Travel Demand Management and its Application at Australian University Campuses

This paper provides an example of how TDM could be applied in Australia with particular reference to university campuses. After considering the different characteristics of Australian university campuses in general, three Melbourne campuses were chosen as representative case studies. These consisted of a inner city campus (University of Melbourne), a inner suburban campus (Swinburne University) and an outer suburban campus (Monash University). Structured interviews were carried out with student and staff representatives involved with transport on campus. The interviews revealed a lack of consideration given to transport as an issue (as opposed to parking) at the three campuses. A subsequent survey was conducted of university administration representatives from campuses around Australia. That larger survey confirmed that Australian university campuses do not have any defined policies or decision making processes focused on campus transport issues. A model campus TDM program is developed based on the review of the available literature and the information on university travel characteristics collected from the three detailed case studies. Although the program is simple, it provides a basis on which individual campuses can establish a TDM program and then develop it further to complement their specific conditions. This paper is to be presented at the 19th ARRB TR Conference to be held in Sydney, 6-11 December 1998

X-ray line coincidence photopumping in a solar flare

Line coincidence photopumping is a process where the electrons of an atomic or molecular species are radiatively excited through the absorption of line emission from another species at a coincident wavelength. There are many instances of line coincidence photopumping in astrophysical sources at optical and ultraviolet wavelengths, with the most famous example being Bowen fluorescence (pumping of O III 303.80 Å by He II), but none to our knowledge in X-rays. However, here we report on a scheme where a He-like line of Ne IX at 11.000 Å is photopumped by He-like Na X at 11.003 Å, which predicts significant intensity enhancement in the Ne IX 82.76 Å transition under physical conditions found in solar flare plasmas. A comparison of our theoretical models with published X-ray observations of a solar flare obtained during a rocket flight provides evidence for line enhancement, with the measured degree of enhancement being consistent with that expected from theory, a truly surprising result. Observations of this enhancement during flares on stars other than the Sun would provide a powerful new diagnostic tool for determining the sizes of flare loops in these distant, spatially unresolved, astronomical sources

CD98hc facilitates B cell proliferation and adaptive humoral immunity.

The proliferation of antigen-specific lymphocytes and resulting clonal expansion are essential for adaptive immunity. We report here that B cell-specific deletion of the heavy chain of CD98 (CD98hc) resulted in lower antibody responses due to total suppression of B cell proliferation and subsequent plasma cell formation. Deletion of CD98hc did not impair early B cell activation but did inhibit later activation of the mitogen-activated protein kinase Erk1/2 and downregulation of the cell cycle inhibitor p27. Reconstitution of CD98hc-deficient B cells with CD98hc mutants showed that the integrin-binding domain of CD98hc was required for B cell proliferation but that the amino acid-transport function of CD98hc was dispensable for this. Thus, CD98hc supports integrin-dependent rapid proliferation of B cells. We propose that the advantage of adaptive immunity favored the appearance of CD98hc in vertebrates

Bordetella Adenylate Cyclase Toxin Mobilizes Its β2 Integrin Receptor into Lipid Rafts to Accomplish Translocation across Target Cell Membrane in Two Steps

Bordetella adenylate cyclase toxin (CyaA) binds the αMβ2 integrin (CD11b/CD18, Mac-1, or CR3) of myeloid phagocytes and delivers into their cytosol an adenylate cyclase (AC) enzyme that converts ATP into the key signaling molecule cAMP. We show that penetration of the AC domain across cell membrane proceeds in two steps. It starts by membrane insertion of a toxin ‘translocation intermediate’, which can be ‘locked’ in the membrane by the 3D1 antibody blocking AC domain translocation. Insertion of the ‘intermediate’ permeabilizes cells for influx of extracellular calcium ions and thus activates calpain-mediated cleavage of the talin tether. Recruitment of the integrin-CyaA complex into lipid rafts follows and the cholesterol-rich lipid environment promotes translocation of the AC domain across cell membrane. AC translocation into cells was inhibited upon raft disruption by cholesterol depletion, or when CyaA mobilization into rafts was blocked by inhibition of talin processing. Furthermore, CyaA mutants unable to mobilize calcium into cells failed to relocate into lipid rafts, and failed to translocate the AC domain across cell membrane, unless rescued by Ca2+ influx promoted in trans by ionomycin or another CyaA protein. Hence, by mobilizing calcium ions into phagocytes, the ‘translocation intermediate’ promotes toxin piggybacking on integrin into lipid rafts and enables AC enzyme delivery into host cytosol

Decellularized Matrix from Tumorigenic Human Mesenchymal Stem Cells Promotes Neovascularization with Galectin-1 Dependent Endothelial Interaction

BACKGROUND: Acquisition of a blood supply is fundamental for extensive tumor growth. We recently described vascular heterogeneity in tumours derived from cell clones of a human mesenchymal stem cell (hMSC) strain (hMSC-TERT20) immortalized by retroviral vector mediated human telomerase (hTERT) gene expression. Histological analysis showed that cells of the most vascularized tumorigenic clone, -BD11 had a pericyte-like alpha smooth muscle actin (ASMA+) and CD146+ positive phenotype. Upon serum withdrawal in culture, -BD11 cells formed cord-like structures mimicking capillary morphogenesis. In contrast, cells of the poorly tumorigenic clone, -BC8 did not stain for ASMA, tumours were less vascularized and serum withdrawal in culture led to cell death. By exploring the heterogeneity in hMSC-TERT20 clones we aimed to understand molecular mechanisms by which mesenchymal stem cells may promote neovascularization. METHODOLOGY/PRINCIPAL FINDINGS: Quantitative qRT-PCR analysis revealed similar mRNA levels for genes encoding the angiogenic cytokines VEGF and Angiopoietin-1 in both clones. However, clone-BD11 produced a denser extracellular matrix that supported stable ex vivo capillary morphogenesis of human endothelial cells and promoted in vivo neovascularization. Proteomic characterization of the -BD11 decellularized matrix identified 50 extracellular angiogenic proteins, including galectin-1. siRNA knock down of galectin-1 expression abrogated the ex vivo interaction between decellularized -BD11 matrix and endothelial cells. More stable shRNA knock down of galectin-1 expression did not prevent -BD11 tumorigenesis, but greatly reduced endothelial migration into -BD11 cell xenografts. CONCLUSIONS: Decellularized hMSC matrix had significant angiogenic potential with at least 50 angiogenic cell surface and extracellular proteins, implicated in attracting endothelial cells, their adhesion and activation to form tubular structures. hMSC -BD11 surface galectin-1 expression was required to bring about matrix-endothelial interactions and for xenografted hMSC -BD11 cells to optimally recruit host vasculature