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Quantitative Methods Colloquium Series: Structural equation modeling approaches for analyzing partially nested data
March 30, 2015

Structural equation modeling approaches for analyzing partially nested data
Sonya Sterba, Quantitative Methods, Vanderbilt Dept. of Psychology & Human Development

Study designs involving clustering in some study arms, but not all study arms, are common in clinical treatment-outcome and educational settings. For instance, in a treatment arm, persons may be nested within therapy groups, whereas in a control arm there are no groups. Methodological approaches for handling such partially nested designs have previously been developed in a multilevel modeling framework (MLM-PN, e.g., Bauer, Sterba, & Hallfors, 2008). Recently, two alternative structural equation modeling (SEM) approaches for analyzing partially nested data were introduced: a multivariate single-level SEM (SSEM-PN) and a multiple-arm multilevel SEM (MSEM-PN) (Sterba, Preacher, Forehand, Hardcastle, Cole, & Compas, 2014). In this talk, I compare and contrast these approaches and show how SSEM-PN and MSEM-PN can produce results equivalent to existing MLM-PNs. I also describe how they can be extended to flexibly accommodate several modeling features that are difficult or impossible to handle in MLM-PN. Importantly, implementation of such features for partially nested designs differs from fully nested designs. An empirical example involving a partially nested depression intervention (Compas et al., 2009, 2011, in press) combines several of these features in an analysis of interest for treatment-outcome studies.

Clinical Science Brown Bag Series: Gloria Han
March 31, 2015

Gloria Han, Department of Psychology (Tomarken Lab), Vanderbilt University

Tuesday, 3/31/15


WH 316

Title and Abstract TBA

CCN Brown Bag Series: Chai-Youn Kim
April 1, 2015

Chai-Youn Kim, Ph.D., Associate Professor, Department of Psychology, Korea University

Wednesday, 4/1/15

12:10 p.m.

Wilson Hall 115

"Determinants of grapheme-color association in synesthesia"

Neuroscience Brown Bag Series: Suzana Herculano-Houzel
April 2, 2015

Professor Suzana Herculano-Houzel, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro

Thursday, 4/2/15

12:10 p.m.

Wilson Hall 316

When larger brains and bodies do not have more neurons: implications for evolution

It has been a basic assumption of comparative and evolutionary neurobiology that larger brains and bodies require larger numbers of neurons to operate them. But do they? And is the relationship between body or brain size and number of neurons across species a product of natural selection acting on a similar relationship across individuals of a same species? Data to be presented in this talk show that, in mammalian, reptile and mollusk species alike, larger brain and body mass are not necessarily correlated with more neurons across individuals. These and other results to be discussed argue that it is not that larger bodies require more neurons, but rather that they allow more neurons to survive; and that evolution happens through selection for step changes in numbers of neurons, rather than by selection for gradual variations.



Department of Psychology Colloquium Series presents Lea Williams
April 2, 2015

Lea Williams, Ph.D., Professor, Stanford University

Thursday  April, 2, 2015

4:10 p.m. 102 Buttrick Hall

"A translational neural circuit model of mental disorder: Implications for classification and treatment”

Complex emotional and cognitive functions rely on the connectivity of large-scale neural circuits. These circuits offer a relevant scale of focus for redefining mental disorders as ³neural circuit types² that reflect different types of neural circuit disconnection and dysfunction. Based on the existing scientific knowledge I will summarize a proposed taxonomy of ³neural circuit types² for depression and anxiety. With regard to clinical translation, I consider how these connectome types may act as biomarkers for helping guide personal treatment selection and for developing novel treatments. I also consider how we might validate a neural circuit model that spans diagnostic categories and will help to translate neuroscience into clinical practice in the real world.



Cancelled - CCN Brown Bag Series
April 8, 2015

Wednesday, 4/8/15

12:10 p.m.

Wilson Hall 115

Title and Abstract TBA

Neuroscience Brown Bag Series: Emily Rockoff
April 9, 2015

Emily Rockoff, Department of Psychology (Kaas Lab), Vanderbilt University

Thursday, 4/9/15

12:10 p.m.

Wilson Hall 316

Title & Abstract TBA

Clinical Science Brown Bag Series: Taylor Benson
April 14, 2015

Taylor Benson, Department of Psychology (Park Lab), Vanderbilt University

Tuesday, 4/14/15


WH 316

Title and Abstract TBA

CCN Brown Bag Series: Kevin Dieter
April 15, 2015

Kevin Dieter, Ph.D., Department of Psychology (Blake Lab), Vanderbilt University

Wednesday, 4/15/15

12:10 p.m.

Wilson Hall 115

“Psychophysical and neural correlates of sensory eye dominance.”

Neuroscience Brown Bag Series: Yuzo Chino
April 16, 2015

Yuzo Chino Ph.D., College of Optometry, University of Houston 

Thursday, 4/16/15

12:10 p.m.

Wilson Hall 316 

“What limits the visual performance of amblyopic primates? : V2 study”

The normal maturation of the primate visual brain requires precise matching of the images in the two eyes. Experiencing interocular decorrelation of cortical inputs early in life, resulting from ocular misalignment (strabismus) or chronic monocular defocus (anisometropia), can cause compromised binocular vision and often amblyopia. Amblyopic humans lose fine spatial vision and show difficulties in perceptual tasks that require precise pooling of local stimulus information (e.g., poor relative position judgments, reduced contour integration, and image distortion). To understand how these perceptual impairments develop in amblyopes requires knowing at what age and where in their visual brain neuronal deficits emerge. Decades of perceptual studies and intense focus on neurophysiological investigations of the striate cortex (V1) have led to the rather surprising, but currently prevailing view that the reduced vision in amblyopes results primarily from neural deficits in visual areas beyond (V1). However, we know very little about information processing in extrastriate visual neurons in the amblyopic brain. In this study, therefore, we created non-human primate models of anisometropic amblyopia and analyzed the receptive-field (RF) properties of neurons in visual area V2 (V2). The receptive fields of V2 neurons in normal monkeys are made up of multiple subunits that are thought to reflect V1 inputs and are capable of encoding the spatial relationship between local stimulus features. Therefore, we compared the RF subunit maps for individual and multiple nearby V2 neurons obtained by using dynamic two-dimensional noise stimuli and reverse correlation methods (LSRC). Unlike in normal monkeys, the subunit maps of V2 neurons in amblyopic monkeys were severely disorganized: subfield maps showed higher heterogeneity within each neuron as well as across nearby neurons. We also analyzed the spiking patterns of these neurons to test the prevailing view from perceptual studies that amblyopic visual brain is ‘noisy’. We found that 1) Fano factor (trial-to-trial fluctuations) was significantly higher in spiking of  individual neurons, and 2) the correlated variability in spiking between pairs of nearby neurons (noise correlation) was elevated in amblyopic monkeys. Under binocular viewing conditions, amblyopic V2 neurons exhibited robust binocular suppression and the strength of suppression was positively correlated with the degree of hereogeneity and the severity of amblyopia in individual monkeys. These results suggest that the disorganized RF subunit maps, spiking noise and robust binocular suppression in V2 are likely to adversely affect the higher stages of cortical processing, resulting in position uncertainty and image distortion in amblyopes.








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