Materials Map

Discover the materials research landscape. Find experts, partners, networks.

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The Materials Map is an open tool for improving networking and interdisciplinary exchange within materials research. It enables cross-database search for cooperation and network partners and discovering of the research landscape.

The dashboard provides detailed information about the selected scientist, e.g. publications. The dashboard can be filtered and shows the relationship to co-authors in different diagrams. In addition, a link is provided to find contact information.

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Materials Map under construction

The Materials Map is still under development. In its current state, it is only based on one single data source and, thus, incomplete and contains duplicates. We are working on incorporating new open data sources like ORCID to improve the quality and the timeliness of our data. We will update Materials Map as soon as possible and kindly ask for your patience.

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in Cooperation with on an Cooperation-Score of 37%

Topics

Publications (7/7 displayed)

  • 2022Pressure-induced shift of effective Ce valence, Fermi energy and phase boundaries in CeOs4Sb121citations
  • 2022Calibration of a Finite Element Forward Model in Eddy Current Inspection.2citations
  • 2021178-OR: Lipotoxicity Stimulates ß-Cell Extracellular Vesicle Secretion Which Induces ß-Cell Dysfunction and Perturbs ß-Cell Transcriptional Identitycitations
  • 2019199-OR: Time-Restricted Feeding Ameliorates Metabolic Dysfunction through the Restoration of Circadian Beta-Cell Function and Transcriptional Identitycitations
  • 2015Influence of destructuration of soft clay on time-dependent settlements:Comparison of some elastic viscoplastic models24citations
  • 2013The influence of destructuration of soft clay on time-dependent settlements – a comparison of some elastic visco-plastic models.citations
  • 2012Impulsively actuated jets from thin liquid films for high-resolution printing applications86citations

Places of action

Chart of shared publication
Tozer, Stanley W.
1 / 1 shared
Goddard, Paul
1 / 8 shared
Coniglio, William
1 / 1 shared
Graf, David Earl
1 / 1 shared
Pearce, Matthew
1 / 1 shared
Singleton, John
1 / 6 shared
Coak, Matthew John
1 / 6 shared
Maple, M. Brian
1 / 4 shared
Götze, Kathrin
1 / 1 shared
Grockowiak, Audrey
1 / 5 shared
Ho, Pei-Chun
1 / 1 shared
Hampton, Joel
1 / 1 shared
Dorn, Oliver
1 / 1 shared
Tesfalem, Henok
1 / 1 shared
Peyton, Anthony
1 / 7 shared
Fletcher, Adam
1 / 1 shared
Javeed, Naureen
1 / 1 shared
Matveyenko, Aleksey
2 / 2 shared
Her, Tracy K.
2 / 2 shared
Nash, David
1 / 6 shared
Nash, David F. T.
1 / 2 shared
Chart of publication period
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2019
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Co-Authors (by relevance)

  • Tozer, Stanley W.
  • Goddard, Paul
  • Coniglio, William
  • Graf, David Earl
  • Pearce, Matthew
  • Singleton, John
  • Coak, Matthew John
  • Maple, M. Brian
  • Götze, Kathrin
  • Grockowiak, Audrey
  • Ho, Pei-Chun
  • Hampton, Joel
  • Dorn, Oliver
  • Tesfalem, Henok
  • Peyton, Anthony
  • Fletcher, Adam
  • Javeed, Naureen
  • Matveyenko, Aleksey
  • Her, Tracy K.
  • Nash, David
  • Nash, David F. T.
OrganizationsLocationPeople

article

178-OR: Lipotoxicity Stimulates ß-Cell Extracellular Vesicle Secretion Which Induces ß-Cell Dysfunction and Perturbs ß-Cell Transcriptional Identity

  • Javeed, Naureen
  • Brown, Matthew
  • Matveyenko, Aleksey
  • Her, Tracy K.
Abstract

<jats:p>Chronically elevated circulating free fatty acids (FFA) contribute to β-cell dysfunction and thus to the onset of obesity-driven type 2 diabetes (T2DM). Prolonged β-cell exposure to FFA is associated with reduced glucose-stimulated insulin secretion (GSIS), alterations in β-cell transcriptional identity, and apoptosis. However, the mechanisms that contribute to the demise of β-cells under lipotoxic conditions have yet to be fully elucidated. Increasing evidence suggests that aberrant release of extracellular vesicles (EV) contribute to the pathogenesis of β-cell failure in T2DM. However, what remains to be deciphered is the role of β-cell-derived EV in lipotoxicity-mediated β-cell failure. We set out to test the hypothesis that lipotoxicity-mediated β-cell dysfunction is mediated in part by paracrine release of ‘toxic’ β-cell-derived EV. To address this, MIN6 β-cells were exposed to palmitate (0.5 mM, 24h) and EV were isolated using differential ultracentrifugation to yield palmitate (PAL) EV (vs. control (CTL) EV). Nanoparticle Tracking Analysis (NTA) revealed a significant increase in PAL EV concentration (~1.5 fold vs. CTL EV) with a reduction in average particle size (CTL EV = 121 nm vs. PAL EV = 75 nm). β-cell functional assessment of mouse islets exposed to PAL EV (48h) resulted in significant suppression of GSIS (~3.4 fold decrease in stimulation index). Global transcriptomic analysis was assessed using RNA-Seq on islets exposed to PAL EV. Over 900 genes were differentially upregulated and ~450 genes downregulated upon PAL EV exposure (p&amp;lt;.05, FC&amp;gt;1.5). Genes upregulated with PAL EV encoded for KEGG pathways regulating protein digestion/absorption, ECM-receptor interaction, and PI3K/Akt signaling, while downregulated genes encode for pathways regulating glycolysis and protein processing in ER (FDR&amp;lt;.05). These data suggest the novel relevance of β-cell-derived EV in free fatty acid-induced β-cell failure in T2DM.</jats:p><jats:sec><jats:title>Disclosure</jats:title><jats:p>T. K. Her: None. M. Brown: None. A. Matveyenko: None. N. Javeed: None.</jats:p></jats:sec><jats:sec><jats:title>Funding</jats:title><jats:p>National Institutes of Health (R01DK098468, T32HL105355)</jats:p></jats:sec>

Topics
  • nanoparticle
  • impedance spectroscopy
  • size-exclusion chromatography