456 research outputs found

    Mare Incognitum: A Glimpse into Future Plankton Diversity and Ecology Research

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    Chust, Guillem ... et al.-- 9 pages, 1 figure.-- Corrigendum: Mare Incognitum: A Glimpse into Future Plankton Diversity and Ecology Research, Frontiers in Marine Science 4: 122 (2017) https://doi.org/10.3389/fmars.2017.00122With global climate change altering marine ecosystems, research on plankton ecology is likely to navigate uncharted seas. Yet, a staggering wealth of new plankton observations, integrated with recent advances in marine ecosystem modeling, may shed light on marine ecosystem structure and functioning. A EuroMarine foresight workshop on the “Impact of climate change on the distribution of plankton functional and phylogenetic diversity” (PlankDiv) identified five grand challenges for future plankton diversity and macroecology research: (1) What can we learn about plankton communities from the new wealth of high-throughput “omics” data? (2) What is the link between plankton diversity and ecosystem function? (3) How can species distribution models be adapted to represent plankton biogeography? (4) How will plankton biogeography be altered due to anthropogenic climate change? and (5) Can a new unifying theory of macroecology be developed based on plankton ecology studies? In this review, we discuss potential future avenues to address these questions, and challenges that need to be tackled along the wayThis research was funded by the EuroMarine Network (http://www.euromarinenetwork.eu), through the organization of the PlankDiv EuroMarine Foresight workshop, held at the Observatoire Océanographique de Villefranche-sur-mer, Villefranche-sur-mer, France, in March 2016, and cofounded by the Basque Government (Department Deputy of Agriculture, Fishing and Food Policy). The PlankDiv workshop was also supported by the Laboratoire d'Océanographie de Villefranche-sur-mer (LOV, UPMC/CNRS), the PlankMed action of WP5 MERMEX/MISTRAL, and by the French national programme EC2CO-LEFE (FunOmics project).Peer Reviewe

    Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group.

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    Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches

    Practical Considerations for Face Recognition System Implementation: Retail Business Use Case

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    COVID-19 pandemic has proven experts’ prediction which stated that traditional retail might not survive in the coming age. During the pandemic, many longstanding retail brands barely survived, and some of them even went out of business. To survive and thrive, implementation of digital technologies to drive a more convenient shopping experience and enhance customer experience has proven to be crucial in gaining customer loyalty. One of the use cases that is gaining popularity nowadays is the implementation of Face Recognition system. The purpose of this study is to propose the practical solutions to three underlying issues of Face Recognition implementation: the simple but effective choice of framework, the discreet but effective way to arrange camera locations, and the light but robust choice of algorithm that could deliver good accuracy with minimum resources. This study used explorative descriptive method, combining authors’ direct experience with literature study. The result of this study is: proposed implementation framework, proposed camera arrangement, and proposed use of Neural Network algorithm with image augmentation. This study hopefully could give context to academics and fellow practitioners of the steps needed to implement Face Recognition to solve real world issues

    The continuum of spreading depolarizations in acute cortical lesion development: Examining Leao's legacy.

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    A modern understanding of how cerebral cortical lesions develop after acute brain injury is based on Aristides Leao's historic discoveries of spreading depression and asphyxial/anoxic depolarization. Treated as separate entities for decades, we now appreciate that these events define a continuum of spreading mass depolarizations, a concept that is central to understanding their pathologic effects. Within minutes of acute severe ischemia, the onset of persistent depolarization triggers the breakdown of ion homeostasis and development of cytotoxic edema. These persistent changes are diagnosed as diffusion restriction in magnetic resonance imaging and define the ischemic core. In delayed lesion growth, transient spreading depolarizations arise spontaneously in the ischemic penumbra and induce further persistent depolarization and excitotoxic damage, progressively expanding the ischemic core. The causal role of these waves in lesion development has been proven by real-time monitoring of electrophysiology, blood flow, and cytotoxic edema. The spreading depolarization continuum further applies to other models of acute cortical lesions, suggesting that it is a universal principle of cortical lesion development. These pathophysiologic concepts establish a working hypothesis for translation to human disease, where complex patterns of depolarizations are observed in acute brain injury and appear to mediate and signal ongoing secondary damage

    The influence of artificial weathering and treatment with FE–DBD plasma in atmospheric conditions on wettability of wood surfaces

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    The treatment of wood surfaces with plasma in atmospheric conditions is a well–known and researched processing technique. In this study, we introduce a new approach of wood surface treatment using a floating electrode dielectric barrier discharge (FE–DBD) plasma. The main principle of this kind of plasma is that wood represents an object for charge storage and the potential of the electrodes is changing according to the surround-ings in the moment of voltage supply from high voltage source. The appearance of the discharge electric fields was firstly simulated with computer software and later analysed in real conditions. Additionally, plasma was characterised by optical emission spectros-copy as elemental analysis of the discharge. The designed FE–DBD technique was ap-plied to some extent artificially weathered common beech (Fagus sylvatica L.) and Nor-way spruce (Picea abies (L.) Karst.) wood surfaces, in order to their re–activation and improvement of their wettability by commercial water-based coating. The results showed that contact angles of the droplets of applied liquids and waterborne coating decreased with weathering time, as well as after performed plasma treatment process

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

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    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.Grants to RDA from the Canadian Heart & Stroke Foundation, National Science Engineering and Research Council and the New Frontiers in Research Fund, to E.F from the National Research, Development and Innovation Office of Hungary, grant no. K134377; and the EU’s Horizon 2020 research and innovation program under grant agreement No. 739593, and to JPD from the DFG (German research Council) (DFG DR323/5-1,DFG DR 323/10-1) BMBF Bundesministerium fuer Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004)

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

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    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.This work was supported by grants from the Heart and Stroke Foundation of Canada and the National Science and Engineering Research Council of Canada to RDA, an NIH grant (NS106901) to CWS, a National Research, Development and Innovation Office of Hungary grant (K1343777) and EU Horizon 2020 research and innovation program (739953) to EF and from DFG Deutsche Forschungsgemeinschaft (German Research Council) (DFG DR 323/5-1), DFG DR 323/10-1, and BMBF Bundesministerium fuer Bildung und Forschung (EraNet Neuron EBio2, with funds from BMBF 01EW2004) to JPD

    Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

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    A rat cortical spreading depression (CSD) model was established to explore whether cerebral mitochondria injury was induced by CSD under both normoxic and hypoxic conditions and whether flunarizine had a protective effect on cerebral mitochondria. SD rats, which were divided into seven groups, received treatment as follows: no intervention (control Group I); 1 M NaCl injections (Group II); 1 M KCl injections (Group III); intraperitoneal flunarizine (3 mg/kg) 30 min before KCl injections (Group IV); 14% O2 inhalation before NaCl injections (Group V); 14% O2 inhalation followed by KCl injections (Group VI); 14% O2 inhalation and intraperitoneal flunarizine followed by KCl injections (Group VII). Following treatment, brains were removed for the analysis of mitochondria transmembrane potential (MMP) and oxidative respiratory function after recording the number, amplitude and duration of CSD. The duration of CSD was significantly longer in Group VI than that in Group III. The number and duration of CSD in Group VII was significantly lower than that in Group VI. MMP in Group VI was significantly lower than that in Group III, and MMP in Group VII was significantly higher than that in Group VI. State 4 respiration in Group VI was significantly higher than that in Group III, and state 3 respiration in Group VII was significantly higher than that in Group VI. Respiration control of rate in Group VII was also significantly higher than that in Group VI. Thus, we concluded that aggravated cerebral mitochondria injury might be attributed to CSD under hypoxic conditions. Flunarizine can alleviate such cerebral mitochondria injury under both normoxic and hypoxic conditions
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