18 research outputs found

    sj-docx-1-spp-10.1177_19485506211070674 – Supplemental material for The Development of Shyness from Late Childhood to Adolescence: A Longitudinal Study of Mexican-Origin Youth

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    Supplemental material, sj-docx-1-spp-10.1177_19485506211070674 for The Development of Shyness from Late Childhood to Adolescence: A Longitudinal Study of Mexican-Origin Youth by Katherine M. Lawson, Brenna L. Barrett, Ryan J. Cerny, Kaitlyn E. Enrici, Juan Eduardo Garcia-Cardenas, Catherine E. Gonzales, Isidro D. Hernandez, Carrina P. Iacobacci, Tiffanie Lin, Nancy Y. Martinez Urieta, Patricia Moreno, Marissa G. Rivera, Devin J. Teichrow, Anabel Vizcarra, Camelia E. Hostinar and Richard W. Robins in Social Psychological and Personality Science</p

    Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

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    Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology 'reverse engineering' approaches. We 'reverse engineered' an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression ('hubs'). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central 'hub' of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

    Interactive Surface Modeling and Analysis

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    Computer Aided Geometric Design (CAGD) is concerned with efficiently modeling physical objects with a surface or a collection of surfaces and has applications in CAD/CAM, computer graphics, robotics, and computer vision. This thesis introduces multi-sided A-patches and investigates their properties. A-patches are smooth and single-sheeted implicit algebraic surface patches in Bernstein-Bézier (BB) form. A new technique is described for filling an n-sided hole smoothly using a single implicit surface patch or a network of implicit patches with a geometrically intuitive compact representation. The free parameters of the A-patches are used to achieve fair surfaces with desirable properties. The main impediments to the widespread use of implicit surfaces for geometric modeling are multiple sheets, self-intersections and several other undesirable singularities. Our A-patch technique provides simple ways to guarantee that the constructed implicit surface is single-sheeted and free of undesirable singularities. The technique uses the zero contouring surfaces of trivariate Bernstein-Bézier polynomials to construct a piecewise smooth surface. We call such iso-splines A-patches, where A stands for algebraic. We have designed four different algorithms to construct smooth A-patch surfaces that interpolate or approximate scattered 3D point data or simple polyhedra of arbitrary topology. In the first algorithm we first construct a Gk curvilinear wire frame and then create implicit surface patches that interpolate the curves. A single patch is used for each triangle, quadrilateral, and pentagon in the input. In the second algorithm we triangulate the quadrilaterals and pentagons. The constructed surface passes through the vertices of the discretization and has the given normals at the vertices. This solution uses piecewise functions defined on a hull that consists of tetrahedra. The third algorithm uses piecewise rational functions defined on a hull that consists of tetrahedra and pyramids. And the fourth algorithm uses piecewise rational functions defined on a hull that consists of prisms

    Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

    No full text
    Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology ‘reverse engineering’ approaches. We ‘reverse engineered’ an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression (‘hubs’). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central ‘hub’ of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

    Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation

    No full text
    Gene expression profiles can be used to infer previously unknown transcriptional regulatory interaction among thousands of genes, via systems biology 'reverse engineering' approaches. We 'reverse engineered' an embryonic stem (ES)-specific transcriptional network from 171 gene expression profiles, measured in ES cells, to identify master regulators of gene expression ('hubs'). We discovered that E130012A19Rik (E13), highly expressed in mouse ES cells as compared with differentiated cells, was a central 'hub' of the network. We demonstrated that E13 is a protein-coding gene implicated in regulating the commitment towards the different neuronal subtypes and glia cells. The overexpression and knock-down of E13 in ES cell lines, undergoing differentiation into neurons and glia cells, caused a strong up-regulation of the glutamatergic neurons marker Vglut2 and a strong down-regulation of the GABAergic neurons marker GAD65 and of the radial glia marker Blbp. We confirmed E13 expression in the cerebral cortex of adult mice and during development. By immuno-based affinity purification, we characterized protein partners of E13, involved in the Polycomb complex. Our results suggest a role of E13 in regulating the division between glutamatergic projection neurons and GABAergic interneurons and glia cells possibly by epigenetic-mediated transcriptional regulation

    Adaptive modification of the cat’s vestibulospinal reflex during sustained and combined roll tilt of the whole animal and forepaw rotation: cerebellar mechanisms.

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    Abstract—In decerebrate cats, the electromyogram (EMG) activity of the forelimb extensor triceps brachii (TB) increases during side-down roll tilt of the whole animal (vestibulospinal reflex, VSR) at about 0.15 Hz. (10°), while decreases during side up tilt. On the other hand, the TB activity increases during dorsal flexion of the ipsilateral forepaw (0.15 Hz, 5°–10°), but decreases during ventral flexion. In six experiments, these stimuli were synergistically associated (side-down tilt coincided with dorsal flexion of the forepaw), so that the EMG modulation of the TB activity was greater than that induced by the individual stimuli. During a 3-h period of this sustained stimulation, the amplitude of the pure VSR progressively increased to reach the maximum value at the end of the third hour and persisted unmodified during the post-adaptation period (1 h). In three experiments, animal tilt and forepaw rotation were antagonistically associated (sidedown tilt coincided with ventral flexion of the forepaw). In these instances the VSR gain remained on the average stable, but, at the end of the 3-h period of combined stimulation, a proportion of TB responses to animal tilt howed a phase reversal. In a digitigrade animal like the cat, a dorsal flexion of the wrist is associated with a decrease in limb length and would occur when the extensor tone is not appropriate to support body weight; we propose, therefore, that somatosensory volleys elicited by wrist rotation modify the gain of VSR so as to maintain postural stability. Inactivation, on the side of muscle recording, of the corticocerebellar region which projects to the lateral vestibular nucleus of Deiters, by local microinjection of the GABA-A agonist muscimol (0.5 l at 16 g/l), decreased the already adapted gain of VSR. In conclusion, the results of this study suggest that somatosensory reafferent inputs to the cerebellar vermis are used to plastically modify the gain of VSR, when external forces produce changes in the final posture of the foot during animal tilt

    A mouse embryonic stem cell bank for inducible overexpression of human chromosome 21 genes.

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    Abstract BACKGROUND: Dosage imbalance is responsible for several genetic diseases, among which Down syndrome is caused by the trisomy of human chromosome 21. RESULTS: To elucidate the extent to which the dosage imbalance of specific human chromosome 21 genes perturb distinct molecular pathways, we developed the first mouse embryonic stem (ES) cell bank of human chromosome 21 genes. The human chromosome 21-mouse ES cell bank includes, in triplicate clones, 32 human chromosome 21 genes, which can be overexpressed in an inducible manner. Each clone was transcriptionally profiled in inducing versus non-inducing conditions. Analysis of the transcriptional response yielded results that were consistent with the perturbed gene's known function. Comparison between mouse ES cells containing the whole human chromosome 21 (trisomic mouse ES cells) and mouse ES cells overexpressing single human chromosome 21 genes allowed us to evaluate the contribution of single genes to the trisomic mouse ES cell transcriptome. In addition, for the clones overexpressing the Runx1 gene, we compared the transcriptome changes with the corresponding protein changes by mass spectroscopy analysis. CONCLUSIONS: We determined that only a subset of genes produces a strong transcriptional response when overexpressed in mouse ES cells and that this effect can be predicted taking into account the basal gene expression level and the protein secondary structure. We showed that the human chromosome 21-mouse ES cell bank is an important resource, which may be instrumental towards a better understanding of Down syndrome and other human aneuploidy disorders
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