Publication Type: Poster
Abstract: Abnormalities in brain development have been reported in dyslexic patients. All four genes thus far linked to developmental dyslexia, DYX1C1, ROBO1, KIAA0319 and DCDC2, participate in brain development. Here, we explored the role of Dcdc2, the member of DCX superfamily, in neuronal migration and dendrite outgrowth in neocortical pyramidal cells. RNAi knock down of Dcdc2, in addition to migration arrest, caused defects in process growth in migrating neurons. We found that Dcdc2 overexpression induced process-like outgrowths in non-neuronal Cos7 cells and exuberant dendrite growth in neocortical pyramidal cells. Additionally, the migration impairment in Dcdc2 knock down was rescued by expression of human Dcdc2 but not by DCX or TAU.

Publication Type: Conference Paper/Unpublished Manuscript

Publication Type: Poster
Review Method: Peer Reviewed
Abstract: Great efforts have been made to develop defined and animal-free conditions for culture of human embryonic stem cells (hESCs) to advance these therapeutically promising cells towards clinic. TeSR1 as a defined medium has been shown to support hESC culture as well as hESC derivation. However, the two hESC lines derived in TeSR1 were karyotypically abnormal, probably due to its formula disfavoring derivation of normal hESCs. Indeed, we found that isolated inner cell mass cells often dissociated in TeSR1, failing to develop to any hESC line. In contrast, the traditional undefined hESC medium co-cultured with mouse embryonic fibroblast allowed us to derive two new hESC lines CT1 and CT2. To identify the important factors responsible for the differences, we analyzed hESC lines CT2 and H9 cultured in the defined versus undefined media via global gene expression profiling and differentiation assays. We found that hESCs cultured in the various conditions had dramatically different levels of several essential signaling pathways as well as different preferences in lineage-specific differentiation. Modification of TeSR1 based on these results may help optimize conditions to enhance the derivation efficiency of hESCs and sustain their unbiased differentiation ability.
Acknowledgements: This work is supported by Connecticut Stem Cell Research grant 06SCD02 to R.X. We thank Anupinder kaur to perform the illumina microarray experiments.

Publication Type: Conference Paper/Unpublished Manuscript
Abstract: This study uses data from the National Longitudinal Study of Adolescent Health (Add Health) to replicate and extend upon current research on gene-environment interactions. We examine whether variation in the DRD2 gene (A2/A2, A1/A2, A1/A1) conditions the effects of stress events on depression among young adults by: (a) controlling for social supports, and 2) examining whether there are gender differences in the gene-environment interaction effect. There are three important findings that emerge from our Poisson analyses. First, the independent effects of DRD2 and stress events consistently increase the likelihood of experiencing depressive symptoms in early adulthood for both males and females. Second, and most importantly, our analyses suggest that the interaction of DRD2 and stress events may have different effects across genders. More specifically, females carrying one or more risk alleles of DRD2 and experiencing a high level of stress events reported a greater likelihood of experiencing depressive symptoms. In contrast, males with one or more risk alleles who experienced a greater number of stress events were less likely to report depressive symptoms. Thus, the interaction between DRD2 and stress events appears to be a risk factor for depressive symptoms among young adult females, but a protective factor against depression for males. Finally, increases in the frequency of marijuana use and prevalence of arrest were significantly related to depressive symptoms for females, but not for males. These findings support the hypothesis that females’ pathway in crime is characterized by greater sensitivity to stressful events, depression, and substance abuse.

Publication Type: Conference Paper/Unpublished Manuscript
Abstract: The last decade has witnessed an outpouring of interest in children’s emotional and behavioral problems from media outlets, the medical profession, and allied mental health disciplines. Little scholarly attention has been given to how the diverse claims of these stakeholders are used by adults to construct a lay understanding of children’s mental health problems. Drawing on social constructionist and claims-making traditions, we analyze the competing frameworks that emerge in public discourse on children’s emotional and behavioral problems. Specifically, using vignette-based data from the 2002 General Social Survey’s National Stigma Study – Children Module, we conduct a latent class analysis of causal attributions for three types of childhood problems: daily trouble, ADHD, and depression. We then evaluate the predictors of those attributions, including characteristics of the child, whether respondents label the problem a mental illness, and respondents’ socio-demographic characteristics. We find that adults construct children’s mental health problems in a manner consistent with public frameworks. And, while socio-demographic characteristics do little to predict group differences, several interesting patterns emerge with regard to the characteristics of the child.