Measurement and structural models for children's problem behaviors

This article considers an analytic strategy for measuring and modeling child and adolescent problem behaviors. The strategy embeds an item response model within a hierarchical model to define an interval scale for the outcomes, to assess dimensionality, and to study how individual and contextual factors relate to multiple dimensions of problem behaviors. To illustrate, the authors analyze data from the primary caregiver ratings of 2,177 children aged 9-15 in 79 urban neighborhoods on externalizing behavior problems using the Child Behavior Checklist 4-18 (T. M. Achenbach, 1991a). Two subscales, Aggression and Delinquency, are highly correlated, and yet unidimensionality must be rejected because these subscales have different associations with key theoretically related covariates.     

Cellular abnormalities and synaptic plasticity in seizure disorders of the immature nervous system

The nervous system has an enhanced capacity to generate seizures during a restricted phase of postnatal development. Studies in animals and particularly in in vitro brain slices from hippocampus and neocortex have been instrumental in furthering an understanding of the underlying processes. Developmental alterations in glutaminergic excitatory synaptic transmission appear to play a key role in the enhanced seizure susceptible of rodents during the second and third week of life. Prior to this period, the number of excitatory synapses is relatively low. The scarcity of connections and the inability of the existing synapses to release glutamate when activated at high frequencies likely contribute importantly to the resistance of neonates to seizures. However, at the beginning of week 2, a dramatic outgrowth of excitatory synapses occurs, and these synapses are able to faithfully follow activation at high frequencies. These changes, coupled with the prolonged nature of synaptic potentials in early life, likely contribute to the ease of seizure generation. After this time, seizure susceptibility declines, patterns of local synaptic connectivity remodel, and some synapses are pruned. Concurrently, the duration of excitatory postsynaptic potentials shortens due at least in part to a switch in the subunit composition of postsynaptic receptors. Other studies have examined the mechanisms underlying chronic epilepsy initiated in early life. Models of both cortical dysplasia and recurrent early-life seizures suggest that alterations in the normal development of excitatory synaptic transmission can contribute importantly to chronic epileptic conditions. In the recurrent early-life seizure model, abnormal use-dependent selection of subpopulations of excitatory synapses may play a role. In experimental cortical dysplasia, alterations in the molecular composition of postsynaptic receptor are observed that favor subunit combinations characteristic of infancy.     

The Female Professional: Parenting,Career, Choices and Compromises

The American Journal of Psychoanalysis -     

Rater bias in psychological research: when is it a problem and what can we do about it?

Rater bias is a substantial source of error in psychological research. Bias distorts observed effect sizes beyond the expected level of attenuation due to intrarater error, and the impact of bias is not accurately estimated using conventional methods of correction for attenuation. Using a model based on multivariate generalizability theory, this article illustrates how bias affects research results. The model identifies 4 types of bias that may affect findings in research using observer ratings, including the biases traditionally termed leniency and halo errors. The impact of bias depends on which of 4 classes of rating design is used, and formulas are derived for correcting observed effect sizes for attenuation (due to bias variance) and inflation (due to bias covariance) in each of these classes. The rater bias model suggests procedures for researchers seeking to minimize adverse impact of bias on study findings.     

Super-learning of Causal Judgements

In three experiments, participants learned which of a variety of foods were capable of causing an allergic reaction in a hypothetical patient during training in which a compound of a treatment and a target food cue was paired with the reaction. In Experiment 1 the causal ratings of the target cue were increased if the treatment cue was pretrained as a preventative cause of the reaction. Experiments 2 and 3 demonstrated that the magnitude of this superlearning is unaffected by the order of compound and treatment cue training. The final study also showed that forward super-learning is not induced solely by simple exposure to the treatment cue prior to compound training but, rather, depends upon training the treatment cue as a preventative cause, whereas retrospective super-learning may be due merely to exposure of the treatment cue. These results are problematic for contingency-based accounts of causal induction but accord with modified and extended associative theories.