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Stephen V. Faraone

Bio: Stephen V. Faraone is an academic researcher from State University of New York Upstate Medical University. The author has contributed to research in topics: Attention deficit hyperactivity disorder & Bipolar disorder. The author has an hindex of 188, co-authored 1427 publications receiving 140298 citations. Previous affiliations of Stephen V. Faraone include University of Bergen & National Institute for Health Research.


Papers
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Journal ArticleDOI
TL;DR: Family genetic studies of ADHD and bipolar I disorder are reviewed to suggest that ADHD plus bipolar comorbidity cannot be accounted for by misdiagnoses, but additional research is needed to rule out artifactual sources of comorebidity.
Abstract: ObjectiveThe existence of comorbidity between attention deficit hyperactivity disorder (ADHD) and bipolar I disorder has been documented in clinical and epidemiological studies, in studies of children and adults, and in diagnosed ADHD and bipolar I patient samples. Yet questions remain about the validity of diagnosing bipolar I disorder in ADHD youth. The authors aim to clarify these issues by reviewing family genetic studies of ADHD and bipolar I disorder.MethodThe authors applied random-effects meta-analysis to family genetic studies of ADHD and bipolar I disorder. Twenty bipolar proband studies provided 37 estimates of the prevalence of ADHD in 4,301 relatives of bipolar probands and 1,937 relatives of comparison probands. Seven ADHD proband studies provided 12 estimates of the prevalence of bipolar I disorder in 1,877 relatives of ADHD probands and 1,601 relatives of comparison probands.ResultsThese studies found a significantly higher prevalence of ADHD among relatives of bipolar probands and a signi...

90 citations

Journal ArticleDOI
TL;DR: Gender was a limited effect modifier of ADHD as a risk factor for ADHD-associated dysfunction in referred children and adolescents and the idea that gender differences in comorbid disorders can be attributed to genes or other familial causes is rejected.

90 citations

Journal ArticleDOI
TL;DR: The data suggested that co-occurrence of ADHD and MP possibly marks a distinct subtype of ADHD, rather than signaling increased severity of disease, but more research will be needed to support that hypothesis.
Abstract: Background Attention-deficit/hyperactivity disorder (ADHD) is frequently accompanied by motor problems (MPs). We investigated a possible shared etiology between the two traits in the Dutch sample of the International Multicenter ADHD Genetics study comprising 275 children with ADHD and their affected or unaffected sibling and 146 unrelated control children. Methods Exploratory data analysis and bivariate structural equation modeling were used to estimate the familiality of MP rated by parents (Developmental Coordination Disorder Questionnaire [DCD-Q]) or teachers (Groningen Motor Observation Scale [GMO]) and to determine the familial and environmental correlation between MP and ADHD. Furthermore, the nature of the familiality was explored by studying the siblings of ADHD-affected children. Results The ADHD-affected children had significantly more MP than their unaffected siblings, who in turn had significantly more MP than the control subjects. The familial component of MP measured by DCD-Q and GMO was 47% and 22%, respectively. The familial correlation between motor performance measures and ADHD was −0.38 for DCD-Q and −0.40 for GMO. Our data suggested that co-occurrence of ADHD and MP possibly marks a distinct subtype of ADHD, rather than signaling increased severity of disease. Conclusions Attention-deficit/hyperactivity disorder and MP have a common basis that may be due to genetic factors and/or shared environmental factors. Attention-deficit/hyperactivity disorder accompanied by MP may behave like a distinct subtype of ADHD, but more research will be needed to support that hypothesis.

90 citations

Journal ArticleDOI
TL;DR: The validity of the Q-LES-QSF as a measure of quality of life in adults with ADHD is supported, and ADHD cases had statistically significantly poorer scores on the Q/SQSF than controls.
Abstract: Objective: The authors assessed the psychometric properties of the Quality of Life Enjoyment and Satisfaction Questionnaire—Short Form (Q-LES-QSF) in adults with ADHD. Method: One hundred fifty ADHD and 134 non-ADHD adults from a case-control study and 173 adults randomized to placebo or methylphenidate were assessed with the Q-LES-QSF and the Social Adjustment Scale (SAS). Response to change was estimated by comparing change in Q-LES-QSF scores in responders and nonresponders in our randomized clinical trial. Results: Internal consistency of the Q-LES-QSF items was .88, and the correlation between the Q-LES-QSF total score and the SAS total T score was .72 in adults with ADHD. ADHD cases had statistically significantly poorer scores on the Q-LES-QSF than controls (76.5 ± 10.9 vs. 59.2 ± 17.3, p < .001), whereas ADHD responders showed Q-LES-QSF improvement compared to nonresponders (76.1 ± 12.0 versus 67.9 ± 14.5, p < .001). Conclusion: These results support the validity of the Q-LES-QSF as a measure of q...

90 citations

Journal ArticleDOI
TL;DR: Behavior and molecular genetics studies of attention deficit hyperactivity disorder (ADHD), along with segregation analyses and molecular genetic studies, all support the hypothesis that both genetic and environmental factors contribute to the etiology of ADHD.
Abstract: In this article we review behavioral and molecular genetics studies of attention deficit hyperactivity disorder (ADHD). Family, twin, and adoption studies, along with segregation analyses and molecular genetic studies, all support the hypothesis that both genetic and environmental factors contribute to the etiology of ADHD. Despite this strong evidence for the familial transmission of ADHD, the mode of transmission requires further clarification. In addition, because ADHD appears to be genetically heterogeneous, more work is needed to delineate genetically homogeneous subtypes and describe the range of expression of their underlying genotypes.

89 citations


Cited by
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28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations

01 Jan 2016
TL;DR: The using multivariate statistics is universally compatible with any devices to read, allowing you to get the most less latency time to download any of the authors' books like this one.
Abstract: Thank you for downloading using multivariate statistics. As you may know, people have look hundreds times for their favorite novels like this using multivariate statistics, but end up in infectious downloads. Rather than reading a good book with a cup of tea in the afternoon, instead they juggled with some harmful bugs inside their laptop. using multivariate statistics is available in our digital library an online access to it is set as public so you can download it instantly. Our books collection saves in multiple locations, allowing you to get the most less latency time to download any of our books like this one. Merely said, the using multivariate statistics is universally compatible with any devices to read.

14,604 citations

Journal Article
TL;DR: For the next few weeks the course is going to be exploring a field that’s actually older than classical population genetics, although the approach it’ll be taking to it involves the use of population genetic machinery.
Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

9,847 citations

Journal ArticleDOI
Paul Burton1, David Clayton2, Lon R. Cardon, Nicholas John Craddock3  +192 moreInstitutions (4)
07 Jun 2007-Nature
TL;DR: This study has demonstrated that careful use of a shared control group represents a safe and effective approach to GWA analyses of multiple disease phenotypes; generated a genome-wide genotype database for future studies of common diseases in the British population; and shown that, provided individuals with non-European ancestry are excluded, the extent of population stratification in theBritish population is generally modest.
Abstract: There is increasing evidence that genome-wide association ( GWA) studies represent a powerful approach to the identification of genes involved in common human diseases. We describe a joint GWA study ( using the Affymetrix GeneChip 500K Mapping Array Set) undertaken in the British population, which has examined similar to 2,000 individuals for each of 7 major diseases and a shared set of similar to 3,000 controls. Case-control comparisons identified 24 independent association signals at P < 5 X 10(-7): 1 in bipolar disorder, 1 in coronary artery disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type 1 diabetes and 3 in type 2 diabetes. On the basis of prior findings and replication studies thus-far completed, almost all of these signals reflect genuine susceptibility effects. We observed association at many previously identified loci, and found compelling evidence that some loci confer risk for more than one of the diseases studied. Across all diseases, we identified a large number of further signals ( including 58 loci with single-point P values between 10(-5) and 5 X 10(-7)) likely to yield additional susceptibility loci. The importance of appropriately large samples was confirmed by the modest effect sizes observed at most loci identified. This study thus represents a thorough validation of the GWA approach. It has also demonstrated that careful use of a shared control group represents a safe and effective approach to GWA analyses of multiple disease phenotypes; has generated a genome-wide genotype database for future studies of common diseases in the British population; and shown that, provided individuals with non-European ancestry are excluded, the extent of population stratification in the British population is generally modest. Our findings offer new avenues for exploring the pathophysiology of these important disorders. We anticipate that our data, results and software, which will be widely available to other investigators, will provide a powerful resource for human genetics research.

9,244 citations