Publications by authors named "Barbara L Thompson"

Infants demonstrate rapid development across the first years of life, which underlies increased human interactions that promote social-emotional development. In particular, gaze, affect, and object exploration are early indicators of engagement and show rapid changes in the first year of life. However, current understanding on developmental trajectories during infancy often comes from majority white, non-Hispanic/Latino samples.

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Development of attention systems is essential for both cognitive and social behavior maturation. Visual behavior has been used to assess development of these attention systems. Yet, given its importance, there is a notable lack of literature detailing successful methods and procedures for using eye-tracking in early infancy to assess oculomotor and attention dynamics.

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Attentional biases to threat-related stimuli, such as fearful and angry facial expressions, are important to survival and emerge early in development. Infants demonstrate an attentional bias to fearful facial expressions by 5-7 months of age and an attentional bias toward anger by 3 years of age that are modulated by experiential factors. In a longitudinal study of 87 mother-infant dyads from families predominantly experiencing low income, we examined whether maternal stress and depressive symptoms were associated with trajectories of attentional biases to threat, assessed during an attention disengagement eye-tracking task when infants were 6-, 9-, and 12-month old.

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Aims: There is limited research on the type and quantity of actions (activities) occupational therapy practitioners utilize when providing sensory integration treatment to children with Autism Spectrum Disorders (ASD).

Methods: A coding scheme identifying specific aspects of sensory integration treatment was developed and used to analyze 34 videos of 9 children with ASD, aged between 18 and 56 months, treated by 8 occupational therapists. Occupational therapists providing sensory integration treatment to children with ASD were behaviorally coded and rated using Observer XT, a software package designed for analysis of behavioral processes.

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by disruptions in social communication and behavioral flexibility. Both genetic and environmental factors contribute to ASD risk. Epidemiologic studies indicate that roadway vehicle exhaust and in utero exposure to diesel particulate matter (DPM) are associated with ASD.

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Objective: In this exploratory longitudinal study we assessed cognitive development in a community sample of infants born into predominantly low-income families from two different urban sites, to identify family and community factors that may associate with outcomes by 1 year of age.

Method: Infant-mother dyads (n = 109) were recruited in Boston and Los Angeles community pediatric practices. Infant cognition was measured using the Mullen Scales of Early Learning when the infant was aged 2, 6, 9, and 12 months.

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Objective: Social-emotional processing is key to daily interactions and routines, yet a challenging construct to quantify. Measuring social and emotional processing in young children, children with language impairments, or non-verbal children, presents additional challenges. This study addresses a pressing need for tools to probe internal responses such as feelings, drives, and motivations that do not rely on intact language skills.

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Importance: Variation in child responses to adversity creates a clinical challenge to identify children most resilient or susceptible to later risk for disturbances in cognition and health. Advances in establishing scalable biomarkers can lead to early identification and mechanistic understanding of the association of early adversity with neurodevelopment.

Objectives: To examine whether maternal reports of stress are associated with patterns in resting electroencephalography at 2 months of age and whether unique electroencephalographic profiles associated with risk and resiliency factors can be identified.

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Background: Our laboratory discovered that the gene encoding the receptor tyrosine kinase, MET, contributes to autism risk. Expression of MET is reduced in human postmortem temporal lobe in autism and Rett Syndrome. Subsequent studies revealed a role for MET in human and mouse functional and structural cortical connectivity.

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Collaborating with patients, families, and communities is a core principle of family medicine. However, the health care system in the United States has grown increasingly complex, fragmented, and difficult to navigate. This system, focused on disease-specific care delivered by specialists, often treats patients as the objects of care rather than as partners in care.

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Affective processing, known to influence attention, motivation, and emotional regulation is poorly understood in young children, especially for those with neurodevelopmental disorders characterized by language impairments. Here we faithfully adapt a well-established animal paradigm used for affective processing, conditioned place preference (CPP) for use in typically developing children between the ages of 30-55 months. Children displayed a CPP, with an average 2.

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Candidate risk genes for autism spectrum disorder (ASD) have been identified, but the challenge of determining their contribution to pathogenesis remains. We previously identified two ASD risk genes encoding the receptor tyrosine kinase MET and the urokinase plasminogen activator receptor (PLAUR), which is thought to modulate availability of the MET ligand. We also reported a role for Met signaling in cortical interneuron development in vitro and a reduction of these neurons in uPAR (mouse ortholog of PLAUR) null mice, suggesting that disruption of either gene impacts cortical development similarly.

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Human cognitive and social-emotional behaviors are heterogeneous, underscoring the challenges in modeling pathogenesis in disorders of neurodevelopmental origin in which these domains are dysfunctional. In general, animal models for these disorders are built to emulate our understanding of the clinical diagnosis, with mixed results. We suggest the utility of model systems lies in the use of different strategies to perturb hierarchical circuit development, to examine the behavioral dimensions that are most impacted, and to discern the capacity for, and heterogeneity of, neuroadaptation that will then inform treatment strategies.

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The mode through which early insults in brain development result in the onset of psychiatric disorders years after impact become a little less mysterious with the report by Niwa et al. that a transient reduction of the schizophrenia risk gene DISC1 can alter prefrontal cortex neurochemistry, architecture, and function.

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Gestational cocaine exposure in a rabbit model leads to a persistent increase in parvalbumin immunoreactive cells and processes, reduces dopamine D1 receptor coupling to Gsalpha by means of improper trafficking of the receptor, changes pyramidal neuron morphology, and disrupts cognitive function. Here, experiments investigated whether changes in parvalbumin neurons were specific, or extended to other subpopulations of interneurons. Additionally, we examined dopamine D1 receptor expression patterns and its overlap with specific interneuron populations in the rabbit prefrontal cortex as a possible correlate for alterations in interneuron development following prenatal cocaine exposure.

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The effects of prenatal exposure to drugs on brain development are complex and are modulated by the timing, dose and route of drug exposure. It is difficult to assess these effects in clinical cohorts as these are beset with problems such as multiple exposures and difficulties in documenting use patterns. This can lead to misinterpretation of research findings by the general public, the media and policy makers, who may mistakenly assume that the legal status of a drug correlates with its biological impact on fetal brain development and long-term clinical outcomes.

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Physician distribution nationally and in Texas trends away from rural toward more urban areas. Consequently, access to health care in rural areas is adversely affected. The University of Texas Medical Branch at Galveston (UTMB) Family Medicine Residency established a rural training track (RTT) in 2000 to combat this trend.

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The formation and function of the mammalian cerebral cortex relies on the complex interplay of a variety of genetic and environmental factors through protracted periods of gestational and postnatal development. Biogenic amine systems are important neuromodulators, both in the adult nervous system, and during critical epochs of brain development. Abnormalities in developmental programming likely contribute to developmental delays and multiple neurological and psychiatric disorders, often with symptom onset much later than the actual induction of pathology.

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Prenatal cocaine exposure in a rabbit intravenous model has revealed selective disruption of brain development and pharmacological responsiveness. We therefore examined the pharmacokinetic properties of cocaine in this model. Dutch-belted rabbits were surgically implanted with a catheter in the carotid artery, allowed to recover, and then injected intravenously with a cocaine bolus.

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The lateral, basal, and central nuclei of the amygdala are part of a circuitry that instantiates many fear and anxious behaviors. One line of support indicates that immediate-early gene (IEG) expression (e.g.

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Our laboratory has previously characterized a rabbit model of gestational cocaine exposure in which permanent alterations in neuronal morphology, cell signaling and psychostimulant-induced behavior are observed. The cellular and molecular neuroadaptations produced by prenatal cocaine occur in brain regions involved in executive function and attention, such as the anterior cingulate and medial prefrontal cortices. Therefore, in the present study, we have measured the effects of prenatal cocaine exposure on specific behavioral tasks in adult offspring whose mothers were treated with cocaine (3mg/kg, twice a day, E16-E25).

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Research has demonstrated that immediate-early genes/inducible transcriptional factors (e.g., c-fos, egr-1) are increased in amygdala nuclei (lateral, basal and central nuclei) known to be involved in fear conditioning, footshock stress and novelty.

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The present study examined the effects of glucocorticoid administration on emotional memory and on corticotropin-releasing hormone (CRH) mRNA expression in the central nucleus of the amygdala (CeA) and the paraventricular nucleus of the hypothalamus (PVN). This was tested by administering repeated corticosterone (CORT) within a contextual fear conditioning paradigm. Rats received 2.

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This article highlights four issues about the neurobiology of emotions: adaptation vs. dysfunction, peripheral and central representations of emotion, the regulation of the internal milieu, and whether emotions are cognitive. It is argued that the emotions evolved to play diverse adaptive roles and are biologically vital sources of information processing.

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