeana Dunn is traditionally used as vegetables, medicinal herbs to treat diseases, and ornamental trees. The current study was performed to evaluate the phytochemicals, total phenolic (TPC) and total flavonoid (TFC) contents, antioxidant activity, and α-glucosidase inhibitability of B× blakeana leaf and flower from Vietnam. Qualitative phytochemical analysis showed positive results for carbohydrates, organic acids, carotenoids, steroids, cardiac glycosides, triterpenoids, saponins, flavonoids, and tannins. The TPC and TFC obtained from B× blakeana leaf were 99.81 ± 0.94 (mg GAE/g E) and 114.93 ± 1.06 (mg RE/g E), respectively, whereas they were 40.45 ± 0.50 (mg GAE/g E) and 59.61 ± 0.85 (mg RE/g E) from B× blakeana flower. The DPPH radical scavenging capacity assay of the crude ethanolic extracts of B× blakeana leaf (IC50 = 266.52 ± 1.03 µg/mL; R² = 0.9864) and flower (IC50 > 1000 µg/mL) was determined. The leaf and flower extracts showed significant α-glucosidase inhibitory activity with IC50 values of 61.88 ± 0.19 µg/mL (R² = 0.9838), 190.79 ± 0.18 µg/mL (R² = 0.9891), respectively. These results indicated that the extract of B× blakeana leaf and flower can be a promising candidate for alternative drug or functional food discovery, and nutritional recommendations for the control of oxidative stress and diabetes. [ABSTRACT FROM AUTHOR]

Published
2023
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8. Striatin heterozygous mice are more sensitive to aldosterone-induced injury

Author

Burhanuddin Moize, Elijah Trefts, Tham M. Yao, Rene Baudrand, Sanjay Ranjit, Gail K. Adler, Thitinan Treesaranuwattana, Isis Katayama Rangel, Luminita H. Pojoga, Amanda E Garza, Jose R. Romero, Gordon H. Williams, and Danielle L Brooks

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Blood Pressure, Nerve Tissue Proteins, 030209 endocrinology & metabolism, Spironolactone, Kidney, striatin, Mice, 03 medical and health sciences, chemistry.chemical_compound, non-genomic, 0302 clinical medicine, Endocrinology, Mineralocorticoid receptor, Internal medicine, medicine, Animals, Pyrroles, Sulfones, mineralocorticoid receptor antagonist, Protein kinase B, Mineralocorticoid Receptor Antagonists, Mice, Knockout, aldosterone, Aldosterone, business.industry, Research, Wild type, Membrane Proteins, cardiac and renal injury, Eplerenone, NG-Nitroarginine Methyl Ester, 030104 developmental biology, medicine.anatomical_structure, chemistry, Second messenger system, Calmodulin-Binding Proteins, business, medicine.drug
Abstract

Aldosterone modulates the activity of both epithelial (specifically renal) and non-epithelial cells. Binding to the mineralocorticoid receptor (MR), activates two pathways: the classical genomic and the rapidly activated non-genomic that is substantially modulated by the level of striatin. We hypothesized that disruption of MR’s non-genomic pathway would alter aldosterone-induced cardiovascular/renal damage. To test this hypothesis, wild type (WT) and striatin heterozygous knockout (Strn+/−) littermate male mice were fed a liberal sodium (1.6% Na+) diet and randomized to either protocol one: 3 weeks of treatment with either vehicle or aldosterone plus/minus MR antagonists, eplerenone or esaxerenone or protocol two: 2 weeks of treatment with either vehicle or L-NAME/AngII plus/minus MR antagonists, spironolactone or esaxerenone. Compared to the WT mice, basally, the Strn+/− mice had greater (~26%) estimated renal glomeruli volume and reduced non-genomic second messenger signaling (pAkt/Akt ratio) in kidney tissue. In response to active treatment, the striatin-associated-cardiovascular/renal damage was limited to volume effects induced by aldosterone infusion: significantly increased blood pressure (BP) and albuminuria. In contrast, with aldosterone or L-NAME/AngII treatment, striatin deficiency did not modify aldosterone-mediated damage: in the heart and kidney, macrophage infiltration, and increases in aldosterone-induced biomarkers of injury. All changes were near-normalized following MR blockade with spironolactone or esaxerenone, except increased BP in the L-NAME/AngII model. In conclusion, the loss of striatin amplified aldosterone-induced damage suggesting that aldosterone’s non-genomic pathway is protective but only related to effects likely mediated via epithelial, but not non-epithelial cells.

Published
2020

11. Elective cancer surgery in COVID-19–Free surgical pathways during the SARS-cov-2 pandemic: An international, multicenter, comparative cohort study

Author

James C Glasbey, Dmitri Nepogodiev, Joana Ff Simoes, Omar Omar, Elizabeth Li, Mary L Venn, Mohammad Abou Chaar, Vita Capizzi, Daoud Chaudhry, Anant Desai, Jonathan G Edwards, Jonathan P Evans, Marco Fiore, Jose Flavio Videria, Samuel J Ford, Ian Ganyli, Ewen A Griffiths, Rohan R Gujjuri, Angelos G Kolias, Haytham Ma Kaafarani, Ana Minaya-Bravo, Siobhan C McKay, Helen M Mohan, Keith Roberts, Carlos San Miguel-Méndez, Peter Pockney, Richard Shaw, Neil J Smart, Grant D Stewart, Sudha Sundar, Raghavan Vidya, Aneel A Bhangu, James C Glasbey, Omar Omar, Aneel A Bhangu, Kwabena Siaw-Acheampong, Ruth A Benson, Edward Bywater, Daoud Chaudhry, Brett E Dawson, Jonathan P Evans, James C Glasbey, Rohan R Gujjuri, Emily Heritage, Conor S Jones, Sivesh K Kamarajah, Chetan Khatri, Rachel A Khaw, James M Keatley, Andrew Knight, Samuel Lawday, Elizabeth Li, Harvinder S Mann, Ella J Marson, Kenneth A McLean, Siobhan C McKay, Emily C Mills, Dmitri Nepogodiev, Gianluca Pellino, Maria Picciochi, Elliott H Taylor, Abhinav Tiwari, Joana Ff Simoes, Isobel M Trout, Mary L Venn, Richard Jw Wilkin, Aneel A Bhangu, James C Glasbey, Neil J Smart, Ana Minaya-Bravo, Jonathan P Evans, Gaetano Gallo, Susan Moug, Francesco Pata, Peter Pockney, Salomone Di Saverio, Abigail Vallance, Dale Vimalchandran, Ewen A Griffiths, Sivesh K Kamarajah, Richard Pt Evans, Philip Townend, Keith Roberts, Siobhan McKay, John Isaac, Sohei Satoi, John Edwards, Aman S Coonar, Adrian Marchbank, Edward J Caruana, Georgia R Layton, Akshay Patel, Alessandro Brunelli, Samuel Ford, Anant Desai, Alessandro Gronchi, Marco Fiore, Max Almond, Fabio Tirotta, Sinziana Dumitra, Angelos Kolias, Stephen J Price, Daniel M Fountain, Michael D Jenkinson, Peter Hutchinson, Hani J Marcus, Rory J Piper, Laura Lippa, Franco Servadei, Ignatius Esene, Christian Freyschlag, Iuri Neville, Gail Rosseau, Karl Schaller, Andreas K Demetriades, Faith Robertson, Alex Alamri, Richard Shaw, Andrew G Schache, Stuart C Winter, Michael Ho, Paul Nankivell, Juan Rey Biel, Martin Batstone, Ian Ganly, Raghavan Vidya, Alex Wilkins, Jagdeep K Singh, Dinesh Thekinkattil, Sudha Sundar, Christina Fotopoulou, Elaine Leung, Tabassum Khan, Luis Chiva, Jalid Sehouli, Anna Fagotti, Paul Cohen, Murat Gutelkin, Rahel Ghebre, Thomas Konney, Rene Pareja, Rob Bristow, Sean Dowdy, T S Shylasree, R Kottayasamy Seenivasagam, Joe Ng, Keiiji Fujiwara, Grant D Stewart, Benjamin Lamb, Krishna Narahari, Alan McNeill, Alexandra Colquhoun, John McGrath, Steve Bromage, Ravi Barod, Veeru Kasivisvanathan, Tobias Klatte, Joana Ff Simoes, Tom Ef Abbott, Sadi Abukhalaf, Michel Adamina, Adesoji O Ademuyiwa, Arnav Agarwal, Murat Akkulak, Ehab Alameer, Derek Alderson, Felix Alakaloko, Markus Albertsmeiers, Osaid Alser, Muhammad Alshaar, Sattar Alshryda, Alexis P Arnaud, Knut Magne Augestad, Faris Ayasra, José Azevedo, Brittany K Bankhead-Kendall, Emma Barlow, David Beard, Ruth A Benson, Ruth Blanco-Colino, Amanpreet Brar, Ana Minaya-Bravo, Kerry A Breen, Chris Bretherton, Igor Lima Buarque, Joshua Burke, Edward J Caruana, Mohammad Chaar, Sohini Chakrabortee, Peter Christensen, Daniel Cox, Moises Cukier, Miguel F Cunha, Giana H Davidson, Anant Desai, Salomone Di Saverio, Thomas M Drake, John G Edwards, Muhammed Elhadi, Sameh Emile, Shebani Farik, Marco Fiore, J Edward Fitzgerald, Samuel Ford, Tatiana Garmanova, Gaetano Gallo, Dhruv Ghosh, Gustavo Mendonça Ataíde Gomes, Gustavo Grecinos, Ewen A Griffiths, Madalegna GrÜndl, Constantine Halkias, Ewen M Harrison, Intisar Hisham, Peter J Hutchinson, Shelley Hwang, Arda Isik, Michael D Jenkinson, Pascal Jonker, Haytham Ma Kaafarani, Debby Keller, Angelos Kolias, Schelto Kruijff, Ismail Lawani, Hans Lederhuber, Sezai Leventoglu, Andrey Litvin, Andrew Loehrer, Markus W Löffler, Maria Aguilera Lorena, Maria Marta Modolo, Piotr Major, Janet Martin, Hassan N Mashbari, Dennis Mazingi, Symeon Metallidis, Ana Minaya-Bravo, Helen M Mohan, Rachel Moore, David Moszkowicz, Susan Moug, Joshua S Ng-Kamstra, Mayaba Maimbo, Ionut Negoi, Milagros Niquen, Faustin Ntirenganya, Maricarmen Olivos, Kacimi Oussama, Oumaima Outani, Marie Dione Parreno-Sacdalanm, Francesco Pata, Carlos Jose Perez Rivera, Thomas D Pinkney, Willemijn van der Plas, Peter Pockney, Ahmad Qureshi, Dejan Radenkovic, Antonio Ramos-De la Medina, Keith Roberts, April C Roslani, Martin Rutegård, Juan José Segura-Sampedro, Irène Santos, Sohei Satoi, Raza Sayyed, Andrew Schache, Andreas A Schnitzbauer, Justina O Seyi-Olajide, Neil Sharma, Richard Shaw, Sebastian Shu, Kjetil Soreide, Antonino Spinelli, Grant D Stewart, Malin Sund, Sudha Sundar, Stephen Tabiri, Philip Townend, Georgios Tsoulfas, Gabrielle H van Ramshorst, Raghavan Vidya, Dale Vimalachandran, Oliver J Warren, Duane Wedderburn, Naomi Wright, C Allemand, L Boccalatte, M Figari, M Lamm, J Larrañaga, C Marchitelli, F Noll, D Odetto, M Perrotta, J Saadi, L Zamora, C Alurralde, E L Caram, D Eskinazi, J P Mendoza, M Usandivaras, R Badra, A Esteban, J S García, P M García, J I Gerchunoff, S M Lucchini, M A NIgra, L Vargas, T Hovhannisyan, A Stepanyan, T Gould, R Gourlay, B Griffiths, S Gananadha, M McLaren, J Cecire, N Joshi, S Salindera, A Sutherland, J H Ahn, G Charlton, S Chen, N Gauri, R Hayhurst, S Jang, F Jia, C Mulligan, W Yang, G Ye, H Zhang, M Ballal, D Gibson, D Hayne, J Moss, T Richards, P Viswambaram, U G Vo, J Bennetts, T Bright, M Brooke-Smith, R Fong, B Gricks, Y H Lam, B S Ong, M Szpytma, D Watson, K Bagraith, S Caird, E Chan, C Dawson, D Ho, E Jeyarajan, S Jordan, A Lim, G J Nolan, A Oar, D Parker, H Puhalla, A Quennell, L Rutherford, P Townend, M Von Papen, M Wullschleger, A Blatt, D Cope, N Egoroff, M Fenton, J Gani, N Lott, P Pockney, N Shugg, M Elliott, D Phung, D Phan, D Townend, C Bong, J Gundara, A Frankel, S Bowman, G R Guerra, J Bolt, K Buddingh, N N Dudi-Venkata, S Jog, H M Kroon, T Sammour, R Smith, C Stranz, M Batstone, K Lah, W McGahan, D Mitchell, A Morton, A Pearce, M Roberts, G Sheahan, B Swinson, N Alam, S Banting, L Chong, P Choong, S Clatworthy, D Foley, A Fox, M W Hii, B Knowles, J Mack, M Read, A Rowcroft, S Ward, G Wright, M Lanner, I Königsrainer, M Bauer, C Freyschlag, M Kafka, F Messner, D Öfner, I Tsibulak, K Emmanuel, M Grechenig, R Gruber, M Harald, L Öhlberger, J Presl, A Wimmer, I Namazov, E Samadov, D Barker, R Boyce, S Corbin, A Doyle, A Eastmond, R Gill, A Haynes, S Millar, M O'Shea, G Padmore, N Paquette, E Phillips, S St John, K Walkes, N Flamey, P Pattyn, W Oosterlinck, J Van den Eynde, R Van den Eynde, A Gatti, C Nardi, R Oliva, R De Cicco, I Cecconello, P Gregorio, L Pontual Lima, U Ribeiro Junior, F Takeda, R M Terra, M Sokolov, B Kidane, S Srinathan, M Boutros, N Caminsky, G Ghitulescu, G Jamjoum, J Moon, J Pelletier, T Vanounou, S Wong, M Boutros, S Dumitra, A Kouyoumdjian, B Johnston, C Russell, M Boutros, S Demyttenaere, R Garfinkle, J Abou-Khalil, C Nessim, J Stevenson, F Heredia, A Almeciga, A Fletcher, A Merchan, L O Puentes, J Mendoza Quevedo, G Bacic, D Karlovic, D Krsul, M Zelic, I Luksic, M Mamic, B Bakmaz, I Coza, E Dijan, Z Katusic, J Mihanovic, I Rakvin, K Frantzeskou, N Gouvas, G Kokkinos, P Papatheodorou, I Pozotou, O Stavrinidou, A Yiallourou, L Martinek, M Skrovina, I Szubota, J Žatecký, V Javurkova, J Klat, T Avlund, P Christensen, J L Harbjerg, L H Iversen, D W Kjaer, Hø Kristensen, M Mekhael, A L Ebbehøj, P Krarup, N Schlesinger, H Smith, A Abdelsamed, A Y Azzam, H Salem, A Seleim, A Abdelmajeed, M Abdou, N E Abosamak, M Al Sayed, F Ashoush, R Atta, E Elazzazy, M Elhoseiny, M Elnemr, M S Elqasabi, M E Elsayed Hewalla, I Elsherbini, E Essam, M Eweda, I Ghallab, E Hassan, M Ibrahim, M Metwalli, M Mourad, M S Qatora, M Ragab, A Sabry, H Saifeldin, M Saleh Mesbah Mohamed Elkaffas, A Samih, A Samir Abdelaal, S Shehata, K Shenit, D Attia, N Kamal, N Osman, A M Abbas, Has Abd Elazeem, M M Abdelkarem, S Alaa, A K Ali, A Ayman, M G Azizeldine, H Elkhayat, S M Elghazaly, F A Monib, M A Nageh, M M Saad, M Salah, M Shahine, E A Yousof, A Youssef, A Eldaly, M ElFiky, A Nabil, G Amira, I Sallam, M Sherief, A Sherif, A Abdelrahman, H Aboulkassem, G Ghaly, R Hamdy, A Morsi, H Salem, G Sherif, H Abdeldayem, I Abdelkader Salama, M Balabel, Y Fayed, A E Sherif, D Bekele, J Kauppila, E Sarjanoja, O Helminen, H Huhta, J H Kauppila, C Beyrne, L Jouffret, L Lugans, L Marie-Macron, E Chouillard, B De Simone, J Bettoni, S Dakpé, B Devauchelle, N Lavagen, S Testelin, S Boucher, R Breheret, A Gueutier, A Kahn, J KÜn-Darbois, A Barrabe, Z Lakkis, A Louvrier, S Manfredelli, P Mathieu, A Chebaro, V Drubay, M El Amrani, C Eveno, K Lecolle, G Legault, L Martin, G Piessen, F R Pruvot, S Truant, P Zerbib, Q Ballouhey, B Barrat, J Laloze, H Salle, A Taibi, J Usseglio, D Bergeat, A Merdrignac, Roy B Le, L O Perotto, A Scalabre, A Aimé, A Ezanno, B Malgras, P Bouche, S Tzedakis, E Cotte, O Glehen, V Kepenekian, J Lifante, G Passot, A D'Urso, E Felli, D Mutter, P Pessaux, B Seeliger, J Bardet, R Berry, G Boddaert, S Bonnet, E Brian, C Denet, D Fuks, D Gossot, M Grigoroiu, A Laforest, Y Levy-Zauberman, C Louis-Sylvestre, A Moumen, G Pourcher, A Seguin-Givelet, E Tribillon, E Duchalais, F Espitalier, C Ferron, O Malard, U Bork, M Distler, J Fritzmann, J Kirchberg, C Praetorius, C Riediger, J Weitz, T Welsch, P Wimberger, K Beyer, C Kamphues, J Lauscher, F N Loch, C Schineis, M Albertsmeier, M Angele, A Kappenberger, H Niess, T Schiergens, J Werner, R Becker, J Jonescheit, I Pergolini, D Reim, C Boeker, I Hakami, J Mall, P Liokatis, W Smolka, K Nowak, T Reinhard, F Hölzle, A Modabber, P Winnand, M Knitschke, P Kauffmann, S Wolfer, J Kleeff, K Lorenz, C Michalski, U Ronellenfitsch, R Schneider, E Bertolani, A Königsrainer, M W Löffler, M Quante, C Steidle, L ÜberrÜck, C Yurttas, C S Betz, J Bewarder, A Böttcher, S Burg, C Busch, M Gosau, A Heuer, J Izbicki, T O Klatte, D Koenig, N Moeckelmann, C Nitschke, M Priemel, R Smeets, U Speth, S Thole, F G Uzunoglu, T Vollkommer, N Zeller, M J Battista, K Gillen, A Hasenburg, S Krajnak, V Linz, R Schwab, K Angelou, D Haidopoulos, A Rodolakis, P Antonakis, K Bramis, L Chardalias, I Contis, N Dafnios, D Dellaportas, G Fragulidis, A Gklavas, M Konstadoulakis, N Memos, I Papaconstantinou, A Polydorou, T Theodosopoulos, A Vezakis, M I Antonopoulou, D K Manatakis, N Tasis, N Arkadopoulos, N Danias, P Economopoulou, P Kokoropoulos, A Larentzakis, N Michalopoulos, J Selmani, T Sidiropoulos, V Tsaousis, P Vassiliu, K Bouchagier, S Klimopoulos, D Paspaliari, G Stylianidis, K Baxevanidou, K Bouliaris, P Chatzikomnitsa, M Efthimiou, A Giaglaras, C Kalfountzos, G Koukoulis, A M Ntziovara, K Petropoulos, K Soulikia, I Tsiamalou, K Zervas, S Zourntou, I Baloyiannis, A Diamantis, E Gkrinia, J Hajiioannou, C Korais, O Koukoura, K Perivoliotis, A Saratziotis, C Skoulakis, D Symeonidis, K Tepetes, G Tzovaras, D Zacharoulis, V Alexoudi, K Antoniades, I Astreidis, P Christidis, D Deligiannidis, T Grivas, O Ioannidis, I Kalaitsidou, L Loutzidou, A Mantevas, D Michailidou, K Paraskevopoulos, S Politis, A Stavroglou, D Tatsis, I Tilaveridis, K Vahtsevanos, G Venetis, I Karaitianos, T Tsirlis, A Charalabopoulos, T Liakakos, E Mpaili, D Schizas, E Spartalis, A Syllaios, C Zografos, C Anthoulakis, C Christou, V Papadopoulos, A Tooulias, D Tsolakidis, G Tsoulfas, D Zouzoulas, E Athanasakis, E Chrysos, J Tsiaoussis, S Xenaki, E Xynos, K Futaba, M F Ho, S F Hon, Twc Mak, Ssm Ng, C C Foo, B Banky, N Suszták, M Aremu, A Canas-Martinez, O Cullivan, C Murphy, P Owens, L Pickett, L Akmenkalne, J Byrne, M Corrigan, C Cullinane, A Daly, C Fleming, P Jordan, S Killeen, N Lynch, A McCarthy, H Mustafa, S O'Brien, P O'Leary, Was Syed, L Vernon, D Callanan, L Huang, A Ionescu, P Sheahan, I Balasubramanian, M Boland, K Conlon, D Evoy, N Fearon, T Gallagher, J Geraghty, H Heneghan, N Kennedy, D Maguire, D McCartan, E W McDermott, R S Prichard, D Winter, D Alazawi, C Barry, T Boyle, W Butt, E M Connolly, N Donlon, C Donohue, B A Fahey, R Farrell, C Fitzgerald, J Kinsella, J O Larkin, P Lennon, P J Maguire, P Mccormick, B J Mehigan, H Mohan, T Nugent, H O'Sullivan, N Ravi, J V Reynolds, A Rogers, P Shokuhi, J Smith, L A Smith, C Timon, Y Bashir, G Bass, T Connelly, B Creavin, H Earley, J A Elliott, A Gillis, D Kavanagh, P Neary, J O'riordan, I S Reynolds, D Rice, P Ridgway, M Umair, M Whelan, P Carroll, C Collins, K Corless, L Finnegan, A Fowler, A Hogan, M Kerin, A Lowery, P McAnena, K McKevitt, K Nizami, É Ryan, A Samy, J C Coffey, R Cunningham, M Devine, D Nally, C Peirce, S Tormey, N Hardy, P Neary, S O'Malley, M Ryan, S Macina, N M Mariani, E Opocher, A Pisani Ceretti, F Ferrari, F Odicino, E Sartori, C Cotsoglou, S Granieri, F Bianco, A Camillo, M Colledan, S Tornese, M F Zambelli, G Bissolotti, S Fusetti, F Lemma, M V Marino, A Mirabella, G Vaccarella, C Agostini, G Alemanno, I Bartolini, C Bergamini, A Bruscino, C Checcucci, R De Vincenti, A Di Bella, M Fambrini, L Fortuna, G Maltinti, P Muiesan, F Petraglia, P Prosperi, M N Ringressi, M Risaliti, F Sorbi, A Taddei, R Tucci, C Bassi, L Bortolasi, T Campagnaro, L Casetti, M De Pastena, A Esposito, M Fontana, A Guglielmi, L Landoni, G Malleo, G Marchegiani, S Nobile, S Paiella, C Pedrazzani, S Rattizzato, A Ruzzenente, R Salvia, G Turri, M Tuveri, P Bellora, G D'Aloisio, M Ferrari, E Francone, S Gentilli, H Nikaj, M Bianchini, M Chiarugi, F Coccolini, G Di Franco, N Furbetta, D Gianardi, S Guadagni, L Morelli, M Palmeri, D Tartaglia, G Anania, P Carcoforo, M Chiozza, A De Troia, M Koleva Radica, M Portinari, M G Sibilla, A Urbani, N Fabbri, C V Feo, S Gennari, S Parini, E Righini, L Ampollini, L Bellanti, M Bergonzani, G Bertoli, G Bocchialini, G D'Angelo, D Lanfranco, L Musini, T Poli, G P Santoro, A Varazzani, L Aguzzoli, G Borgonovo, C Castro Ruiz, S Coiro, G Falco, V D Mandato, V Mastrofilippo, M T Montella, V Annessi, M Zizzo, U Grossi, S Novello, M Romano, S Rossi, G Zanus, G Esposito, F Frongia, A Pisanu, M Podda, C Belluco, A Lauretta, G Montori, L Moras, M Olivieri, F Bussu, A G Carta, M L Cossu, P Cottu, A Fancellu, C F Feo, G C Ginesu, G Giuliani, M Madonia, T Perra, A Piras, A Porcu, D Rizzo, A M Scanu, A Tedde, M Tedde, P Delrio, D Rega, G Badalamenti, G Campisi, A Cordova, M Franza, G Maniaci, G Rinaldi, F Toia, M Calabrò, F Farnesi, E G Lunghi, A Muratore, N S Pipitone Federico, F Bàmbina, G D'Andrea, P Familiari, V Picotti, G De Palma, G Luglio, G Pagano, F P Tropeano, L Baldari, G A Beltramini, L Boni, E Cassinotti, A Gianni, L Pignataro, S Torretta, C Abatini, M Baia, D Biasoni, G Bogani, P Cadenelli, V Capizzi, Spb Cioffi, D Citterio, L V Comini, M Cosimelli, M Fiore, S Folli, M Gennaro, L Giannini, A Gronchi, M Guaglio, A Macchi, F Martinelli, V Mazzaferro, A Mosca, S Pasquali, C Piazza, F Raspagliesi, L Rolli, R Salvioni, G Sarpietro, C Sarre, L Sorrentino, A Agnes, S Alfieri, F Belia, A Biondi, V Cozza, A D'Amore, D D'Ugo, V De Simone, A Fagotti, G Gasparini, L Gordini, F Litta, C P Lombardi, L Lorenzon, A A Marra, F Marzi, A Moro, A Parello, E Perrone, R 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Hernandez, I Lasa, F Mendoza-Moreno, N Morales Palacios, E Ovejero Merino, C Vera Mansilla, F Acebes García, M Bailón, A D Bueno Cañones, E Choolani Bhojwani, P Marcos-Santos, T Miguel, D Pacheco Sánchez, B Pérez-Saborido, J Sanchez Gonzalez, F J Tejero-Pintor, F Alconchel, A Conesa, J Gil Martínez, A I Gutiérrez Fernández, A Lopez Abad, T Nicolás-López, P Ramirez Romero, M J Roca Calvo, K Rodrigues, J J Ruiz Manzanera, A I Soriano, A Cano, L Capitan-Morales, J Cintas Catena, J Gomez-Rosado, F Oliva Mompean, M A Pérez Sánchez, F D Río Lafuente, C Torres Arcos, J Valdes-Hernandez, H Cholewa, S Domingo, M Frasson, V Lago, T Marina Martin, C Martínez Chicote, J Sancho-Muriel, A Landaluce-Olavarria, D Lecumberri, A Abad Gurumeta, A Abad-Motos, E Martínez-Hurtado, J Ripollés-Melchor, A Ruiz Escobar, A Cuadrado-García, L Garcia-Sancho Tellez, J Heras Aznar, P Maté, I Ortega Vázquez, A L Picardo, J A Rojo López, F Sanchez Cabezudo Noguera, D Serralta de Colsa, J Anchuelo Latorre, C Cagigas Fernandez, R Caiña Ruiz, M Gomez Ruiz, F Hernanz, J Jimeno Fraile, P Martínez-Pérez, C Poch, S Santarrufina Martinez, V Valbuena Jabares, C Moliner-Sánchez, L Pingarron-Martin, J Rey-Biel, I Ruiz Martin, J L Blas Laina, B Cros, J Escartin, J Garcia Egea, A Nogués, I Talal El-Abur, C Yánez, E P Cagigal Ortega, I Cervera, P Díaz Peña, Gdcr Elena, D Enjuto, P Fernández Bernabé, R Garcés García, J Gonzalez, I Hernández, N Herrera-Merino, M Marqueta De Salas, P Martinez Pascual, M Perez Gonzalez, A Ramos Bonilla, L Rodríguez Gómez, C Bescós, R Blanco-Colino, I Brana, B Caimari, A De Pablo García-Cuenca, F Duran-Valles, E Espin-Basany, J Giralt Lóez de Sagredo, J Pamias, G Pellino, N Prat, R Pujol Pina, M Saez Barba, A Arulanantham, Gbk Bandara, U Jayarajah, S Ravindrakumar, V S Rodrigo, S Srishankar, A A Ali Karar, P Elbe, E K Lindqvist, H Taflin, A Älgå, G Heinius, M Nordberg, E Pieniowski, I Gkekas, N Löfgren, M Rutegård, M Sund, M Arigoni, M Bernasconi, D Christoforidis, M Di Giuseppe, D La Regina, F Mongelli, M Chevallay, O Dwidar, E Gialamas, M Sauvain, F Klenke, A Kollàr, C Kurze, M Adamina, T Bächler, A S Crugnale, M Giardini, L Guglielmetti, G Peros, F Solimene, A Aghayeva, I Hamzaoglu, I Sahin, E Akaydin, Z Aliyeva, E Aytac, B Baca, O DÜlgeroğlu, V Ozben, B B Ozmen, C Uras, A E Arikan, I A Bilgin, B Bozkirli, G O Ceyhan, H Kara, T Karahasanoglu, C Uras, H Celik, M M Meydanli, H Akilli, A Ayhan, E Kuscu, M A Onan, U Akgor, H A Dincer, T Erol, M Gultekin, N Orhan, N Ozgul, M C Salman, B Soyak, A Alhamed, S ErgÜn, M F OZcelik, A N Sanli, S S Uludag, M Velidedeoglu, A K Zengin, M A Bozkurt, Y Kara, A Kocatas, B Cimenoglu, R Demirhan, K Saracoglu, I F Azamat, E Balik, D Bugra, B Giray, C B Kulle, C Taskiran, D Vatansever, K Gözal, S A GÜler, H Köken, O C Tatar, N Z Utkan, A Yildirim, E YÜksel, E Akin, F Altintoprak, Z Bayhan, G Cakmak, R Çapoglu, F Çelebi, H Demir, E Dikicier, N Firat, E GönÜllÜ, M B Kamburoglu, B Kocer, I F KÜçÜk, B Mantoglu, E Çolak, G O Kucuk, M S Uyanik, B Göksoy, E Bozkurt, B Citgez, M Mihmanli, M Tanal, G Yetkin, M Akalin, C Arican, E K Avci, C Aydin, S Demirli Atici, M Emiroglu, T Kaya, E Kebabçi, G Kilinc, Y Kirmizi, H Ogucu, S Salimoglu, I Sert, C Tugmen, K Tuncer, G Uslu, D Yesilyurt, E Karaman, A Kolusari, A Yildiz, O Benson, H Lule, J Agilinko, A Ahmeidat, M Barabasz, M Bekheit, L K Cheung, T Colloc, W Cymes, M Elhusseini, G Gradinariu, A Hannah, B S Kamera, G Mignot, S Shaikh, P Sharma, I Abu-Nayla, A Agrawal, A Al-Mohammad, S Ali, J Ashcroft, A Azizi, O Baker, A Balakrishnan, M Byrne, A Colquhoun, A Cotter, P Coughlin, R J Davies, A Durrani, M Elshaer, S Fordington, P Forouhi, F Georgiades, H Grimes, A Habeeb, V Hudson, P Hutchinson, E Irune, A Jah, D Z Khan, A Kolias, H Kyriacou, B Lamb, S Liau, L Luke, R Mahmoud, R Mannion, L Masterson, C G Mitrofan, M Mohan, A Morris, S Murphy, R O'Neill, S Price, J Pushpa-Rajah, W Raby-Smith, J Ramzi, S Rooney, T Santarius, A Singh, G D Stewart, X S Tan, A Townson, E Tweedle, C Walker, S Waseem, S Yordanov, T Jones, A Kattakayam, C Loh, R Lunevicius, S Pringle, A Schache, R Shaw, A Sheel, C Rossborough, D Angelou, M Choynowski, B McAree, A McCanny, D Neely, G Tutoveanu, S Ahad, Mfi De La Cruz Monroy, F Mosley, V Oktseloglou, A Alanbuki, M Patel, A Shabana, E Perera, D Raveendran, K Ravi-Shankar, J Thiruchelvam, L Arrowsmith, W Campbell, T Grove, C Kontovounisios, O Warren, P Rolland, A Aggarwal, S Brown, C Jelley, N Neal, R Clifford, N Eardley, E Krishnan, N Manu, E Martin, S Roy Mahapatra, O L Serevina, C Smith, D Vimalachandran, M Bordenave, R Houston, G Putnam, A Robson, H Tustin, K Emslie, P L Labib, A Marchbank, D Miller, G Minto, J Natale, H Nwinee, P Panahi, L Rogers, A Abubakar, M M Akhter Rahman, E Chan, Kyk Ko, H O'Brien, K Sasapu, H Woodun, R Inglis, H J Ng, A De Gea Rico, N Ghazali, J Lambert, G Markose, S Math, I Sarantitis, D Shrestha, A Sultana, M Taggarsi, S Timbrell, O P Vaz, L Vitone, A Day, H Dent, M Fahim, S Waheed, A Hunt, N Laskar, A Gupta, J Steinke, S Thrumurthy, E Massie, K McGivern, D Rutherford, M Wilson, J Hardie, S Kazzaz, S Handa, M Kaushal, A Kler, P Patel, J Redfern, S Tezas, Y Aawsaj, S Amonkar, C Barry, L Blackwell, D Blake, J Carter, H Emerson, A Fisher, M Katory, P Korompelis, W McCormick, A Mustafa, L Pearce, N Ratnavelu, R Reehal, L Kretzmer, L Lalou, B Manku, I Parwaiz, J Stafford, M Abdelkarim, A Asqalan, T Gala, S Ibrahim, A Maw, R Mithany, R Morgan, G Sundaram Venkatesan, K Ang, E J Caruana, M F Chowdhry, A Mohammad, A Nakas, S Rathinam, M Boal, O Brown, S Dwerryhouse, S Higgs, A Vallance, E Boyd, V Irvine, A Kirk, G Bakolas, A Boulton, A Chandock, T Khan, M Kumar, P Agoston, A Bille, B Challacombe, S Fraser, K Harrison-Phipps, J King, G Mehra, L Mills, M Najdy, R Nath, L Okiror, J Pilling, V Rizzo, T Routledge, A Sayasneh, L Stroman, A Wali, M Fehervari, C Fotopoulou, N Habib, S Hamrang-Yousefi, Z Jawad, L Jiao, M Pai, J Ploski, P Rajagopal, S Saso, M Sodergren, D Spalding, S Laws, C Hardie, C McNaught, R Alam, A Budacan, J Cahill, M Kalkat, S Karandikar, L Kenyon, D Naumann, A Patel, J Ayorinde, T Chase, T Cuming, A Ghanbari, L Humphreys, S Tayeh, A Aboelkassem Ibrahim, R Bichoo, H Cao, Akw Chai, J Choudhury, C Evans, H Fitzjohn, H Ikram, M Langstroth, M Loubani, A McMillan, S Nazir, Ssa Qadri, A Robinson, E Ross, T Sehgal, A Wilkins, J Dixon, J Dunning, K Freystaetter, M Jha, S Lester, A Madhavan, S V Thulasiraman, Y Viswanath, T Curl-Roper, C Delimpalta, Ccl Liao, V Velchuru, E Westwood, E Belcher, G Bond-Smith, S Chidambaram, F Di Chiara, K Fasanmade, L Fraser, H Fu, M Ganau, S Gore, J Graystone, D Jeyaretna, H Khatkar, M Lami, M Maher, S Mastoridis, R Mihai, R Piper, S Prabhu, Obf Risk, U Selbong, K Shah, R Smillie, H Soleymani Majd, S Sravanam, D Stavroulias, G D Tebala, M Vatish, C Verberne, K Wallwork, S Winter, M I Bhatti, H Boyd-Carson, E Elsey, E Gemmill, P Herrod, M Jibreel, E Lenzi, T Saafan, D Sapre, T Sian, N Watson, A Athanasiou, G Bourke, L Bradshaw, A Brunelli, J Burke, P Coe, F Costigan, H Elkadi, M Ho, J Johnstone, A Kanatas, V Kantola, A Kaufmann, A Laios, S Lam, E MacInnes, S Munot, C Nahm, M Otify, C Pompili, I Smith, G Theophilou, G Toogood, R Wade, D Ward, C West, S Annamalai, C Ashmore, A Boddy, T Hossain, A Kourdouli, A Gvaramadze, A Jibril, L Prusty, D Thekkinkattil, A Harky, M Shackcloth, A Askari, C Chan, N Cirocchi, S Kudchadkar, K Patel, J Sagar, S Shaw, R Talwar, M Abdalla, R Edmondson, O Ismail, D Jones, K Newton, N Stylianides, A Aderombi, U Andaleeb, O Bajomo, K Beatson, W Garrett, M Mehmood, V Ng, R Al-Habsi, G S Divya, B Keeler, B Al-Sarireh, R Egan, R Harries, A Henry, M Kittur, Z Li, K Parkins, F Soliman, N Spencer, D Thompson, C Burgess, C Gemmell, C Grieco, M Hollyman, L Hunt, J Morrison, S Ojha, N Ryan, F Abbadessa, S Barnard, C Chan, N Dawe, J Hammond, Ali F Mahmoud, I McPherson, C Mellor, J Moir, S Pandanaboyana, J Powell, B Rai, A Rogers, C Roy, A Sachdeva, C Saleh, S Tingle, T Williams, J Manickavasagam, C McDonald, N McGrath, N McSorley, K Ragupathy, L Ramsay, A Solth, O Kakisi, K Seebah, I Shaikh, L Sreedharan, M Youssef, J Shah, P Ameerally, N McLarty, S Mills, A Shenfine, K Sahnan, J Abu, E Addae-Boateng, D Bratt, L Brock, N Burnside, S Cadwell-Sneath, K Gajjar, C Gan, C Grundy, K Hallam, K Hassell, M Hawari, A Joshi, H Khout, K Konstantinidi, Rxn Lee, D Nunns, R Schiemer, T Walton, H Weaver, L Whisker, K Williamson, J McVeigh, R Myatt, M A Williams, R Kaur, E Leung, S Sundar, M Michel, S Patil, S Ravindran, J Sarveswaran, L Scott, M Edmond, E King, M Almond, A Bhangu, O Breik, L D Cato, A Desai, S Ford, E Griffiths, M Idle, M Kamal, A Kisiel, R Kulkarni, Jkc Mak, T Martin, P Nankivell, A Parente, S Parmar, A M Pathanki, L Phelan, P Praveen, S Saeed, N Sharma, J Singh, F Tirotta, D Vijayan, A Geddes, J McCaul, J McMahon, A H Khan, F Khan, A Mansuri, S Mukherjee, M Patel, M Sarigul, S Singh, K L Tan, A Woodham, A Adiamah, H Brewer, A Chowdhury, J Evans, D Humes, J Jackman, A Koh, C Lewis-Lloyd, O Oyende, J Reilly, D Worku, P Cool, G Cribb, K Shepherd, C Bisset, S Moug, N Elson, G Faulkner, P Saleh, C Underwood, G Brixton, L Findlay, T Klatte, A Majkowska, J Manson, R Potter, A Bhalla, Z Chia, P Daliya, A Goyal, E Grimley, A Hamad, A Kumar, F L Malcolm, E Theophilidou, J Bowden, N Campain, I Daniels, C Evans, G Fowler, J John, L Massey, F McDermott, J McGrath, A McLennan, M Ng, J Pascoe, N Rajaretnam, S Bulathsinhala, B Davidson, G Fusai, C Hidalgo Salinas, N Machairas, T Pissanou, J M Pollok, D A Raptis, F Soggiu, H Tzerbinis, S E Xyda, A Beamish, E Davies, R Foulkes, D Magowan, H Nassa, R Ooi, C Price, L Smith, F Solari, A Tang, G Williams, Y Al-Tamimi, A Bacon, N Beasley, D Chew, M Crank, N Ilenkovan, M Macdonald, B Narice, O Rominiyi, A Thompson, I Varley, T Drake, E Harrison, G Linder, J Mayes, R McGregor, R Skipworth, V Zamvar, E Davies, P Hawkin, T Raymond, O Ryska, R Baron, D Dunne, S Gahunia, C Halloran, N Howes, R McKinney, F McNicol, J Russ, P Szatmary, J R Tan, A Thomas, P Whelan, A Anzak, A Banerjee, O Fuwa, F Hughes, J D Jayasinghe, C Knowles, H Kocher, I Leal Silva, F S Ledesma, A Minicozzi, L Navaratne, R Rahman, R Ramamoorthy, C Sohrabi, M Thaha, B Thakur, M Venn, V Yip, R Baumber, J Parry, S Evans, L Jeys, G Morris, M Parry, J Stevenson, N Ahmadi, G Aresu, Z M Barrett-Brown, A S Coonar, H Durio Yates, D Gearon, J Hogan, M King, A Peryt, I S Pradeep, C Smith, M Adishesh, R Atherton, K Baxter, M Brocklehurst, M Chaudhury, N Krishnamohan, J McAleer, G Owens, E Parkin, P Patkar, I Phang, A Aladeojebi, M Ali, B Barmayehvar, A Gaunt, M Gowda, E Halliday, M Kitchen, F Mansour, M Thomas, D Zakai, N Abbassi-Ghadi, H Assalaarachchi, A Currie, M Flavin, A Frampton, M Hague, C Hammer, J Hopper, J Horsnell, S Humphries, A Kamocka, T K Madhuri, S Preston, P Singh, J Stebbing, A Tailor, D Walker, F Aljanadi, M Jones, P Mhandu, C O'Donnell, R Turkington, Z Al-Ishaq, S Bhasin, A S Bodla, A Burahee, A Crichton, R Fossett, N Pigadas, S Pickford, E Rahman, D Snee, R Vidya, N Yassin, F Colombo, D Fountain, M T Hasan, K Karabatsou, R Laurente, O Pathmanaban, A Al-Mukhtar, S Brown, J Edwards, A Giblin, C Kelty, M Lee, G Lye, T Newman, A Sharkey, C Steele, N Sureshkumar Shah, E Whitehall, R Athwal, A Baker, L Jones, C Konstantinou, S Ramcharan, S Singh, J Vatish, R Wilkin, M Ethunandan, G K Sekhon, H Shields, R Singh, F Wensley, S Lawday, A Lyons, T Abbott, S Anwar, K Ghufoor, C Sohrabi, E Chung, R Hagger, A Hainsworth, A Karim, H Owen, A Ramwell, K Williams, C Baker, A Davies, J Gossage, M Kelly, W Knight, J Hall, G Harris, G James, C Kang, D J Lin, A D Rajgor, T Royle, R Scurrah, B Steel, L J Watson, D Choi, R Hutchison, A Jain, V Luoma, H Marcus, R May, A Menon, B Pramodana, L Webber, I A Aneke, P Asaad, B Brown, J Collis, S Duff, A Khan, F Moura, B Wadham, H Warburton, T Elmoslemany, M Jenkinson, C Millward, R Zakaria, S Mccluney, C Parmar, S Shah, J Allison, M S Babar, B Collard, S Goodrum, K Lau, A Patel, R Scott, E Thomas, H Whitmore, D Balasubramaniam, B Jayasankar, S Kapoor, A Ramachandran, A Elhamshary, Smb Imam, K Kapriniotis, V Kasivisvanathan, J Lindsay, S Rakhshani-Moghadam, N Beech, M Chand, L Green, N Kalavrezos, H Kiconco, R McEwen, C Schilling, D Sinha, J Pereca, J Singh, S Chopra, D Egbeare, R Thomas, T Combellack, Sef Jones, M Kornaszewska, M Mohammed, A Sharma, G Tahhan, V Valtzoglou, J Williams, P Eskander, K Gash, L Gourbault, M Hanna, T Maccabe, C Newton, J Olivier, S Rozwadowski, E Teh, D West, H Al-Omishy, M Baig, H Bates, G Di Taranto, K Dickson, N Dunne, C Gill, D Howe, D Jeevan, A Khajuria, K Martin-Ucar AMcEvoy, P Naredla, V Ng, S Robertson, M Sait, D R Sarma, S Shanbhag, T Shortland, S Simmonds, J Skillman, N Tewari, G Walton, M A Akhtar, A Brunt, J McIntyre, K Milne, M M Rashid, A Sgro, K E Stewart, A Turnbull, M Aguilar Gonzalez, S Talukder, C Boyle, D Fernando, K Gallagher, A Laird, D Tham, M Bath, P Patki, C Sohrabi, C Tanabalan, T Arif, C Magee, T Nambirajan, S Powell, R Vinayagam, I Flindall, A Hanson, V Mahendran, S Green, M Lim, L MacDonald, V Miu, L Onos, K Sheridan, R Young, F Alam, O Griffiths, C Houlden, R Jones, V S Kolli, A K Lala, S Leeson, R Peevor, Z Seymour, L Chen, E Henderson, A Loehrer, K Brown, D Fleming, A Haynes, C Heron, C Hill, H Kay, E Leede, K McElhinney, K Olson, E C Osterberg, C Riley, P Srikanth, M Thornhill, D Blazer, G DiLalla, E S Hwang, W Lee, M Lidsky, J Plichta, L Rosenberger, R Scheri, K Shah, K Turnage, J Visgauss, S Zani, J Farma, J Clark, D Kwon, E Etchill, H E Gabre-Kidan AJenny, A Kent, M Ladd, C Long, H Malapati, A Margalit, S Rapaport, J Rose, K Stevens, L Tsai, D Vervoort, P Yesantharao, A Dehal, D Klaristenfeld, K Huynh, L Brown, I Ganly, J Mullinax, N Gusani, J Hazelton, J Maines, J S Oh, A Ssentongo, P Ssentongo, M Azam, A Choudhry, W Marx, J Fleming, A Fuson, J Gigliotti, A Ovaitt, Y Ying, M K Abel, V Andaya, K Bigay, M A Boeck, L Chen, H Chern, C Corvera, I El-Sayed, A Glencer, P Ha, Bcs Hamilton, C Heaton, K Hirose, D M Jablons, K Kirkwood, L Z Kornblith, J R Kratz, R Lee, P N Miller, E Nakakura, B Nunez-Garcia, R O'Donnell, D Ozgediz, P Park, B Robinson, A Sarin, B Sheu, M Varma, K Wai, R Wustrack, M J Xu, D Beswick, J Goddard, J Manor, J Song, T Fullmer, C Gaskill, N Gross, K Kiong, C L Roland, S N Zafar, M Abdallah, A Abouassi, M Almasri, G Kulkarni, H Marwan, M Mehdi, S Aoun, V S Ban, H H Batjer, J Caruso, D Abbott, A Acher, T Aiken, J Barrett, E Foley, P Schwartz, S N Zafar, A Hawkins, A Maiga, J Laufer, S Scasso

Subjects
Aged, 80 and over, Male, Critical Care, SARS-CoV-2, International Cooperation, COVID-19, Middle Aged, Cohort Studies, Logistic Models, Postoperative Complications, Elective Surgical Procedures, Neoplasms, Outcome Assessment, Health Care, Humans, Female, Epidemics, Aged
Abstract

PURPOSE As cancer surgery restarts after the first COVID-19 wave, health care providers urgently require data to determine where elective surgery is best performed. This study aimed to determine whether COVID-19–free surgical pathways were associated with lower postoperative pulmonary complication rates compared with hospitals with no defined pathway. PATIENTS AND METHODS This international, multicenter cohort study included patients who underwent elective surgery for 10 solid cancer types without preoperative suspicion of SARS-CoV-2. Participating hospitals included patients from local emergence of SARS-CoV-2 until April 19, 2020. At the time of surgery, hospitals were defined as having a COVID-19–free surgical pathway (complete segregation of the operating theater, critical care, and inpatient ward areas) or no defined pathway (incomplete or no segregation, areas shared with patients with COVID-19). The primary outcome was 30-day postoperative pulmonary complications (pneumonia, acute respiratory distress syndrome, unexpected ventilation). RESULTS Of 9,171 patients from 447 hospitals in 55 countries, 2,481 were operated on in COVID-19–free surgical pathways. Patients who underwent surgery within COVID-19–free surgical pathways were younger with fewer comorbidities than those in hospitals with no defined pathway but with similar proportions of major surgery. After adjustment, pulmonary complication rates were lower with COVID-19–free surgical pathways (2.2% v 4.9%; adjusted odds ratio [aOR], 0.62; 95% CI, 0.44 to 0.86). This was consistent in sensitivity analyses for low-risk patients (American Society of Anesthesiologists grade 1/2), propensity score–matched models, and patients with negative SARS-CoV-2 preoperative tests. The postoperative SARS-CoV-2 infection rate was also lower in COVID-19–free surgical pathways (2.1% v 3.6%; aOR, 0.53; 95% CI, 0.36 to 0.76). CONCLUSION Within available resources, dedicated COVID-19–free surgical pathways should be established to provide safe elective cancer surgery during current and before future SARS-CoV-2 outbreaks.

Published
2021

13. Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice

Author

Pojoga, Luminita H., Yao, Tham M., Sinha, Sumi, Ross, Reagan L., Lin, Jeffery C., Raffetto, Joseph D., Adler, Gail K., Williams, Gordon H., and Khalil, Raouf A.

Subjects
Sodium in the body -- Physiological aspects, Sodium in the body -- Health aspects, Vasoconstriction -- Causes of, Vascular endothelium -- Properties, Vascular endothelium -- Health aspects, Membrane proteins -- Physiological aspects, Membrane proteins -- Chemical properties, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

Changes in dietary sodium intake are associated with changes in vascular volume and reactivity that may be mediated, in part, by alterations in endothelial nitric oxide synthase (eNOS) activity. Caveolin-1 (Cav-1), a transmembrane anchoring protein in the plasma membrane caveolae, binds eNOS and limits its translocation and activation. To test the hypothesis that endothelial Car-1 participates in the dietary sodium-mediated effects on vascular function, we assessed vascular responses and nitric oxide (NO)-mediated mechanisms of vascular relaxation in Cav-1 knockout mice ([Car-1.sup.-/-]) and wild-type control mice (WT; [Cav-1.sup.+/+]) placed on a high-salt (HS; 4% NaCl) or low-salt (LS; 0.08% NaCl) diet for 16 days. After the systolic blood pressure was measured, the thoracic aorta was isolated for measurement of vascular reactivity and NO production, and the heart was used for measurement of eNOS expression and/or activity. The blood pressure was elevated in HS mice treated with [N.sup.G]-nitro-L-arginine methyl ester and more so in [Cav-1.sup.-/-] than WT mice and was significantly reduced during the LS diet. Phenylephrine caused vascular contraction that was significantly reduced in [Cav-1.sup.-/-] (maximum 0.25 [+ or -] 0.06 g/mg) compared with WT (0.75 [+ or -] 0.22 g/mg) on the HS diet, and the differences were eliminated with the LS diet. Also, vascular contraction in response to membrane depolarization by high KCl (96 mM) was reduced in [Cav-1.sup.-/-] (0.27 [+ or -] 0.05 g/mg) compared with WT mice (0.53 [+ or -] 0.12 g/mg) on the HS diet, suggesting that the reduced vascular contraction is not limited to a particular receptor. Acetylcholine ([10.sup.-5] M) caused aortic relaxation in WT mice on HS (23.6 [+ or -] 3.5%) and LS (23.7 [+ or -] 5.5%) that was enhanced in [Cav-1.sup.-/-] HS (72.6 [+ or -] 6.1%) and more so in [Cav-1.sup.-/-] LS mice (93.6 [+ or -] 3.5%). RT-PCR analysis indicated increased eNOS mRNA expression in the aorta and heart, and Western blots indicated increased total eNOS and phosphorylated eNOS in the heart of [Cav-1.sup.-/-] compared with WT mice on the HS diet, and the genotypic differences were less apparent during the LS diet. Thus Cav-1 deficiency during the HS diet is associated with decreased vasoconstriction, increased vascular relaxation, and increased eNOS expression and activity, and these effects are altered during the LS diet. The data support the hypothesis that endothelial Cav-1, likely through an effect on eNOS activity, plays a prominent role in the regulation of vascular function during substantial changes in dietary sodium intake. endothelium; nitric oxide; vascular smooth muscle; blood pressure; hypertension

Published
2008

17. Striatin heterozygous mice are more sensitive to aldosterone-induced injury

Author

Garza, Amanda E, primary, Trefts, Elijah, additional, Katayama Rangel, Isis A, additional, Brooks, Danielle, additional, Baudrand, Rene, additional, Moize, Burhanuddin, additional, Romero, Jose R, additional, Ranjit, Sanjay, additional, Treesaranuwattana, Thitinan, additional, Yao, Tham M, additional, Adler, Gail K, additional, Pojoga, Luminita H, additional, and Williams, Gordon H, additional

Published
2020
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20. Regulation of aldosterone secretion by mineralocorticoid receptor–mediated signaling

Author

Anis Amalina Abdul Hamid, Luminita H. Pojoga, Gordon H. Williams, Amanda E Garza, Cherish Chong, Jose R. Romero, Gail K. Adler, and Tham M. Yao

Subjects
Male, 0301 basic medicine, Aldosterone synthase, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, 030209 endocrinology & metabolism, Article, 03 medical and health sciences, chemistry.chemical_compound, Receptors, Glucocorticoid, 0302 clinical medicine, Endocrinology, Mineralocorticoid receptor, Zona fasciculata, Corticosterone, Internal medicine, medicine, Animals, Rats, Wistar, Aldosterone, biology, Adrenal cortex, Sodium, Dietary, Zona Reticularis, Rats, Receptors, Mineralocorticoid, 030104 developmental biology, medicine.anatomical_structure, chemistry, Zona glomerulosa, biology.protein, Zona Glomerulosa, Zona reticularis, Signal Transduction
Abstract

We posit the existence of a paracrine/autocrine negative feedback loop, mediated by the mineralocorticoid receptor (MR), regulating aldosterone secretion. To assess this hypothesis, we asked whether altering MR activity in zona glomerulosa (ZG) cells affects aldosterone production. To this end, we studiedex vivoZG cells isolated from male Wistar rats fed chow containing either high (1.6% Na+(HS)) or low (0.03% Na+(LS)) amount of sodium. Western blot analyses demonstrated that MR was present in both the ZG and zona fasciculata/zona reticularis (ZF/ZR/ZR). In ZG cells isolated from rats on LS chow, MR activation by fludrocortisone produced a 20% and 60% reduction in aldosterone secretion basally and in response to angiotensin II (ANGII) stimulation, respectively. Corticosterone secretion was increased in these cells suggesting that aldosterone synthase activity was being reduced by fludrocortisone. In contrast, canrenoic acid, an MR antagonist, enhanced aldosterone production by up to 30% both basally and in response to ANGII. Similar responses were observed in ZG cells from rats fed HS. Modulating glucocorticoid receptor (GR) activity did not alter aldosterone production by ZG cells; however, altering GR activity did modify corticosterone production from ZF/ZR/ZR cells both basally and in response to adrenocorticotropic hormone (ACTH). Additionally, activating the MR in ZF/ZR/ZR cells strikingly reduced corticosterone secretion. In summary, these data support the hypothesis that negative ultra-short feedback loops regulate adrenal steroidogenesis. In the ZG, aldosterone secretion is regulated by the MR, but not the GR, an effect that appears to be secondary to a change in aldosterone synthase activity.

Published
2017

27. Histone demethylase LSD1 deficiency and biological sex: impact on blood pressure and aldosterone production

Author

Gail K. Adler, Pei Yee Ting, Yuefei Huang, Jonathan S. Williams, Tsuyoshi Homma, Luminita H. Pojoga, Gordon H. Williams, Danielle L Brooks, Jose R. Romero, Isis Katayama Rangel, and Tham M. Yao

Subjects
0301 basic medicine, Male, medicine.medical_specialty, animal structures, medicine.drug_class, Endocrinology, Diabetes and Metabolism, Blood Pressure, 030204 cardiovascular system & hematology, Article, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, Mineralocorticoid receptor, Sex Factors, Risk Factors, Internal medicine, medicine, Albuminuria, Animals, Humans, Salt intake, Sodium Chloride, Dietary, Aldosterone, Histone Demethylases, Mice, Knockout, business.industry, Age Factors, medicine.disease, Mice, Inbred C57BL, 030104 developmental biology, Blood pressure, medicine.anatomical_structure, chemistry, Estrogen, Zona glomerulosa, Cardiovascular Diseases, Microalbuminuria, Female, Zona Glomerulosa, business, Ex vivo
Abstract

Human risk allele carriers of lysine-specific demethylase 1 (LSD1) and LSD1-deficient mice have salt-sensitive hypertension for unclear reasons. We hypothesized that LSD1 deficiency causes dysregulation of aldosterone’s response to salt intake resulting in increased cardiovascular risk factors (blood pressure and microalbumin). Furthermore, we determined the effect of biological sex on these potential abnormalities. To test our hypotheses, LSD1 male and female heterozygote-knockout (LSD1+/−) and WT mice were assigned to two age groups: 18 weeks and 36 weeks. Plasma aldosterone levels and aldosterone production from zona glomerulosa cells studied ex vivo were greater in both male and female LSD1+/− mice consuming a liberal salt diet as compared to WT mice consuming the same diet. However, salt-sensitive blood pressure elevation and increased microalbuminuria were only observed in male LSD1+/− mice. These data suggest that LSD1 interacts with aldosterone’s secretory response to salt intake. Lack of LSD1 causes inappropriate aldosterone production on a liberal salt diet; males appear to be more sensitive to this aldosterone increase as males, but not females, develop salt sensitivity of blood pressure and increased microalbuminuria. The mechanism responsible for the cardiovascular protective effect in females is uncertain but may be related to estrogen modulating the effect of mineralocorticoid receptor activation.

Published
2018

32. Cooperative Role of Mineralocorticoid Receptor and Caveolin-1 in Regulating the Vascular Response to Low Nitric Oxide–High Angiotensin II–Induced Cardiovascular Injury

Author

Ossama M. Reslan, Luminita H. Pojoga, Lauren A. Opsasnick, Gordon H. Williams, Waleed T. Siddiqui, Raouf A. Khalil, Tham M. Yao, and Gail K. Adler

Subjects
Male, Models, Molecular, medicine.medical_specialty, Receptor expression, Caveolin 1, Blood Pressure, Spironolactone, Cardiovascular, Nitric Oxide, Cardiovascular System, Nitric oxide, Renin-Angiotensin System, Mice, chemistry.chemical_compound, Mineralocorticoid receptor, Internal medicine, Renin–angiotensin system, medicine, Animals, Cyclic GMP, Aorta, Mineralocorticoid Receptor Antagonists, Pharmacology, Aldosterone, Renal sodium reabsorption, Angiotensin II, Eplerenone, Vasodilation, NG-Nitroarginine Methyl Ester, Receptors, Mineralocorticoid, Endocrinology, Heart Injuries, chemistry, Vasoconstriction, cardiovascular system, Nucleic Acid Conformation, Molecular Medicine, Sodium nitroprusside, Signal Transduction, medicine.drug
Abstract

Aldosterone interacts with mineralocorticoid receptor (MR) to stimulate sodium reabsorption in renal tubules and may also affect the vasculature. Caveolin-1 (cav-1), an anchoring protein in plasmalemmal caveolae, binds steroid receptors and also endothelial nitric oxide synthase, thus limiting its translocation and activation. To test for potential MR/cav-1 interaction in the vasculature, we investigated if MR blockade in cav-1-replete or -deficient states would alter vascular function in a mouse model of low nitric oxide (NO)-high angiotensin II (AngII)-induced cardiovascular injury. Wild-type (WT) and cav-1 knockout mice (cav-1(-/-)) consuming a high salt diet (4% NaCl) received Nω-nitro-l-arginine methyl ester (L-NAME) (0.1-0.2 mg/ml in drinking water at days 1-11) plus AngII (0.7-2.8 mg/kg per day via an osmotic minipump at days 8-11) ± MR antagonist eplerenone (EPL) 100 mg/kg per day in food. In both genotypes, blood pressure increased with L-NAME + AngII. EPL minimally changed blood pressure, although its dose was sufficient to block MR and reverse cardiac expression of the injury markers cluster of differentiation 68 and plasminogen activator inhibitor-1 in L-NAME+AngII treated mice. In aortic rings, phenylephrine and KCl contraction was enhanced with EPL in L-NAME+AngII treated WT mice, but not cav-1(-/-) mice. AngII-induced contraction was not different, and angiotensin type 1 receptor expression was reduced in L-NAME + AngII treated WT and cav-1(-/-) mice. In WT mice, acetylcholine-induced relaxation was enhanced with L-NAME + AngII treatment and reversed with EPL. Acetylcholine relaxation in cav-1(-/-) mice was greater than in WT mice, not modified by L-NAME + AngII or EPL, and blocked by ex vivo L-NAME, 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ), or endothelium removal, suggesting the role of NO-cGMP. Cardiac endothelial NO synthase was increased in cav-1(-/-) versus WT mice, further increased with L-NAME + AngII, and not affected by EPL. Vascular relaxation to the NO donor sodium nitroprusside was increased with L-NAME + AngII in WT mice but not in cav-1(-/-) mice. Plasma aldosterone levels increased and cardiac MR expression decreased in L-NAME + AngII treated WT and cav-1(-/-) mice and did not change with EPL. Thus, during L-NAME + AngII induced hypertension, MR blockade increases contraction and alters vascular relaxation via NO-cGMP, and these changes are absent in cav-1 deficiency states. The data suggest a cooperative role of MR and cav-1 in regulating vascular contraction and NO-cGMP-mediated relaxation during low NO-high AngII-dependent cardiovascular injury.

Published
2015

33. Variants in Striatin Gene Are Associated With Salt-Sensitive Blood Pressure in Mice and Humans

Author

Burhanuddin Moize, Jessica Lasky-Su, Gordon H. Williams, Jose R. Romero, Rene Baudrand, Gail K. Adler, Bei Sun, Jonathan S. Williams, Luminita H. Pojoga, Chevon M. Rariy, Wan M. Hafiz, Amanda E Garza, Claudio Ferri, Tham M. Yao, and Paul N. Hopkins

Subjects
Epithelial sodium channel, medicine.medical_specialty, Mouse, Genotype, Knockout, Messenger, Blotting, Western, Dietary, Blood Pressure, Nerve Tissue Proteins, Biology, Polymerase Chain Reaction, Article, Mice, Mineralocorticoid receptor, Internal medicine, Internal Medicine, medicine, Animals, Humans, RNA, Messenger, Polymorphism, Salt intake, Receptor, Protein kinase B, Single Nucleotide, Striatin Protein, Calmodulin-Binding Proteins, Disease Models, Animal, Hypertension, Membrane Proteins, Mice, Knockout, Phenotype, Signal Transduction, Sodium, Dietary, Gene Expression Regulation, Blotting, Animal, Sodium, Heterozygote advantage, Endocrinology, Mineralocorticoid receptor activity, Disease Models, Knockout mouse, RNA, Western
Abstract

Striatin is a novel protein that interacts with steroid receptors and modifies rapid, nongenomic activity in vitro. We tested the hypothesis that striatin would in turn affect mineralocorticoid receptor function and consequently sodium, water, and blood pressure homeostasis in an animal model. We evaluated salt sensitivity of blood pressure in novel striatin heterozygote knockout mice. Compared with wild type, striatin heterozygote exhibited a significant increase in blood pressure when sodium intake was increased from restricted (0.03%) to liberal (1.6%) sodium. Furthermore, renal expression of mineralocorticoid receptor and its genomic downstream targets serum/glucocorticoid-regulated kinase 1, and epithelial sodium channel was increased in striatin heterozygote versus wild-type mice on liberal sodium intake while the pAkt/Akt ratio, readout of mineralocorticoid receptor’s rapid, nongenomic pathway, was reduced. To determine the potential clinical relevance of these findings, we tested the association between single nucleotide polymorphic variants of striatin gene and salt sensitivity of blood pressure in 366 white hypertensive subjects. HapMap-derived tagging single nucleotide polymorphisms identified an association of rs2540923 with salt sensitivity of blood pressure (odds ratio, 6.25; 95% confidence interval, 1.7–20; P =0.01). These data provide the first in vivo evidence in humans and rodents that associates striatin with markers of mineralocorticoid receptor activity. The data also support the hypothesis that the rapid, nongenomic mineralocorticoid receptor pathway (mediated via striatin) has a role in modulating the interaction between salt intake and blood pressure.

Published
2015

37. Combined Salt and Caloric Restrictions: Potential Adverse Outcomes

Author

Jose R. Romero, Gail K. Adler, Gordon H. Williams, Korapat Mayurasakorn, Anis Amalina Abdul Hamid, Yuefei Huang, Nurul Mahamad Rodi, Mika Homma, Tsuyoshi Homma, Luminita H. Pojoga, Shelley Hurwitz, and Tham M. Yao

Subjects
0301 basic medicine, Blood Glucose, Male, Time Factors, Blood Pressure, 030204 cardiovascular system & hematology, Kidney, Renin-Angiotensin System, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, insulin resistance, Renin, Insulin, insulin action, Nicotinamide Phosphoribosyltransferase, Aldosterone, Original Research, 2. Zero hunger, chemistry.chemical_classification, Diet, Sodium-Restricted, salt intake, Cardiovascular Diseases, Hypertension, Endothelium/Vascular Type/Nitric Oxide, Cytokines, Animal Nutritional Physiological Phenomena, Zona Glomerulosa, mineralocorticoids, Adiponectin, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Adverse outcomes, Salt (chemistry), Nutritional Status, Risk Assessment, ACE/Angiotension Receptors/Renin Angiotensin System, 03 medical and health sciences, Insulin resistance, Internal medicine, medicine, Animals, Salt intake, Rats, Wistar, Caloric Restriction, Caloric restrictions, business.industry, Hemodynamics, Caloric theory, Sodium, Dietary, medicine.disease, NAD, 030104 developmental biology, Blood pressure, Endocrinology, Metabolism, chemistry, Animal Models of Human Disease, business, Biomarkers, high blood pressure
Abstract

Background We hypothesized that caloric restriction ( CR ) and salt restriction (ResS) would have similar effects on reducing cardiovascular risk markers and that combining CR and ResS would be synergistic in modulating these markers. Methods and Results To test our hypothesis, rats were randomized into 2 groups: ad libitum liberal salt diet (ad libitum/high‐sodium, 1.6% sodium) or ResS diet (ad libitum/ResS, 0.03% sodium). CR was initiated in half of the rats in each group by reducing caloric intake to 60% while maintaining sodium intake constant ( CR /high‐sodium, 2.7% sodium or CR /ResS, 0.05% sodium) for 4 weeks. CR in rats on a high‐sodium diet improved metabolic parameters, renal transforming growth factor‐β and collagen‐1α1 and increased plasma adiponectin and renal visfatin and NAD + protein levels. Although CR produced some beneficial cardiovascular effects (increased sodium excretion and reduced blood pressure), it also was associated with potentially adverse cardiovascular effects. Adrenal zona glomerulosa cell responsiveness and aldosterone levels and activation were inappropriately increased for the volume state of the rodent. Like CR on HS , CR on a ResS diet also produced relative increased zona glomerulosa responsiveness and an increased blood pressure with no improvement in metabolic parameters. Conclusions These results suggest that combining CR and ResS may decrease the beneficial effects of each alone. Furthermore, CR , regardless of dietary salt intake, inappropriately activates aldosterone production. Thus, caution should be used in combining ResS and CR because the combination may lead to increased cardiovascular risk.

Published
2017

41. Dissociation of Hyperglycemia from Altered Vascular Contraction and Relaxation Mechanisms in Caveolin-1 Null Mice

Author

Raouf A. Khalil, Gordon H. Williams, Gail K. Adler, Amanda E Garza, Tham M. Yao, Ossama M. Reslan, Luminita H. Pojoga, and Lauren A. Opsasnick

Subjects
Male, medicine.medical_specialty, Nitric Oxide Synthase Type III, endocrine system diseases, Endothelium, Caveolin 1, Vasodilation, AMP-Activated Protein Kinases, Cardiovascular, Muscle, Smooth, Vascular, Mice, Internal medicine, medicine, Animals, Hypoglycemic Agents, Glucose homeostasis, Enzyme Inhibitors, Phosphorylation, Endothelial dysfunction, Aorta, Mice, Knockout, Pharmacology, business.industry, nutritional and metabolic diseases, AMPK, medicine.disease, Metformin, Endocrinology, medicine.anatomical_structure, Guanylate Cyclase, Vasoconstriction, Hyperglycemia, Hypertension, cardiovascular system, Molecular Medicine, Endothelium, Vascular, Sodium nitroprusside, medicine.symptom, business, Protein Processing, Post-Translational, medicine.drug
Abstract

Hyperglycemia and endothelial dysfunction are associated with hypertension, but the specific causality and genetic underpinning are unclear. Caveolin-1 (cav-1) is a plasmalemmal anchoring protein and modulator of vascular function and glucose homeostasis. Cav-1 gene variants are associated with reduced insulin sensitivity in hypertensive individuals, and cav-1(-/-) mice show endothelial dysfunction, hyperglycemia, and increased blood pressure (BP). On the other hand, insulin-sensitizing therapy with metformin may inadequately control hyperglycemia while affecting the vascular outcome in certain patients with diabetes. To test whether the pressor and vascular changes in cav-1 deficiency states are related to hyperglycemia and to assess the vascular mechanisms of metformin under these conditions, wild-type (WT) and cav-1(-/-) mice were treated with either placebo or metformin (400 mg/kg daily for 21 days). BP and fasting blood glucose were in cav-1(-/-)WT and did not change with metformin. Phenylephrine (Phe)- and KCl-induced aortic contraction was in cav-1(-/-)WT; endothelium removal, the nitric-oxide synthase (NOS) blocker L-NAME (N(ω)-nitro-L-arginine methyl ester), or soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) enhanced Phe contraction, and metformin blunted this effect. Acetylcholine-induced relaxation was in cav-1(-/-)WT, abolished by endothelium removal, L-NAME or ODQ, and reduced with metformin. Nitric oxide donor sodium nitroprusside was more potent in inducing relaxation in cav-1(-/-) than in WT, and metformin reversed this effect. Aortic eNOS, AMPK, and sGC were in cav-1(-/-)WT, and metformin decreased total and phosphorylated eNOS and AMPK in cav-1(-/-). Thus, metformin inhibits both vascular contraction and NO-cGMP-dependent relaxation but does not affect BP or blood glucose in cav-1(-/-) mice, suggesting dissociation of hyperglycemia from altered vascular function in cav-1-deficiency states.

Published
2013

42. Exploring the function of online narratives to develop critical thinking and localisation of knowledge in an international science program

Author

Hicks, M, Tham, M, Brookes, R, Hicks, M, Tham, M, and Brookes, R

Abstract

e‐learning practitioners have long recognised the benefits of using online training to achieve knowledge transfer, less is understood about facilitating the sharing of values, attitudes, critical thinking, and localisation using online platforms. In this article an online learning platform in the context of an international scientific program was evaluated. The platform uses a narrative approach to convey stories with the explicit aim of developing critical thinking and localisation. The platform embeds formative assessment within the stories to transfer the tacit understandings of the program to project site staff. Some of the challenges this approach encounters, particularly with regard to the expression of localisation was explored.

Published
2017

43. Industrial applications of a new adaptive estimator for inferential control

Author

Morris, A. J., Tham, M. T., Montague, G. A., Thoma, M., editor, Wyner, A., editor, Brebbia, C. A., editor, Orszag, S. A., editor, Argyris, J., editor, Bathe, K. -J., editor, Cakmak, A. S., editor, Connor, J., editor, McCrory, R., editor, Desai, C. S., editor, Holz, K. -P., editor, Leckie, F. A., editor, Pinder, G., editor, Pont, A. R. S., editor, Seinfeld, J. H., editor, Silvester, P., editor, Spanos, P., editor, Wunderlich, W., editor, Yip, S., editor, Shah, Sirish L., editor, and Dumont, Guy, editor

Published
1989
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45. Abstract 097: Effects of Lysine-specific Demethylase 1 Deficiency on Aldosterone Production and Salt-sensitive Hypertension in Female Mice

Author

Pei Yee Ting, Luminita H. Pojoga, Tham M. Yao, Jia Wei Tan, Gail K. Adler, Amanda E Garza, Jose R. Romero, Yuefei Huang, Isis Katayama Rangel, Paul Loutraris, and Gordon H. Williams

Subjects
endocrine system, medicine.medical_specialty, chemistry.chemical_compound, animal structures, Endocrinology, Aldosterone, Chemistry, Internal medicine, Salt sensitivity, Internal Medicine, medicine, LYSINE-SPECIFIC DEMETHYLASE 1
Abstract

Lysine-Specific Demethylase1 (LSD1) is an epigenetic factor modulated by salt intake. Previously, we documented the male heterozygote LSD1 knockout mice (LSD1+/-) had dysregulation of aldosterone (ALDO) production on a liberal salt diet (1.6% Na+) associated with salt-sensitive hypertension. This study assessed if: 1) female LSD1+/- mice have a similar phenotype; and 2) the effect of aging on this phenotype. Methods: Female LSD1+/- and wild type mice (LSD1+/+) were randomly assigned for sacrifice at the ages of 18-week, 52-week, and 75-week and the following were assessed at each time point: blood pressure (BP); plasma renin activity (PRA) and ALDO; urine albumin; and ex vivo ALDO production from isolated adrenal zona glomerulosa cells. Results: BP and urine albumin in the LSD1+/- compared to the LSD1+/+ were not different at any age (Table). However, the LSD1+/- had greater ALDO/PRA ratios at 18 weeks compared with the LSD1+/+, but lower ALDO levels and ex vivo ALDO production at 52 and 75 weeks. Associated with this phenotype, the LSD1+/- showed significantly higher rate of all-cause mortality than the LSD1+/+. Conclusion: Lack of LSD1 caused dysregulation of ALDO production in both male and female mice. But the cardiovascular outcomes are different. The LSD1+/- females in contrast to males do not develop hypertension or albuminuria even at 75 weeks of age. However, the females do die at a faster rate than the males of a variety of causes. Thus, there is considerable sexual dimorphism in the pathogenesis of cardiovascular outcomes associated with dysregulation of adrenal ALDO production mediated by lack of LSD1.

Published
2016

46. Response to Letter Regarding Article, 'Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects'

Author

Tham M. Yao, Xavier Jeunemaitre, Rene Baudrand, Anand Vaidya, Gail K. Adler, Gordon H. Williams, Paul A. Vöhringer, Amanda E Garza, Luminita H. Pojoga, Jonathan S. Williams, and Paul N. Hopkins

Subjects
medicine.medical_specialty, Aldosterone, business.industry, Sodium, chemistry.chemical_element, 030209 endocrinology & metabolism, Context (language use), 030204 cardiovascular system & hematology, Statin treatment, medicine.disease, Angiotensin II, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, chemistry, Physiology (medical), Internal medicine, Diabetes mellitus, Renin–angiotensin system, Medicine, Cardiology and Cardiovascular Medicine, business, Low sodium
Abstract

We thank Dr Campbell for his interest in our study,1 and the fair and helpful comments from the accompanying editorial by Andersson and Vasan, as well.2 We are in agreement with Dr Campbell that statins may influence adrenal steroidogenesis via a multitude of effects. Our study focused mainly on the regulation of aldosterone by using a series of complex physiological maneuvers that included manipulation of angiotensin II and potassium. The subjects in our study were not taking antihypertensive therapy or were withdrawn of therapy, thus allowing investigation of their native physiology. In this context, our use of extreme sodium diets permitted the study of aldosterone when the renin-angiotensin system was maximally suppressed on high sodium and maximally stimulated on low sodium intake in the context of a fixed potassium diet. Therefore, all our assessments of aldosterone were conducted under conditions whereby the …

Published
2016

47. Mineralocorticoid Receptor Blockade Reverses Obesity-Related Changes in Expression of Adiponectin, Peroxisome Proliferator-Activated Receptor-γ, and Proinflammatory Adipokines

Author

Patricia Coutinho, Gordon H. Williams, Christine Guo, Jose R. Romero, Gail K. Adler, Tham M. Yao, Bill Q. Lian, Jianmin Li, and Vincent Ricchiuti

Subjects
chemistry.chemical_classification, medicine.medical_specialty, Adiponectin, medicine.drug_class, business.industry, Adipokine, Peroxisome proliferator-activated receptor, Adipose tissue, Eplerenone, Proinflammatory cytokine, Mineralocorticoid receptor, Endocrinology, chemistry, Mineralocorticoid, Physiology (medical), Internal medicine, medicine, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

Background— In obesity, decreases in adiponectin and increases in proinflammatory adipokines are associated with heart disease. Because adipocytes express mineralocorticoid receptor (MR) and MR blockade reduces cardiovascular inflammation and injury, we tested the hypothesis that MR blockade reduces inflammation and expression of proinflammatory cytokines in adipose tissue and increases adiponectin expression in adipose tissue and hearts of obese mice. Methods and Results— We determined the effect of MR blockade (eplerenone, 100 mg/kg per day for 16 weeks) on gene expression in retroperitoneal adipose and heart tissue from obese, diabetic db / db mice (n=8) compared with untreated obese, diabetic db / db mice (n=10) and lean, nondiabetic db /+ littermates (n=11). Expression of tumor necrosis factor-α, monocyte chemoattractant protein-1, plasminogen activator inhibitor type 1, and macrophage protein CD68 increased, and expression of adiponectin and peroxisome proliferator-activated receptor-γ decreased in retroperitoneal adipose tissue from obese versus lean mice. In addition, adiponectin expression in heart was reduced in obese versus lean mice. MR blockade prevented these obesity-related changes in gene expression. Furthermore, treatment of undifferentiated preadipocytes with aldosterone (10 −8 mol/L for 24 hours) increased mRNA levels of tumor necrosis factor-α and monocyte chemoattractant protein-1 and reduced mRNA and protein levels of peroxisome proliferator-activated receptor-γ and adiponectin, supporting a direct aldosterone effect on gene expression. Conclusions— MR blockade reduced expression of proinflammatory and prothrombotic factors in adipose tissue and increased expression of adiponectin in heart and adipose tissue of obese, diabetic mice. These effects on adiponectin and adipokine gene expression may represent a novel mechanism for the cardioprotective effects of MR blockade.

Published
2008

48. Statin Use And Adrenal Aldosterone Production In Hypertensive And Diabetic Subjects

Author

Anand Vaidya, Jonathan S. Williams, Paul A. Vöhringer, Gordon H. Williams, Paul N. Hopkins, Luminita H. Pojoga, Xavier Jeunemaitre, Amanda E Garza, Tham M. Yao, Gail K. Adler, and Rene Baudrand

Subjects
Adult, Male, medicine.medical_specialty, Statin, medicine.drug_class, Stimulation, Pharmacology, chemistry.chemical_compound, Corticosterone, Physiology (medical), Internal medicine, Diabetes mellitus, Adrenal Glands, Diabetes Mellitus, medicine, Animals, Humans, cardiovascular diseases, Rats, Wistar, Aldosterone, business.industry, nutritional and metabolic diseases, Diet, Sodium-Restricted, Middle Aged, medicine.disease, Rats, Endocrinology, chemistry, Hypertension, Female, lipids (amino acids, peptides, and proteins), Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, business, Ex vivo, Hormone, Low sodium
Abstract

Background— Statins substantially reduce cardiovascular mortality and appear to have beneficial effects independent of their lipid-lowering properties. We evaluated the hypothesis that statin use may modulate the secretion of aldosterone, a well-known contributor to cardiovascular disease. Methods and Results— We measured adrenal hormones in 2 intervention studies. In study 1 in hypertensive subjects, aldosterone was analyzed at baseline and after angiotensin II stimulation on both high- and low-sodium diets (1122 observations, 15% on statins for >3 months). Statin users had 33% lower aldosterone levels in adjusted models ( P P P =0.006), particularly those using lipophilic statins. Ex vivo studies in rat adrenal glomerulosa cells confirmed that lipophilic statins acutely inhibited aldosterone, but not corticosterone, in response to different secretagogues. Conclusions— Statin use among hypertensive and diabetic subjects was associated with lower aldosterone secretion in response to angiotensin II and a low-sodium diet in 2 human intervention studies. This effect appeared to be most pronounced with lipophilic statins and higher doses. Future studies to evaluate whether aldosterone inhibition may partially explain the robust cardioprotective effects of statins are warranted.

Published
2015

49. Mineralocorticoid Receptor Antagonist Reduces Renal Injury in Rodent Models of Types 1 and 2 Diabetes Mellitus

Author

Maria F. Toniolo, Tham M. Yao, Vincent Ricchiuti, Gordon H. Williams, Luminita H. Pojoga, Eveline Oestreicher, Christine Guo, Nathalie Lapointe, Diego Martinez-Vasquez, Gail K. Adler, Taisuke Kikuchi, and Gonzalo P. Mendez

Subjects
Male, medicine.medical_specialty, Systole, Spironolactone, Kidney, Streptozocin, Diabetes Mellitus, Experimental, Mice, chemistry.chemical_compound, Endocrinology, Mineralocorticoid receptor, Diabetes mellitus, Internal medicine, Albuminuria, Animals, Medicine, Diabetic Nephropathies, RNA, Messenger, Rats, Wistar, Mineralocorticoid Receptor Antagonists, business.industry, Type 2 Diabetes Mellitus, Hypertrophy, medicine.disease, Streptozotocin, Eplerenone, Rats, Mice, Inbred C57BL, Diabetes Mellitus, Type 1, Receptors, Mineralocorticoid, medicine.anatomical_structure, Diabetes Mellitus, Type 2, chemistry, Osteopontin, medicine.symptom, business, medicine.drug
Abstract

To determine whether mineralocorticoid receptor (MR) activation plays a role in diabetic renal injury and whether this role differs in types 1 and 2 diabetes mellitus, we examined the effect of a MR antagonist on renal injury in rodent models of type 1 (streptozotocin-treated rat) and type 2 (db/db mouse) diabetes. We studied three groups of 8-wk-old, uninephrectomized Wistar rats for 4 wk: diabetic streptozotocin- (55 mg/kg) treated rats (n = 11), diabetic streptozotocin-treated rats receiving the MR antagonist eplerenone (n = 15), and nondiabetic rats (n = 9). In addition, we studied three groups of 8-wk-old mice for 16 wk: diabetic db/db mice (n = 10), diabetic db/db mice treated with eplerenone (n = 8), and nondiabetic, db/+ littermates (n = 11). Diabetic rats and mice developed albuminuria and histopathological evidence of renal injury, including glomerular hypertrophy, mesangial expansion, and tubulointerstitial injury as well as increased renal cortical levels of MR protein, MR mRNA, TGFβ mRNA, and osteopontin mRNA. All of these changes were significantly reduced by treatment with eplerenone except for the elevated MR levels. The beneficial effects of eplerenone were not attributable to changes in blood pressure or glycemia. In summary, MR expression was increased in kidneys of diabetic rodents, and MR antagonists effectively reduced diabetic renal injury irrespective of the species or specific cause of the diabetes. Thus, these data suggest that MR activation is a critical factor in the early pathogenesis of renal disease in both type 1 and type 2 diabetes mellitus.

Published
2006

50. Histone demethylase LSD1 deficiency and biological sex: impact on blood pressure and aldosterone production.

Author

Yuefei Huang, Pei Yee Ting, Yao, Tham M., Homma, Tsuyoshi, Brooks, Danielle, Rangel, Isis Katayama, Adler, Gail K., Romero, Jose R., Williams, Jonathan S., Pojoga, Luminita H., and Williams, Gordon H.

Subjects
SEX (Biology), BLOOD pressure, AGE groups, ALDOSTERONE
Abstract

Human risk allele carriers of lysine-specific demethylase 1 (LSD1) and LSD1-deficient mice have salt-sensitive hypertension for unclear reasons. We hypothesized that LSD1 deficiency causes dysregulation of aldosterone's response to sal t intake resulting in increased cardiovascular risk factors (blood pressure and microalbumin). Furthermore, we determined the effect of biological sex on these potential ab normalities. To test our hypotheses, LSD1 male and female heterozygote-knockout (LSD1+/-) and WT mice were assigned to two age groups: 18 weeks and 36 weeks. Plasma aldosterone levels and aldosterone production from zona glomerulosa cells studied ex vivo were greater in both male and female LSD1+/- mice consuming a liberal salt diet as compared to WT mice consuming the same diet. However, salt-sensitive blood pressure elevation and increased microalbuminuria were only observed in male LSD1+/- mice. These data suggest that LSD1 interacts with aldosterone's secretory response to salt intake. Lack of LSD1 causes inappropriate aldosterone production on a liberal salt diet; males appear to be more sensitive to this aldosterone increase as males, but not females, develop salt sensitivity of blood pressure and increased microalbuminuria. The mechanism responsible for the cardiovascular protective effect in females is uncertain but may be related to estrogen modulating the effect of mineralocorticoid r eceptor activation. [ABSTRACT FROM AUTHOR]

Published
2019
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