Biomedical subjects

H Glidden

Publications and source records attributed to H Glidden.

4 recordsLinked to original sources

PubMed2000

Processing affective stimuli in children with attention-deficit hyperactivity disorder.

Neuropsychological investigations have suggested a contribution of right hemisphere dysfunction in attention-deficit hyperactivity disorder (ADHD). Right hemisphere dysfunction has been implicated in deficits of attention, motor impersistence, and processing emotion-laden stimuli. The current study investigated the ability of ADHD children to perceive emotional stimuli in the form of facial expressions and speech intonation. The subjects consisted of 37 ADHD and 37 control children aged 7 to 12 years. ANCOVA analysis indicated that ADHD children demonstrate mild-to-moderate deficits in the perception of affect. Furthermore, deficits in attention may contribute to inaccurate or incomplete encoding of stimulus properties. The results lend tentative support for the notion that the right cerebral hemisphere may play a critical role in ADHD.

Attention↗

PubMed1994

Emotional behavior as an agenda in neuropsychological evaluation.

In an effort to objectify neuropsychologic evaluations, consideration of a patient's emotional behavior has often been neglected. An extensive literature review is undertaken in an effort to document lateralized emotional behaviors commonly found in brain injury populations. This evidence is contrasted with the psychiatric symptoms and lateralized neuropsychologic impairments seen in major depression and schizophrenia. A theoretical model is then proposed that attempts to integrate these "functional" vs. "organic" symptoms based upon reciprocal inhibition of lateralized emotional functioning in brain injury and psychiatric disorders. This opponent process model not only seems to account for some of the discrepant findings in the literature, but additionally provides a cogent and useful marker to neurophychologically differentiate "neuronal" vs. "metabolic" disorders. The model further suggests new ways of envisioning treatment and recovery from both psychiatric illness and brain injury.

Brain Injuries↗

PubMed1980

A new Pk phenotype in the P blood group system.

A healthy 22-year-old woman was noted to have erythrocytes of the Pk phenotype: a strong Pk antigen, no detectable P antigen and anti-P antibody in her serum. Her erythrocytes contained four to six times as much Pk glycolipid (globotriaosylceramide or CTH) and approximately half as much P glycolipid (globotetraosylceramide or globoside) as normal red cells. The structures of CTH and globoside were characterized by analysis of permethylated sugars and complement fixation, in addition to chromatographic mobility and sugar composition. Inasmuch as the erythrocytes of two Pk individuals that were analysed previously (Marcus et al., 1976) contained no detectable globoside, these abnormalities appear to represent a new phenotype in the P blood group system.

Adult↗

PubMedDate not supplied

Studies on the blood of an MiV/Mk proposita and her family.

An individual (J-1) was shown to be heterozygous for the MiV and Mk genes. Her red cells typed as M+(weak), N-, S-, s+(strong), U+, Hil+, Wr(a-b-), En(a+weak). Polyacrylamide gel electrophoresis analysis of her red cell membranes revealed absence of PAS-staining bands corresponding to normal MN and Ss sialoglycoprotein (SGP), and presence of a hybrid MNSs SGP [(alpha-delta)MiV] similar but not identical to that reported for an MiV homozygote. However, J-1 cannot be homozygous for MiV since the red cells of two of her children are Hil- and s-, carry only a single dose of M antigen, and have a sialic acid content that is consistent with the presumption that they are Mk heterozygotes. J-1's hybrid MNSs SGP is considered to be gene-fusion product resulting from unequal crossover between a normal alpha M and delta gene, and her red cells lack that portion of the Ena antigen that is resistant to ficin. Her hybrid MNSs SGP differs, therefore, from that reported for the MiV homozygote, which probably arose from unequal crossover between alpha N and delta genes. Further, the red cells of the MiV homozygote carry the ficin-resistant Ena determinant.

Aged↗