ABSTRACT
The validity of a Personality Inventory for Children-Revised edition (PIC-R) typology was examined in a sample of 323 children aged 6-16 years. These children had been referred to a children's mental health centre for neuropsychological assessment. In study 1, K-means cluster analysis (k = 12) was applied to the PIC clinical scales in an attempt to replicate the 12 clusters identified by Gdowski, Lachar, and Kline (1985). Partial cluster replication was achieved. Examination of the obtained clusters revealed significant overlap, suggesting that fewer clusters would represent an optimal solution. In study 2, a two-stage cluster analysis yielded a seven-cluster solution consistent with several key forms of psychopathology previously reported in the literature using specific neuropsychological populations. Identified subtypes included profiles characterized as: normal, cognitive deficit, cognitive deficit with internalized psychopathology, cognitive deficit with social impairment, cognitive deficit with hyperactivity, cognitive deficit with both internalized and externalized psychopathology, and combined internalized and externalized psychopathology without a cognitive deficit component.
Subject(s)
Child Behavior Disorders/diagnosis , Cognition Disorders/diagnosis , Learning Disabilities/diagnosis , Neuropsychological Tests/statistics & numerical data , Personality Inventory/statistics & numerical data , Referral and Consultation , Adolescent , Attention Deficit Disorder with Hyperactivity/diagnosis , Attention Deficit Disorder with Hyperactivity/psychology , Child , Child Behavior Disorders/psychology , Cluster Analysis , Cognition Disorders/psychology , Comorbidity , Female , Humans , Internal-External Control , Learning Disabilities/psychology , Male , Psychometrics/statistics & numerical data , Psychopathology , Socialization , Statistics as TopicABSTRACT
Impaired cognitive functioning impedes the development of age-appropriate adaptive behavior, thus adding to the burdens of many children with epilepsy. Detailed neuropsychological assessment can identify the underlying ability-related impairments that contribute to the adaptive behavior deficiencies evidenced, particularly in the home and school settings. This information can serve as the basis for a multidisciplinary treatment plan tailored to individual needs. Ideally, the need for such a treatment plan should be perceived early in childhood, so that it can be developed and applied preventively. The same remedial principles also apply in older children and are here set out in detail.
Subject(s)
Adaptation, Psychological , Cognition Disorders/diagnosis , Epilepsy/psychology , Neuropsychological Tests , Activities of Daily Living , Child , Cognition Disorders/rehabilitation , Epilepsy/rehabilitation , Female , Humans , Learning Disabilities/diagnosis , Learning Disabilities/rehabilitation , Male , Parents/education , Patient Care Planning , Patient Care Team , Primary Prevention , Social AdjustmentABSTRACT
The genes encoding the periplasmic [Fe] hydrogenase from Desulfovibrio vulgaris subsp. oxamicus Monticello were cloned by exploiting their homology with the hydAB genes from D. vulgaris subsp. vulgaris Hildenborough, in which this enzyme is present as a heterologous dimer of alpha and beta subunits. Nucleotide sequencing showed that the enzyme is encoded by an operon in which the gene for the 46-kilodalton (kDa) alpha subunit precedes that of the 13.5-kDa beta subunit, exactly as in the Hildenborough strain. The pairs of hydA and hydB genes are highly homologous; both alpha subunits (420 amino acid residues) share 79% sequence identity, while the unprocessed beta subunits (124 and 123 amino acid residues, respectively) share 71% sequence identity. In contrast, there appears to be no sequence homology outside these coding regions, with the exception of a possible promoter element, which was found approximately 90 base pairs upstream from the translational start of the hydA gene. The recently discovered hydC gene, which may code for a 65.8-kDa fusion protein (gamma) of the alpha and beta subunits and is present immediately downstream from the hydAB genes in the Hildenborough strain, was found to be absent from the Monticello strain. The implication of this result for the possible function of the hydC gene product in Desulfovibrio species is discussed.
