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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: A comparison of family resemblance sex ratios in unipolar and bipolar studies revealed that X linkage was not a good fit to the unipolar data, and this sex effect may help clarify genetic transmission and heterogeneity.
Abstract: Epidemiological studies have consistently found women to be at greater risk than men for affective disorders. This sex effect may help clarify genetic transmission and heterogeneity. Data from eight family studies of unipolar and eight family studies of bipolar probands were used to calculate family resemblance sex ratios. These observed sex ratios were then compared to sex ratios predicted by X-linked and nonfamilial effects models. Maximum likelihood estimation of competing models revealed that X linkage was not a good fit to the unipolar data. The bipolar studies were not consistent with either the X-linked or the nonfamilial effects model.

28 citations

Journal ArticleDOI
TL;DR: Findings are consistent with the hypothesis that ADHD and PSUD are transmitted independently in families, and the hypothesis stating that ADHDand PSUD represent variable expressions of a common underlying risk factor cannot be ruled out.
Abstract: Objective To test hypotheses about patterns of familial association between attention-deficit/hyperactivity disorder (ADHD) and psychoactive substance use disorders (PSUDs) by using the family study method. Design The first-degree relatives of clinically referred children and adolescents with ADHD (131 probands, 413 relatives) and healthy control probands (106 probands, 323 relatives) were assessed by blind raters. Results After stratifying the probands with ADHD and the control probands into those with PSUD (group 1 and group 3, respectively) and those without PSUD (group 2 and group 4, respectively), familial risk analyses revealed the following: (1) the risk for ADHD was not significantly different between relatives of group 2 and group 1 probands (19.6% vs 18.0%; P =.88), but these 2 risks were significantly greater than the risk to relatives of group 3 probands (1.0%; P =.01 and P =.02, respectively) and group 4 probands (7.0%; P =.001 and P =.01, respectively); (2) there were no significant differences in the risk for PSUD between relatives of group 1 (47.5%) and group 3 probands (39.7%; P =.40), but these risks were greater than the risk to relatives of group 2 (30.0%; P =.32) and group 4 probands (20.9%; P Conclusions These findings are consistent with the hypothesis that ADHD and PSUD are transmitted independently in families. Because the probands were young adolescents, many have not lived through the age at risk for PSUD. Thus, the hypothesis stating that ADHD and PSUD represent variable expressions of a common underlying risk factor cannot be ruled out.

28 citations

Journal ArticleDOI
TL;DR: The FSPD group had more inadequate rapport; the groups did not differ in the frequency of any other symptoms of SPD and there was a higher risk of bipolar disorder in the relatives of NFSPDs and higher risk for anxiety disorders in the relative of FSPDs.
Abstract: In order to investigate possible heterogeneity in schizotypal personality disorder (SPD), two groups of schizotypals, one related to schizophrenic probands (FSPD) (n = 34) and one related to affective disorder probands (NFSPD) (n = 14), ascertained in the same family study, were compared. The FSPD group had more inadequate rapport; the groups did not differ in the frequency of any other symptoms of SPD. NFSPDs had higher rates of comorbid histrionic PD and a trend for higher rates of impulsive/dramatic cluster PDs. FSPDs had a trend for higher rates of anxiety disorders. There was a higher risk of bipolar disorder in the relatives of NFSPDs and higher risk for anxiety disorders in the relatives of FSPDs. The relatives of NFSPDs had higher rates for histrionic, narcissistic, and atypical PDs and for having at least one PD.

28 citations

Journal ArticleDOI
TL;DR: Individuals with ADHD showed thinner bilateral medial temporal cortex throughout adolescence and young adulthood compared to healthy controls, and there was no association between CT and stimulant treatment.
Abstract: Objective Attention-deficit/hyperactivity disorder (ADHD) has been associated with widespread changes in cortical thickness (CT). Findings have been inconsistent, however, possibly due to age differences between samples. Cortical changes have also been suggested to be reduced or to disappear with stimulant treatment. We investigated differences in CT between adolescents/young adults with and without ADHD in the largest ADHD sample to date, the NeuroIMAGE sample. Second, we investigated how such differences were related to age and stimulant treatment. Method Participants (participants with ADHD = 306; healthy controls = 184, 61% male, 8–28 years of age, mean age = 17 years) underwent structural magnetic resonance imaging. Participants and pharmacies provided detailed information regarding lifetime stimulant treatment, including cumulative intake and age of treatment initiation and cessation. Vertexwise statistics were performed in Freesurfer, modeling the main effect of diagnosis on CT and its interaction with age. Effects of stimulant treatment parameters on CT were modeled within the sample with ADHD. Results After correction for multiple comparisons, participants with ADHD showed decreased medial temporal CT in both left ( p CLUSTER = .008) and right ( p CLUSTER = .038) hemispheres. These differences were present across different ages and were associated with symptoms of hyperactivity and prosocial behavior. There were no age-by-diagnosis interaction effects. None of the treatment parameters predicted CT within ADHD. Conclusion Individuals with ADHD showed thinner bilateral medial temporal cortex throughout adolescence and young adulthood compared to healthy controls. We found no association between CT and stimulant treatment. The cross-sectional design of the current study warrants cautious interpretation of the findings.

28 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