The Automated Delimitation of Maritime Boundaries - An Australian Perspective

Determining the accurate location of maritime boundaries and computing the outer limits of the extended continental shelf can be a mathematically demanding and computationally intensive task. This paper considers the relevant issues, particularly from an Australian perspective. An efficient and automated solution to maritime boundary and extended continental shelf delimitation has been designed and implemented in the form of a software package known as MarZone. This paper introduces the MarZone software. In the design of MarZone, emphasis was placed on a geodetically rigorous methodology while at the same time maintaining strict agreement with the relevant provisions of the United Nations Convention on the Law of the Sea. The reasons for such an emphasis are explained in the paper

A Committee to Manage Innovative Learning Spaces: Balancing Committee Size, Cross-Campus Representation, and Decision-Making Power

The growth in active learning classrooms represents a major shift in the pedagogy and built environment of higher education. While a robust literature exists to discuss the development, use, and evaluation of these innovative learning spaces, the practical considerations of managing innovative learning spaces has not received the same level of attention. This article describes the management model at _____ University, outlining key workflow considerations: committee size, cross-campus representation, and decision-making power. The conclusion sets out future research opportunities related to the institutional dynamics of innovative learning space management

A Semantic Grid Oriented to E-Tourism

With increasing complexity of tourism business models and tasks, there is a clear need of the next generation e-Tourism infrastructure to support flexible automation, integration, computation, storage, and collaboration. Currently several enabling technologies such as semantic Web, Web service, agent and grid computing have been applied in the different e-Tourism applications, however there is no a unified framework to be able to integrate all of them. So this paper presents a promising e-Tourism framework based on emerging semantic grid, in which a number of key design issues are discussed including architecture, ontologies structure, semantic reconciliation, service and resource discovery, role based authorization and intelligent agent. The paper finally provides the implementation of the framework.Comment: 12 PAGES, 7 Figure

Randomized multicentre pilot study of sacubitril/valsartan versus irbesartan in patients with chronic kidney disease: United Kingdom Heart and Renal Protection (HARP)- III—rationale, trial design and baseline data

BACKGROUND: Patients with chronic kidney disease (CKD) are at risk of progression to end-stage renal disease and cardiovascular disease. Data from other populations and animal experiments suggest that neprilysin inhibition (which augments the natriuretic peptide system) may reduce these risks, but clinical trials among patients with CKD are required to test this hypothesis. METHODS: UK Heart and Renal Protection III (HARP-III) is a multicentre, double-blind, randomized controlled trial comparing sacubitril/valsartan 97/103 mg two times daily (an angiotensin receptor-neprilysin inhibitor) with irbesartan 300 mg one time daily among 414 patients with CKD. Patients ≥18 years of age with an estimated glomerular filtration rate (eGFR) of ≥45 but <60 mL/min/1.73 m2 and urine albumin:creatinine ratio (uACR) >20 mg/mmol or eGFR ≥20 but <45 mL/min/1.73 m2 (regardless of uACR) were invited to be screened. Following a 4- to 7-week pre-randomization single-blind placebo run-in phase (during which any current renin-angiotensin system inhibitors were stopped), willing and eligible participants were randomly assigned either sacubitril/valsartan or irbesartan and followed-up for 12 months. The primary aim was to compare the effects of sacubitril/valsartan and irbesartan on measured GFR after 12 months of therapy. Important secondary outcomes include effects on albuminuria, change in eGFR over time and the safety and tolerability of sacubitril/valsartan in CKD. RESULTS: Between November 2014 and January 2016, 620 patients attended a screening visit and 566 (91%) entered the pre-randomization run-in phase. Of these, 414 (73%) participants were randomized (mean age 63 years; 72% male). The mean eGFR was 34.0 mL/min/1.73 m2 and the median uACR was 58.5 mg/mmol. CONCLUSIONS: UK HARP-III will provide important information on the short-term effects of sacubitril/valsartan on renal function, tolerability and safety among patients with CKD

Onset of Superfluidity in 4He Films Adsorbed on Disordered Substrates

We have studied 4He films adsorbed in two porous glasses, aerogel and Vycor, using high precision torsional oscillator and DC calorimetry techniques. Our investigation focused on the onset of superfluidity at low temperatures as the 4He coverage is increased. Torsional oscillator measurements of the 4He-aerogel system were used to determine the superfluid density of films with transition temperatures as low as 20 mK. Heat capacity measurements of the 4He-Vycor system probed the excitation spectrum of both non-superfluid and superfluid films for temperatures down to 10 mK. Both sets of measurements suggest that the critical coverage for the onset of superfluidity corresponds to a mobility edge in the chemical potential, so that the onset transition is the bosonic analog of a superconductor-insulator transition. The superfluid density measurements, however, are not in agreement with the scaling theory of an onset transition from a gapless, Bose glass phase to a superfluid. The heat capacity measurements show that the non-superfluid phase is better characterized as an insulator with a gap.Comment: 15 pages (RevTex), 21 figures (postscript

Mott Transition in Degenerate Hubbard Models: Application to Doped Fullerenes

The Mott-Hubbard transition is studied for a Hubbard model with orbital degeneracy N, using a diffusion Monte-Carlo method. Based on general arguments, we conjecture that the Mott-Hubbard transition takes place for U/W \propto \sqrt{N}, where U is the Coulomb interaction and W is the band width. This is supported by exact diagonalization and Monte-Carlo calculations. Realistic parameters for the doped fullerenes lead to the conclusion that stoichiometric A_3 C_60 (A=K, Rb) are near the Mott-Hubbard transition, in a correlated metallic state.Comment: 4 pages, revtex, 1 eps figure included, to be published in Phys.Rev.B Rapid Com

Direct CP violation and the ΔI=1/2 rule in K→ππ decay from the standard model

We present a lattice QCD calculation of the ΔI=1/2, K→ππ decay amplitude A0 and ϵ′, the measure of direct CP violation in K→ππ decay, improving our 2015 calculation [1] of these quantities. Both calculations were performed with physical kinematics on a 323×64 lattice with an inverse lattice spacing of a-1=1.3784(68)  GeV. However, the current calculation includes nearly 4 times the statistics and numerous technical improvements allowing us to more reliably isolate the ππ ground state and more accurately relate the lattice operators to those defined in the standard model. We find Re(A0)=2.99(0.32)(0.59)×10-7  GeV and Im(A0)=-6.98(0.62)(1.44)×10-11  GeV, where the errors are statistical and systematic, respectively. The former agrees well with the experimental result Re(A0)=3.3201(18)×10-7  GeV. These results for A0 can be combined with our earlier lattice calculation of A2 [2] to obtain Re(ϵ′/ϵ)=21.7(2.6)(6.2)(5.0)×10-4, where the third error represents omitted isospin breaking effects, and Re(A0)/Re(A2)=19.9(2.3)(4.4). The first agrees well with the experimental result of Re(ϵ′/ϵ)=16.6(2.3)×10-4. A comparison of the second with the observed ratio Re(A0)/Re(A2)=22.45(6), demonstrates the standard model origin of this “ΔI=1/2 rule” enhancement.We present a lattice QCD calculation of the $\Delta I=1/2$, $K\to\pi\pi$ decay amplitude $A_0$ and $\varepsilon'$, the measure of direct CP-violation in $K\to\pi\pi$ decay, improving our 2015 calculation of these quantities. Both calculations were performed with physical kinematics on a $32^3\times 64$ lattice with an inverse lattice spacing of $a^{-1}=1.3784(68)$ GeV. However, the current calculation includes nearly four times the statistics and numerous technical improvements allowing us to more reliably isolate the $\pi\pi$ ground-state and more accurately relate the lattice operators to those defined in the Standard Model. We find ${\rm Re}(A_0)=2.99(0.32)(0.59)\times 10^{-7}$ GeV and ${\rm Im}(A_0)=-6.98(0.62)(1.44)\times 10^{-11}$ GeV, where the errors are statistical and systematic, respectively. The former agrees well with the experimental result ${\rm Re}(A_0)=3.3201(18)\times 10^{-7}$ GeV. These results for $A_0$ can be combined with our earlier lattice calculation of $A_2$ to obtain ${\rm Re}(\varepsilon'/\varepsilon)=21.7(2.6)(6.2)(5.0) \times 10^{-4}$, where the third error represents omitted isospin breaking effects, and Re$(A_0)$/Re$(A_2) = 19.9(2.3)(4.4)$. The first agrees well with the experimental result of ${\rm Re}(\varepsilon'/\varepsilon)=16.6(2.3)\times 10^{-4}$. A comparison of the second with the observed ratio Re$(A_0)/$Re$(A_2) = 22.45(6)$, demonstrates the Standard Model origin of this "$\Delta I = 1/2$ rule" enhancement

Limited Lifespan of Fragile Regions in Mammalian Evolution

An important question in genome evolution is whether there exist fragile regions (rearrangement hotspots) where chromosomal rearrangements are happening over and over again. Although nearly all recent studies supported the existence of fragile regions in mammalian genomes, the most comprehensive phylogenomic study of mammals (Ma et al. (2006) Genome Research 16, 1557-1565) raised some doubts about their existence. We demonstrate that fragile regions are subject to a "birth and death" process, implying that fragility has limited evolutionary lifespan. This finding implies that fragile regions migrate to different locations in different mammals, explaining why there exist only a few chromosomal breakpoints shared between different lineages. The birth and death of fragile regions phenomenon reinforces the hypothesis that rearrangements are promoted by matching segmental duplications and suggests putative locations of the currently active fragile regions in the human genome

Apoptosis in the Nervous System in Experimental Allergic Encephalomyelitis

We report here for the first time the occurrence of apoptosis of cells in the spinal cord in experimental allergic encephalomyelitis (EAE), an autoimmune, T-cell-mediated demyelinating disease. Four different forms of EAE were studied in the Lewis rat: (i) acute EAE induced by inoculation with whole spinal cord and adjuvants; (ii) acute EAE induced by inoculation with myelin basic protein (MBP) and adjuvants; (iii) acute EAE induced by the passive transfer of MBP-sensitized spleen cells; (iv) chronic relapsing EAE induced by inoculation with whole spinal cord and adjuvants followed by treatment with low-dose cyclosporin A. Cells undergoing apoptosis were recognized at light and electron microscopy by the presence of either crescentic masses of condensed chromatin lying against the nuclear envelope or rounded masses of uniformly dense chromatin. They were found in both the white and grey matter of the spinal cord in all 4 forms of this disease. Although it was not possible to identify definitively the types of cells undergoing apoptosis, the size and location of some of the affected cells suggested that they were oligodendrocytes. As there is now a large body of evidence that T-cell-induced target cell death takes the form of apoptosis, it is attractive to hypothesize that oligodendrocyte apoptosis is occurring in EAE as a result of oligodendrocyte-directed T-cell cytotoxicity. However, other apoptotic cells were located within the myelin sheath, meninges and perivascular spaces and were clearly not oligodendrocytes but were most likely blood-derived mononuclear cells. The sparsity of their cytoplasm and the absence of phagocytosed material suggested that they were mainly lymphocytes rather than macrophages. Apoptosis has been shown to be involved in deleting autoreactive T-cells during the normal development of tolerance. Thus apoptotic deletion of myelin/oligodendrocyte-specific lymphocytes in the central nervous system in EAE might explain both the subsidence of inflammation and the acquisition of tolerance in this autoimmune disease