Anatomy and physiology of organs involved in food ingestion in the lobster, Homarus gammarus L.

The dissertation describes the gross neuromuscular anatomy of the labrum (upper lip) and oesophagus of the lobster Homarus gammarue as a pre-requisite for studies on the mechanisms and control of food ingestion. Sense organs of the area are also described. Of particular interest are two paired sensors (the anterior and posterior oesophageal sensors) which are bilaterally situated at the oesophageal/cardiac sac valve. These are similar to contact chemoreceptors previously described in insects, and are classified as such on morphological grounds and with indirect electrophysiological evidence. The labrum undergoes rhythmical retraction/protraction movements during feeding and can be shown to participate in both the mandibular rhythm and oesophageal peristalsis. Its role in feeding is discussed. Subsequently, small labral protractions are used as an indication of the duration and frequency of oesophageal peristalsis. Oesophageal peristalsis is effected by the co-ordinated contraction of the oesophageal musculature. This is controlled by rhythmical bursting neuronal activity which can be recorded from the nerve trunks in the area, A characteristic burst recorded from the superior oesophageal nerve is used as an indication of oesophageal dilatation during peristalsis for studies on the feedback effects of the oesophageal sensors. Electrical and chemical stimulation of the posterior oesophageal sensors can initiate and increase the frequency of oesophageal peristalsis, while stimulation of the anterior oesophageal sensors can slow and terminate oesophageal peristalsis. The results are discussed and, in conclusion, a model of the role of the oesophageal sensors in feeding is presented

Stress Preconditioning of Spreading Depression in the Locust CNS

Cortical spreading depression (CSD) is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG) of locusts. Using K+ -sensitive microelectrodes, we measured extracellular K+ concentration ([K+]o) in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K+ in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na+/K+ ATPase impairment, K+ injection) was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45°C) and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K+ that was not linked to changes in ATP levels or total Na+/K+ ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin

Thermal preconditioning and heat-shock protein 72 preserve synaptic transmission during thermal stress

As with other tissues, exposing the mammalian CNS to nonlethal heat stress (i.e., thermal preconditioning) increases levels of heat-shock proteins (Hsps) such as Hsp70 and enhances the viability of neurons under subsequent stress. Using a medullary slice preparation from a neonatal mouse, including the site of the neural network that generates respiratory rhythm (the pre-Bö tzinger complex), we show that thermal preconditioning has an additional fundamental effect, protection of synaptic function. Relative to 30°C baseline, initial thermal stress (40°C) greatly increased the frequency of synaptic currents recorded without pharmacological manipulation by ϳ17-fold ( p Ͻ 0.01) and of miniature postsynaptic currents (mPSCs) elicited by GABA (20-fold) glutamate (10-fold), and glycine (36-fold). Thermal preconditioning (15 min at 40°C) eliminated the increase in frequency of overall synaptic transmission during acute thermal stress and greatly attenuated the frequency increases of GABAergic, glutamatergic, and glycinergic mPSCs (for each, p Ͻ 0.05). Moreover, without thermal preconditioning, incubation of slices in solution containing inducible Hsp70 (Hsp72) mimicked the effect of thermal preconditioning on the stressinduced release of neurotransmitter. That preconditioning and exogenous Hsp72 can affect and preserve normal physiological function has important therapeutic implications. Key words: hyperthermia; heat shock; synaptic transmission; miniature postsynaptic current; GABA; glutamate; glycine The discovery that preconditioning with mild stress protects neural tissue from severe stresses such as hyperthermia or hypoxia has yielded new ideas on how to mitigate brain damage by ischemia and strok

Cerium dioxide nanoparticles exacerbate house dust mite induced type II airway inflammation

Background Nanomaterial inhalation represents a potential hazard for respiratory conditions such as asthma. Cerium dioxide nanoparticles (CeO2NPs) have the ability to modify disease outcome but have not been investigated for their effect on models of asthma and inflammatory lung disease. The aim of this study was to examine the impact of CeO2NPs in a house dust mite (HDM) induced murine model of asthma. Results Repeated intranasal instillation of CeO2NPs in the presence of HDM caused the induction of a type II inflammatory response, characterised by increased bronchoalveolar lavage eosinophils, mast cells, total plasma IgE and goblet cell metaplasia. This was accompanied by increases in IL-4, CCL11 and MCPT1 gene expression together with increases in the mucin and inflammatory regulators CLCA1 and SLC26A4. CLCA1 and SLC26A4 were also induced by CeO2NPs + HDM co-exposure in air liquid interface cultures of human primary bronchial epithelial cells. HDM induced airway hyperresponsiveness and airway remodelling in mice were not altered with CeO2NPs co-exposure. Repeated HMD instillations followed by a single exposure to CeO2NPs failed to produce changes in type II inflammatory endpoints but did result in alterations in the neutrophil marker CD177. Treatment of mice with CeO2NPs in the absence of HDM did not have any significant effects. RNA-SEQ was used to explore early effects 24 h after single treatment exposures. Changes in SAA3 expression paralleled increased neutrophil BAL levels, while no changes in eosinophil or lymphocyte levels were observed. HDM resulted in a strong induction of type I interferon and IRF3 dependent gene expression, which was inhibited with CeO2NPs co-exposure. Changes in the expression of genes including CCL20, CXCL10, NLRC5, IRF7 and CLEC10A suggest regulation of dendritic cells, macrophage functionality and IRF3 modulation as key early events in how CeO2NPs may guide pulmonary responses to HDM towards type II inflammation. Conclusions CeO2NPs were observed to modulate the murine pulmonary response to house dust mite allergen exposure towards a type II inflammatory environment. As this type of response is present within asthmatic endotypes this finding may have implications for how occupational or incidental exposure to CeO2NPs should be considered for those susceptible to disease

Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization

Background Within 2 min of severe ischemia, spreading depolarization (SD) propagates like a wave through compromised gray matter of the higher brain. More SDs arise over hours in adjacent tissue, expanding the neuronal damage. This period represents a therapeutic window to inhibit SD and so reduce impending tissue injury. Yet most neuroscientists assume that the course of early brain injury can be explained by glutamate excitotoxicity, the concept that immediate glutamate release promotes early and downstream brain injury. There are many problems with glutamate release being the unseen culprit, the most practical being that the concept has yielded zero therapeutics over the past 30 years. But the basic science is also flawed, arising from dubious foundational observations beginning in the 1950s Methods Literature pertaining to excitotoxicity and to SD over the past 60 years is critiqued. Results Excitotoxicity theory centers on the immediate and excessive release of glutamate with resulting neuronal hyperexcitation. This instigates poststroke cascades with subsequent secondary neuronal injury. By contrast, SD theory argues that although SD evokes some brief glutamate release, acute neuronal damage and the subsequent cascade of injury to neurons are elicited by the metabolic stress of SD, not by excessive glutamate release. The challenge we present here is to find new clinical targets based on more informed basic science. This is motivated by the continuing failure by neuroscientists and by industry to develop drugs that can reduce brain injury following ischemic stroke, traumatic brain injury, or sudden cardiac arrest. One important step is to recognize that SD plays a central role in promoting early neuronal damage. We argue that uncovering the molecular biology of SD initiation and propagation is essential because ischemic neurons are usually not acutely injured unless SD propagates through them. The role of glutamate excitotoxicity theory and how it has shaped SD research is then addressed, followed by a critique of its fading relevance to the study of brain injury. Conclusions Spreading depolarizations better account for the acute neuronal injury arising from brain ischemia than does the early and excessive release of glutamate

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

Background: When a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD. Methods: In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na+/K+ pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate. Results: We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na+/K+ ATPase elicits SD. Elevated K+ or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling. Conclusions: Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory. © 2022, The Author(s)

Dynamic Crystallization Pathways of Polymorphic Pharmaceuticals Revealed in Segmented Flow with Inline Powder X-ray Diffraction

Understanding the transitions between polymorphs is essential in the development of strategies for manufacturing and maximizing the efficiency of pharmaceuticals. However, this can be extremely challenging: crystallization can be influenced by subtle changes in environment, such as temperature and mixing intensity or even imperfections in the crystallizer walls. Here, we highlight the importance of in situ measurements in understanding crystallization mechanisms, where a segmented flow crystallizer was used to study the crystallization of the pharmaceuticals urea: barbituric acid (UBA) and carbamazepine (CBZ). The reactor provides highly reproducible reaction conditions, while in situ synchrotron powder X-ray diffraction (PXRD) enables us to monitor the evolution of this system. UBA has two polymorphs of almost equivalent free-energy and so is typically obtained as a polymorphic mixture. In situ PXRD analysis uncovered a progression of polymorphs from UBA III to the thermodynamic polymorph UBA I, where different positions along the length of the tubular flow crystallizer correspond to different reaction times. Addition of UBA I seed crystals modified this pathway such that only UBA I was observed throughout, while transformation from UBA III into UBA I still occurred in the presence of UBA III seeds. Information regarding the mixing-dependent kinetics of the CBZ form II to III transformation was also uncovered in a series of seeded and unseeded flow crystallization runs, despite atypical habit expression. These results illustrate the importance of coupling controlled reaction environments with in situ XRD to study the phase relationships in polymorphic materials

Glial Hsp70 Protects K+ Homeostasis in the Drosophila Brain during Repetitive Anoxic Depolarization

Neural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat shock pre-conditioned flies were resistant to ouabain treatment. To control the timing of repeated loss of ion homeostasis we subjected flies to repetitive anoxia while recording extracellular [K+] in the brain. We show that targeted expression of the chaperone protein Hsp70 in glial cells delays a permanent loss of ion homeostasis associated with repetitive anoxic stress and suggest that this is a useful model for investigating molecular mechanisms of neuroprotection

Crop Updates 2007 - Lupins, Pulses and Oilseeds

This session covers forty eight papers from different authors: 2006 REGIONAL ROUNDUP 1. South east agricultural region, Mark Seymour1 and Jacinta Falconer2, 1Department of Agriculture and Food, 2Cooperative Bulk Handling Group 2. Central agricultural region, Ian Pritchard, Department of Agriculture and Food 3. Great Southern and Lakes region, Rodger Beermier, Department of Agriculture and Food 4. Northern agricultural region, Wayne Parker and Martin Harries, Department of Agriculture and Food LUPINS 5. Development of anthracnose resistant and early flowering albus lupins (Lupinus albus L) in Western Australia, Kedar Adhikari and Geoff Thomas, Department of Agriculture and Food 6. New lupins adapted to the south coast, Peter White, Bevan Buirchell and Mike Baker, Department of Agriculture and Food 7. Lupin species and row spacing interactions by environment, Martin Harries, Peter White, Bob French, Jo Walker, Mike Baker and Laurie Maiolo, Department of Agriculture and Food 8. The interaction of lupin species row spacing and soil type, Martin Harries, Bob French, Laurie Maiolo and Jo Walker, Department of Agriculture and Food 9. The effects of row spacing and crop density on competitiveness of lupins with wild radish, Bob French and Laurie Maiolo, Department of Agriculture and Food 10. The effect of time of sowing and radish weed density on lupin yield, Martin Harries and Jo Walker, Department of Agriculture and Food 11. Interaction of time of sowing and weed management in lupins, Martin Harries and Jo Walker, Department of Agriculture and Food 12. Delayed sowing as a strategy to manage annual ryegrass, Bob French and Laurie Maiolo, Department of Agriculture and Food 13. Is delayed sowing a good strategy for weed management in lupins? Bob French, Department of Agriculture and Food 14. Lupins aren’t lupins when it comes to simazine, Peter White and Leigh Smith, Department of Agriculture and Food 15. Seed yield and anthracnose resistance of Tanjil mutants tolerant to metribuzin, Ping Si1, Bevan Buirchell1,2 and Mark Sweetingham1,2, 1Centre for Legumes in Mediterranean Agriculture, Australia; 2Department of Agriculture and Food 16. The effect of herbicides on nodulation in lupins, Lorne Mills1, Harmohinder Dhammu2 and Beng Tan1, 1Curtin University of Technology and 2Department of Agriculture and Food 17. Effect of fertiliser placements and watering regimes on lupin growth and seed yield in the central grain belt of Western Australia, Qifu Ma1, Zed Rengel1, Bill Bowden2, Ross Brennan2, Reg Lunt2 and Tim Hilder2, 1Soil Science & Plant Nutrition UWA, 2Department of Agriculture and Food 18. Development of a forecasting model for Bean Yellow Mosaic Virus in lupins, T. Maling1,2, A. Diggle1, D. Thackray1,2, R.A.C. Jones2, and K.H.M. Siddique1, 1Centre for Legumes in Mediterranean Agriculture, The University of Western Australia; 2Department of Agriculture and Food 19. Manufacturing of lupin tempe,Vijay Jayasena1,4, Leonardus Kardono2,4, Ken Quail3,4 and Ranil Coorey1,4, 1Curtin University of Technology, Perth, Australia, 2Indonesian Institute of Sciences (LIPI), Indonesia, 3BRI Australia Ltd, Sydney, Australia, 4Grain Foods CRC, Sydney, Australia 20. The impact of lupin based ingredients in ice-cream, Hannah Williams, Lee Sheer Yap and Vijay Jayasena, Curtin University of Technology, Perth WA 21. The acceptability of muffins substituted with varying concentrations of lupin flour, Anthony James, Don Elani Jayawardena and Vijay Jayasena, Curtin University of Technology, PerthWA PULSES 22. Chickpea variety evaluation, Kerry Regan1, Rod Hunter1, Tanveer Khan1,2and Jenny Garlinge1, 1Department of Agriculture and Food, 2CLIMA, The University of Western Australia 23. Advanced breeding trials of desi chickpea, Khan, T.N.1, Siddique, K.H.M.3, Clarke, H.2, Turner, N.C.2, MacLeod, W.1, Morgan, S.1, and Harris, A.1, 1Department of Agriculture and Food, 2Centre for Legumes in Mediterranean Agriculture, 3TheUniversity of Western Australia 24. Ascochyta resistance in chickpea lines in Crop Variety Testing (CVT) of 2006, Tanveer Khan1 2, Bill MacLeod1, Alan Harris1, Stuart Morgan1and Kerry Regan1, 1Department of Agriculture and Food, 2CLIMA, The University of Western Australia 25. Yield evaluation of ascochyta blight resistant Kabuli chickpeas, Kerry Regan1and Kadambot Siddique2, 1Department of Agriculture and Food, 2Institute of Agriculture, The University of Western Australia 26. Pulse WA Chickpea Industry Survey 2006, Mark Seymour1, Ian Pritchard1, Wayne Parker1and Alan Meldrum2, 1Department of Agriculture and Food, 2Pulse Australia 27. Genes from the wild as a valuable genetic resource for chickpea improvement, Heather Clarke1, Helen Bowers1and Kadambot Siddique2, 1Centre for Legumes in Mediterranean Agriculture, 2Institute of Agriculture, The University of Western Australia 28. International screening of chickpea for resistance to Botrytis grey mould, B. MacLeod1, Dr T. Khan1, Prof. K.H.M. Siddique2and Dr A. Bakr3, 1Department of Agriculture and Food, 2The University of Western Australia, 3Bangladesh Agricultural Research Institute 29. Balance® in chickpea is safest applied post sowing to a level seed bed, Wayne Parker, Department of Agriculture and Food, 30. Demonstrations of Genesis 510 chickpea, Wayne Parker, Department of Agriculture and Food 31. Field pea 2006, Ian Pritchard, Department of Agriculture and Food 32. Field pea variety evaluation, Kerry Regan1, Rod Hunter1, Tanveer Khan1,2 and Jenny Garlinge1, 1Department of Agriculture and Food, 2CLIMA, The University of Western Australia 33. Breeding highlights of the Australian Field Pea Improvement Program (AFPIP),Kerry Regan1, Tanveer Khan1,2, Phillip Chambers1, Chris Veitch1, Stuart Morgan1 , Alan Harris1and Tony Leonforte3, 1Department of Agriculture and Food, 2CLIMA, The University of Western Australia, 3Department of Primary Industries, Victoria 34. Field pea germplasm enhancement for black spot resistance, Tanveer Khan, Kerry Regan, Stuart Morgan, Alan Harris and Phillip Chambers, Department of Agriculture and Food 35. Validation of Blackspot spore release model and testing moderately resistant field pea line, Mark Seymour, Ian Pritchard, Rodger Beermier, Pam Burgess and Leanne Young, Department of Agriculture and Food 36. Yield losses from sowing field pea seed infected with Pea Seed-borne Mosaic Virus, Brenda Coutts, Donna O’Keefe, Rhonda Pearce, Monica Kehoe and Roger Jones, Department of Agriculture and Food 37. Faba bean in 2006, Mark Seymour, Department of Agriculture and Food 38. Germplasm evaluation – faba bean, Mark Seymour1, Terri Jasper1, Ian Pritchard1, Mike Baker1 and Tim Pope1,2, 1Department of Agriculture and Food, , 2CLIMA, The University of Western Australia 39. Breeding highlights of the Coordinated Improvement Program for Australian Lentils (CIPAL), Kerry Regan1, Chris Veitch1, Phillip Chambers1 and Michael Materne2, 1Department of Agriculture and Food, 2Department of Primary Industries, Victoria 40. Screening pulse lentil germplasm for tolerance to alternate herbicides, Ping Si1, Mike Walsh2 and Mark Sweetingham1,3, 1Centre for Legumes in Mediterranean Agriculture, 2West Australian Herbicide Resistance Initiative, 3Department of Agriculture and Food 41. Genomic synteny in legumes: Application to crop breeding, Phan, H.T.T.1, Ellwood, S.R.1, Hane, J.1, Williams, A.1, Ford, R.2, Thomas, S.3 and Oliver R1, 1Australian Centre of Necrotrophic Plant Pathogens, Murdoch University, 2BioMarka, University of Melbourne, 3NSW Department of Primary Industries 42. Tolerance of lupins, chickpeas and canola to Balanceâ(Isoxaflutole) and Galleryâ (Isoxaben), Leigh Smith and Peter White, Department of Agriculture and Food CANOLA AND OILSEEDS 43. The performance of TT Canola varieties in the National Variety Test (NVT),WA,2006,Katie Robinson, Research Agronomist, Agritech Crop Research 44. Evaluation of Brassica crops for biodiesel in Western Australia, Mohammad Amjad, Graham Walton, Pat Fels and Andy Sutherland, Department of Agriculture and Food 45. Production risk of canola in different rainfall zones in Western Australia, Imma Farré1, Michael Robertson2 and Senthold Asseng3, 1Department of Agriculture and Food, 2CSIRO Sustainable Ecosystems, 3CSIRO Plant Industry 46. Future directions of blackleg management – dynamics of blackleg susceptibility in canola varieties, Ravjit Khangura, Moin Salam and Bill MacLeod, Department of Agriculture and Food 47. Appendix 1: Contributors 48. Appendix 2: List of common acronym