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Contributors
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- By Phillip L. Ackerman, Neil Anderson, Jens B. Asendorpf, R. Michael Bagby, Michael Harris Bond, Gregory J. Boyle, Andrea L. Briggs, Giles St J. Burch, Turhan Canli, David Canter, Gianvittorio Caprara, Charles S. Carver, Douglas F. Cellar, Gordon Claridge, Susan Cloninger, Elisabeth D. Conradt, Philip J. Corr, Sharon Dawe, Ian J. Deary, Boele De Raad, Edward L. Deci, Colin G. DeYoung, M. Brent Donnellan, Juris G. Draguns, Marko Elovainio, Aurelio José Figueredo, David C. Funder, Paul Gladden, Rapson Gomez, Samuel D. Gosling, Jeremy R. Gray, Robert D. Hare, B. Austin Harley, Edward Helmes, Robert Hogan, Lauri A. Jensen-Campbell, Daniel Nelson Jones, Mika Kivimäki, Jennifer M. Knack, James T. Lamiell, Natalie J. Loxton, Geoff MacDonald, Gerald Matthews, Robert R. McCrae, Mario Mikulincer, Stephanie N. Mullins-Sweatt, Marcus R. Munafò, Vickie Nam, Craig S. Newmann, Rainer Reisenzein, Madeline Rex-Lear, Richard W. Robins, Michael D. Robinson, Mary K. Rothbart, Richard M. Ryan, Gerard Saucier, Michael F. Scheier, Constantine Sedikides, Phillip R. Shaver, Brad E. Sheese, Yuichi Shoda, Ronald E. Smith, Alice F. Stuhlmacher, Rhonda Swickert, Avril Thorne, David D. Vachon, Geneva Vásquez, Michele Vecchione, Seth A. Wagerman, Fiona Warren, Hannelore Weber, Thomas A. Widiger, Pedro Sofio Abril Wolf, Donna Youngs, Moshe Zeidner
- Edited by Philip J. Corr, University of East Anglia, Gerald Matthews, University of Cincinnati
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- Book:
- The Cambridge Handbook of Personality Psychology
- Published online:
- 05 June 2012
- Print publication:
- 16 July 2009, pp xv-xvii
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“Masked” pulmonary venous obstruction in patients with isomerism of the right atrial appendages: an overstated association
- C. Becket Mahnke, George G. Sandor, Gerard J. Boyle, Steven A. Webber
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- Journal:
- Cardiology in the Young / Volume 12 / Issue 2 / March 2002
- Published online by Cambridge University Press:
- 15 August 2006, pp. 113-118
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- Article
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Isomerism of the right atrial appendages is associated with anomalies of pulmonary venous return, which may be obstructive. The associated pulmonary arterial obstruction, however, has been reported to “mask” the pulmonary venous obstruction, with resultant pulmonary edema following augmentation of the flow of blood to the lungs. We postulated that the frequency of “masked” pulmonary venous obstruction has been overreported in the literature. To ascertain the true situation, we evaluated the frequency of “masked” pulmonary venous obstruction in a large, unselected, group of patients with isomerism of the right atrial appendages. We evaluated the clinical, anatomic, and radiographic data of 65 newborns seen with this syndrome since 1970. Development of pulmonary venous obstruction, both before and after systemic-to-pulmonary shunting and/or infusion of prostaglandin E1, was determined and correlated to clinical and radiographic findings. Of the 65 patients, 19 (29%) were ultimately diagnosed with pulmonary venous obstruction. The pulmonary veins themselves connected in infradiaphragmatic fashion in 10 patients, supracardiac in 3, to the atriums directly in 1, and in mixed fashion in the other 5. Pulmonary venous obstruction was readily apparent in 15 of the 19, as demonstrated by pulmonary edema on initial chest radiography. The remaining four cases ultimately diagnosed with pulmonary venous obstruction received augmentation of pulmonary blood flow with resultant pulmonary edema. Of these four severely cyanosed patients, pulmonary vascular markings on the initial chest radiograph had been normal in one but increased in three. Due to the presence of these clinical markers, they do not truly represent “masked” pulmonary venous obstruction. Except for two patients with minimally obstructed pulmonary arterial blood flow, 44 patients without pulmonary venous obstruction had normal or decreased pulmonary vascular markings at presentation. Of these 44, 14 received infusions of prostaglandin E1, with none developing pulmonary edema. We conclude that pulmonary venous obstruction is usually readily apparent at time of presentation in patients with right isomerism, and that “masked” pulmonary venous is a very rare event which has been over-emphasized in the literature. Careful evaluation of clinical and radiographic findings at time of presentation can correctly identify pulmonary venous obstruction in such patients.
Polymorphisms in cytokine genes do not predict progression to end-stage heart failure in children
- Steven A. Webber, Gerard J. Boyle, Steven Gribar, Yuk Law, Pamela Bowman, Susan A. Miller, Mohammed R. Awad, Mamun Ahmed, Joan Martell, Adriana Zeevi
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- Journal:
- Cardiology in the Young / Volume 12 / Issue 5 / October 2002
- Published online by Cambridge University Press:
- 15 August 2006, pp. 461-464
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- Article
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A number of cytokines have been implicated in the pathophysiology of congestive heart failure. Genetic polymorphisms of several cytokine genes are known to result in altered gene expression, enabling us to characterize patients as "high" or "low" producers of specific cytokines. We speculate that the cytokine genotypes for a population of children who underwent heart transplantation for end-stage ventricular failure due to cardiomyopathy or congenital heart disease would be enriched for "high producers" of pro-inflammatory cytokines and "low producers" of anti-inflammatory cytokines. Methods: Cytokine genotyping was performed for the following cytokines on 94 transplanted children using polymerase chain reaction-sequence specific technique: tumor necrosis factor-α (−308), interleukin 10 (−1082, −819, −592), interleukin 6 (−174), transforming growth factor-β1(codons 10 & 25), and interferon-γ (+874). Patients with ventricular failure after transplantation for dilated cardiomyopathy, numbering 37, or for congenital heart disease, numbering 34, were compared to 15 children transplanted for structural disease, such as hypoplastic left heart syndrome, without ventricular failure, and to data from healthy children. An additional 8 children with restrictive or hypertrophic cardiomyopathy were also studied. Results: No differences in genotypic distribution were seen between the groups, and all patients were comparable to genotypic distributions as assessed from published normal data. Conclusion: No evidence is found to support the hypothesis that these polymorphisms for cytokine genes influence progression to end-stage heart failure in children undergoing transplantation because of cardiomyopathy or congenital heart disease.