Search

Your search keyword '"Oreland, L."' showing total 965 results
Start Over Author "Oreland, L."
965 results on '"Oreland, L."'

2. The Development of Mental State Attributions in Women with X-Monosomy, and the Role of Monoamine Oxidase B in the Sociocognitive Phenotype

Author

Lawrence, K., Jones, A., and Oreland, L.

Abstract

We hypothesized that women with Turner syndrome (45,X) with a single X-chromosome inherited from their mother may show mentalizing deficits compared to women of normal karyotype with two X-chromosomes (46,X). Simple geometrical animation events (two triangles moving with apparent intention in relation to each other) which usually elicit mental-state descriptions in normally developing people, did not do so to the same extent in women with Turner syndrome. We then investigated the potential role in this deficit played by monoamine oxidase B enzymatic activity. MAO-B activity reflects central serotonergic activity, and by implication the functional integrity of neural circuits implicated in mentalizing. Platelet MAO-B was substantially reduced in Turner syndrome. However, contrary to prediction, in this (relatively small) sample there was no association between MAO-B enzymatic activity and mentalizing skills in participants with and without Turner syndrome.

Published
2007
Full Text
View/download PDF

4. Reactive gliosis and monoamine oxidase B

Author

Ekblom, J., Jossan, S. S., Oreland, L., Walum, E., Aquilonius, S.-M., Tipton, K. F., editor, Youdim, M. B. H., editor, Barwell, C. J., editor, Callingham, B. A., editor, and Lyles, G. A., editor

Published
1994
Full Text
View/download PDF

41. Association between Transcription Factor AP-2B genotype, obesity, insulin resistance and dietary intake in a longitudinal birth cohort study Transcription Factor AP-2B associated with obesity

Author

Joost, U., Harro, J., Veidebaum, L., Oreland, L., Comasco, E., and Villa, I.

Abstract

This is a post-peer-review, pre-copyedit version of an article published in International Journal of Obesity., The development of obesity has a large genetic component, and the gene encoding the transcription factor 2 beta (TFAP2B) has been identified as one of the responsible factors. We investigated the effect of TFAP2B intron 2 variable number tandem repeat (VNTR) genotype on obesity, insulin resistance and dietary intake from 15 to 33 years of age.

Published
2019

49. Supplementary Material for: Genetic and Functional Study of L-Type Amino Acid Transporter 1 in Schizophrenia

Author

Comasco, E., Vumma, R., Toffoletto, S., Johansson, J., Flyckt, L., Lewander, T., Oreland, L., Bjerkenstedt, L., Andreou, D., Söderman, E., Terenius, L., Agartz, I., Jönsson, E.G., and Venizelos, N.

Abstract

Schizophrenia involves neural catecholaminergic dysregulation. Tyrosine is the precursor of catecholamines, and its major transporter, according to studies on fibroblasts, in the brain is the L-type amino acid transporter 1 (LAT1). The present study assessed haplotype tag single-nucleotide polymorphisms (SNPs) of the SLC7A5/LAT1 gene in 315 patients with psychosis within the schizophrenia spectrum and 233 healthy controls to investigate genetic vulnerability to the disorder as well as genetic relationships to homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenylglycol (MHPG), the major catecholamine metabolites in the cerebrospinal fluid (CSF). Moreover, the involvement of the different isoforms of the system L in tyrosine uptake and LAT1 tyrosine kinetics were studied in fibroblast cell lines of 10 patients with schizophrenia and 10 healthy controls. The results provide suggestive evidence of individual vulnerability to schizophrenia related to the LAT1 SNP rs9936204 genotype. A number of SNPs were nominally associated with CSF HVA and MHPG concentrations but did not survive correction for multiple testing. The LAT1 isoform was confirmed as the major tyrosine transporter in patients with schizophrenia. However, the kinetic parameters (maximal transport capacity, affinity of the binding sites, and diffusion constant of tyrosine transport through the LAT1 isoform) did not differ between patients with schizophrenia and controls. The present genetic findings call for independent replication in larger samples, while the functional study seems to exclude a role of LAT1 in the aberrant transport of tyrosine in fibroblasts of patients with schizophrenia.

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results