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Sökning: WFRF:(Deck R.)

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  • Davies, N., et al. (författare)
  • Report of the 14th Genomic Standards Consortium Meeting, Oxford, UK, September 17-21, 2012
  • 2014
  • Ingår i: Standards in Genomic Sciences. - : Springer Science and Business Media LLC. - 1944-3277. ; 9:3, s. 1236-1250
  • Tidskriftsartikel (refereegranskat)abstract
    • This report summarizes the proceedings of the 14th workshop of the Genomic Standards Consortium (GSC) held at the University of Oxford in September 2012. The primary goal of the workshop was to work towards the launch of the Genomic Observatories (GOs) Network under the GSC. For the first time, it brought together potential GOs sites, GSC members, and a range of interested partner organizations. It thus represented the first meeting of the GOs Network (GOs1). Key outcomes include the formation of a core group of “champions” ready to take the GOs Network forward, as well as the formation of working groups. The workshop also served as the first meeting of a wide range of participants in the Ocean Sampling Day (OSD) initiative, a first GOs action. Three projects with complementary interests – COST Action ES1103, MG4U and Micro B3 – organized joint sessions at the workshop. A two-day GSC Hackathon followed the main three days of meetings.
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  • Davies, Neil, et al. (författare)
  • The founding charter of the Genomic Observatories Network
  • 2014
  • Ingår i: GigaScience. - 2047-217X. ; 3:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract The co-authors of this paper hereby state their intention to work together to launch the Genomic Observatories Network (GOs Network) for which this document will serve as its Founding Charter. We define a Genomic Observatory as an ecosystem and/or site subject to long-term scientific research, including (but not limited to) the sustained study of genomic biodiversity from single-celled microbes to multicellular organisms.An international group of 64 scientists first published the call for a global network of Genomic Observatories in January 2012. The vision for such a network was expanded in a subsequent paper and developed over a series of meetings in Bremen (Germany), Shenzhen (China), Moorea (French Polynesia), Oxford (UK), Pacific Grove (California, USA), Washington (DC, USA), and London (UK). While this community-building process continues, here we express our mutual intent to establish the GOs Network formally, and to describe our shared vision for its future. The views expressed here are ours alone as individual scientists, and do not necessarily represent those of the institutions with which we are affiliated.
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5.
  • Deck, C., et al. (författare)
  • Protection capability of bicycle helmets under oblique impact assessed with two separate brain FE models
  • 2017
  • Ingår i: Conference proceedings International Research Council on the Biomechanics of Injury, IRCOBI. - : International Research Council on the Biomechanics of Injury. ; , s. 190-200
  • Konferensbidrag (refereegranskat)abstract
    • The present study proposes a bicycle helmet evaluation under oblique impact based on a coupled experimental versus numerical test method using two separate brain FE models. For each of the 17 helmet types three oblique impacts have been conducted and the 6D headform acceleration curves have been considered as the initial conditions of the brain injury risk assessment based on the FE simulation. The study gives a new insight into helmet protection capability under oblique loading and shows that adequate protection is offered by most of the helmets when impacts leading to rotation around X and Y are concerned. However when impact leads to rotation around Z axis the protection is critical for nearly all helmets. The study considers two separate brain FE models for the assessment of brain injury risk and thus permits a comparative analysis of brain FE modeling. When impact induces rotation around X and Y axis the computed results are comparable. However when rotation around Z axis are concerned significant differences are observed which demonstrate that further efforts are needed in the domain of model based brain injury criteria harmonization. 
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6.
  • Deck, M, et al. (författare)
  • Physiology of PNS axons relies on glycolytic metabolism in myelinating Schwann cells
  • 2022
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 17:10, s. e0272097-
  • Tidskriftsartikel (refereegranskat)abstract
    • While lactate shuttle theory states that glial cells metabolize glucose into lactate to shuttle it to neurons, how glial cells support axonal metabolism and function remains unclear. Lactate production is a common occurrence following anaerobic glycolysis in muscles. However, several other cell types, including some stem cells, activated macrophages and tumor cells, can produce lactate in presence of oxygen and cellular respiration, using Pyruvate Kinase 2 (PKM2) to divert pyruvate to lactate dehydrogenase. We show here that PKM2 is also upregulated in myelinating Schwann cells (mSC) of mature mouse sciatic nerve versus postnatal immature nerve. Deletion of this isoform in PLP-expressing cells in mice leads to a deficit of lactate in mSC and in peripheral nerves. While the structure of myelin sheath was preserved, mutant mice developed a peripheral neuropathy. Peripheral nerve axons of mutant mice failed to maintain lactate homeostasis upon activity, resulting in an impaired production of mitochondrial ATP. Action potential propagation was not altered but axonal mitochondria transport was slowed down, muscle axon terminals retracted and motor neurons displayed cellular stress. Additional reduction of lactate availability through dichloroacetate treatment, which diverts pyruvate to mitochondrial oxidative phosphorylation, further aggravated motor dysfunction in mutant mice. Thus, lactate production through PKM2 enzyme and aerobic glycolysis is essential in mSC for the long-term maintenance of peripheral nerve axon physiology and function.
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  • Hollerhage, M., et al. (författare)
  • Piericidin A Aggravates Tau Pathology in P301S Transgenic Mice
  • 2014
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 9:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The P301S mutation in exon 10 of the tau gene causes a hereditary tauopathy. While mitochondrial complex I inhibition has been linked to sporadic tauopathies. Piericidin A is a prototypical member of the group of the piericidins, a class of biologically active natural complex I inhibitors, isolated from streptomyces spp. with global distribution in marine and agricultural habitats. The aim of this study was to determine whether there is a pathogenic interaction of the environmental toxin piericidin A and the P301S mutation. Methods: Transgenic mice expressing human tau with the P301S-mutation (P301S(+/+)) and wild-type mice at 12 weeks of age were treated subcutaneously with vehicle (N=10 P301S(+/+), N = 7 wild-type) or piericidin A (N = 9 P301S(+/+), N = 9 wild-type mice) at a dose of 0.5 mg/kg/d for a period of 28 days via osmotic minipumps. Tau pathology was measured by stereological counts of cells immunoreative with antibodies against phosphorylated tau (AD2, AT8, AT180, and AT100) and corresponding Western blot analysis. Results: Piericidin A significantly increased the number of phospho-tau immunoreactive cells in the cerebral cortex in P301S(+/+) mice, but only to a variable and mild extent in wild-type mice. Furthermore, piericidin A led to increased levels of pathologically phosphorylated tau only in P301S(+/+) mice. While we observed no apparent cell loss in the frontal cortex, the synaptic density was reduced by piericidin A treatment in P301S(+/+) mice. Discussion: This study shows that exposure to piericidin A aggravates the course of genetically determined tau pathology, providing experimental support for the concept of gene-environment interaction in the etiology of tauopathies.
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  • Peng, Yong, et al. (författare)
  • A Study of Adult Pedestrian Head Impact Conditions and Injury Risks in Passenger Car Collisions Based on Real-World Accident Data
  • 2013
  • Ingår i: Traffic Injury Prevention. - : Informa UK Limited. - 1538-957X .- 1538-9588. ; 14:6, s. 639-646
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The aim of the current study was to study the kinematics of adult pedestrians and assess head injury risks based on real-world accidents. Methods: A total of 43 passenger car versus pedestrian accidents, in which the pedestrian's head impacted the windscreen, were selected from accident databases for simulation study. According to real-world accident investigation, accident reconstructions were conducted using multibody system (MBS) pedestrian and car models under MADYMO environment (Strasbourg University) to calculate head impact conditions in terms of head impact velocity, head position, and head orientation. Pedestrian head impact conditions from MADYMO simulation results were then used to set the initial conditions in a simulation of a head striking a windscreen using finite element (FE) approach. Results: The results showed strong correlations between vehicle impact velocity and head contact time, throw distance, and head impact velocity using a quadratic regression model. In the selected samples, the results indicated that Abbreviated Injury Scale (AIS) 2+ and AIS 3+ severe head injuries with probability of 50 percent were caused by head impact velocity at about 33 and 49km/h, respectively. Further, the predicted head linear acceleration (head injury criterion, HIC) value, resultant angular velocity, and resultant angular acceleration for 50 percent probability of AIS 2+ and AIS 3+ head injury risk were 116 g, 825, 40 rad/s, 11,368 rad/s(2) and 162 g, 1442, 55 rad/s, 18,775 rad/s(2), respectively, and the predicted value of 50 percent probability of skull fracture was 135 g. Conclusions: The present study provides new insight into pedestrian head impact conditions in terms of velocity, angle, and impact location based on a number of real-world cases. Therefore, it may perform a critical analysis for current pedestrian head standard tests.
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  • Peng, Yong, et al. (författare)
  • Development of head injury risk functions based on real-world accident reconstruction
  • 2014
  • Ingår i: International Journal of Crashworthiness. - : Informa UK Limited. - 1358-8265 .- 1754-2111. ; 19:2, s. 105-114
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective of this study is to assess head injury risks of adult pedestrians using computer reconstructions of the accidents. For this purpose, accident reconstructions were developed based on the real-world pedestrian accidents. The impact conditions, which were obtained from the previous study [Y. Peng, C. Deck, J.K. Yang, D. Otte, and R. Willinger, A study of adult pedestrian head impact conditions and injury risks in passenger car collisions based on real world accident data, Traffic Inj. Prev., doi: 10.1080/15389588.2012.733841] including head impact velocity, head position and head orientation, were defined as initial loading conditions in a simulation of the head striking to a windscreen by using a finite element (FE) Hybrid III head model. Logistic regression models were developed to study brain injury risk with respect to injury related variables: the head linear acceleration, HIC value, skull fracture correlate (SFC), resultant angular acceleration and head impact power (HIP). The results from Hybrid III head impact simulations indicated that the predicted head linear acceleration, HIC value, resultant angular acceleration and HIP for 50% probability of AIS 2+ and AIS 3+head injury risk are 116g, 825, 11368 rad/s(2), 37 kW and 162g, 1442, 18775 rad/s(2), 68 kW, respectively, and the predicted values of 50% probability of skull fracture is 135g. The knowledge from this study could be a prerequisite for developing guidelines to improve pedestrian safety.
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