Julia S. Noland
Vanderbilt University
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Featured researches published by Julia S. Noland.
Alcoholism: Clinical and Experimental Research | 2003
Julia S. Noland; Lynn T. Singer; Robert Arendt; Sonia Minnes; Elizabeth J. Short; Cynthia F. Bearer
BACKGROUND Reports from clinical and experimental (animal) research converge on the suggestion that prenatal exposure to alcohol, cocaine, or marijuana undermines executive functioning (EF) and its neurological underpinnings. However, large, adequately controlled, prospective studies of alcohol and marijuana effects on EF have reported conflicting findings, and there have been no such studies of cocaine exposure. METHODS EF was investigated in a cohort (n = 316) of 4-year-old children the majority of whose mothers had used varying combinations of cocaine, alcohol, and marijuana during pregnancy. With use of postpartum maternal report and biological assay, children were assigned to overlapping prenatal cocaine-exposed, alcohol-exposed, and marijuana-exposed groups and to complementary control groups. The postnatal environmental assessment included measures of maternal intellectual and psychosocial functioning, current drug or alcohol use, and home environment. RESULTS The children in the alcohol-exposed group had worse tapping-inhibition performance than children in the non-alcohol-exposed group, and this effect persisted when potential confounding environmental variables, other drug variables, and concurrent verbal intelligence were controlled for. CONCLUSIONS Prenatal alcohol is predictive of decreased EF in early childhood that could not be attributed to environmental factors. The results are discussed in terms of the age and overall high-risk status of the children.
Developmental Science | 2010
Julia S. Noland; J. Steven Reznick; Wendy L. Stone; Tedra A. Walden; Elisabeth H. Sheridan
We compared working memory (WM) for the location of social versus non-social targets in infant siblings of children with Autism Spectrum Disorders (sibs-ASD, n = 25) and of typically developing children (sibs-TD, n = 30) at 6.5 and 9 months of age. There was a significant interaction of risk group and target type on WM, in which the sibs-ASD had better WM for non-social targets as compared with controls. There was no group by stimulus interaction on two non-memory measures. The results suggest that the increased competency of sibs-ASD in WM (creating, updating and using transient representations) for non-social stimuli distinguishes them from sibs-TD by 9 months of age. This early emerging strength is discussed as a developmental pathway that may have implications for social attention and learning in children at risk for ASD.
Developmental Neuropsychology | 2003
Julia S. Noland; Lynn T. Singer; Sudhir Ken Mehta; Dennis M. Super
Executive functioning in cocaine/polydrug (marijuana, alcohol, tobacco) exposed infants was assessed in a single session, occurring between 9.5 and 12.5 months of age. In an A-not-B task, infants searched, after performance-adjusted delays, for an object hidden in a new location. Overall, the cocaine-exposed (CE) infants did not differ from non-CE controls recruited from the same at-risk population. However, comparison of heavier-CE (n = 9) to the combined group of lighter-CE (n = 10) and non-CE (n = 32) infants revealed significant differences on A-not-B performance, as well as on global tests of mental and motor development. Covariates investigated included socioeconomic status, marital status, race, maternal age, years of education, weeks of gestation, birth weight, as well as severity of prenatal marijuana, alcohol, and tobacco exposure. The relationship of heavier-CE status to motor development was mediated by length of gestation, and the relationship of heavier-CE status to mental development was confounded with maternal gestational use of cigarettes. The relationship of heavier-CE status to A-not-B performance remained significant after controlling for potentially confounded variables and mediators, but was not statistically significant after controlling for the variance associated with global mental development.
Child Neuropsychology | 2008
Julia S. Noland
At 8 to 11 months of age, infants are more successful in negotiating opaque relative to transparent barriers. However, 7-month-old infants have more difficulty with opaque barriers relative to semitransparent barriers. Here, 8-month-old infants spent more time in ineffective direct reaches with more the transparent barriers (Experiments 1 & 2) and were faster with the fully opaque barrier (Experiment 2). This demonstration of the graded effects of transparency confirms the working memory and/or response inhibition demands of the object retrieval task.
Child Neuropsychology | 2012
Julia S. Noland; Nikita P. Rodrigues
Current interpretation of the object retrieval task (Diamond, 1990) as an infant assessment of response inhibition requires evidence that younger infants make more ineffective attempts to retrieve toys through clear barriers. On two 30-second trials, infants (9 or 11 months of age) saw an inaccessible toy in the front or back of a clear box. The location of the infants touches corresponded with the toys location and, on the second trial, the younger infants touched the box more. In previous research nonhuman primates with orbital-frontal, but not dorsa-lateral, lesions also made ineffective barrier touches. The current developmental decreases in barrier touches may selectively tap developmental increases in inhibitory control supported by the developing orbital-frontal cortex.
International Review of Research in Mental Retardation | 2004
Robert Arendt; Julia S. Noland; Elizabeth J. Short; Lynn T. Singer
Publisher Summary This chapter discusses prenatal drug exposure and mental retardation. Prenatal exposure to cocaine is a behavioral teratogen. The early “rush to judgement” that occurred with crack cocaine can be replaced by sound research. As is evident from studies of cocaine exposure, even in cases where no birth defects are obvious, long-term follow-up may be needed to detect and ameliorate neurobehavioral effects. At both the individual and the societal levels, even in situations where etiology and pathogenesis are well-known, developmental disorders such as mental retardation do not emerge as a result of a single factor or at a single point in development. Neither a prenatal teratogenic environment nor a postnatal rearing environment model of development following prenatal cocaine exposure has total explanatory power. At each stage in development, the human brain is uniquely susceptible to exposure of teratogenic compounds. It is also readily apparent that prevention and treatment of conditions arising from exposure to teratogenic substances will be largely dictated by the stage or stages in which the exposure occurs. The chapter discusses several drawbacks of the traditional etiological classification of mental retardation—prenatal, perinatal, or postnatal.
Neurotoxicology and Teratology | 2005
Julia S. Noland; Lynn T. Singer; Elizabeth J. Short; Sonia Minnes; Robert Arendt; H. Lester Kirchner; Cynthia F. Bearer
Infant Behavior & Development | 2005
Lynn T. Singer; Laurie J. Eisengart; Sonia Minnes; Julia S. Noland; Arthur Jey; Courtney Lane; Meeyoung O. Min
Infancy | 2007
Julia S. Noland
Infant Behavior & Development | 1996
Julia S. Noland