Turner syndrome: Neuroimaging findings: Structural and functional
ABSTRACT Neuroimaging studies of Turner syndrome can advance our understanding of the X chromosome in brain development, and the modulatory influence of endocrine factors. There is increasing evidence from neuroimaging studies that TX individuals have significant differences in the anatomy, function, and metabolism of a number of brain regions; including the parietal lobe; cerebellum, amygdala, hippocampus; and basal ganglia; and perhaps differences in "connectivity" between frontal and parieto-occipital regions. Finally, there is preliminary evidence that genomic imprinting, sex hormones and growth hormone have significant modulatory effects on brain maturation in TS.
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ABSTRACT: A new kind of light beam called the elliptical Hermite–Gaussian beam (EHGB) is introduced in this paper by using tensor method. The EHGB can be used to describe the generalized higher-order laser beams, such as hollow laser beams and the twisted Hermite–Gaussian beams conveniently. It includes the conventional Hermite–Gaussian beams as special cases. Using the generalized Collins integral, we derive the propagation formula of the EHGB passing through axially non-symmetrical paraxial optical systems. The EHGB allows us to treat the propagation and transformation of some complicated laser beams analytically. As an application example, we treat the elliptical flattened Gaussian beams by expressing it as superposition of a series of EHGBs by using polynomial expansion.Optics Communications 06/2002; 207(1-6):139-147. DOI:10.1016/S0030-4018(02)01533-X · 1.54 Impact Factor
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ABSTRACT: Genomic imprinting is the phenomenon where the expression of a locus differs between the maternally and paternally inherited alleles. Typically, this manifests as transcriptional silencing of one of the alleles, although many genes are imprinted in a tissue- or isoform-specific manner. Diseases associated with imprinted genes include various cancers, disorders of growth and metabolism, and disorders in neurodevelopment, cognition, and behavior, including certain major psychiatric disorders. In many cases, the disease phenotypes associated with dysfunction at particular imprinted loci can be understood in terms of the evolutionary processes responsible for the origin of imprinting. Imprinted gene expression represents the outcome of an intragenomic evolutionary conflict, where natural selection favors different expression strategies for maternally and paternally inherited alleles. This conflict is reasonably well understood in the context of the early growth effects of imprinted genes, where paternally inherited alleles are selected to place a greater demand on maternal resources than are maternally inherited alleles. Less well understood are the origins of imprinted gene expression in the brain, and their effects on cognition and behavior. This chapter reviews the genetic diseases that are associated with imprinted genes, framed in terms of the evolutionary pressures acting on gene expression at those loci. We begin by reviewing the phenomenon and evolutionary origins of genomic imprinting. We then discuss diseases that are associated with genetic or epigenetic defects at particular imprinted loci, many of which are associated with abnormalities in growth and/or feeding behaviors that can be understood in terms of the asymmetric pressures of natural selection on maternally and paternally inherited alleles. We next described the evidence for imprinted gene effects on adult cognition and behavior, and the possible role of imprinted genes in the etiology of certain major psychiatric disorders. Finally, we conclude with a discussion of how imprinting, and the evolutionary-genetic conflicts that underlie it, may enhance both the frequency and morbidity of certain types of diseases.Progress in molecular biology and translational science 01/2011; 101:401-45. DOI:10.1016/B978-0-12-387685-0.00013-5 · 3.11 Impact Factor
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ABSTRACT: There is little debate that mammalian sexual differentiation starts from the perspective of two primary sexes that correspond to differential sex chromosomes (X versus Y) that lead to individuals with sex typical characteristics. Sex steroid hormones account for most aspects of brain sexual differentiation, however, a growing literature has raised important questions about the role of sex chromosomal genes separate from sex steroid actions. Several important model animals are being used to address these issues and, in particular, they are taking advantage of molecular genetic approaches using different mouse strains. The current review examines the cooperation of genetic and endocrine influences from the perspective of behavioral and morphological hypothalamic sexual differentiation, first in adults and then in development. In the final analysis, there is an ongoing need to account for the influence of hormones in the context of underlying genetic circumstances and null hormone conditions.Frontiers in Neuroendocrinology 02/2011; 32(2):137-45. DOI:10.1016/j.yfrne.2011.02.009 · 7.58 Impact Factor