Making the Case to Protect Australia's Coral Sea

The Coral Sea Conservation Zone (referred to in this report as the Coral Sea) is bounded on the west by the Great Barrier Reef Marine Park, on the east by the edge of Australia's Exclusive Economic Zone, on the north by the Torres Strait Protection Zone and on the south by the same southern latitude line as the Great Barrier Reef Marine Park. The area comprises 972,000 km2 . The Coral Sea hosts a high diversity of habitats, ecosystems and species. Only a small portion of this area has been studied, but knowledge gained to date indicates that there are important habitats, migration corridors and ecological processes that sustain unique biological communities. This review draws together the available scientific research to provide a comprehensive description of the physical and biological characteristics of the Coral Sea. The seabed of the Coral Sea is characterised by a vast plain over 4,000 m deep to the northeast, several plateaux and slopes etched by undersea canyons and separated by deep ocean trenches, and, to the south, the northern end of a chain of undersea volcanoes. Eighteen coral reef systems, many with multiple small reefs, emerge from structural high points on the plateaux or from the tops of the volcanoes. Forty-nine small islands and cays form the only terrestrial habitats. At the ocean's surface, the westwardflowing South Equatorial Current enters the Coral Sea as a series of jets between the network of islands that form the Solomon Islands, Vanuatu and New Caledonia. As this current approaches the Great Barrier Reef, it splits in two to form the Hiri Current to the north and the East Australian Current to the south. This latter current brings warm, low-nutrient water and tropical species southward as a series of eddies. Very little is known about how small-scale circulation patterns affect the Coral Sea's ecology, but slow eddies, which may retain fauna and promote the development of species that do not occur anywhere else, have been discovered over some of the plateaux. The islets and cays of the Coral Sea support a variety of life, ranging from simple food chains based on carrion and detritus to well developed thick forests of Pisonia trees. The cays provide habitat for nesting and roosting seabirds (many of which are of conservation significance) and nesting endangered green turtles. In general, highly exposed reef zones in the Coral Sea are dominated by species that are robust enough to withstand strong wave action, while more sheltered reef habitats have a greater amount of live coral cover (30–50%) and host a larger abundance of fish and invertebrates. Coral, fish and invertebrate populations show key differences from those on the Great Barrier Reef and some affinities with those on the reefs of the western Pacific and the Arafura and Timor Seas. Recent research has uncovered coralline sponges, considered 'living fossils,' in the shallow caves of Osprey Reef. Some reefs support high densities of sharks (~4.4 individuals per hectare) and other predators, and protection in existing no-take Commonwealth Reserves in the Coral Sea has led to healthy populations of otherwise exploited species. Preliminary explorations of deeper Coral Sea reef ecosystems (from 30–40 m to over 150 m) have revealed a great diversity of geological formations along with coral communities that have adapted to low light. Soft corals are an important feature of these deeper coral communities, and gorgonians (sea fans) tend to be very abundant. These mesophotic (low light) communities may act as refugia during disturbance events such as cyclones and bleaching, and may provide larvae during the recovery of these highly isolated reefs

Australia's Coral Sea: A Biophysical Profile

Details the diverse ecosystems, habitats, and species found in Australia's Coral Sea, including humpback and dwarf minke whales, green turtles, seabirds, and deep-water sharks, and the Coral Sea's advantages for large-scale conservation and research

Destruction of dimethyl ether and methyl formate by collisions with He+^+

To correctly model the abundances of interstellar complex organic molecules (iCOMS) in different environments, both formation and destruction routes should be appropriately accounted for. While several scenarios have been explored for the formation of iCOMs via grain and gas-phase processes, much less work has been devoted to understanding the relevant destruction pathways, with special reference to (dissociative) charge exchange or proton transfer reactions with abundant atomic and molecular ions such as He$^+$, H$_3^+$ and HCO$^+$. By using a combined experimental and theoretical methodology we provide new values for the rate coefficients and branching ratios (BRs) of the reactions of He$^+$ ions with two important iCOMs, namely dimethyl ether (DME) and methyl formate (MF). We also review the destruction routes of DME and MF by other two abundant ions, namely H$_3^+$ and HCO$^+$. Based on our recent laboratory measurements of cross sections and BRs for the DME/MF + He$^+$ reactions over a wide collision energy range, we extend our theoretical insights on the selectivity of the microscopic dynamics to calculate the rate coefficients $k(T)$ in the temperature range from 10 to 298 K. We implement these new and revised kinetic data in a general model of cold and warm gas, simulating environments where DME and MF have been detected. Due to stereodynamical effects present at low collision energies, the rate coefficients, BRs and temperature dependences here proposed differ substantially from those reported in KIDA and UDfA, two of the most widely used astrochemical databases. These revised rates impact the predicted abundances of DME and MF, with variations up to 40% in cold gases and physical conditions similar to those present in prestellar coresComment: accepted for publication in Astronomy and Astrophysics (manuscript no. AA/2018/34585), 10 pages, 3 figure

New V. cholerae atypical El Tor variant emerged during the 2006 epidemic outbreak in Angola

<p>Abstract</p> <p>Background</p> <p><it>V. cholerae </it>is the etiological agent of cholera, a major public health concern in most developing countries. Virulence of <it>V. cholerae </it>relies on the powerful cholera toxin, encoded by the CTX prophage. The emergence of new pathogenic variants in the recent years has been mostly associated with new CTX prophage rearrangements.</p> <p>Results</p> <p>In this retrospective study, we show that the epidemic <it>V. cholerae </it>O1 El Tor strain responsible for the 2006 outbreak in Angola is clonally and genetically different from El Tor strains circulating in the 1990s in the same area. Strains from 2006 carry ICE<it>Vch</it>Ang3 of the SXT/R391 family. This ICE is associated with a narrower multidrug resistance profile compared to the one conferred by plasmid p3iANG to strains of the 1990s. The CTX prophage carried by 2006 El Tor strains is characterized by <it>rstR^ET</it>and <it>ctxB^Cla</it>alleles organized in a RS1-RS2-Core array on chromosome I. Interestingly, the newly emerging atypical strain belongs to a clade previously known to comprise only clinical isolates from the Indian subcontinent that also contain the same ICE of the SXT/R391 family.</p> <p>Conclusions</p> <p>Our findings remark the appearance of a novel <it>V. cholerae </it>epidemic variant in Africa with a new CTXΦ arrangement previously described only in the Indian Subcontinent.</p

New <i>V. cholerae</i> atypical El Tor variant emerged during the 2006 epidemic outbreak in Angola

Background V. cholerae is the etiological agent of cholera, a major public health concern in most developing countries. Virulence of V. cholerae relies on the powerful cholera toxin, encoded by the CTX prophage. The emergence of new pathogenic variants in the recent years has been mostly associated with new CTX prophage rearrangements. Results In this retrospective study, we show that the epidemic V. cholerae O1 El Tor strain responsible for the 2006 outbreak in Angola is clonally and genetically different from El Tor strains circulating in the 1990s in the same area. Strains from 2006 carry ICEVchAng3 of the SXT/R391 family. This ICE is associated with a narrower multidrug resistance profile compared to the one conferred by plasmid p3iANG to strains of the 1990s. The CTX prophage carried by 2006 El Tor strains is characterized by rstRET and ctxBCla alleles organized in a RS1-RS2-Core array on chromosome I. Interestingly, the newly emerging atypical strain belongs to a clade previously known to comprise only clinical isolates from the Indian subcontinent that also contain the same ICE of the SXT/R391 family. Conclusions Our findings remark the appearance of a novel V. cholerae epidemic variant in Africa with a new CTXΦ arrangement previously described only in the Indian Subcontinent.</br

a cost effective approach for improving the quality of soil sealing change detection from landsat imagery

The aim of this study is to develop a cost-effective approach for soil sealing change detection integrating radiometric analysis, multi-resolution segmentation and object-based classifiers in two study areas in Italy: Campania region and Veneto region. The integrated approach uses multi-temporal satellite images and CORINE Land Cover (CLC) maps. A good overall accuracy was obtained for the soil sealing maps produced. The results show an improvement in terms of size of the minimum mapping unit and of the changed object (1,44 ha in both cases) in respect to the CLC. The approach proves to be cost-effective given the data which are provided at low or no cost and as well as the level of automation achievable

Beyond Glycemic Control in Diabetes Mellitus: Effects of Incretin-Based Therapies on Bone Metabolism

Diabetes mellitus (DM) and osteoporosis (OP) are common disorders with a significant health burden, and an increase in fracture risk has been described both in type 1 (T1DM) and in type 2 (T2DM) diabetes. The pathogenic mechanisms of impaired skeletal strength in diabetes remain to be clarified in details and they are only in part reflected by a variation in bone mineral density. In T2DM, the occurrence of low bone turnover together with a decreased osteoblast activity and compromised bone quality has been shown. Of note, some antidiabetic drugs (e.g., thiazolidinediones, insulin) may deeply affect bone metabolism. In addition, the recently introduced class of incretin-based drugs (i.e., GLP-1 receptor agonists and DPP-4 inhibitors) is expected to exert potentially beneficial effects on bone health, possibly due to a bone anabolic activity of GLP-1, that can be either direct or indirect through the involvement of thyroid C cells. Here we will review the established as well as the putative effects of incretin hormones and of incretin-based drugs on bone metabolism, both in preclinical models and in man, taking into account that such therapeutic strategy may be effective not only to achieve a good glycemic control, but also to improve bone health in diabetic patients

A Highly Stable Plastidic-Type Ferredoxin-NADP(H) Reductase in the Pathogenic Bacterium Leptospira interrogans

Leptospira interrogans is a bacterium that is capable of infecting animals and humans, and its infection causes leptospirosis with a range of symptoms from flu-like to severe illness and death. Despite being a bacteria, Leptospira interrogans contains a plastidic class ferredoxin-NADP(H) reductase (FNR) with high catalytic efficiency, at difference from the bacterial class FNRs. These flavoenzymes catalyze the electron transfer between NADP(H) and ferredoxins or flavodoxins. The inclusion of a plastidic FNR in Leptospira metabolism and in its parasitic life cycle is not currently understood. Bioinformatic analyses of the available genomic and proteins sequences showed that the presence of this enzyme in nonphotosynthetic bacteria is restricted to the Leptospira genus and that a [4Fe-4S] ferredoxin (LB107) encoded by the Leptospira genome may be the natural substrate of the enzyme. Leptospira FNR (LepFNR) displayed high diaphorase activity using artificial acceptors and functioned as a ferric reductase. LepFNR displayed cytochrome c reductase activity with the Leptospira LB107 ferredoxin with an optimum at pH 6.5. Structural stability analysis demonstrates that LepFNR is one of the most stable FNRs analyzed to date. The persistence of a native folded LepFNR structure was detected in up to 6 M urea, a condition in which the enzyme retains 38% activity. In silico analysis indicates that the high LepFNR stability might be due to robust interactions between the FAD and the NADP+ domains of the protein. The limited bacterial distribution of plastidic class FNRs and the biochemical and structural properties of LepFNR emphasize the uniqueness of this enzyme in the Leptospira metabolism. Our studies show that in L. interrogans a plastidic-type FNR exchanges electrons with a bacterial-type ferredoxin, process which has not been previously observed in nature

Structural and mutational analyses of the Leptospira interrogans virulence-related heme oxygenase provide insights into its catalytic mechanism

© 2017 Soldano et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Heme oxygenase from Leptospira interrogans is an important virulence factor. During catalysis, redox equivalents are provided to this enzyme by the plastidic-type ferredoxin-NADP+ reductase also found in L. interrogans. This process may have evolved to aid this bacterial pathogen to obtain heme-iron from their host and enable successful colonization. Herein we report the crystal structure of the heme oxygenase-heme complex at 1.73 Å resolution. The structure reveals several distinctive features related to its function. A hydrogen bonded network of structural water molecules that extends from the catalytic site to the protein surface was cleared observed. A depression on the surface appears to be the H+ network entrance from the aqueous environment to the catalytic site for O2 activation, a key step in the heme oxygenase reaction. We have performed a mutational analysis of the F157, located at the above-mentioned depression. The mutant enzymes were unable to carry out the complete degradation of heme to biliverdin since the reaction was arrested at the verdoheme stage. We also observed that the stability of the oxyferrous complex, the efficiency of heme hydroxylation and the subsequent conversion to verdoheme was adversely affected. These findings underscore a long-range communication between the outer fringes of the hydrogen-bonded network of structural waters and the heme active site during catalysis. Finally, by analyzing the crystal structures of ferredoxin-NADP+ reductase and heme oxygenase, we propose a model for the productive association of these proteins