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Article ; Online: Computational modeling of anoctamin 1 calcium-activated chloride channels as pacemaker channels in interstitial cells of Cajal.

Lees-Green, Rachel / Gibbons, Simon J / Farrugia, Gianrico / Sneyd, James / Cheng, Leo K

American journal of physiology. Gastrointestinal and liver physiology

2014 Volume 306, Issue 8, Page(s) G711–27

Abstract: Interstitial cells of Cajal (ICC) act as pacemaker cells in the gastrointestinal tract by generating electrical slow waves to regulate rhythmic smooth muscle contractions. Intrinsic Ca(2+) oscillations in ICC appear to produce the slow waves by ... ...

Abstract	Interstitial cells of Cajal (ICC) act as pacemaker cells in the gastrointestinal tract by generating electrical slow waves to regulate rhythmic smooth muscle contractions. Intrinsic Ca(2+) oscillations in ICC appear to produce the slow waves by activating pacemaker currents, currently thought to be carried by the Ca(2+)-activated Cl(-) channel anoctamin 1 (Ano1). In this article we present a novel model of small intestinal ICC pacemaker activity that incorporates store-operated Ca(2+) entry and a new model of Ano1 current. A series of simulations were carried out with the ICC model to investigate current controversies about the reversal potential of the Ano1 Cl(-) current in ICC and to predict the characteristics of the other ion channels that are necessary to generate slow waves. The model results show that Ano1 is a plausible pacemaker channel when coupled to a store-operated Ca(2+) channel but suggest that small cyclical depolarizations may still occur in ICC in Ano1 knockout mice. The results predict that voltage-dependent Ca(2+) current is likely to be negligible during the slow wave plateau phase. The model shows that the Cl(-) equilibrium potential is an important modulator of slow wave morphology, highlighting the need for a better understanding of Cl(-) dynamics in ICC.
MeSH term(s)	Animals ; Anoctamin-1 ; Calcium/metabolism ; Chloride Channels/metabolism ; Computer Simulation ; Gastrointestinal Motility/physiology ; Interstitial Cells of Cajal/physiology ; Mice ; Models, Biological ; Muscle Contraction/physiology ; Muscle, Smooth/metabolism
Chemical Substances	ANO1 protein, mouse ; Anoctamin-1 ; Chloride Channels ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00449.2013
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Article ; Online: Biophysically based modeling of the interstitial cells of cajal: current status and future perspectives.

Lees-Green, Rachel / Du, Peng / O'Grady, Gregory / Beyder, Arthur / Farrugia, Gianrico / Pullan, Andrew J

Frontiers in physiology

2011 Volume 2, Page(s) 29

Abstract: Gastrointestinal motility research is progressing rapidly, leading to significant advances in the last 15 years in understanding the cellular mechanisms underlying motility, following the discovery of the central role played by the interstitial cells of ... ...

Abstract	Gastrointestinal motility research is progressing rapidly, leading to significant advances in the last 15 years in understanding the cellular mechanisms underlying motility, following the discovery of the central role played by the interstitial cells of Cajal (ICC). As experimental knowledge of ICC physiology has expanded, biophysically based modeling has become a valuable tool for integrating experimental data, for testing hypotheses on ICC pacemaker mechanisms, and for applications in in silico studies including in multiscale models. This review is focused on the cellular electrophysiology of ICC. Recent evidence from both experimental and modeling domains have called aspects of the existing pacemaker theories into question. Therefore, current experimental knowledge of ICC pacemaker mechanisms is examined in depth, and current theories of ICC pacemaking are evaluated and further developed. Existing biophysically based ICC models and their physiological foundations are then critiqued in light of the recent advances in experimental knowledge, and opportunities to improve these models are identified. The review concludes by examining several potential clinical applications of biophysically based ICC modeling from the subcellular through to the organ level, including ion channelopathies and ICC network degradation.
Language	English
Publishing date	2011-07-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X ; 1664-042X
ISSN (online)	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2011.00029
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Article ; Online: Tissue-specific mathematical models of slow wave entrainment in wild-type and 5-HT(2B) knockout mice with altered interstitial cells of Cajal networks.

Du, Peng / O'Grady, Greg / Gibbons, Simon J / Yassi, Rita / Lees-Green, Rachel / Farrugia, Gianrico / Cheng, Leo K / Pullan, Andrew J

Biophysical journal

2010 Volume 98, Issue 9, Page(s) 1772–1781

Abstract: Gastrointestinal slow waves are generated within networks of interstitial cells of Cajal (ICCs). In the intact tissue, slow waves are entrained to neighboring ICCs with higher intrinsic frequencies, leading to active propagation of slow waves. ... ...

Abstract	Gastrointestinal slow waves are generated within networks of interstitial cells of Cajal (ICCs). In the intact tissue, slow waves are entrained to neighboring ICCs with higher intrinsic frequencies, leading to active propagation of slow waves. Degradation of ICC networks in humans is associated with motility disorders; however, the pathophysiological mechanisms of this relationship are uncertain. A recently developed biophysically based mathematical model of ICC was adopted and updated to simulate entrainment of slow waves. Simulated slow wave propagation was successfully entrained in a one-dimensional model, which contained a gradient of intrinsic frequencies. Slow wave propagation was then simulated in tissue models which contained a realistic two-dimensional microstructure of the myenteric ICC networks translated from wild-type (WT) and 5-HT(2B) knockout (degraded) mouse jejunum. The results showed that the peak current density in the WT model was 0.49 muA mm(-2) higher than the 5-HT(2B) knockout model, and the intracellular Ca(2+) density after 400 ms was 0.26 mM mm(-2) higher in the WT model. In conclusion, tissue-specific models of slow waves are presented, and simulations quantitatively demonstrated physiological differences between WT and 5-HT(2B) knockout models. This study provides a framework for evaluating how ICC network degradation may impair slow wave propagation and ultimately motility and transit.
MeSH term(s)	Animals ; Biophysical Phenomena ; Gastrointestinal Tract/cytology ; Gastrointestinal Tract/metabolism ; Gastrointestinal Tract/physiology ; Interstitial Cells of Cajal/cytology ; Interstitial Cells of Cajal/metabolism ; Intestine, Small/cytology ; Intestine, Small/metabolism ; Intestine, Small/physiology ; Kinetics ; Mice ; Mice, Knockout ; Models, Biological ; Myenteric Plexus/cytology ; Myenteric Plexus/metabolism ; Myenteric Plexus/physiology ; Organ Specificity ; Receptor, Serotonin, 5-HT2B/deficiency ; Receptor, Serotonin, 5-HT2B/genetics ; Receptor, Serotonin, 5-HT2B/metabolism
Chemical Substances	Receptor, Serotonin, 5-HT2B
Language	English
Publishing date	2010-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2010.01.009
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Article ; Online: The neuropsychopharmacology of cannabis: A review of human imaging studies.

Bloomfield, Michael A P / Hindocha, Chandni / Green, Sebastian F / Wall, Matthew B / Lees, Rachel / Petrilli, Katherine / Costello, Harry / Ogunbiyi, M Olabisi / Bossong, Matthijs G / Freeman, Tom P

Pharmacology & therapeutics

2018 Volume 195, Page(s) 132–161

Abstract: The laws governing cannabis are evolving worldwide and associated with changing patterns of use. The main psychoactive drug in cannabis is ... ...

Abstract	The laws governing cannabis are evolving worldwide and associated with changing patterns of use. The main psychoactive drug in cannabis is Δ
MeSH term(s)	Animals ; Brain/blood supply ; Brain/diagnostic imaging ; Brain/drug effects ; Brain/growth & development ; Cannabis ; Diagnostic Imaging ; Dronabinol/toxicity ; Human Development/drug effects ; Humans ; Marijuana Abuse/epidemiology ; Psychotropic Drugs/toxicity
Chemical Substances	Psychotropic Drugs ; Dronabinol (7J8897W37S)
Language	English
Publishing date	2018-10-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2018.10.006
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Article ; Online: Biophysically-based modelling of the interstitial cells of Cajal

AndrewPullan / RachelLees-Green / GregO'Grady / ArthurBeyder

Frontiers in Physiology, Vol

Current status and future perspectives

2011 Volume 2

Abstract	Gastrointestinal motility research is progressing rapidly, leading to significant advances in the last 15 years in understanding the cellular mechanisms underlying motility, following the discovery of the central role played by the interstitial cells of Cajal (ICC). As experimental knowledge of ICC physiology has expanded, biophysically-based modelling has become a valuable tool for integrating experimental data, for testing hypotheses on ICC pacemaker mechanisms, and for applications in in silico studies including in multiscale models. This review is focused on the cellular electrophysiology of ICC. Recent evidence from both experimental and modelling domains have called aspects of the existing pacemaker theories into question. Therefore, current experimental knowledge of ICC pacemaker mechanisms is examined in depth, and current theories of ICC pacemaking are evaluated and further developed. Existing biophysically-based ICC models and their physiological foundations are then critiqued in light of the recent advances in experimental knowledge, and opportunities to improve these models are identified. The review concludes by examining several potential clinical applications of biophysically-based ICC modelling from the subcellular through to the organ level, including ion channelopathies and ICC network degradation.
Keywords	Electrophysiology ; Gastrointestinal Motility ; Interstitial Cells of Cajal ; Ion Channels ; Mathematical Models ; pacemaker ; physiome ; Physiology ; QP1-981 ; Science ; Q
Language	English
Publishing date	2011-07-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Predictors of anti-TNF treatment failure in anti-TNF-naive patients with active luminal Crohn's disease: a prospective, multicentre, cohort study.

Kennedy, Nicholas A / Heap, Graham A / Green, Harry D / Hamilton, Benjamin / Bewshea, Claire / Walker, Gareth J / Thomas, Amanda / Nice, Rachel / Perry, Mandy H / Bouri, Sonia / Chanchlani, Neil / Heerasing, Neel M / Hendy, Peter / Lin, Simeng / Gaya, Daniel R / Cummings, J R Fraser / Selinger, Christian P / Lees, Charlie W / Hart, Ailsa L /

Parkes, Miles / Sebastian, Shaji / Mansfield, John C / Irving, Peter M / Lindsay, James / Russell, Richard K / McDonald, Timothy J / McGovern, Dermot / Goodhand, James R / Ahmad, Tariq

The lancet. Gastroenterology & hepatology

2019 Volume 4, Issue 5, Page(s) 341–353

Abstract: Background: Anti-TNF drugs are effective treatments for the management of Crohn's disease but treatment failure is common. We aimed to identify clinical and pharmacokinetic factors that predict primary non-response at week 14 after starting treatment, ... ...

Abstract	Background: Anti-TNF drugs are effective treatments for the management of Crohn's disease but treatment failure is common. We aimed to identify clinical and pharmacokinetic factors that predict primary non-response at week 14 after starting treatment, non-remission at week 54, and adverse events leading to drug withdrawal. Methods: The personalised anti-TNF therapy in Crohn's disease study (PANTS) is a prospective observational UK-wide study. We enrolled anti-TNF-naive patients (aged ≥6 years) with active luminal Crohn's disease at the time of first exposure to infliximab or adalimumab between March 7, 2013, and July 15, 2016. Patients were evaluated for 12 months or until drug withdrawal. Demographic data, smoking status, age at diagnosis, disease duration, location, and behaviour, previous medical and drug history, and previous Crohn's disease-related surgeries were recorded at baseline. At every visit, disease activity score, weight, therapy, and adverse events were recorded; drug and total anti-drug antibody concentrations were also measured. Treatment failure endpoints were primary non-response at week 14, non-remission at week 54, and adverse events leading to drug withdrawal. We used regression analyses to identify which factors were associated with treatment failure. Findings: We enrolled 955 patients treated with infliximab (753 with originator; 202 with biosimilar) and 655 treated with adalimumab. Primary non-response occurred in 295 (23·8%, 95% CI 21·4-26·2) of 1241 patients who were assessable at week 14. Non-remission at week 54 occurred in 764 (63·1%, 60·3-65·8) of 1211 patients who were assessable, and adverse events curtailed treatment in 126 (7·8%, 6·6-9·2) of 1610 patients. In multivariable analysis, the only factor independently associated with primary non-response was low drug concentration at week 14 (infliximab: odds ratio 0·35 [95% CI 0·20-0·62], p=0·00038; adalimumab: 0·13 [0·06-0·28], p<0·0001); the optimal week 14 drug concentrations associated with remission at both week 14 and week 54 were 7 mg/L for infliximab and 12 mg/L for adalimumab. Continuing standard dosing regimens after primary non-response was rarely helpful; only 14 (12·4% [95% CI 6·9-19·9]) of 113 patients entered remission by week 54. Similarly, week 14 drug concentration was also independently associated with non-remission at week 54 (0·29 [0·16-0·52] for infliximab; 0·03 [0·01-0·12] for adalimumab; p<0·0001 for both). The proportion of patients who developed anti-drug antibodies (immunogenicity) was 62·8% (95% CI 59·0-66·3) for infliximab and 28·5% (24·0-32·7) for adalimumab. For both drugs, suboptimal week 14 drug concentrations predicted immunogenicity, and the development of anti-drug antibodies predicted subsequent low drug concentrations. Combination immunomodulator (thiopurine or methotrexate) therapy mitigated the risk of developing anti-drug antibodies (hazard ratio 0·39 [95% CI 0·32-0·46] for infliximab; 0·44 [0·31-0·64] for adalimumab; p<0·0001 for both). For infliximab, multivariable analysis of immunododulator use, and week 14 drug and anti-drug antibody concentrations showed an independent effect of immunomodulator use on week 54 non-remission (odds ratio 0·56 [95% CI 0·38-0·83], p=0·004). Interpretation: Anti-TNF treatment failure is common and is predicted by low drug concentrations, mediated in part by immunogenicity. Clinical trials are required to investigate whether personalised induction regimens and treatment-to-target dose intensification improve outcomes. Funding: Guts UK, Crohn's and Colitis UK, Cure Crohn's Colitis, AbbVie, Merck Sharp and Dohme, Napp Pharmaceuticals, Pfizer, and Celltrion.
MeSH term(s)	Adalimumab/immunology ; Adalimumab/metabolism ; Adalimumab/therapeutic use ; Adult ; Age Factors ; Antibodies/immunology ; Azathioprine/therapeutic use ; Cohort Studies ; Crohn Disease/drug therapy ; Crohn Disease/epidemiology ; Drug Therapy, Combination ; Female ; Humans ; Immunosuppressive Agents/therapeutic use ; Infliximab/immunology ; Infliximab/metabolism ; Infliximab/therapeutic use ; Leukocyte Count ; Male ; Mercaptopurine/therapeutic use ; Methotrexate/therapeutic use ; Middle Aged ; Proportional Hazards Models ; Prospective Studies ; Risk Factors ; Serum Albumin/metabolism ; Smoking/epidemiology ; Treatment Failure ; Treatment Outcome ; Tumor Necrosis Factor Inhibitors/immunology ; Tumor Necrosis Factor Inhibitors/metabolism ; Tumor Necrosis Factor Inhibitors/therapeutic use ; Young Adult
Chemical Substances	Antibodies ; Immunosuppressive Agents ; Serum Albumin ; Tumor Necrosis Factor Inhibitors ; Infliximab (B72HH48FLU) ; Mercaptopurine (E7WED276I5) ; Adalimumab (FYS6T7F842) ; Azathioprine (MRK240IY2L) ; Methotrexate (YL5FZ2Y5U1)
Language	English
Publishing date	2019-02-27
Publishing country	Netherlands
Document type	Journal Article ; Multicenter Study ; Observational Study ; Research Support, Non-U.S. Gov't
ISSN	2468-1253
ISSN (online)	2468-1253
DOI	10.1016/S2468-1253(19)30012-3
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Article ; Online: Safety and immunogenicity of the ChAdOx1 nCoV-19 vaccine against SARS-CoV-2

Folegatti, Pedro M / Ewer, Katie J / Aley, Parvinder K / Angus, Brian / Becker, Stephan / Belij-Rammerstorfer, Sandra / Bellamy, Duncan / Bibi, Sagida / Bittaye, Mustapha / Clutterbuck, Elizabeth A / Dold, Christina / Faust, Saul N / Finn, Adam / Flaxman, Amy L / Hallis, Bassam / Heath, Paul / Jenkin, Daniel / Lazarus, Rajeka / Makinson, Rebecca /

Minassian, Angela M / Pollock, Katrina M / Ramasamy, Maheshi / Robinson, Hannah / Snape, Matthew / Tarrant, Richard / Voysey, Merryn / Green, Catherine / Douglas, Alexander D / Hill, Adrian V S / Lambe, Teresa / Gilbert, Sarah C / Pollard, Andrew J / Aboagye, Jeremy / Adams, Kelly / Ali, Aabidah / Allen, Elizabeth / Allison, Jennifer L. / Anslow, Rachel / Arbe-Barnes, Edward H. / Babbage, Gavin / Baillie, Kenneth / Baker, Megan / Baker, Natalie / Baker, Philip / Baleanu, Ioana / Ballaminut, Juliana / Barnes, Eleanor / Barrett, Jordan / Bates, Louise / Batten, Alexander / Beadon, Kirsten / Beckley, Rebecca / Berrie, Eleanor / Berry, Lisa / Beveridge, Amy / Bewley, Kevin R. / Bijker, Else Margreet / Bingham, Tracey / Blackwell, Luke / Blundell, Caitlin L. / Bolam, Emma / Boland, Elena / Borthwick, Nicola / Bower, Thomas / Boyd, Amy / Brenner, Tanja / Bright, Philip D. / Brown-O'Sullivan, Charlie / Brunt, Emily / Burbage, Jamie / Burge, Sharon / Buttigieg, Karen R. / Byard, Nicholas / Cabera Puig, Ingrid / Calvert, Anna / Camara, Susana / Cao, Michelangelo / Cappuccini, Federica / Carr, Melanie / Carroll, Miles W. / Carter, Victoria / Cathie, Katrina / Challis, Ruth J. / Charlton, Sue / Chelysheva, Irina / Cho, Jee-Sun / Cicconi, Paola / Cifuentes, Liliana / Clark, Helen / Clark, Elizabeth / Cole, Tom / Colin-Jones, Rachel / Conlon, Christopher P. / Cook, Aislinn / Coombes, Naomi S. / Cooper, Rachel / Cosgrove, Catherine A. / Coy, Karen / Crocker, Wendy E.M. / Cunningham, Christina J. / Damratoski, Brad E. / Dando, Lynne / Datoo, Mehreen S. / Davies, Hannah / De Graaf, Hans / Demissie, Tesfaye / Di Maso, Claudio / Dietrich, Isabelle / Dong, Tao / Donnellan, Francesca R. / Douglas, Naomi / Downing, Charlotte / Drake, Jonathan / Drake-Brockman, Rachael / Drury, Ruth Elizabeth / Dunachie, Susanna Jane / Edwards, Nick J. / Edwards, Frances D.L. / Edwards, Chris J. / Elias, Sean C. / Elmore, Michael J. / Emary, Katherine R.W. / English, Marcus Rex / Fagerbrink, Susanne / Felle, Sally / Feng, Shuo / Field, Samantha / Fixmer, Carine / Fletcher, Clare / Ford, Karen J. / Fowler, Jamie / Fox, Polly / Francis, Emma / Frater, John / Furze, Julie / Fuskova, Michelle / Galiza, Eva / Gbesemete, Diane / Gilbride, Ciaran / Godwin, Kerry / Gorini, Giacomo / Goulston, Lyndsey / Grabau, Caroline / Gracie, Lara / Gray, Zoe / Guthrie, Lucy Belle / Hackett, Mark / Halwe, Sandro / Hamilton, Elizabeth / Hamlyn, Joseph / Hanumunthadu, Brama / Harding, Irasha / Harris, Stephanie A. / Harris, Andrew / Harrison, Daisy / Harrison, Clare / Hart, Thomas C. / Haskell, Louise / Hawkins, Sophia / Head, Ian / Henry, John Aaron / Hill, Jennifer / Hodgson, Susanne H.C. / Hou, Mimi M. / Howe, Elizabeth / Howell, Nicola / Hutlin, Cecilia / Ikram, Sabina / Isitt, Catherine / Iveson, Poppy / Jackson, Susan / Jackson, Frederic / James, Sir William / Jenkins, Megan / Jones, Elizabeth / Jones, Kathryn / Jones, Christine E. / Jones, Bryony / Kailath, Reshma / Karampatsas, Konstantinos / Keen, Jade / Kelly, Sarah / Kelly, Dearbhla / Kerr, David / Kerridge, Simon / Khan, Liaquat / Khan, Uzma / Killen, Annabel / Kinch, Jasmin / King, Thomas B. / King, Lloyd / King, Jade / Kingham-Page, Lucy / Klenerman, Paul / Knapper, Francesca / Knight, Julian C. / Knott, Daniel / Koleva, Stanislava / Kupke, Alexandra / Larkworthy, Colin W. / Larwood, Jessica P.J. / Laskey, Anna / Lawrie, Alison M. / Lee, Arlene / Ngan Lee, Kim Yee / Lees, Emily A / Legge, Helen / Lelliott, Alice / Lemm, Nana-Marie / Lias, Amelia M. / Linder, Aline / Lipworth, Samuel / Liu, Xinxue / Liu, Shuchang / Lopez Ramon, Raquel / Lwin, May / Mabesa, Francesca / Madhavan, Meera / Mallett, Garry / Mansatta, Kushal / Marcal, Ines / Marinou, Spyridoula / Marlow, Emma / Marshall, Julia L. / Martin, Jane / McEwan, Joanne / McInroy, Lorna / Meddaugh, Gretchen / Mentzer, Alexander J. / Mirtorabi, Neginsadat / Moore, Maria / Moran, Edward / Morey, Ella / Morgan, Victoria / Morris, Susan Jane / Morrison, Hazel / Morshead, Gertraud / Morter, Richard / Mujadidi, Yama F. / Muller, Jilly / Munera-Huertas, Tatiana / Munro, Claire / Munro, Alasdair / Murphy, Sarah / Munster, Vincent J. / Mweu, Philomena / Noé, Andrés / Nugent, Fay L. / Nuthall, Elizabeth / O'Brien, Katie / O'Connor, Daniel / Oguti, Blanché / Oliver, Jennifer L. / Oliveira, Catarina / O'Reilly, Peter John / Osborn, Mairead / Osborne, Piper / Owen, Cathy / Owens, Daniel / Owino, Nelly / Pacurar, Mihaela / Parker, Kaye / Parracho, Helena / Patrick-Smith, Maia / Payne, Victoria / Pearce, Jennifer / Peng, Yanchun / Peralta Alvarez, Marco Polo / Perring, James / Pfafferott, Katja / Pipini, Dimitra / Plested, Emma / Pluess-Hall, Helen / Pollock, Katrina / Poulton, Ian / Presland, Laura / Provstgaard-Morys, Samuel / Pulido, David / Radia, Kajal / Ramos Lopez, Fernando / Rand, Jade / Ratcliffe, Helen / Rawlinson, Thomas / Rhead, Sarah / Riddell, Amy / Ritchie, Adam John / Roberts, Hannah / Robson, Joanna / Roche, Sophie / Rohde, Cornelius / Rollier, Christine S. / Romani, Rossana / Rudiansyah, Indra / Saich, Stephen / Sajjad, Sara / Salvador, Stephannie / Sanchez Riera, Lidia / Sanders, Helen / Sanders, Katherine / Sapaun, Shari / Sayce, Chloe / Schofield, Ella / Screaton, Gavin / Selby, Beatrice / Semple, Calum / Sharpe, Hannah R. / Shaik, Imam / Shea, Adam / Shelton, Holly / Silk, Sarah / Silva-Reyes, Laura / Skelly, Donal T. / Smee, Heather / Smith, Catherine C. / Smith, David J. / Song, Rinn / Spencer, Alexandra J. / Stafford, Elizabeth / Steele, Amy / Stefanova, Elena / Stockdale, Lisa / Szigeti, Anna / Tahiri-Alaoui, Abdessamad / Tait, Moira / Talbot, Helen / Tanner, Rachel / Taylor, Iona Jennifer / Taylor, Victoria / Te Water Naude, Rebecca / Thakur, Nazia / Themistocleous, Yrene / Themistocleous, Andreas / Thomas, Merin / Thomas, Tonia M. / Thompson, Amber / Thomson-Hill, Samantha / Tomlins, Jennifer / Tonks, Susan / Towner, James / Tran, Nguyen / Tree, Julia A. / Truby, Adam / Turkentine, Kate / Turner, Cheryl / Turner, Nicola / Turner, Sally / Tuthill, Toby / Ulaszewska, Marta / Varughese, Rachel / Van Doremalen, Neeltje / Veighey, Kristin / Verheul, Marije K. / Vichos, Iason / Vitale, Elia / Walker, Laura / Watson, Marion E.E. / Welham, Benjamin / Wheat, Julie / White, Caroline / White, Rachel / Worth, Andrew T. / Wright, Danny / Wright, Suzie / Yao, Xin Li / Yau, Yasmine

The Lancet

a preliminary report of a phase 1/2, single-blind, randomised controlled trial

2020 Volume 396, Issue 10249, Page(s) 467–478

Keywords	General Medicine ; covid19
Language	English
Publisher	Elsevier BV
Publishing country	us
Document type	Article ; Online
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/s0140-6736(20)31604-4
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Article ; Online: Genome-wide association study of CNVs in 16,000 cases of eight common diseases and 3,000 shared controls.

Craddock, Nick / Hurles, Matthew E / Cardin, Niall / Pearson, Richard D / Plagnol, Vincent / Robson, Samuel / Vukcevic, Damjan / Barnes, Chris / Conrad, Donald F / Giannoulatou, Eleni / Holmes, Chris / Marchini, Jonathan L / Stirrups, Kathy / Tobin, Martin D / Wain, Louise V / Yau, Chris / Aerts, Jan / Ahmad, Tariq / Andrews, T Daniel /

Arbury, Hazel / Attwood, Anthony / Auton, Adam / Ball, Stephen G / Balmforth, Anthony J / Barrett, Jeffrey C / Barroso, Inês / Barton, Anne / Bennett, Amanda J / Bhaskar, Sanjeev / Blaszczyk, Katarzyna / Bowes, John / Brand, Oliver J / Braund, Peter S / Bredin, Francesca / Breen, Gerome / Brown, Morris J / Bruce, Ian N / Bull, Jaswinder / Burren, Oliver S / Burton, John / Byrnes, Jake / Caesar, Sian / Clee, Chris M / Coffey, Alison J / Connell, John M C / Cooper, Jason D / Dominiczak, Anna F / Downes, Kate / Drummond, Hazel E / Dudakia, Darshna / Dunham, Andrew / Ebbs, Bernadette / Eccles, Diana / Edkins, Sarah / Edwards, Cathryn / Elliot, Anna / Emery, Paul / Evans, David M / Evans, Gareth / Eyre, Steve / Farmer, Anne / Ferrier, I Nicol / Feuk, Lars / Fitzgerald, Tomas / Flynn, Edward / Forbes, Alistair / Forty, Liz / Franklyn, Jayne A / Freathy, Rachel M / Gibbs, Polly / Gilbert, Paul / Gokumen, Omer / Gordon-Smith, Katherine / Gray, Emma / Green, Elaine / Groves, Chris J / Grozeva, Detelina / Gwilliam, Rhian / Hall, Anita / Hammond, Naomi / Hardy, Matt / Harrison, Pile / Hassanali, Neelam / Hebaishi, Husam / Hines, Sarah / Hinks, Anne / Hitman, Graham A / Hocking, Lynne / Howard, Eleanor / Howard, Philip / Howson, Joanna M M / Hughes, Debbie / Hunt, Sarah / Isaacs, John D / Jain, Mahim / Jewell, Derek P / Johnson, Toby / Jolley, Jennifer D / Jones, Ian R / Jones, Lisa A / Kirov, George / Langford, Cordelia F / Lango-Allen, Hana / Lathrop, G Mark / Lee, James / Lee, Kate L / Lees, Charlie / Lewis, Kevin / Lindgren, Cecilia M / Maisuria-Armer, Meeta / Maller, Julian / Mansfield, John / Martin, Paul / Massey, Dunecan C O / McArdle, Wendy L / McGuffin, Peter / McLay, Kirsten E / Mentzer, Alex / Mimmack, Michael L / Morgan, Ann E / Morris, Andrew P / Mowat, Craig / Myers, Simon / Newman, William / Nimmo, Elaine R / O'Donovan, Michael C / Onipinla, Abiodun / Onyiah, Ifejinelo / Ovington, Nigel R / Owen, Michael J / Palin, Kimmo / Parnell, Kirstie / Pernet, David / Perry, John R B / Phillips, Anne / Pinto, Dalila / Prescott, Natalie J / Prokopenko, Inga / Quail, Michael A / Rafelt, Suzanne / Rayner, Nigel W / Redon, Richard / Reid, David M / Renwick / Ring, Susan M / Robertson, Neil / Russell, Ellie / St Clair, David / Sambrook, Jennifer G / Sanderson, Jeremy D / Schuilenburg, Helen / Scott, Carol E / Scott, Richard / Seal, Sheila / Shaw-Hawkins, Sue / Shields, Beverley M / Simmonds, Matthew J / Smyth, Debbie J / Somaskantharajah, Elilan / Spanova, Katarina / Steer, Sophia / Stephens, Jonathan / Stevens, Helen E / Stone, Millicent A / Su, Zhan / Symmons, Deborah P M / Thompson, John R / Thomson, Wendy / Travers, Mary E / Turnbull, Clare / Valsesia, Armand / Walker, Mark / Walker, Neil M / Wallace, Chris / Warren-Perry, Margaret / Watkins, Nicholas A / Webster, John / Weedon, Michael N / Wilson, Anthony G / Woodburn, Matthew / Wordsworth, B Paul / Young, Allan H / Zeggini, Eleftheria / Carter, Nigel P / Frayling, Timothy M / Lee, Charles / McVean, Gil / Munroe, Patricia B / Palotie, Aarno / Sawcer, Stephen J / Scherer, Stephen W / Strachan, David P / Tyler-Smith, Chris / Brown, Matthew A / Burton, Paul R / Caulfield, Mark J / Compston, Alastair / Farrall, Martin / Gough, Stephen C L / Hall, Alistair S / Hattersley, Andrew T / Hill, Adrian V S / Mathew, Christopher G / Pembrey, Marcus / Satsangi, Jack / Stratton, Michael R / Worthington, Jane / Deloukas, Panos / Duncanson, Audrey / Kwiatkowski, Dominic P / McCarthy, Mark I / Ouwehand, Willem / Parkes, Miles / Rahman, Nazneen / Todd, John A / Samani, Nilesh J / Donnelly, Peter

Nature

2010 Volume 464, Issue 7289, Page(s) 713–720

Abstract: Copy number variants (CNVs) account for a major proportion of human genetic polymorphism and have been predicted to have an important role in genetic susceptibility to common disease. To address this we undertook a large, direct genome-wide study of ... ...

Abstract	Copy number variants (CNVs) account for a major proportion of human genetic polymorphism and have been predicted to have an important role in genetic susceptibility to common disease. To address this we undertook a large, direct genome-wide study of association between CNVs and eight common human diseases. Using a purpose-designed array we typed approximately 19,000 individuals into distinct copy-number classes at 3,432 polymorphic CNVs, including an estimated approximately 50% of all common CNVs larger than 500 base pairs. We identified several biological artefacts that lead to false-positive associations, including systematic CNV differences between DNAs derived from blood and cell lines. Association testing and follow-up replication analyses confirmed three loci where CNVs were associated with disease-IRGM for Crohn's disease, HLA for Crohn's disease, rheumatoid arthritis and type 1 diabetes, and TSPAN8 for type 2 diabetes-although in each case the locus had previously been identified in single nucleotide polymorphism (SNP)-based studies, reflecting our observation that most common CNVs that are well-typed on our array are well tagged by SNPs and so have been indirectly explored through SNP studies. We conclude that common CNVs that can be typed on existing platforms are unlikely to contribute greatly to the genetic basis of common human diseases.
MeSH term(s)	Arthritis, Rheumatoid/genetics ; Case-Control Studies ; Crohn Disease/genetics ; DNA Copy Number Variations/genetics ; Diabetes Mellitus/genetics ; Disease ; Gene Frequency/genetics ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis ; Pilot Projects ; Polymorphism, Single Nucleotide/genetics ; Quality Control
Language	English
Publishing date	2010-03-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature08979
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Article ; Online: Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants.

Burton, Paul R / Clayton, David G / Cardon, Lon R / Craddock, Nick / Deloukas, Panos / Duncanson, Audrey / Kwiatkowski, Dominic P / McCarthy, Mark I / Ouwehand, Willem H / Samani, Nilesh J / Todd, John A / Donnelly, Peter / Barrett, Jeffrey C / Davison, Dan / Easton, Doug / Evans, David M / Leung, Hin-Tak / Marchini, Jonathan L / Morris, Andrew P /

Spencer, Chris C A / Tobin, Martin D / Attwood, Antony P / Boorman, James P / Cant, Barbara / Everson, Ursula / Hussey, Judith M / Jolley, Jennifer D / Knight, Alexandra S / Koch, Kerstin / Meech, Elizabeth / Nutland, Sarah / Prowse, Christopher V / Stevens, Helen E / Taylor, Niall C / Walters, Graham R / Walker, Neil M / Watkins, Nicholas A / Winzer, Thilo / Jones, Richard W / McArdle, Wendy L / Ring, Susan M / Strachan, David P / Pembrey, Marcus / Breen, Gerome / St Clair, David / Caesar, Sian / Gordon-Smith, Katharine / Jones, Lisa / Fraser, Christine / Green, Elaine K / Grozeva, Detelina / Hamshere, Marian L / Holmans, Peter A / Jones, Ian R / Kirov, George / Moskivina, Valentina / Nikolov, Ivan / O'Donovan, Michael C / Owen, Michael J / Collier, David A / Elkin, Amanda / Farmer, Anne / Williamson, Richard / McGuffin, Peter / Young, Allan H / Ferrier, I Nicol / Ball, Stephen G / Balmforth, Anthony J / Barrett, Jennifer H / Bishop, Timothy D / Iles, Mark M / Maqbool, Azhar / Yuldasheva, Nadira / Hall, Alistair S / Braund, Peter S / Dixon, Richard J / Mangino, Massimo / Stevens, Suzanne / Thompson, John R / Bredin, Francesca / Tremelling, Mark / Parkes, Miles / Drummond, Hazel / Lees, Charles W / Nimmo, Elaine R / Satsangi, Jack / Fisher, Sheila A / Forbes, Alastair / Lewis, Cathryn M / Onnie, Clive M / Prescott, Natalie J / Sanderson, Jeremy / Matthew, Christopher G / Barbour, Jamie / Mohiuddin, M Khalid / Todhunter, Catherine E / Mansfield, John C / Ahmad, Tariq / Cummings, Fraser R / Jewell, Derek P / Webster, John / Brown, Morris J / Lathrop, Mark G / Connell, John / Dominiczak, Anna / Marcano, Carolina A Braga / Burke, Beverley / Dobson, Richard / Gungadoo, Johannie / Lee, Kate L / Munroe, Patricia B / Newhouse, Stephen J / Onipinla, Abiodun / Wallace, Chris / Xue, Mingzhan / Caulfield, Mark / Farrall, Martin / Barton, Anne / Bruce, Ian N / Donovan, Hannah / Eyre, Steve / Gilbert, Paul D / Hilder, Samantha L / Hinks, Anne M / John, Sally L / Potter, Catherine / Silman, Alan J / Symmons, Deborah P M / Thomson, Wendy / Worthington, Jane / Dunger, David B / Widmer, Barry / Frayling, Timothy M / Freathy, Rachel M / Lango, Hana / Perry, John R B / Shields, Beverley M / Weedon, Michael N / Hattersley, Andrew T / Hitman, Graham A / Walker, Mark / Elliott, Kate S / Groves, Christopher J / Lindgren, Cecilia M / Rayner, Nigel W / Timpson, Nicolas J / Zeggini, Eleftheria / Newport, Melanie / Sirugo, Giorgio / Lyons, Emily / Vannberg, Fredrik / Hill, Adrian V S / Bradbury, Linda A / Farrar, Claire / Pointon, Jennifer J / Wordsworth, Paul / Brown, Matthew A / Franklyn, Jayne A / Heward, Joanne M / Simmonds, Matthew J / Gough, Stephen C L / Seal, Sheila / Stratton, Michael R / Rahman, Nazneen / Ban, Maria / Goris, An / Sawcer, Stephen J / Compston, Alastair / Conway, David / Jallow, Muminatou / Rockett, Kirk A / Bumpstead, Suzannah J / Chaney, Amy / Downes, Kate / Ghori, Mohammed J R / Gwilliam, Rhian / Hunt, Sarah E / Inouye, Michael / Keniry, Andrew / King, Emma / McGinnis, Ralph / Potter, Simon / Ravindrarajah, Rathi / Whittaker, Pamela / Widden, Claire / Withers, David / Cardin, Niall J / Ferreira, Teresa / Pereira-Gale, Joanne / Hallgrimsdo'ttir, Ingeleif B / Howie, Bryan N / Su, Zhan / Teo, Yik Ying / Vukcevic, Damjan / Bentley, David / Mitchell, Sarah L / Newby, Paul R / Brand, Oliver J / Carr-Smith, Jackie / Pearce, Simon H S / McGinnis, R / Keniry, A / Deloukas, P / Reveille, John D / Zhou, Xiaodong / Sims, Anne-Marie / Dowling, Alison / Taylor, Jacqueline / Doan, Tracy / Davis, John C / Savage, Laurie / Ward, Michael M / Learch, Thomas L / Weisman, Michael H / Brown, Mathew

Nature genetics

2007 Volume 39, Issue 11, Page(s) 1329–1337

Abstract: We have genotyped 14,436 nonsynonymous SNPs (nsSNPs) and 897 major histocompatibility complex (MHC) tag SNPs from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC). ... ...

Abstract	We have genotyped 14,436 nonsynonymous SNPs (nsSNPs) and 897 major histocompatibility complex (MHC) tag SNPs from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC). Comparing these data against a common control dataset derived from 1,500 randomly selected healthy British individuals, we report initial association and independent replication in a North American sample of two new loci related to ankylosing spondylitis, ARTS1 and IL23R, and confirmation of the previously reported association of AITD with TSHR and FCRL3. These findings, enabled in part by increased statistical power resulting from the expansion of the control reference group to include individuals from the other disease groups, highlight notable new possibilities for autoimmune regulation and suggest that IL23R may be a common susceptibility factor for the major 'seronegative' diseases.
MeSH term(s)	Aminopeptidases/genetics ; Autoimmunity/genetics ; Breast Neoplasms/epidemiology ; Breast Neoplasms/genetics ; Case-Control Studies ; Chromosome Mapping ; Genetics, Population ; Genotype ; Haplotypes/genetics ; Humans ; Linkage Disequilibrium ; Minor Histocompatibility Antigens ; Multiple Sclerosis/epidemiology ; Multiple Sclerosis/genetics ; North America/epidemiology ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide/genetics ; Receptors, Immunologic/genetics ; Receptors, Interleukin/genetics ; Spondylitis, Ankylosing/epidemiology ; Spondylitis, Ankylosing/genetics ; Thyroiditis, Autoimmune/epidemiology ; Thyroiditis, Autoimmune/genetics
Chemical Substances	FCRL3 protein, human ; IL23R protein, human ; Minor Histocompatibility Antigens ; Receptors, Immunologic ; Receptors, Interleukin ; Aminopeptidases (EC 3.4.11.-) ; ERAP1 protein, human (EC 3.4.11.-)
Language	English
Publishing date	2007-10-21
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/ng.2007.17
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes

Zeggini, Eleftheria / Ahmad, Tariq / Ardern-Jones, A / Attwood, Antony P / Ball, Stephen G / Balmforth, Anthony J / Ban, Maria / Barbour, Jamie / Barrett, Jeffrey C / Barrett, Jennifer H / Barton, Anne / Bentley, David / Berg, J / Bishop, D. Timothy / Boorman, James P / Bradbury, Linda A / Bradshaw, N / Brady, A / Braga Marcano, Carolina A /

Braund, Peter S / Bredin, Francesca / Breen, Gerome / Brewer, C / Brice, G / Brown, Matthew A / Brown, Morris J / Bruce, Ian N / Bullman, B / Bumpstead, Suzannah J / Burke, Beverley / Burton, Paul R / Caesar, Sian / Campbell, J / Cant, Barbara / Cardin, Niall J / Cardon, Lon R / Castle, B / Caulfield, Mark / Cetnarsryj, R / Chaney, Amy / Chapman, C / Chu, C / Clayton, David G / Coates, N / Cole, T / Collier, David A / Compston, Alastair / Compston, Alistair / Connell, John / Conway, David / Craddock, Nick / Cummings, Fraser R / Davidson, R / Davison, Dan / Deloukas, Panos / Dixon, Richard J / Dobson, Richard / Dominiczak, Anna / Donaldson, A / Doney, Alex S.F / Donnelly, Peter / Donovan, Hannah / Dorkins, H / Douglas, F / Downes, Kate / Drummond, Hazel / Duncanson, Audrey / Dunger, David B / Easton, Doug / Eccles, D / Eeles, R / Elkin, Amanda / Ellard, Sian / Elliott, Katherine S / Elmslie, F / Evans, D.G / Evans, David / Everson, Ursula / Eyre, Steve / Farmer, Anne / Farrall, Martin / Farrar, Claire / Ferreira, Teresa / Ferrier, I. Nicol / Fisher, Sheila A / Forbes, Alastair / Franklyn, Jayne A / Fraser, Christine / Frayling, Timothy M / Freathy, Rachel M / Ghori, Mohammed J.R / Gilbert, Paul D / Goff, S / Goodman, S / Gordon-Smith, Katherine / Goris, An / Goudie, D / Gough, Stephen C.L / Gray, J / Green, Elaine K / Greenhalgh, L / Gregory, H / Groves, Christopher J / Grozeva, Detelina / Gungadoo, Johannie / Gwilliam, Rhian / Hall, Alistair S / HallgrimsdoÌttir, Ingeleif B / Hamshere, Marian L / Harries, Lorna W / Hattersley, Andrew T / Heward, Joanne M / Hider, Samantha L / Hill, Adrian V.S / Hinks, Anne M / Hitman, Graham A / Hodgson, S.V / Holmans, Peter A / Homfray, T / Houlston, R.S / Howie, Bryan N / Hunt, Sarah E / Hussey, Judith M / Iles, Mark M / Inouye, Michael / Isaacs, John D / Izatt, L / Jackson, L / Jallow, Muminatou / Jeffers, L / Jewell, Derek P / John, Sally L / Johnson-Roffey, V / Jolley, Jennifer D / Jones, Ian R / Jones, Lisa / Jones, Richard W / Kavalier, F / Keniry, Andrew / King, Emma / Kirk, C / Kirov, George / Knight, Alexandra S / Knight, Beatrice / Koch, Kerstin / Kwiatkowski, Dominic P / Lalloo, F / Langman, C / Lango, Hana / Lathrop, G. Mark / Lee, Kate L / Lees, Charles W / Leung, Hin-Tak / Lewis, Cathryn M / Lindgren, Cecilia M / Locke, I / Longmuir, M / Lyons, Emily / Mackay, J / Magee, A / Mangino, Massimo / Mansfield, John C / Mansour, S / Maqbool, Azhar / Marchini, Jonathan L / Mathew, Christopher G / McArdle, Wendy L / McCarthy, Mark I / McGinnis, Ralph / McGuffin, Peter / Meech, Elizabeth / Miedzybrodzka, Z / Miller, J / Mohiuddin, M. Khalid / Morgan, Ann W / Morris, Andrew D / Morris, Andrew P / Morrison, P / Moskvina, Valentina / Munroe, Patricia B / Murday, V / Newhouse, Stephen J / Newport, Melanie / Nikolov, Ivan / Nimmo, Elaine R / Nutland, Sarah / O'Donovan, Michael C / Onipinla, Abiodun / Onnie, Clive M / Ouwehand, Nilesh J / Ouwehand, Willem H / Owen, Katharine R / Owen, Michael J / Parkes, Miles / Paterson, J / Pembrey, Marcus / Pereira-Gale, Joanne / Perry, John R.B / Pichert, G / Pointon, Jennifer J / Porteous, M / Potter, Catherine / Potter, Simon / Prescott, Natalie J / Prowse, Christopher V / Rahman, N / Rahman, Nazneen / Ravindrarajah, Rathi / Rayner, Nigel W / Ring, Susan M / Rockett, Kirk A / Rogers, M / Rowe, S / Saggar, A / Samani, Michael R / Samani, Nilesh J / Sanderson, Jeremy / Satsangi, Jack / Sawcer, Stephen J / Scott, G / Seal, Sheila / Shanley, S / Shields, Beverley / Side, L / Silman, Alan J / Simmonds, Matthew J / Sirugo, Giorgio / Snadden, L / Spencer, Chris C.A / St. Clair, David / Steel, M / Stevens, Helen E / Stevens, Suzanne / Strachan, David P / Stratton, Michael R / Su, Zhan / Symmons, Deborah P.M / Taylor, Niall C / Teo, Yik Ying / Thomas, M / Thomas, S / Thompson, John R / Thomson, Wendy / Timpson, Nicholas J / Tobin, Martin D / Todd, John A / Todhunter, Catherine E / Tremelling, Mark / Vannberg, Fredrik / Vukcevic, Damjan / Walker, Mark / Walker, Neil M / Wallace, Chris / Walters, Graham R / Watkins, Nicholas A / Webster, John / Weedon, Michael N / Whittaker, Pamela / Widden, Claire / Widmer, Barry / Williamson, Richard / Wilson, Gerry D / Winzer, Thilo / Withers, David / Wordsworth, Paul / Worthington, Jane / Xue, Mingzhan / Young, Allan H / Yuldasheva, Nadira

Science. 2007 June 1, v. 316, no. 5829

2007

Abstract: The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set ... ...

Abstract	The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set out to detect replicated diabetes association signals through analysis of 3757 additional cases and 5346 controls and by integration of our findings with equivalent data from other international consortia. We detected diabetes susceptibility loci in and around the genes CDKAL1, CDKN2A/CDKN2B, and IGF2BP2 and confirmed the recently described associations at HHEX/IDE and SLC30A8. Our findings provide insight into the genetic architecture of type 2 diabetes, emphasizing the contribution of multiple variants of modest effect. The regions identified underscore the importance of pathways influencing pancreatic beta cell development and function in the etiology of type 2 diabetes.
Keywords	etiology ; genes ; genotype ; islets of Langerhans ; loci ; noninsulin-dependent diabetes mellitus ; risk ; United Kingdom
Language	English
Dates of publication	2007-0601
Size	p. 1336-1341.
Publishing place	American Association for the Advancement of Science
Document type	Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.1142364
Database	NAL-Catalogue (AGRICOLA)

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