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.

Evidence of Familial Association Between Attention Deficit Disorder and Major Affective Disorders

Abstract: • With the use of family study methods and assessments by "blinded" raters, we tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and affective disorders (AFFs) among first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 24 (33%) met criteria for AFFs (major depression, n = 15 [21%]; bipolar disorder, n = 8 [11%]; and dysthymia, n = 1 [1%]). After stratification of the ADD sample into those with AFFs (ADD+AFF) and those without AFF (ADD), familial risk analyses revealed the following: (1) the relatives of each ADD proband subgroup were at significantly greater risk for ADD than were relatives of normal controls; (2) the agecorrected morbidity risk for ADD was not significantly different between relatives of ADD and ADD+AFF (27% vs 22%); however, these two risks were significantly greater than the risk to relatives of normal controls (5%); (3) the risk for any AFF (bipolar disorder, major depressive disorder, or dysthymia) was not significantly different between relatives of ADD probands and ADD+AFF probands (28% and 25%), but these two risks were significantly greater than the risk to relatives of normal controls (4%); (4) ADD and AFFs did not cosegregate within families; and (5) there was no evidence for nonrandom mating. These findings are consistent with the hypothesis that ADD and AFFs may share common familial vulnerabilities.

Separation of DSM-III attention deficit disorder and conduct disorder: evidence from a family-genetic study of American child psychiatric patients.

Abstract: Using family study methodology and assessments by blind raters, this study tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and antisocial disorders (childhood conduct (CD) and oppositional disorder (OPD) and adult antisocial personality disorder) among 457 first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives), psychiatric (26 probands, 101 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 33 (45%) met criteria for OPD, 24 (33%) met criteria for CD, and 16 (22%) had no antisocial diagnosis. After stratifying the ADD sample into those with CD (ADD + CD), those with OPD (ADD + OPD) and those with neither (ADD) familial risk analysis revealed the following: (1) relatives of each ADD proband subgroup were at significantly greater risk for ADD than relatives of both psychiatric and normal controls: (2) the morbidity risk for ADD was highest among relatives of ADD + CD probands (38%), moderate among relatives of ADD + OPD (17%) and ADD probands (24%) and lowest among relatives of psychiatric and normal controls (5% for both); (3) the risk for any antisocial disorder was highest among relatives of ADD + CD (34%) and ADD + OPD (24%) which were significantly greater than the risk to relatives of ADD probands (11%), psychiatric (7%) and normal controls (4%); and (4) both ADD and antisocial disorders occurred in the same relatives more often than expected by chance alone. Although these findings suggest that ADD with and without antisocial disorders may be aetiologically distinct disorders, they are also consistent with a multifactorial hypothesis in which ADD, ADD + OPD and ADD + CD fall along a continuum of increasing levels of familial aetiological factors and, correspondingly, severity of illness.

Psychiatric Comorbidity among Referred Juveniles with Major Depression: Fact or Artifact?

Abstract: Objective The high levels of psychiatric comorbidity reported in juveniles meeting operational definitions at depressive disorders raise both substantive and methodological concerns about whether depression with comorbid disorders should be classified as two disorders or as different manifestations of the same condition. Our purpose was to clarify issues of diagnostic heterogeneity and diagnostic overlap in juvenile depression. Method The sample consisted of consecutively referred children and adolescents ( N = 424) comprehensively evaluated with structured diagnostic interviews and psychosocial assessments. Results A clinical picture compatible with the diagnosis of major depression was identified in 40% of these referred youths. Children meeting criteria for major depression had prototypical symptoms of the disorder, a chronic course, and severe psychosocial dysfunction. In addition, they frequently met criteria for attention-deficit hyperactivity disorder, conduct disorder, and anxiety disorders. These comorbidity findings were not due to symptom overlap among major depression and the co-occurring disorders. For the most part, comorbid disorders preceded the onset of major depression by several years. Conclusions Juvenile depression has a chronic course, severe dysfunction, and high levels of psychiatric comorbidity. Despite symptom overlap, our work suggests that major depression and other conditions may represent different disorders.

Patterns of alcohol and drug use in adolescents can be predicted by parental substance use disorders.

Abstract: Objective. To examine the specificity of risk for alcohol or drug abuse or dependence (substance use disorders [SUDs]) in offspring exposed to particular subtypes of parental SUDs. Methods. The original sample was derived from 2 groups of index children: 140 attention-deficit/hyperactivity disorder (ADHD) probands and 120 non-ADHD comparison probands. These groups had 174 and 129 biological siblings and 279 and 240 parents, respectively. Results. Independent of familial risk, exposure to parental SUDs predicted SUDs in the offspring. Controlling for duration of exposure, we found that adolescence was a critical developmental period for exposure to parental SUDs. Because all our analyses controlled for social class, ADHD status, and parental lifetime history of SUDs, these results show that exposure to parental SUDs predicts offspring SUDs independently of these risk factors. Conclusions. These results support the critical importance of familial environmental risk factors for the development of SUDs in youth in general and particularly in those at high risk for these disorders. These results highlight adolescence as a critical period for the deleterious effects of exposure to parental SUDs, supporting the need to develop preventive and early intervention strategies targeted at adolescents at high risk for SUDs.

Presenting ADHD Symptoms, Subtypes, and Comorbid Disorders in Clinically Referred Adults with ADHD

Abstract: Objective Despite the increasing presentation of ADHD in adults, many practitioners remain reluctant to assess individuals for ADHD, in part related to the relative lack of data on the presenting symptoms of ADHD in adulthood. Comorbidity among adults with ADHD is also of great interest due to the high rates of psychiatric comorbidity, which can lead to a more persistent ADHD among adults.

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

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。

Using Multivariate Statistics

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Human biochemical genetics

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

Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls

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.