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G Hanten

Publications and source records attributed to G Hanten.

7 recordsLinked to original sources
PubMed2001

A developmental phonological short-term memory deficit: a case study.

A developmental case of phonological short-term memory deficit was studied in a highly educated subject. The subject, BS, who had obtained a Ph.D. in molecular biology, demonstrated striking deficits on some short-term memory tasks, particularly for auditorily presented nonword lists. With visual presentation and with meaningful words, he often scored at a normal level. The results indicate a deficit in retaining phonological information but an ability to use visual, lexical, and semantic information to boost recall. Despite this phonological short-term memory deficit, BS scored at a normal level on a syntactic comprehension test and on reading of nonwords. He was impaired, however, on repeated list learning, learning of foreign vocabulary, and transcribing dictated materials. The implications of these results for models of short-term memory and the uses of phonological retention in cognitive processing are discussed.

Adult↗
PubMed2000

Metacognition following pediatric traumatic brain injury: a preliminary study.

Metacognition is one of the cognitive processes included under the general term executive functions. The executive functions are widely held to be under the control of the prefrontal cortex, an area often damaged after severe traumatic brain injury (TBI). We examined the metacognitive processing of a group of 9 children with TBI, and a group of 9 healthy, age-matched control children. Children with TBI showed significant impairments in their accuracy of prediction of the ease with which an item would be learned and their ability to predict recall of an item after a 2-hr delay. No significant differences in recall performance between the TBI and control groups were exhibited. The results are interpreted as suggesting an impairment in metacognitive processing resulting from frontal lobe damage after TBI in children. Additional research is necessary to confirm the relation of frontal lobe pathology and severity of injury to metacognitive impairments.

Adolescent↗
PubMed1997

Diverse genetic regulatory motifs required for murine adenosine deaminase gene expression in the placenta.

Murine adenosine deaminase (ADA) is a ubiquitous purine catabolic enzyme whose expression is subject to developmental and tissue-specific regulation. ADA is enriched in trophoblast cells of the chorioallantoic placenta and is essential for embryonic and fetal development. To begin to understand the genetic pathway controlling Ada gene expression in the placenta, we have identified and characterized a 770-base pair fragment located 5.4 kilobase pairs upstream of the Ada transcription initiation site, which directs reporter gene expression to the placenta of transgenic mice. The expression pattern of the reporter gene reflected that of the endogenous Ada gene in the placenta. Sequence analysis revealed potential binding sites for bHLH and GATA transcription factors. DNase I footprinting defined three protein binding regions, one of which was placenta-specific. Mutations in the potential protein binding sites and footprinting regions resulted in loss of placental expression in transgenic mice. These findings indicate that multiple protein binding motifs are necessary for Ada expression in the placenta.

Adenosine Deaminase↗
PubMed1991

FVB/N: an inbred mouse strain preferable for transgenic analyses.

FVB/N mice offer a system suitable for most transgenic experiments and subsequent genetic analyses. The inbred FVB/N strain is characterized by vigorous reproductive performance and consistently large litters. Moreover, fertilized FVB/N eggs contain large and prominent pronuclei, which facilitate microinjection of DNA. The phenotype of large pronuclei in the zygote is a dominant trait associated with the FVB/N oocyte but not the FVB/N sperm. In experiments to generate transgenic mice, the same DNA constructs were injected into three different types of zygotes: FVB/N, C57BL/6J, and (C57BL/6J x SJL/J)F1. FVB/N zygotes survived well after injection, and transgenic animals were obtained with efficiencies similar to the F1 zygotes and much better than the C57BL/6J zygotes. Genetic markers of the FVB/N strain have been analyzed for 44 loci that cover 15 chromosomes and were compared with those of commonly used inbred strains. In addition to the albino FVB/N strain, pigmented congenic strains of FVB/N are being constructed. These features make the FVB/N strain advantageous to use for research with transgenic mice.

Alleles↗
PubMed1991

Coinjection strategy for visual identification of transgenic mice.

Transgenic mice were generated by coinjection of a dominant marker gene that induces fur and eye pigmentation (a tyrosinase minigene) plus an unrelated DNA construction that has a gamma-glutamyl transferase (gamma GT) promoter linked to a ras oncogene. Mice transgenic for gamma GT-ras could be identified in the first and all subsequent generations by simple visual inspection for pigmentation. Furthermore, the gamma-glutamyl transferase promoter was active in kidney but not skin of the transgenic mice, indicating that the cointegrated DNA was active and independently expressed. These results confirm that the tyrosinase minigene can be used for coinjections to allow rapid visual identification of transgenic mice.

Animals↗
PubMed1990

Tissue-specific expression in transgenic mice directed by the 5'-flanking sequences of the human gene encoding interphotoreceptor retinoid-binding protein.

Interphotoreceptor retinoid-binding protein (IRBP) is an extracellular protein that has been suggested to participate in the visual process as a carrier for visual retinoids. A chimeric gene composed of the human IRBP promoter fused to the bacterial reporter gene chloramphenicol acetyltransferase (CAT) was used to generate transgenic mice. Analysis of six transgenic families revealed that the CAT gene, concomitant with the endogenous IRBP gene, was expressed primarily in the retina and, to a lesser extent, in the pineal gland. These results establish that a 1.3-kilobase fragment from the 5' end of the human IRBP gene is sufficient to direct transgene expression to a visual subdivision of the central nervous system.

Animals↗