297 research outputs found
A Design Methodology for Early Education Facility Prototypes in Hawai‘i.
D.Arch. Thesis. University of Hawaiʻi at Mānoa 2017
Schwinger variational principle applied to long-range potentials
We discuss an adaptation of the Schwinger variational principle which is particularly suitable for dealing with long-range potentials. The method treats the direct interaction potential exactly by numerical integration and assumes a separable representation of the Schwinger type for the exchange potential. The method should be very effective for obtaining the electronic continuum solutions of strongly polar molecular ions. The related photoionization cross sections can be shown to be variationally stable
Amino-termini Isoforms Of Slack K(Na) Channel Differentially Influence The Rate Of Neuronal Adaptation.
Regulation of Insulin-like Growth Factor I Receptor Dephosphorylation by SHPS-1 and the Tyrosine Phosphatase SHP-2
Activation of insulin-like growth factor I receptor (IGF-IR) kinase is an important site of control of IGF-I-linked intracellular signaling pathways. One potentially important regulatory variable is IGF-IR dephosphorylation. It has been shown that SHP-2, a tyrosine phosphatase, can bind to the activated IGF-IR in vitro; however, its role in IGF-IR dephosphorylation in whole cells is unknown. These studies were undertaken to determine whether SHP-2 was a candidate for mediating IGF-IR dephosphorylation. The IGF-IR in smooth muscle cells was dephosphorylated rapidly beginning 10 min after ligand addition, and this was temporally associated with SHP-2 binding to the receptor. IGF-I stimulated SHPS-1 phosphorylation and the subsequent recruitment of SHP-2. In cells expressing a SHPS-1 mutant that did not bind SHP-2 there was no recruitment of SHP-2 to the IGF-IR. Cells expressing a catalytically inactive form of SHP-2 showed SHP-2 recruitment to SHPS-1, but this did not result in SHPS-1 dephosphorylation, and there was a prolonged IGF-IR phosphorylation response after IGF-I stimulation. These studies indicate that IGF-IR stimulates phosphorylation of SHPS-1 which is critical for SHP-2 recruitment to the plasma membrane and for its recruitment to the IGF-IR. Recruitment of SHP-2 to the receptor then results in receptor dephosphorylation. The regulation of this process may be an important determinant of IGF-IR-mediated signaling
Studies of the photoionization cross section of the 2pi level of nitric oxide
We present photoionization cross sections and asymmetry parameters for the 2pi level of nitric oxide which are obtained from the direct solution of the e+NO+ collisional equations at the static-exchange level. These cross sections differ significantly from those obtained previously using a moment theory approach [J. J. Delaney, I. H. Hillier, and V. R. Saunders, J. Phys. B 15, 1477 (1982)]. The calculated cross sections show a broad nonresonant feature at a photon energy of 29 eV which is not as pronounced as observed experimentally. The sigma shape resonance in our cross section occurs at 14 eV which is about 5 eV below the feature in the measured cross sections attributed to this shape resonance. The probable role of autoionization and vibrational averaging on these cross sections is also discussed
CoastalImageLib: An open- source Python package for creating common coastal image products
CoastalImageLib is a Python library that produces common coastal image products intended for quantitative analysis of coastal environments. This library contains functions to georectify and merge multiple oblique camera views, produce statistical image products for a given set of images, and create subsampled pixel instruments for use in bathymetric inversion, surface current estimation, run-up calculations, and other quantitative analyses. This package intends to be an open-source broadly generalizable front end to future coastal imaging applications, ultimately expanding user accessibility to optical remote sensing of coastal environments. This package was developed and tested on data collected from the Argus Tower, a 43 m tall observation structure in Duck, North Carolina at the US Army Engineer Research and Development Center’s Field Research Facility that holds six stationary cameras which collect twice-hourly coastal image products. Thus, CoastalImageLib also contains functions designed to interface with the file storage and collection system implemented at the Argus Tower
Glucose Regulation of Thrombospondin and Its Role in the Modulation of Smooth Muscle Cell Proliferation
Smooth muscle cells (SMC) maintained in high glucose are more responsive to IGF-I than those in normal glucose. There is significantly more thrombospondin-1 (TSP-1) in extracellular matrix surrounding SMC grown in 25 mM glucose. In this study we investigated 1) the mechanism by which glucose regulates TSP-1 levels and 2) the mechanism by which TS-1 enhances IGF-I signaling. The addition of TSP-1 to primary SMC was sufficient to enhance IGF-I responsiveness in normal glucose. Reducing TSP-1 protein levels inhibited IGF-I signaling in SMC maintained in high glucose. We determined that TSP-1 protected IAP/CD47 from cleavage and thereby facilitated its association with SHP substrate-1 (SHPS-1). We have shown previously that the hyperglycemia induced protection of IAP from cleavage is an important component of the ability of hyperglycemia to enhance IGF-I signaling. Furthermore we determined that TSP-1 also enhanced phosphorylation of the β3 subunit of the αVβ3 integrin, another molecular event that we have shown are critical for SMC response to IGF-I in high glucose. Our studies also revealed that the difference in the amount of TSP-1 in the two different glucose conditions was due, at least in part, to a difference in the cellular uptake and degradation of TSP-1
Structural analysis of the role of the (β)3 subunit of the (α)V(β)3 integrin in IGF-I signaling
The disintegrin echistatin inhibits ligand occupancy of the (α)V(β)3 integrin and reduces Insulin-like growth factor I (IGF-I) stimulated migration, DNA synthesis, and receptor autophosphorylation in smooth muscle cells. This suggests that ligand occupancy of the (α)V(β)3 receptor is required for full activation of the IGF-I receptor. Transfection of the full-length (β)3 subunit into CHO cells that have no endogenous (β)3 and do not migrate in response to IGF-I was sufficient for IGF-I to stimulate migration of these anchorage dependent cells. In contrast, transfection of either of two truncated mutant forms of (β)3 (terminating at W(715) or E(731)) or a mutant with substitutions for Tyr(747) Tyr(759) (YY) into either CHO or into porcine smooth muscle cells did not restore the capacity of these cells to migrate across a surface in response to IGF-I. This effect was not due to loss of IGF-I receptor autophosphorylation since the response of the receptor to IGF-I was similar in cells expressing either the full-length or any of the mutant forms of the (β)3 subunit. Echistatin reduced IGF-I receptor phosphorylation in cells expressing the full-length or the YY mutant forms of (β)3 subunit, but it had no effect in cells expressing either of two truncated forms of (β)3. A cell-permeable peptide homologous to the C-terminal region of the (β)3 subunit (amino acids 747–762) reduced IGF-I stimulated migration and receptor autophosphorylation of non-transfected porcine smooth muscle cells. These results demonstrate that the full-length (β)3 with intact tyrosines at positions 747 and 759 is required for CHO cells to migrate in response to IGF-I. Furthermore, a region of critical amino acids between residues 742–762 is required for echistatin to induce its regulatory effect on receptor phosphorylation. Since the IGF-I receptor does not bind to (α)V(β)3 the results suggest that specific but distinct regions of the (β)3 subunit interact with intermediary proteins to facilitate IGF-I stimulated cell migration and echistatin induced inhibition of IGF-I signal transduction
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