A review of the dodo and its ecosystem: insights from a vertebrate concentration Lagerstätte in Mauritius

The dodo Raphus cucullatus Linnaeus, an extinct and flightless, giant pigeon endemic to Mauritius, has fascinated people since its discovery, yet has remained surprisingly poorly known. Until the mid-19th century, almost all that was known about the dodo was based on illustrations and written accounts by 17th century mariners, often of questionable accuracy. Furthermore, only a few fragmentary remains of dodos collected prior to the bird's extinction exist. Our understanding of the dodo's anatomy was substantially enhanced by the discovery in 1865 of subfossil bones in a marsh called the Mare aux Songes, situated in southeastern Mauritius. However, no contextual information was recorded during early excavation efforts, and the majority of excavated material comprised larger dodo bones, almost all of which were unassociated. Here we present a modern interdisciplinary analysis of the Mare aux Songes, a 4200-year-old multitaxic vertebrate concentration Lagerstätte. Our analysis of the deposits at this site provides the first detailed overview of the ecosystem inhabited by the dodo. The interplay of climatic and geological conditions led to the exceptional preservation of the animal and associated plant remains at the Mare aux Songes and provides a window into the past ecosystem of Mauritius. This interdisciplinary research approach provides an ecological framework for the dodo, complementing insights on its anatomy derived from the only associated dodo skeletons known, both of which were collected by Etienne Thirioux and are the primary subject of this memoir.publishedVersio

Crop Updates 2009 - Cereals

This session covers twenty seven papers from different authors: PLENARY 1. Building soil carbon for productivity and implications for carbon accounting, Jeff Baldock, CSIRO Land and Water, Adelaide, SA 2. Fact or Fiction: Who is telling the truth and how to tell the difference, Doug Edmeades, agKnowledge Ltd, Hamilton 3. Four decades of crop sequence trials in Western Australia, Mark Seymour,Department of Agriculture and Food BREAK CROPS 4. 2008 Break Crops survey Report, Paul Carmody,Development Officer, Department of Agriculture and Food 5. Attitudes of Western Australian wheatbelt growers to ‘Break Crops’, Paul Carmody and Ian Pritchard, Development Officers, Department of Agriculture and Food 6. The value of organic nitrogen from lupins, Alan Meldrum, Pulse Australia 7.The area of break crops on farm: What farmers are doing compared to estimates based on maximising profit, Michael Robertson and Roger Lawes,CSIRO Floreat, Rob Sands,FARMANCO Farm Consultants, Peter White,Department of Agriculture and Food, Western Australia, Felicity Byrne and Andrew Bathgate,Farming Systems Analysis CROP SPECIFIC Breeding 8. Identification of WALAB2014 as a potential albus lupin variety for northern agricultural region of Western Australia, Kedar Adhikari, Department of Agriculture and Food 9. Enhancement of black spot resistance in field pea, Kedar Adhikari, Tanveer Khan, Stuart Morgan and Alan Harris, Department of Agriculture and Food 10. Desi chickpea breeding: Evaluation of advanced line, Khan, TN1, Harris, A1, Gaur, P2, Siddique, KHM3, Clarke, H4, Turner, NC4, MacLeod, W1, Morgan, S1 1Department of Agriculture and Food, Western Australia, 2International Crop Research Institute for the Semi Arid Tropics (ICRISAT), 3The University of Western Australia, 4Centre for Legumes in Mediterranean Agriculture 11. Pulse Breeding Australia-Australian Field Pea Improvement Program (AFPIP), Ian Pritchard1, Chris Veitch1, Stuart Morgan1, Alan Harris1 and Tony Leonforte 2 1 Department of Agriculture and Food, Western Australia, 2 Department off Primary Industries, Victoria Disease 12. Interaction between wheat varieties and fungicides to control stripe rust for grain and quality, Kith Jayasena, Geoff Thomas, Rob Loughman, Kazue Tanaka and Bill MacLeod, Department of Agriculture and Food 13. Findings of canola disease survey 2008 and its implications for better disease management in 2009, Ravjit Khangura, WJ MacLeod, P White, P Carmody and M Amjad, Department of Agriculture and Food 14. Combating wheat leaf diseases using genome sequencing and functional genomics, Richard Oliver, Australian Centre for Necrotrophic Fungal Pathogens, Murdoch University 15. Distribution and survival of wheat curl mite (Aceria tosichella), vector of Wheat Streak Mosaic Virus, in the WA grainbelt during 2008, Dusty Severtson, Peter Mangano, John Botha and Brenda Coutts, Department of Agriculture and Food 16. Partial resistance to Stagonspora (Septoria) Partial resistance to Stagonospora (Septoria) nodorum blotch and response to fungicide in a severe epidemic scenario, Manisha Shankar1, Richard Oliver2, Kasia Rybak2and Rob Loughman1 1Department of Agriculture and Food, Western Australia, 2Australian Centre for Necrotrophic Fungal Pathogens, Murdoch University, Western Australia 17. Black pod syndrome in lupins can be reduced by regular insecticide sprays, Peter White and Michael Baker,Department of Agriculture and Food Variety performance 18. Incorporating new herbicide tolerant juncea canola into low rainfall cropping systems in Western Australia, Mohammad Amjad, Department of Agriculture and Food 19. Varietal differences in germ end staining of barley, Andrea Hills,Department of Agriculture and Food 20. Wheat variety performance in the Central Agricultural Region in 2008, Shahajahan Miyan, Department of Agriculture and Food 21. Barley variety identification using DNA fingerprinting, Peter Portmann, Agriconnect, Perth WA Dr Nicole Rice, Southern Cross University, Lismore NSW Prof Robert Henry, Southern Cross University, Lismore NSW 22. Forecast disease resistance profile for the Western Australian barley crop over the next three years, Jeff J. Russell, Department of Agriculture and Food 23. Malting barley varieties differ in their flowering date and their response to changes in sowing date, BH Paynter and Jeff J. Russell,Department of Agriculture and Food 24. Market development for new barley varieties, Linda Price,Barley Australia 25. Response of wheat varieties to sowing time at Mt Barker, Katanning and Newdegate in 2008, Brenda Shackley and Vicki Scanlan,Department of Agriculture and Food 26. Flowering dates of wheat varieties in 2008 at three locations in Western Australia, Darshan Sharma, Brenda Shackley and Christine Zaicou-Kunesch, Department of Agriculture and Food 27. Agronomic responses of new wheat varieties in the norther agricultural region in 2008, Christine Zaicou-Kunesch, Department of Agriculture and Foo

Upregulation of Glycolytic Enzymes, Mitochondrial Dysfunction and Increased Cytotoxicity in Glial Cells Treated with Alzheimer’s Disease Plasma

<div><p>Alzheimer’s disease (AD) is a neurodegenerative disorder associated with increased oxidative stress and neuroinflammation. Markers of increased protein, lipid and nucleic acid oxidation and reduced activities of antioxidant enzymes have been reported in AD plasma. Amyloid plaques in the AD brain elicit a range of reactive inflammatory responses including complement activation and acute phase reactions, which may also be reflected in plasma. Previous studies have shown that human AD plasma may be cytotoxic to cultured cells. We investigated the effect of pooled plasma (n = 20 each) from healthy controls, individuals with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) on cultured microglial cells. AD plasma and was found to significantly decrease cell viability and increase glycolytic flux in microglia compared to plasma from healthy controls. This effect was prevented by the heat inactivation of complement. Proteomic methods and isobaric tags (iTRAQ) found the expression level of complement and other acute phase proteins to be altered in MCI and AD plasma and an upregulation of key enzymes involved in the glycolysis pathway in cells exposed to AD plasma. Altered expression levels of acute phase reactants in AD plasma may alter the energy metabolism of glia.</p></div

Cell viability of microglial cells after 48 hour incubation with human complement components (C1q, C1 inhibitor, C4, C5 and C9), both individually and in combination with each other; and a human complement standard containing complement components C1q, C2, C3, C4, C5, C6, C7, C8, C9 and factor B.

<p>Cell viability was determined by MTT assay of cell proliferation and intracellular NAD levels (for complement standard samples). Replicates included n = 6 for cell proliferation measurements and, n = 3 for NAD concentrations.</p><p>* p ≤ 0.05 vs Control,</p><p>** p ≤ 0.01 vs Control</p><p>Cell viability of microglial cells after 48 hour incubation with human complement components (C1q, C1 inhibitor, C4, C5 and C9), both individually and in combination with each other; and a human complement standard containing complement components C1q, C2, C3, C4, C5, C6, C7, C8, C9 and factor B.</p

Chromatogram of fractionation using Hu6 column and 1D SDS/PAGE of these fractions.

<p>Low abundant proteins are eluted first (first peak on chromatogram) and high abundant proteins are eluted after (second peak). Gel shows significant depletion of high abundant proteins in the low abundant fractions. Loading was 50 μg/lane. First and last lanes contained molecular weight markers. Each fraction was run in duplicate.</p

Summary of previous studies showing changes in acute phase proteins in Alzheimer’s disease.

<p>Summary of previous studies showing changes in acute phase proteins in Alzheimer’s disease.</p

Effects of human plasma on cellular bioenergetics in a microglial cell line.

<p><b>(A)</b> Effect of human plasma on oxygen consumption rates (OCR) in a microglial cell line for 48 hours. *p<0.05 compared to non-treated cells (control); (n = 4 for each treatment group). <b>(B)</b> Effect of human plasma on extracellular acidification rates (ECAR) in a microglial cell line for 48 hours. *p<0.05 compared to non-treated cells (control); (n = 4 for each treatment group). <b>(C)</b> Effect of human plasma on the basal control ratio (BCR) in a microglial cell line for 48 hours. *p<0.05 compared to non-treated cells (control); (n = 4 for each treatment group). <b>(D)</b> Effect of human plasma on the uncoupling ratio (UCR) in a microglial cell line for 48 hours. *p<0.05 compared to non-treated cells (control); (n = 4 for each treatment group).</p

Fractionation of non heat inactivated control plasma into protein and metabolite fractions and the effects of plasma treatment on cell proliferation.

<p>Panel A: Fractionation of non heat inactivated control plasma into protein and metabolite fractions using PD10 column Panel B: Effect of these fractions on cell proliferation. Three replicates were performed. Plasma used for the measurements were obtained from the pooled plasma of 20 patients from each of the three groups (Control, MCI and AD). * p ≤ 0.01 vs Control, ** p ≤ 0.001 vs Control. Panel C: Images of microglia after 48 hour incubation with non heat inactivated 20% control plasma (left) and 20% AD plasma (right), showing increased toxicity and reduced cell proliferation in the AD plasma treated cells.</p

Dysregulated proteins in glial cells treated with human control, MCI and AD plasma compared to FBS (non human serum control) following iTRAQ analysis.

<p>Cells were incubated with plasma in two 24 well plates, 3 wells for each of the plasma types were pooled from each plate to obtain two biological replicates for the 8-plex iTRAQ experiment. iTRAQ reporter ratios and p-values for altered proteins are shown for both replicates. Proteins found to be dysregulated in MCI and AD treated cells are shown in table. Proteins dysregulated only in cells treated with AD plasma are highlighted in bold. Full list of identified proteins can be found in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116092#pone.0116092.s004" target="_blank">S2 Table</a>.</p><p>* p ≤ 0.05 vs Fetal Bovine Serum Control</p><p>Dysregulated proteins in glial cells treated with human control, MCI and AD plasma compared to FBS (non human serum control) following iTRAQ analysis.</p

Cell viability as measured by MTT absorbance (abs) at 570nm, LDH release and intracellular NAD levels of microglial cells after 48 hour incubation in pooled, non heat inactivated and heat inactivated MCI and AD plasma.

<p>* p ≤ 0.05 vs Control,</p><p>** p ≤ 0.01 vs Control</p><p>Cell viability was determined by measurement of cell proliferation, intracellular NAD levels and LDH activity in cell culture media and cell lysate homogenates. n = 9 (nine replicates) for cell proliferation measurements, n = 6 (six replicates) for NAD concentration and LDH activity. Plasma used for the measurements were obtained from the pooled plasma of 20 patients from each of the three groups (Control, MCI and AD) investigated. Three concentration levels of plasma were tested: 5%, 10% and 20% plasma as a percentage of total media volume.</p><p>Cell viability as measured by MTT absorbance (abs) at 570nm, LDH release and intracellular NAD levels of microglial cells after 48 hour incubation in pooled, non heat inactivated and heat inactivated MCI and AD plasma.</p