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Institution

University of Iowa

EducationIowa City, Iowa, United States
About: University of Iowa is a education organization based out in Iowa City, Iowa, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 49229 authors who have published 109171 publications receiving 5021465 citations. The organization is also known as: UI & The University of Iowa.


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Journal ArticleDOI
TL;DR: Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation, which may be implicated in the pathogenesis of hypertension and heart failure in this condition.
Abstract: Background—Patients with obstructive sleep apnea (OSA) experience repetitive episodic hypoxemia with consequent sympathetic activation and marked blood pressure surges, each of which may impair endothelial function. We tested the hypothesis that patients with OSA have impaired endothelium-dependent vasodilation, even in the absence of overt cardiovascular disease. Methods and Results—We studied 8 patients with OSA (age 44 64 years) and 9 obese control subjects (age 4863 years). Patients with OSA were newly diagnosed, never treated for OSA, on no medications, and free of any other known diseases. All obese control subjects underwent complete overnight polysomnographic studies to exclude occult OSA. Resistance-vessel function was tested by use of forearm blood flow responses to intra-arterial infusions of acetylcholine (a vasodilator that stimulates endothelial release of nitric oxide), sodium nitroprusside (an exogenous nitric oxide donor), and verapamil (a calcium channel blocker). Conduit-vessel function was also evaluated by ultrasonography. Brachial artery diameter was measured under baseline conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent vasodilator). Patients with OSA had a blunted vasodilation in response to acetylcholine ( P,0.007), but responses to sodium nitroprusside and verapamil were not significantly different from those of control subjects. No significant difference in conduit-vessel dilation was evident between OSA patients and obese control subjects. Conclusions—Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation. This may be implicated in the pathogenesis of hypertension and heart failure in this condition. (Circulation. 2000;102:26072610.)

711 citations

Journal ArticleDOI
Angela M. Wood1, Stephen Kaptoge1, Adam S. Butterworth1, Peter Willeit1, Samantha Warnakula1, Thomas Bolton1, Ellie Paige2, Dirk S. Paul1, Michael J. Sweeting1, Stephen Burgess1, Steven Bell1, William J. Astle1, David Stevens1, Albert Koulman1, Randi Selmer3, W. M. Monique Verschuren4, Shinichi Sato, Inger Njølstad5, Mark Woodward6, Mark Woodward7, Mark Woodward8, Veikko Salomaa9, Børge G. Nordestgaard10, Børge G. Nordestgaard11, Bu B. Yeap12, Bu B. Yeap13, Bu B. Yeap14, Astrid E. Fletcher15, Olle Melander16, Lewis H. Kuller17, B. Balkau18, Michael Marmot19, Wolfgang Koenig20, Wolfgang Koenig21, Edoardo Casiglia22, Cyrus Cooper23, Volker Arndt24, Oscar H. Franco25, Patrik Wennberg26, John Gallacher27, Agustín Gómez de la Cámara, Henry Völzke28, Christina C. Dahm29, Caroline Dale19, Manuela M. Bergmann, Carlos J. Crespo30, Yvonne T. van der Schouw4, Rudolf Kaaks24, Leon A. Simons31, Pagona Lagiou32, Pagona Lagiou33, Josje D. Schoufour25, Jolanda M. A. Boer, Timothy J. Key6, Beatriz L. Rodriguez34, Conchi Moreno-Iribas, Karina W. Davidson35, James O. Taylor, Carlotta Sacerdote, Robert B. Wallace36, J. Ramón Quirós, Rosario Tumino, Dan G. Blazer37, Allan Linneberg11, Makoto Daimon38, Salvatore Panico, Barbara V. Howard39, Guri Skeie5, Timo E. Strandberg40, Timo E. Strandberg41, Elisabete Weiderpass, Paul J. Nietert42, Bruce M. Psaty43, Bruce M. Psaty44, Daan Kromhout45, Elena Salamanca-Fernández46, Stefan Kiechl, Harlan M. Krumholz47, Sara Grioni, Domenico Palli48, José María Huerta, Jackie F. Price49, Johan Sundström50, Larraitz Arriola51, Hisatomi Arima52, Hisatomi Arima53, Ruth C. Travis6, Demosthenes B. Panagiotakos54, Anna Karakatsani33, Antonia Trichopoulou33, Tilman Kühn24, Diederick E. Grobbee4, Elizabeth Barrett-Connor55, Natasja M. van Schoor56, Heiner Boeing, Kim Overvad29, Kim Overvad57, Jussi Kauhanen58, Nicholas J. Wareham1, Claudia Langenberg1, Nita G. Forouhi1, Maria Wennberg26, Jean-Pierre Després59, Mary Cushman60, Jackie A. Cooper19, Carlos J. Rodriguez61, Carlos J. Rodriguez62, Masaru Sakurai63, Jonathan E. Shaw64, Matthew Knuiman14, Trudy Voortman25, Christa Meisinger, Anne Tjønneland, Hermann Brenner24, Hermann Brenner65, Luigi Palmieri66, Jean Dallongeville67, Eric J. Brunner19, Gerd Assmann, Maurizio Trevisan68, Richard F. Gillum69, Ian Ford70, Naveed Sattar70, Mariana Lazo8, Simon G. Thompson1, Pietro Ferrari71, David A. Leon15, George Davey Smith72, Richard Peto6, Rod Jackson73, Emily Banks2, Emanuele Di Angelantonio1, John Danesh1 
University of Cambridge1, Australian National University2, Norwegian Institute of Public Health3, Utrecht University4, University of Tromsø5, University of Oxford6, The George Institute for Global Health7, Johns Hopkins University8, National Institutes of Health9, Copenhagen University Hospital10, University of Copenhagen11, Fiona Stanley Hospital12, Harry Perkins Institute of Medical Research13, University of Western Australia14, University of London15, Lund University16, University of Pittsburgh17, French Institute of Health and Medical Research18, University College London19, University of Ulm20, Technische Universität München21, University of Padua22, University of Southampton23, German Cancer Research Center24, Erasmus University Medical Center25, Umeå University26, Cardiff University27, Greifswald University Hospital28, Aarhus University29, Portland State University30, University of New South Wales31, Harvard University32, National and Kapodistrian University of Athens33, University of Hawaii34, Columbia University35, University of Iowa36, Duke University37, Yamagata University38, Tuskegee University39, University of Oulu40, University of Helsinki41, Medical University of South Carolina42, University of Washington43, Kaiser Permanente44, University of Groningen45, University of Granada46, Yale University47, Prevention Institute48, University of Edinburgh49, Uppsala University50, Basque Government51, Royal Prince Alfred Hospital52, Kyushu University53, Harokopio University54, University of California, San Diego55, VU University Medical Center56, Aalborg University57, University of Eastern Finland58, Laval University59, University of Vermont60, Wake Forest Baptist Medical Center61, Wake Forest University62, Kanazawa Medical University63, Baker IDI Heart and Diabetes Institute64, Heidelberg University65, Istituto Superiore di Sanità66, Pasteur Institute67, City College of New York68, Howard University69, University of Glasgow70, International Agency for Research on Cancer71, University of Bristol72, University of Auckland73
TL;DR: Current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week, and data support limits for alcohol consumption that are lower than those recommended in most current guidelines.

711 citations

Journal ArticleDOI
TL;DR: An overview of the gene–environment contributions to nonsyndromic forms of clefting and their implications for developmental biology and clinical counseling is presented.
Abstract: Craniofacial anomalies, and in particular cleft lip and palate, are major human birth defects with a worldwide frequency of 1 in 700 and substantial clinical impact. A wide range of studies in developmental biology has contributed to a better knowledge of how both genes and environmental exposures impact head organogenesis. Specific causes have now been identified for some forms of cleft lip and palate, and we are at the beginning of a time in which the common nonsyndromic forms may also have specific etiologies identified. Mouse models have an especially important role in disclosing cleft etiologies and providing models for environmental cotriggers or interventions. An overview of the gene-environment contributions to nonsyndromic forms of clefting and their implications for developmental biology and clinical counseling is presented.

709 citations

Journal ArticleDOI
TL;DR: This study showed that VX-770 was associated with within-subject improvements in CFTR and lung function and provides support for further studies of pharmacologic potentiation of CFTR as a means to treat cystic fibrosis.
Abstract: Background A new approach in the treatment of cystic fibrosis involves improving the function of mutant cystic fibrosis transmembrane conductance regulator (CFTR). VX-770, a CFTR potentiator, has been shown to increase the activity of wild-type and defective cellsurface CFTR in vitro. Methods We randomly assigned 39 adults with cystic fibrosis and at least one G551D-CFTR allele to receive oral VX-770 every 12 hours at a dose of 25, 75, or 150 mg or placebo for 14 days (in part 1 of the study) or VX-770 every 12 hours at a dose of 150 or 250 mg or placebo for 28 days (in part 2 of the study). Results At day 28, in the group of subjects who received 150 mg of VX-770, the median change in the nasal potential difference (in response to the administration of a chloride-free isoproterenol solution) from baseline was −3.5 mV (range, −8.3 to 0.5; P = 0.02 for the within-subject comparison, P = 0.13 vs. placebo), and the median change in the level of sweat chloride was −59.5 mmol per liter (range, −66.0 to −19.0; P = 0.008 within-subject, P = 0.02 vs. placebo). The median change from baseline in the percent of predicted forced expiratory volume in 1 second was 8.7% (range, 2.3 to 31.3; P = 0.008 for the within-subject comparison, P = 0.56 vs. placebo). None of the subjects withdrew from the study. Six severe adverse events occurred in two subjects (diffuse macular rash in one subject and five incidents of elevated blood and urine glucose levels in one subject with diabetes). All severe adverse events resolved without the discontinuation of VX-770. Conclusions This study to evaluate the safety and adverse-event profile of VX-770 showed that VX-770 was associated with within-subject improvements in CFTR and lung function. These findings provide support for further studies of pharmacologic potentiation of CFTR as a means to treat cystic fibrosis. (Funded by Vertex Pharmaceuticals and others; ClinicalTrials.gov number, NCT00457821.)

709 citations


Authors

Showing all 49661 results

NameH-indexPapersCitations
Stephen V. Faraone1881427140298
Jie Zhang1784857221720
D. M. Strom1763167194314
Bradley T. Hyman169765136098
John H. Seinfeld165921114911
David Jonathan Hofman1591407140442
Stephen J. O'Brien153106293025
John T. Cacioppo147477110223
Mark Raymond Adams1471187135038
E. L. Barberio1431605115709
Andrew Ivanov142181297390
Stephen J. Lippard141120189269
Russell Richard Betts140132395678
Barry Blumenfeld1401909105694
Marcus Hohlmann140135694739
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023154
2022727
20214,129
20203,902
20193,763
20183,659