Jackson State University's Center for Spatial Data Research and Applications: New facilities and new paradigms

Jackson State University recently established the Center for Spatial Data Research and Applications, a Geographical Information System (GIS) and remote sensing laboratory. Taking advantage of new technologies and new directions in the spatial (geographic) sciences, JSU is building a Center of Excellence in Spatial Data Management. New opportunities for research, applications, and employment are emerging. GIS requires fundamental shifts and new demands in traditional computer science and geographic training. The Center is not merely another computer lab but is one setting the pace in a new applied frontier. GIS and its associated technologies are discussed. The Center's facilities are described. An ARC/INFO GIS runs on a Vax mainframe, with numerous workstations. Image processing packages include ELAS, LIPS, VICAR, and ERDAS. A host of hardware and software peripheral are used in support. Numerous projects are underway, such as the construction of a Gulf of Mexico environmental data base, development of AI in image processing, a land use dynamics study of metropolitan Jackson, and others. A new academic interdisciplinary program in Spatial Data Management is under development, combining courses in Geography and Computer Science. The broad range of JSU's GIS and remote sensing activities is addressed. The impacts on changing paradigms in the university and in the professional world conclude the discussion

Upper bounds for inverse domination in graphs

In any graph $G$, the domination number $\gamma(G)$ is at most the independence number $\alpha(G)$. The \emph{Inverse Domination Conjecture} says that, in any isolate-free $G$, there exists pair of vertex-disjoint dominating sets $D, D\u27$ with $|D|=\gamma(G)$ and $|D\u27| \leq \alpha(G)$. Here we prove that this statement is true if the upper bound $\alpha(G)$ is replaced by $\frac{3}{2}\alpha(G) - 1$ (and $G$ is not a clique). We also prove that the conjecture holds whenever $\gamma(G)\leq 5$ or $|V(G)|\leq 16$

Facile Protocol for Water-Tolerant “Frustrated Lewis Pair”-Catalyzed Hydrogenation

Despite rapid advances in the field of metal-free, “frustrated Lewis pair” (FLP)-catalyzed hydrogenation, the need for strictly anhydrous reaction conditions has hampered wide-scale uptake of this methodology. Herein, we report that, despite the generally perceived moisture sensitivity of FLPs, 1,4-dioxane solutions of B(C6F5)3 actually show appreciable moisture tolerance and can catalyze hydrogenation of a range of weakly basic substrates without the need for rigorously inert conditions. In particular, reactions can be performed directly in commercially available nonanhydrous solvents without subsequent drying or use of internal desiccants

High-Throughput, Whole-Genome Sequencing

Since the completion of the Human Genome Project, research focusing on the consequence of known human genetic code has advanced by leaps and bounds. The development of personalized medicine, a field focused on enumerating the effects of individual genetic variations, termed SNPs, has become a reality for those researching the molecular basis of disease. With clinical correlates between genotype and prognosis becoming ever more common, the utility of personal genetic screening has become impossible to ignore. In this report, we present PennBio: a whole-genome sequencing company utilizing a novel single-molecule, real time sequencing-by-synthesis technology. Using unique zero-mode waveguides, which have revolutionized single-molecule detection, individual enzymes polymerizing novel phospholinked fluorescence labeled nucleotides can be observed as they sequence genomic template DNA. Modern optical techniques record these fragmented sequences, which are then analyzed by highly efficient alignment algorithms. A personal genomic code will ultimately allow consumers to be aware of their genetic predispositions as the medical community continues to discover them

Microenvironmental regulation of the sinusoidal endothelial cell phenotype in vitro

Author Manuscript: 2010 June 23.Liver sinusoidal endothelial cells (LSECs) differ, both structurally and functionally, from endothelial cells (ECs) lining blood vessels of other tissues. For example, in contrast to other ECs, LSECs possess fenestrations, have low detectable levels of platelet endothelial cell adhesion molecule 1 expression, and in rat tissue, they distinctively express a cell surface marker recognized by the SE-1 antibody. These unique phenotypic characteristics seen in hepatic tissue are lost over time upon culture in vitro; therefore, this study sought to systematically examine the effects of microenvironmental stimuli—namely, extracellular matrix and neighboring cells, on the LSEC phenotype in vitro. In probing the role of the underlying extracellular matrix, we identified collagen I and collagen III as well as mixtures of collagen I/collagen IV/fibronectin as having a positive effect on LSEC survival. Furthermore, using a stable hepatocellular model (hepatocyte–fibroblast) we were able to prolong the expression of both SE-1 and phenotypic functions of LSEC such as factor VIII activity and AcLOL uptake in cocultured LSECs through the production of short-range paracrine signals. In the course of these experiments, we identified the antigen recognized by SE-1 as CD32b. Conclusion: Collectively, this study has identified several microenvironmental regulators of liver sinusoidal endothelial cells that prolong their phenotypic functions for up to 2 weeks in culture, enabling the development of better in vitro models of liver physiology and disease

Synthesis, Photochemical, and Redox Properties of Gold(I) and Gold(III) Pincer Complexes Incorporating a 2,2′:6′,2″-Terpyridine Ligand Framework

Reaction of [Au(C6F5)(tht)] (tht = tetrahydrothiophene) with 2,2′:6′,2″-terpyridine (terpy) leads to complex [Au(C6F5)(η1-terpy)] (1). The chemical oxidation of complex (1) with 2 equiv of [N(C6H4Br-4)3](PF6) or using electrosynthetic techniques affords the Au(III) complex [Au(C6F5)(η3-terpy)](PF6)2 (2). The X-ray diffraction study of complex 2 reveals that the terpyridine acts as tridentate chelate ligand, which leads to a slightly distorted square-planar geometry. Complex 1 displays fluorescence in the solid state at 77 K due to a metal (gold) to ligand (terpy) charge transfer transition, whereas complex 2 displays fluorescence in acetonitrile due to excimer or exciplex formation. Time-dependent density functional theory calculations match the experimental absorption spectra of the synthesized complexes. In order to further probe the frontier orbitals of both complexes and study their redox behavior, each compound was separately characterized using cyclic voltammetry. The bulk electrolysis of a solution of complex 1 was analyzed by spectroscopic methods confirming the electrochemical synthesis of complex 2

Identification of Novel Compounds That Increase SMN Protein Levels Using an Improved SMN2 Reporter Cell Assay

Spinal muscular atrophy (SMA) is a neurodegenerative disorder that is characterized by progressive loss of motor neuron function. It is caused by the homozygous loss of the SMN1 (survival of motor neuron 1) gene and a decrease in full-length SMN protein. SMN2 is a nearly identical homolog of SMN1 that, due to alternative splicing, expresses predominantly truncated SMN protein. SMN2 represents an enticing therapeutic target. Increasing expression of full-length SMN from the SMN2 gene might represent a treatment for SMA. We describe a newly designed cell-based reporter assay that faithfully and reproducibly measures full-length SMN expression from the SMN2 gene. This reporter can detect increases of SMN protein by an array of compounds previously shown to regulate SMN2 expression and by the overexpression of proteins that modulate SMN2 splicing. It also can be used to evaluate changes at both the transcriptional and splicing level. This assay can be a valuable tool for the identification of novel compounds that increase SMN2 protein levels and the optimization of compounds already known to modulate SMN2 expression. We present here preliminary data from a high-throughput screen using this assay to identify novel compounds that increase expression of SMN2

Neuronal clusterin expression is associated with cognitive protection in amyotrophic lateral sclerosis

Research Funding Medical Research Council. Grant Number: MR/L016400/1 Academy of Medical Sciences. Grant Number: 210JMG 3102 R45620 MND Scotland Motor Neurone Disease Association Amyotrophic Lateral Sclerosis AssociationPeer reviewedPublisher PD