---
_id: '1895'
abstract:
- lang: eng
  text: Major histocompatibility complex class I (MHCI) molecules were recently identified
    as novel regulators of synaptic plasticity. These molecules are expressed in various
    brain areas, especially in regions undergoing activity-dependent synaptic plasticity,
    but their role in the nucleus accumbens (NAc) is unknown. In this study, we investigated
    the effects of genetic disruption of MHCI function, through deletion of β2-microblobulin,
    which causes lack of cell surface expression of MHCI. First, we confirmed that
    MHCI molecules are expressed in the NAc core in wild-type mice. Second, we performed
    electrophysiological recordings with NAc core slices from wild-type and β2-microglobulin
    knock-out mice lacking cell surface expression of MHCI. We found that low frequency
    stimulation induced long-term depression in wild-type but not knock-out mice,
    whereas high frequency stimulation induced long-term potentiation in both genotypes,
    with a larger magnitude in knock-out mice. Furthermore, we demonstrated that knock-out
    mice showed more persistent behavioral sensitization to cocaine, which is a NAc-related
    behavior. Using this model, we analyzed the density of total AMPA receptors and
    their subunits GluR1 and GluR2 in the NAc core, by SDS-digested freeze-fracture
    replica labeling. After repeated cocaine exposure, the density of GluR1 was increased,
    but there was no change in total AMPA receptors and GluR2 levels in wildtype mice.
    In contrast, following repeated cocaine exposure, increased densities of total
    AMPA receptors, GluR1 and GluR2 were observed in knock-out mice. These results
    indicate that functional deficiency of MHCI enhances synaptic potentiation, induced
    by electrical and pharmacological stimulation.
acknowledgement: This work was supported in part by a Grant-in-Aid for Scientific
  Research on Innovative Areas (Comprehensive Brain Science Network) and (B) 17330153,
  from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
article_number: e107099
author:
- first_name: Mitsuhiro
  full_name: Edamura, Mitsuhiro
  last_name: Edamura
- first_name: Gen
  full_name: Murakami, Gen
  last_name: Murakami
- first_name: Hongrui
  full_name: Meng, Hongrui
  last_name: Meng
- first_name: Makoto
  full_name: Itakura, Makoto
  last_name: Itakura
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Atsuo
  full_name: Fukuda, Atsuo
  last_name: Fukuda
- first_name: Daiichiro
  full_name: Nakahara, Daiichiro
  last_name: Nakahara
citation:
  ama: Edamura M, Murakami G, Meng H, et al. Functional deficiency of MHC class i
    enhances LTP and abolishes LTD in the nucleus accumbens of mice. <i>PLoS One</i>.
    2014;9(9). doi:<a href="https://doi.org/10.1371/journal.pone.0107099">10.1371/journal.pone.0107099</a>
  apa: Edamura, M., Murakami, G., Meng, H., Itakura, M., Shigemoto, R., Fukuda, A.,
    &#38; Nakahara, D. (2014). Functional deficiency of MHC class i enhances LTP and
    abolishes LTD in the nucleus accumbens of mice. <i>PLoS One</i>. Public Library
    of Science. <a href="https://doi.org/10.1371/journal.pone.0107099">https://doi.org/10.1371/journal.pone.0107099</a>
  chicago: Edamura, Mitsuhiro, Gen Murakami, Hongrui Meng, Makoto Itakura, Ryuichi
    Shigemoto, Atsuo Fukuda, and Daiichiro Nakahara. “Functional Deficiency of MHC
    Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” <i>PLoS
    One</i>. Public Library of Science, 2014. <a href="https://doi.org/10.1371/journal.pone.0107099">https://doi.org/10.1371/journal.pone.0107099</a>.
  ieee: M. Edamura <i>et al.</i>, “Functional deficiency of MHC class i enhances LTP
    and abolishes LTD in the nucleus accumbens of mice,” <i>PLoS One</i>, vol. 9,
    no. 9. Public Library of Science, 2014.
  ista: Edamura M, Murakami G, Meng H, Itakura M, Shigemoto R, Fukuda A, Nakahara
    D. 2014. Functional deficiency of MHC class i enhances LTP and abolishes LTD in
    the nucleus accumbens of mice. PLoS One. 9(9), e107099.
  mla: Edamura, Mitsuhiro, et al. “Functional Deficiency of MHC Class i Enhances LTP
    and Abolishes LTD in the Nucleus Accumbens of Mice.” <i>PLoS One</i>, vol. 9,
    no. 9, e107099, Public Library of Science, 2014, doi:<a href="https://doi.org/10.1371/journal.pone.0107099">10.1371/journal.pone.0107099</a>.
  short: M. Edamura, G. Murakami, H. Meng, M. Itakura, R. Shigemoto, A. Fukuda, D.
    Nakahara, PLoS One 9 (2014).
date_created: 2018-12-11T11:54:35Z
date_published: 2014-09-30T00:00:00Z
date_updated: 2021-01-12T06:53:54Z
day: '30'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1371/journal.pone.0107099
file:
- access_level: open_access
  checksum: 1f3be936be93114596d61ba44cacee69
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:09:01Z
  date_updated: 2020-07-14T12:45:20Z
  file_id: '4724'
  file_name: IST-2016-439-v1+1_journal.pone.0107099.pdf
  file_size: 6262085
  relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: '         9'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '5200'
pubrep_id: '439'
scopus_import: 1
status: public
title: Functional deficiency of MHC class i enhances LTP and abolishes LTD in the
  nucleus accumbens of mice
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '1896'
abstract:
- lang: eng
  text: 'Biopolymer length regulation is a complex process that involves a large number
    of biological, chemical, and physical subprocesses acting simultaneously across
    multiple spatial and temporal scales. An illustrative example important for genomic
    stability is the length regulation of telomeres - nucleoprotein structures at
    the ends of linear chromosomes consisting of tandemly repeated DNA sequences and
    a specialized set of proteins. Maintenance of telomeres is often facilitated by
    the enzyme telomerase but, particularly in telomerase-free systems, the maintenance
    of chromosomal termini depends on alternative lengthening of telomeres (ALT) mechanisms
    mediated by recombination. Various linear and circular DNA structures were identified
    to participate in ALT, however, dynamics of the whole process is still poorly
    understood. We propose a chemical kinetics model of ALT with kinetic rates systematically
    derived from the biophysics of DNA diffusion and looping. The reaction system
    is reduced to a coagulation-fragmentation system by quasi-steady-state approximation.
    The detailed treatment of kinetic rates yields explicit formulas for expected
    size distributions of telomeres that demonstrate the key role played by the J
    factor, a quantitative measure of bending of polymers. The results are in agreement
    with experimental data and point out interesting phenomena: an appearance of very
    long telomeric circles if the total telomere density exceeds a critical value
    (excess mass) and a nonlinear response of the telomere size distributions to the
    amount of telomeric DNA in the system. The results can be of general importance
    for understanding dynamics of telomeres in telomerase-independent systems as this
    mode of telomere maintenance is similar to the situation in tumor cells lacking
    telomerase activity. Furthermore, due to its universality, the model may also
    serve as a prototype of an interaction between linear and circular DNA structures
    in various settings.'
acknowledgement: The work was supported by the VEGA Grant No. 1/0459/13 (R.K. and
  K.B.).
article_number: '032701'
article_processing_charge: No
author:
- first_name: Richard
  full_name: Kollár, Richard
  last_name: Kollár
- first_name: Katarína
  full_name: Bod'ová, Katarína
  id: 2BA24EA0-F248-11E8-B48F-1D18A9856A87
  last_name: Bod'ová
  orcid: 0000-0002-7214-0171
- first_name: Jozef
  full_name: Nosek, Jozef
  last_name: Nosek
- first_name: Ľubomír
  full_name: Tomáška, Ľubomír
  last_name: Tomáška
citation:
  ama: Kollár R, Bodova K, Nosek J, Tomáška Ľ. Mathematical model of alternative mechanism
    of telomere length maintenance. <i>Physical Review E Statistical Nonlinear and
    Soft Matter Physics</i>. 2014;89(3). doi:<a href="https://doi.org/10.1103/PhysRevE.89.032701">10.1103/PhysRevE.89.032701</a>
  apa: Kollár, R., Bodova, K., Nosek, J., &#38; Tomáška, Ľ. (2014). Mathematical model
    of alternative mechanism of telomere length maintenance. <i>Physical Review E
    Statistical Nonlinear and Soft Matter Physics</i>. American Institute of Physics.
    <a href="https://doi.org/10.1103/PhysRevE.89.032701">https://doi.org/10.1103/PhysRevE.89.032701</a>
  chicago: Kollár, Richard, Katarina Bodova, Jozef Nosek, and Ľubomír Tomáška. “Mathematical
    Model of Alternative Mechanism of Telomere Length Maintenance.” <i>Physical Review
    E Statistical Nonlinear and Soft Matter Physics</i>. American Institute of Physics,
    2014. <a href="https://doi.org/10.1103/PhysRevE.89.032701">https://doi.org/10.1103/PhysRevE.89.032701</a>.
  ieee: R. Kollár, K. Bodova, J. Nosek, and Ľ. Tomáška, “Mathematical model of alternative
    mechanism of telomere length maintenance,” <i>Physical Review E Statistical Nonlinear
    and Soft Matter Physics</i>, vol. 89, no. 3. American Institute of Physics, 2014.
  ista: Kollár R, Bodova K, Nosek J, Tomáška Ľ. 2014. Mathematical model of alternative
    mechanism of telomere length maintenance. Physical Review E Statistical Nonlinear
    and Soft Matter Physics. 89(3), 032701.
  mla: Kollár, Richard, et al. “Mathematical Model of Alternative Mechanism of Telomere
    Length Maintenance.” <i>Physical Review E Statistical Nonlinear and Soft Matter
    Physics</i>, vol. 89, no. 3, 032701, American Institute of Physics, 2014, doi:<a
    href="https://doi.org/10.1103/PhysRevE.89.032701">10.1103/PhysRevE.89.032701</a>.
  short: R. Kollár, K. Bodova, J. Nosek, Ľ. Tomáška, Physical Review E Statistical
    Nonlinear and Soft Matter Physics 89 (2014).
date_created: 2018-12-11T11:54:35Z
date_published: 2014-03-04T00:00:00Z
date_updated: 2022-08-01T10:50:10Z
day: '04'
department:
- _id: NiBa
- _id: GaTk
doi: 10.1103/PhysRevE.89.032701
intvolume: '        89'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://arxiv.org/abs/1402.0430
month: '03'
oa: 1
oa_version: Submitted Version
publication: Physical Review E Statistical Nonlinear and Soft Matter Physics
publication_status: published
publisher: American Institute of Physics
publist_id: '5198'
scopus_import: '1'
status: public
title: Mathematical model of alternative mechanism of telomere length maintenance
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 89
year: '2014'
...
---
_id: '1897'
abstract:
- lang: eng
  text: GNOM is one of the most characterized membrane trafficking regulators in plants,
    with crucial roles in development. GNOM encodes an ARF-guanine nucleotide exchange
    factor (ARF-GEF) that activates small GTPases of the ARF (ADP ribosylation factor)
    class to mediate vesicle budding at endomembranes. The crucial role of GNOM in
    recycling of PIN auxin transporters and other proteins to the plasma membrane
    was identified in studies using the ARF-GEF inhibitor brefeldin A (BFA). GNOM,
    the most prominent regulator of recycling in plants, has been proposed to act
    and localize at so far elusive recycling endosomes. Here, we report the GNOM localization
    in context of its cellular function in Arabidopsis thaliana. State-of-the-art
    imaging, pharmacological interference, and ultrastructure analysis show that GNOM
    predominantly localizes to Golgi apparatus. Super-resolution confocal live imaging
    microscopy identified GNOM and its closest homolog GNOM-like 1 at distinct subdomains
    on Golgi cisternae. Short-term BFA treatment stabilizes GNOM at the Golgi apparatus,
    whereas prolonged exposures results in GNOM translocation to trans-Golgi network
    (TGN)/early endosomes (EEs). Malformed TGN/EE in gnom mutants suggests a role
    for GNOM in maintaining TGN/EE function. Our results redefine the subcellular
    action of GNOM and reevaluate the identity and function of recycling endosomes
    in plants.
acknowledgement: This work was supported by the Odysseus Program of the Research Foundation-Flanders
  (J.F.).
author:
- first_name: Satoshi
  full_name: Naramoto, Satoshi
  last_name: Naramoto
- first_name: Marisa
  full_name: Otegui, Marisa
  last_name: Otegui
- first_name: Natsumaro
  full_name: Kutsuna, Natsumaro
  last_name: Kutsuna
- first_name: Riet
  full_name: De Rycke, Riet
  last_name: De Rycke
- first_name: Tomoko
  full_name: Dainobu, Tomoko
  last_name: Dainobu
- first_name: Michael
  full_name: Karampelias, Michael
  last_name: Karampelias
- first_name: Masaru
  full_name: Fujimoto, Masaru
  last_name: Fujimoto
- first_name: Elena
  full_name: Feraru, Elena
  last_name: Feraru
- first_name: Daisuke
  full_name: Miki, Daisuke
  last_name: Miki
- first_name: Hiroo
  full_name: Fukuda, Hiroo
  last_name: Fukuda
- first_name: Akihiko
  full_name: Nakano, Akihiko
  last_name: Nakano
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Naramoto S, Otegui M, Kutsuna N, et al. Insights into the localization and
    function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus
    in Arabidopsis. <i>Plant Cell</i>. 2014;26(7):3062-3076. doi:<a href="https://doi.org/10.1105/tpc.114.125880">10.1105/tpc.114.125880</a>
  apa: Naramoto, S., Otegui, M., Kutsuna, N., De Rycke, R., Dainobu, T., Karampelias,
    M., … Friml, J. (2014). Insights into the localization and function of the membrane
    trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis. <i>Plant
    Cell</i>. American Society of Plant Biologists. <a href="https://doi.org/10.1105/tpc.114.125880">https://doi.org/10.1105/tpc.114.125880</a>
  chicago: Naramoto, Satoshi, Marisa Otegui, Natsumaro Kutsuna, Riet De Rycke, Tomoko
    Dainobu, Michael Karampelias, Masaru Fujimoto, et al. “Insights into the Localization
    and Function of the Membrane Trafficking Regulator GNOM ARF-GEF at the Golgi Apparatus
    in Arabidopsis.” <i>Plant Cell</i>. American Society of Plant Biologists, 2014.
    <a href="https://doi.org/10.1105/tpc.114.125880">https://doi.org/10.1105/tpc.114.125880</a>.
  ieee: S. Naramoto <i>et al.</i>, “Insights into the localization and function of
    the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis,”
    <i>Plant Cell</i>, vol. 26, no. 7. American Society of Plant Biologists, pp. 3062–3076,
    2014.
  ista: Naramoto S, Otegui M, Kutsuna N, De Rycke R, Dainobu T, Karampelias M, Fujimoto
    M, Feraru E, Miki D, Fukuda H, Nakano A, Friml J. 2014. Insights into the localization
    and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus
    in Arabidopsis. Plant Cell. 26(7), 3062–3076.
  mla: Naramoto, Satoshi, et al. “Insights into the Localization and Function of the
    Membrane Trafficking Regulator GNOM ARF-GEF at the Golgi Apparatus in Arabidopsis.”
    <i>Plant Cell</i>, vol. 26, no. 7, American Society of Plant Biologists, 2014,
    pp. 3062–76, doi:<a href="https://doi.org/10.1105/tpc.114.125880">10.1105/tpc.114.125880</a>.
  short: S. Naramoto, M. Otegui, N. Kutsuna, R. De Rycke, T. Dainobu, M. Karampelias,
    M. Fujimoto, E. Feraru, D. Miki, H. Fukuda, A. Nakano, J. Friml, Plant Cell 26
    (2014) 3062–3076.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-07-01T00:00:00Z
date_updated: 2021-01-12T06:53:55Z
day: '01'
department:
- _id: JiFr
doi: 10.1105/tpc.114.125880
intvolume: '        26'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145132/
month: '07'
oa: 1
oa_version: Submitted Version
page: 3062 - 3076
publication: Plant Cell
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '5199'
scopus_import: 1
status: public
title: Insights into the localization and function of the membrane trafficking regulator
  GNOM ARF-GEF at the Golgi apparatus in Arabidopsis
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2014'
...
---
_id: '1899'
abstract:
- lang: eng
  text: Asymmetric cell divisions allow stem cells to balance proliferation and differentiation.
    During embryogenesis, murine epidermis expands rapidly from a single layer of
    unspecified basal layer progenitors to a stratified, differentiated epithelium.
    Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation
    protein LGN, but little is known about how the apical localization of LGN is regulated.
    Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to
    explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas
    loss of each gene alone leads to randomized division angles, combined loss of
    Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of
    LGN. These findings lend experimental support for the hitherto untested model
    that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular
    divisions. Finally, we uncover a developmental switch between delamination-driven
    early stratification and spindle-orientation-dependent differentiation that occurs
    around E15, revealing a two-step mechanism underlying epidermal maturation.
article_processing_charge: No
article_type: original
author:
- first_name: Scott
  full_name: Williams, Scott
  last_name: Williams
- first_name: Lyndsay
  full_name: Ratliff, Lyndsay
  last_name: Ratliff
- first_name: Maria P
  full_name: Postiglione, Maria P
  id: 2C67902A-F248-11E8-B48F-1D18A9856A87
  last_name: Postiglione
- first_name: Juergen
  full_name: Knoblich, Juergen
  last_name: Knoblich
- first_name: Elaine
  full_name: Fuchs, Elaine
  last_name: Fuchs
citation:
  ama: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and
    Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. <i>Nature
    Cell Biology</i>. 2014;16(8):758-769. doi:<a href="https://doi.org/10.1038/ncb3001">10.1038/ncb3001</a>
  apa: Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., &#38; Fuchs, E.
    (2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
    through LGN. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncb3001">https://doi.org/10.1038/ncb3001</a>
  chicago: Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich,
    and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal
    Cell Divisions through LGN.” <i>Nature Cell Biology</i>. Nature Publishing Group,
    2014. <a href="https://doi.org/10.1038/ncb3001">https://doi.org/10.1038/ncb3001</a>.
  ieee: S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc
    and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,”
    <i>Nature Cell Biology</i>, vol. 16, no. 8. Nature Publishing Group, pp. 758–769,
    2014.
  ista: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc
    and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN.
    Nature Cell Biology. 16(8), 758–769.
  mla: Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented
    Epidermal Cell Divisions through LGN.” <i>Nature Cell Biology</i>, vol. 16, no.
    8, Nature Publishing Group, 2014, pp. 758–69, doi:<a href="https://doi.org/10.1038/ncb3001">10.1038/ncb3001</a>.
  short: S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature
    Cell Biology 16 (2014) 758–769.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-07-13T00:00:00Z
date_updated: 2021-01-12T06:53:55Z
day: '13'
department:
- _id: SiHi
doi: 10.1038/ncb3001
external_id:
  pmid:
  - '25016959'
intvolume: '        16'
issue: '8'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/
month: '07'
oa: 1
oa_version: Submitted Version
page: 758 - 769
pmid: 1
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5196'
quality_controlled: '1'
scopus_import: 1
status: public
title: Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
  through LGN
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '1904'
abstract:
- lang: eng
  text: We prove a Strichartz inequality for a system of orthonormal functions, with
    an optimal behavior of the constant in the limit of a large number of functions.
    The estimate generalizes the usual Strichartz inequality, in the same fashion
    as the Lieb-Thirring inequality generalizes the Sobolev inequality. As an application,
    we consider the Schrödinger equation with a time-dependent potential and we show
    the existence of the wave operator in Schatten spaces.
author:
- first_name: Rupert
  full_name: Frank, Rupert
  last_name: Frank
- first_name: Mathieu
  full_name: Lewin, Mathieu
  last_name: Lewin
- first_name: Élliott
  full_name: Lieb, Élliott
  last_name: Lieb
- first_name: Robert
  full_name: Seiringer, Robert
  id: 4AFD0470-F248-11E8-B48F-1D18A9856A87
  last_name: Seiringer
  orcid: 0000-0002-6781-0521
citation:
  ama: Frank R, Lewin M, Lieb É, Seiringer R. Strichartz inequality for orthonormal
    functions. <i>Journal of the European Mathematical Society</i>. 2014;16(7):1507-1526.
    doi:<a href="https://doi.org/10.4171/JEMS/467">10.4171/JEMS/467</a>
  apa: Frank, R., Lewin, M., Lieb, É., &#38; Seiringer, R. (2014). Strichartz inequality
    for orthonormal functions. <i>Journal of the European Mathematical Society</i>.
    European Mathematical Society. <a href="https://doi.org/10.4171/JEMS/467">https://doi.org/10.4171/JEMS/467</a>
  chicago: Frank, Rupert, Mathieu Lewin, Élliott Lieb, and Robert Seiringer. “Strichartz
    Inequality for Orthonormal Functions.” <i>Journal of the European Mathematical
    Society</i>. European Mathematical Society, 2014. <a href="https://doi.org/10.4171/JEMS/467">https://doi.org/10.4171/JEMS/467</a>.
  ieee: R. Frank, M. Lewin, É. Lieb, and R. Seiringer, “Strichartz inequality for
    orthonormal functions,” <i>Journal of the European Mathematical Society</i>, vol.
    16, no. 7. European Mathematical Society, pp. 1507–1526, 2014.
  ista: Frank R, Lewin M, Lieb É, Seiringer R. 2014. Strichartz inequality for orthonormal
    functions. Journal of the European Mathematical Society. 16(7), 1507–1526.
  mla: Frank, Rupert, et al. “Strichartz Inequality for Orthonormal Functions.” <i>Journal
    of the European Mathematical Society</i>, vol. 16, no. 7, European Mathematical
    Society, 2014, pp. 1507–26, doi:<a href="https://doi.org/10.4171/JEMS/467">10.4171/JEMS/467</a>.
  short: R. Frank, M. Lewin, É. Lieb, R. Seiringer, Journal of the European Mathematical
    Society 16 (2014) 1507–1526.
date_created: 2018-12-11T11:54:38Z
date_published: 2014-08-23T00:00:00Z
date_updated: 2021-01-12T06:53:58Z
day: '23'
department:
- _id: RoSe
doi: 10.4171/JEMS/467
intvolume: '        16'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://arxiv.org/abs/1306.1309
month: '08'
oa: 1
oa_version: Submitted Version
page: 1507 - 1526
project:
- _id: 26450934-B435-11E9-9278-68D0E5697425
  name: NSERC Postdoctoral fellowship
publication: Journal of the European Mathematical Society
publication_status: published
publisher: European Mathematical Society
publist_id: '5191'
quality_controlled: '1'
scopus_import: 1
status: public
title: Strichartz inequality for orthonormal functions
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '1906'
abstract:
- lang: eng
  text: In this paper, we introduce a novel scene representation for the visualization
    of large-scale point clouds accompanied by a set of high-resolution photographs.
    Many real-world applications deal with very densely sampled point-cloud data,
    which are augmented with photographs that often reveal lighting variations and
    inaccuracies in registration. Consequently, the high-quality representation of
    the captured data, i.e., both point clouds and photographs together, is a challenging
    and time-consuming task. We propose a two-phase approach, in which the first (preprocessing)
    phase generates multiple overlapping surface patches and handles the problem of
    seamless texture generation locally for each patch. The second phase stitches
    these patches at render-time to produce a high-quality visualization of the data.
    As a result of the proposed localization of the global texturing problem, our
    algorithm is more than an order of magnitude faster than equivalent mesh-based
    texturing techniques. Furthermore, since our preprocessing phase requires only
    a minor fraction of the whole data set at once, we provide maximum flexibility
    when dealing with growing data sets.
acknowledgement: This research was supported by the Austrian Research Promotion Agency
  (FFG) project REPLICATE (no. 835948), the EU FP7 project HARVEST4D (no. 323567).
author:
- first_name: Murat
  full_name: Arikan, Murat
  last_name: Arikan
- first_name: Reinhold
  full_name: Preiner, Reinhold
  last_name: Preiner
- first_name: Claus
  full_name: Scheiblauer, Claus
  last_name: Scheiblauer
- first_name: Stefan
  full_name: Jeschke, Stefan
  id: 44D6411A-F248-11E8-B48F-1D18A9856A87
  last_name: Jeschke
- first_name: Michael
  full_name: Wimmer, Michael
  last_name: Wimmer
citation:
  ama: Arikan M, Preiner R, Scheiblauer C, Jeschke S, Wimmer M. Large-scale point-cloud
    visualization through localized textured surface reconstruction. <i>IEEE Transactions
    on Visualization and Computer Graphics</i>. 2014;20(9):1280-1292. doi:<a href="https://doi.org/10.1109/TVCG.2014.2312011">10.1109/TVCG.2014.2312011</a>
  apa: Arikan, M., Preiner, R., Scheiblauer, C., Jeschke, S., &#38; Wimmer, M. (2014).
    Large-scale point-cloud visualization through localized textured surface reconstruction.
    <i>IEEE Transactions on Visualization and Computer Graphics</i>. IEEE. <a href="https://doi.org/10.1109/TVCG.2014.2312011">https://doi.org/10.1109/TVCG.2014.2312011</a>
  chicago: Arikan, Murat, Reinhold Preiner, Claus Scheiblauer, Stefan Jeschke, and
    Michael Wimmer. “Large-Scale Point-Cloud Visualization through Localized Textured
    Surface Reconstruction.” <i>IEEE Transactions on Visualization and Computer Graphics</i>.
    IEEE, 2014. <a href="https://doi.org/10.1109/TVCG.2014.2312011">https://doi.org/10.1109/TVCG.2014.2312011</a>.
  ieee: M. Arikan, R. Preiner, C. Scheiblauer, S. Jeschke, and M. Wimmer, “Large-scale
    point-cloud visualization through localized textured surface reconstruction,”
    <i>IEEE Transactions on Visualization and Computer Graphics</i>, vol. 20, no.
    9. IEEE, pp. 1280–1292, 2014.
  ista: Arikan M, Preiner R, Scheiblauer C, Jeschke S, Wimmer M. 2014. Large-scale
    point-cloud visualization through localized textured surface reconstruction. IEEE
    Transactions on Visualization and Computer Graphics. 20(9), 1280–1292.
  mla: Arikan, Murat, et al. “Large-Scale Point-Cloud Visualization through Localized
    Textured Surface Reconstruction.” <i>IEEE Transactions on Visualization and Computer
    Graphics</i>, vol. 20, no. 9, IEEE, 2014, pp. 1280–92, doi:<a href="https://doi.org/10.1109/TVCG.2014.2312011">10.1109/TVCG.2014.2312011</a>.
  short: M. Arikan, R. Preiner, C. Scheiblauer, S. Jeschke, M. Wimmer, IEEE Transactions
    on Visualization and Computer Graphics 20 (2014) 1280–1292.
date_created: 2018-12-11T11:54:39Z
date_published: 2014-09-09T00:00:00Z
date_updated: 2021-01-12T06:53:59Z
day: '09'
ddc:
- '000'
department:
- _id: ChWo
doi: 10.1109/TVCG.2014.2312011
file:
- access_level: open_access
  checksum: 5bf58942d2eb20adf03c7f9ea2e68124
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:17:41Z
  date_updated: 2020-07-14T12:45:20Z
  file_id: '5297'
  file_name: IST-2016-573-v1+1_arikan-2014-pcvis-draft.pdf
  file_size: 13594598
  relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: '        20'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Submitted Version
page: 1280 - 1292
project:
- _id: 25357BD2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P 24352-N23
  name: 'Deep Pictures: Creating Visual and Haptic Vector Images'
publication: IEEE Transactions on Visualization and Computer Graphics
publication_status: published
publisher: IEEE
publist_id: '5189'
pubrep_id: '573'
scopus_import: 1
status: public
title: Large-scale point-cloud visualization through localized textured surface reconstruction
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 20
year: '2014'
...
---
_id: '1907'
abstract:
- lang: eng
  text: 'Most cryptographic security proofs require showing that two systems are indistinguishable.
    A central tool in such proofs is that of a game, where winning the game means
    provoking a certain condition, and it is shown that the two systems considered
    cannot be distinguished unless this condition is provoked. Upper bounding the
    probability of winning such a game, i.e., provoking this condition, for an arbitrary
    strategy is usually hard, except in the special case where the best strategy for
    winning such a game is known to be non-adaptive. A sufficient criterion for ensuring
    the optimality of non-adaptive strategies is that of conditional equivalence to
    a system, a notion introduced in [1]. In this paper, we show that this criterion
    is not necessary to ensure the optimality of non-adaptive strategies by giving
    two results of independent interest: 1) the optimality of non-adaptive strategies
    is not preserved under parallel composition; 2) in contrast, conditional equivalence
    is preserved under parallel composition.'
article_number: '6875125'
author:
- first_name: Grégory
  full_name: Demay, Grégory
  last_name: Demay
- first_name: Peter
  full_name: Gazi, Peter
  id: 3E0BFE38-F248-11E8-B48F-1D18A9856A87
  last_name: Gazi
- first_name: Ueli
  full_name: Maurer, Ueli
  last_name: Maurer
- first_name: Björn
  full_name: Tackmann, Björn
  last_name: Tackmann
citation:
  ama: 'Demay G, Gazi P, Maurer U, Tackmann B. Optimality of non-adaptive strategies:
    The case of parallel games. In: <i>IEEE International Symposium on Information
    Theory</i>. IEEE; 2014. doi:<a href="https://doi.org/10.1109/ISIT.2014.6875125">10.1109/ISIT.2014.6875125</a>'
  apa: 'Demay, G., Gazi, P., Maurer, U., &#38; Tackmann, B. (2014). Optimality of
    non-adaptive strategies: The case of parallel games. In <i>IEEE International
    Symposium on Information Theory</i>. Honolulu, USA: IEEE. <a href="https://doi.org/10.1109/ISIT.2014.6875125">https://doi.org/10.1109/ISIT.2014.6875125</a>'
  chicago: 'Demay, Grégory, Peter Gazi, Ueli Maurer, and Björn Tackmann. “Optimality
    of Non-Adaptive Strategies: The Case of Parallel Games.” In <i>IEEE International
    Symposium on Information Theory</i>. IEEE, 2014. <a href="https://doi.org/10.1109/ISIT.2014.6875125">https://doi.org/10.1109/ISIT.2014.6875125</a>.'
  ieee: 'G. Demay, P. Gazi, U. Maurer, and B. Tackmann, “Optimality of non-adaptive
    strategies: The case of parallel games,” in <i>IEEE International Symposium on
    Information Theory</i>, Honolulu, USA, 2014.'
  ista: 'Demay G, Gazi P, Maurer U, Tackmann B. 2014. Optimality of non-adaptive strategies:
    The case of parallel games. IEEE International Symposium on Information Theory.
    IEEE International Symposium on Information Theory Proceedings, 6875125.'
  mla: 'Demay, Grégory, et al. “Optimality of Non-Adaptive Strategies: The Case of
    Parallel Games.” <i>IEEE International Symposium on Information Theory</i>, 6875125,
    IEEE, 2014, doi:<a href="https://doi.org/10.1109/ISIT.2014.6875125">10.1109/ISIT.2014.6875125</a>.'
  short: G. Demay, P. Gazi, U. Maurer, B. Tackmann, in:, IEEE International Symposium
    on Information Theory, IEEE, 2014.
conference:
  end_date: 2014-07-04
  location: Honolulu, USA
  name: IEEE International Symposium on Information Theory Proceedings
  start_date: 2014-06-29
date_created: 2018-12-11T11:54:39Z
date_published: 2014-01-01T00:00:00Z
date_updated: 2021-01-12T06:53:59Z
day: '01'
department:
- _id: KrPi
doi: 10.1109/ISIT.2014.6875125
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://eprint.iacr.org/2014/299
month: '01'
oa: 1
oa_version: Submitted Version
publication: IEEE International Symposium on Information Theory
publication_status: published
publisher: IEEE
publist_id: '5188'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Optimality of non-adaptive strategies: The case of parallel games'
type: conference
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
year: '2014'
...
---
_id: '1908'
abstract:
- lang: eng
  text: In large populations, multiple beneficial mutations may be simultaneously
    spreading. In asexual populations, these mutations must either arise on the same
    background or compete against each other. In sexual populations, recombination
    can bring together beneficial alleles from different backgrounds, but tightly
    linked alleles may still greatly interfere with each other. We show for well-mixed
    populations that when this interference is strong, the genome can be seen as consisting
    of many effectively asexual stretches linked together. The rate at which beneficial
    alleles fix is thus roughly proportional to the rate of recombination and depends
    only logarithmically on the mutation supply and the strength of selection. Our
    scaling arguments also allow us to predict, with reasonable accuracy, the fitness
    distribution of fixed mutations when the mutational effect sizes are broad. We
    focus on the regime in which crossovers occur more frequently than beneficial
    mutations, as is likely to be the case for many natural populations.
author:
- first_name: Daniel
  full_name: Weissman, Daniel
  id: 2D0CE020-F248-11E8-B48F-1D18A9856A87
  last_name: Weissman
- first_name: Oskar
  full_name: Hallatschek, Oskar
  last_name: Hallatschek
citation:
  ama: Weissman D, Hallatschek O. The rate of adaptation in large sexual populations
    with linear chromosomes. <i>Genetics</i>. 2014;196(4):1167-1183. doi:<a href="https://doi.org/10.1534/genetics.113.160705">10.1534/genetics.113.160705</a>
  apa: Weissman, D., &#38; Hallatschek, O. (2014). The rate of adaptation in large
    sexual populations with linear chromosomes. <i>Genetics</i>. Genetics Society
    of America. <a href="https://doi.org/10.1534/genetics.113.160705">https://doi.org/10.1534/genetics.113.160705</a>
  chicago: Weissman, Daniel, and Oskar Hallatschek. “The Rate of Adaptation in Large
    Sexual Populations with Linear Chromosomes.” <i>Genetics</i>. Genetics Society
    of America, 2014. <a href="https://doi.org/10.1534/genetics.113.160705">https://doi.org/10.1534/genetics.113.160705</a>.
  ieee: D. Weissman and O. Hallatschek, “The rate of adaptation in large sexual populations
    with linear chromosomes,” <i>Genetics</i>, vol. 196, no. 4. Genetics Society of
    America, pp. 1167–1183, 2014.
  ista: Weissman D, Hallatschek O. 2014. The rate of adaptation in large sexual populations
    with linear chromosomes. Genetics. 196(4), 1167–1183.
  mla: Weissman, Daniel, and Oskar Hallatschek. “The Rate of Adaptation in Large Sexual
    Populations with Linear Chromosomes.” <i>Genetics</i>, vol. 196, no. 4, Genetics
    Society of America, 2014, pp. 1167–83, doi:<a href="https://doi.org/10.1534/genetics.113.160705">10.1534/genetics.113.160705</a>.
  short: D. Weissman, O. Hallatschek, Genetics 196 (2014) 1167–1183.
date_created: 2018-12-11T11:54:39Z
date_published: 2014-04-01T00:00:00Z
date_updated: 2021-01-12T06:53:59Z
day: '01'
department:
- _id: NiBa
doi: 10.1534/genetics.113.160705
ec_funded: 1
intvolume: '       196'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://arxiv.org/abs/1307.0737
month: '04'
oa: 1
oa_version: Submitted Version
page: 1167 - 1183
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '250152'
  name: Limits to selection in biology and in evolutionary computation
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '5187'
quality_controlled: '1'
scopus_import: 1
status: public
title: The rate of adaptation in large sexual populations with linear chromosomes
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 196
year: '2014'
...
---
_id: '1909'
abstract:
- lang: eng
  text: 'Summary: Phenotypes are often environmentally dependent, which requires organisms
    to track environmental change. The challenge for organisms is to construct phenotypes
    using the most accurate environmental cue. Here, we use a quantitative genetic
    model of adaptation by additive genetic variance, within- and transgenerational
    plasticity via linear reaction norms and indirect genetic effects respectively.
    We show how the relative influence on the eventual phenotype of these components
    depends on the predictability of environmental change (fast or slow, sinusoidal
    or stochastic) and the developmental lag τ between when the environment is perceived
    and when selection acts. We then decompose expected mean fitness into three components
    (variance load, adaptation and fluctuation load) to study the fitness costs of
    within- and transgenerational plasticity. A strongly negative maternal effect
    coefficient m minimizes the variance load, but a strongly positive m minimises
    the fluctuation load. The adaptation term is maximized closer to zero, with positive
    or negative m preferred under different environmental scenarios. Phenotypic plasticity
    is higher when τ is shorter and when the environment changes frequently between
    seasonal extremes. Expected mean population fitness is highest away from highest
    observed levels of phenotypic plasticity. Within- and transgenerational plasticity
    act in concert to deliver well-adapted phenotypes, which emphasizes the need to
    study both simultaneously when investigating phenotypic evolution.'
acknowledgement: 'Engineering and Physical Sciences Research Council. Grant Number:
  EP/H031928/1'
author:
- first_name: Thomas
  full_name: Ezard, Thomas
  last_name: Ezard
- first_name: Roshan
  full_name: Prizak, Roshan
  id: 4456104E-F248-11E8-B48F-1D18A9856A87
  last_name: Prizak
- first_name: Rebecca
  full_name: Hoyle, Rebecca
  last_name: Hoyle
citation:
  ama: Ezard T, Prizak R, Hoyle R. The fitness costs of adaptation via phenotypic
    plasticity and maternal effects. <i>Functional Ecology</i>. 2014;28(3):693-701.
    doi:<a href="https://doi.org/10.1111/1365-2435.12207">10.1111/1365-2435.12207</a>
  apa: Ezard, T., Prizak, R., &#38; Hoyle, R. (2014). The fitness costs of adaptation
    via phenotypic plasticity and maternal effects. <i>Functional Ecology</i>. Wiley-Blackwell.
    <a href="https://doi.org/10.1111/1365-2435.12207">https://doi.org/10.1111/1365-2435.12207</a>
  chicago: Ezard, Thomas, Roshan Prizak, and Rebecca Hoyle. “The Fitness Costs of
    Adaptation via Phenotypic Plasticity and Maternal Effects.” <i>Functional Ecology</i>.
    Wiley-Blackwell, 2014. <a href="https://doi.org/10.1111/1365-2435.12207">https://doi.org/10.1111/1365-2435.12207</a>.
  ieee: T. Ezard, R. Prizak, and R. Hoyle, “The fitness costs of adaptation via phenotypic
    plasticity and maternal effects,” <i>Functional Ecology</i>, vol. 28, no. 3. Wiley-Blackwell,
    pp. 693–701, 2014.
  ista: Ezard T, Prizak R, Hoyle R. 2014. The fitness costs of adaptation via phenotypic
    plasticity and maternal effects. Functional Ecology. 28(3), 693–701.
  mla: Ezard, Thomas, et al. “The Fitness Costs of Adaptation via Phenotypic Plasticity
    and Maternal Effects.” <i>Functional Ecology</i>, vol. 28, no. 3, Wiley-Blackwell,
    2014, pp. 693–701, doi:<a href="https://doi.org/10.1111/1365-2435.12207">10.1111/1365-2435.12207</a>.
  short: T. Ezard, R. Prizak, R. Hoyle, Functional Ecology 28 (2014) 693–701.
date_created: 2018-12-11T11:54:40Z
date_published: 2014-06-01T00:00:00Z
date_updated: 2021-01-12T06:54:00Z
day: '01'
ddc:
- '570'
department:
- _id: NiBa
- _id: GaTk
doi: 10.1111/1365-2435.12207
file:
- access_level: open_access
  checksum: 3cbe8623174709a8ceec2103246f8fe0
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:45Z
  date_updated: 2020-07-14T12:45:20Z
  file_id: '5167'
  file_name: IST-2016-419-v1+1_Ezard_et_al-2014-Functional_Ecology.pdf
  file_size: 536154
  relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: '        28'
issue: '3'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 693 - 701
publication: Functional Ecology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5186'
pubrep_id: '419'
scopus_import: 1
status: public
title: The fitness costs of adaptation via phenotypic plasticity and maternal effects
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 28
year: '2014'
...
---
_id: '1912'
abstract:
- lang: eng
  text: Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the
    embryo along its left-right (LR) axis. Regional differences in cell shape within
    the lumen-lining KV epithelium are essential for its LR patterning function. However,
    the processes by which KV cells acquire their characteristic shapes are largely
    unknown. Here, we show that the notochord induces regional differences in cell
    shape within KV by triggering extracellular matrix (ECM) accumulation adjacent
    to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts
    apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen
    growth. Our study provides mechanistic insight into the processes by which KV
    translates global embryonic patterning into regional cell shape differences required
    for its LR symmetry-breaking function.
acknowledgement: We are grateful to members of the C.-P.H. lab, M. Concha, D. Siekhaus,
  and J. Vermot for comments on the manuscript and to M. Furutani-Seiki for sharing
  reagents. This work was supported by the Institute of Science and Technology Austria
  and an Alexander von Humboldt Foundation fellowship to J.C.
article_processing_charge: No
author:
- first_name: Julien
  full_name: Compagnon, Julien
  id: 2E3E0988-F248-11E8-B48F-1D18A9856A87
  last_name: Compagnon
- first_name: Vanessa
  full_name: Barone, Vanessa
  id: 419EECCC-F248-11E8-B48F-1D18A9856A87
  last_name: Barone
  orcid: 0000-0003-2676-3367
- first_name: Srivarsha
  full_name: Rajshekar, Srivarsha
  last_name: Rajshekar
- first_name: Rita
  full_name: Kottmeier, Rita
  last_name: Kottmeier
- first_name: Kornelija
  full_name: Pranjic-Ferscha, Kornelija
  id: 4362B3C2-F248-11E8-B48F-1D18A9856A87
  last_name: Pranjic-Ferscha
- first_name: Martin
  full_name: Behrndt, Martin
  id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
  last_name: Behrndt
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Compagnon J, Barone V, Rajshekar S, et al. The notochord breaks bilateral symmetry
    by controlling cell shapes in the Zebrafish laterality organ. <i>Developmental
    Cell</i>. 2014;31(6):774-783. doi:<a href="https://doi.org/10.1016/j.devcel.2014.11.003">10.1016/j.devcel.2014.11.003</a>
  apa: Compagnon, J., Barone, V., Rajshekar, S., Kottmeier, R., Pranjic-Ferscha, K.,
    Behrndt, M., &#38; Heisenberg, C.-P. J. (2014). The notochord breaks bilateral
    symmetry by controlling cell shapes in the Zebrafish laterality organ. <i>Developmental
    Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.devcel.2014.11.003">https://doi.org/10.1016/j.devcel.2014.11.003</a>
  chicago: Compagnon, Julien, Vanessa Barone, Srivarsha Rajshekar, Rita Kottmeier,
    Kornelija Pranjic-Ferscha, Martin Behrndt, and Carl-Philipp J Heisenberg. “The
    Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish
    Laterality Organ.” <i>Developmental Cell</i>. Cell Press, 2014. <a href="https://doi.org/10.1016/j.devcel.2014.11.003">https://doi.org/10.1016/j.devcel.2014.11.003</a>.
  ieee: J. Compagnon <i>et al.</i>, “The notochord breaks bilateral symmetry by controlling
    cell shapes in the Zebrafish laterality organ,” <i>Developmental Cell</i>, vol.
    31, no. 6. Cell Press, pp. 774–783, 2014.
  ista: Compagnon J, Barone V, Rajshekar S, Kottmeier R, Pranjic-Ferscha K, Behrndt
    M, Heisenberg C-PJ. 2014. The notochord breaks bilateral symmetry by controlling
    cell shapes in the Zebrafish laterality organ. Developmental Cell. 31(6), 774–783.
  mla: Compagnon, Julien, et al. “The Notochord Breaks Bilateral Symmetry by Controlling
    Cell Shapes in the Zebrafish Laterality Organ.” <i>Developmental Cell</i>, vol.
    31, no. 6, Cell Press, 2014, pp. 774–83, doi:<a href="https://doi.org/10.1016/j.devcel.2014.11.003">10.1016/j.devcel.2014.11.003</a>.
  short: J. Compagnon, V. Barone, S. Rajshekar, R. Kottmeier, K. Pranjic-Ferscha,
    M. Behrndt, C.-P.J. Heisenberg, Developmental Cell 31 (2014) 774–783.
date_created: 2018-12-11T11:54:41Z
date_published: 2014-12-22T00:00:00Z
date_updated: 2023-09-07T12:05:08Z
day: '22'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2014.11.003
external_id:
  pmid:
  - '25535919'
intvolume: '        31'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pubmed/25535919
month: '12'
oa: 1
oa_version: Published Version
page: 774 - 783
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '5182'
quality_controlled: '1'
related_material:
  record:
  - id: '961'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish
  laterality organ
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2014'
...
---
_id: '1913'
abstract:
- lang: eng
  text: 'Deposits of phosphorylated tau protein and convergence of pathology in the
    hippocampus are the hallmarks of neurodegenerative tauopathies. Thus we aimed
    to evaluate whether regional and cellular vulnerability patterns in the hippocampus
    distinguish tauopathies or are influenced by their concomitant presence. Methods:
    We created a heat map of phospho-tau (AT8) immunoreactivity patterns in 24 hippocampal
    subregions/layers in individuals with Alzheimer''s disease (AD)-related neurofibrillary
    degeneration (n = 40), Pick''s disease (n = 8), progressive supranuclear palsy
    (n = 7), corticobasal degeneration (n = 6), argyrophilic grain disease (AGD, n
    = 18), globular glial tauopathy (n = 5), and tau-astrogliopathy of the elderly
    (n = 10). AT8 immunoreactivity patterns were compared by mathematical analysis.
    Results: Our study reveals disease-specific hot spots and regional selective vulnerability
    for these disorders. The pattern of hippocampal AD-related tau pathology is strongly
    influenced by concomitant AGD. Mathematical analysis reveals that hippocampal
    involvement in primary tauopathies is distinguishable from early-stage AD-related
    neurofibrillary degeneration. Conclusion: Our data demonstrate disease-specific
    AT8 immunoreactivity patterns and hot spots in the hippocampus even in tauopathies,
    which primarily do not affect the hippocampus. These hot spots can be shifted
    to other regions by the co-occurrence of tauopathies like AGD. Our observations
    support the notion that globular glial tauopathies and tau-astrogliopathy of the
    elderly are distinct entities.'
acknowledgement: This study was supported by the European Commission’s 7th Framework
  Programme under GA No. 278486, ‘DEVELAGE’.
article_processing_charge: No
article_type: original
author:
- first_name: Ivan
  full_name: Milenković, Ivan
  last_name: Milenković
- first_name: Tatjana
  full_name: Petrov, Tatjana
  id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
  last_name: Petrov
  orcid: 0000-0002-9041-0905
- first_name: Gábor
  full_name: Kovács, Gábor
  last_name: Kovács
citation:
  ama: Milenković I, Petrov T, Kovács G. Patterns of hippocampal tau pathology differentiate
    neurodegenerative dementias. <i>Dementia and Geriatric Cognitive Disorders</i>.
    2014;38(5-6):375-388. doi:<a href="https://doi.org/10.1159/000365548">10.1159/000365548</a>
  apa: Milenković, I., Petrov, T., &#38; Kovács, G. (2014). Patterns of hippocampal
    tau pathology differentiate neurodegenerative dementias. <i>Dementia and Geriatric
    Cognitive Disorders</i>. Karger Publishers. <a href="https://doi.org/10.1159/000365548">https://doi.org/10.1159/000365548</a>
  chicago: Milenković, Ivan, Tatjana Petrov, and Gábor Kovács. “Patterns of Hippocampal
    Tau Pathology Differentiate Neurodegenerative Dementias.” <i>Dementia and Geriatric
    Cognitive Disorders</i>. Karger Publishers, 2014. <a href="https://doi.org/10.1159/000365548">https://doi.org/10.1159/000365548</a>.
  ieee: I. Milenković, T. Petrov, and G. Kovács, “Patterns of hippocampal tau pathology
    differentiate neurodegenerative dementias,” <i>Dementia and Geriatric Cognitive
    Disorders</i>, vol. 38, no. 5–6. Karger Publishers, pp. 375–388, 2014.
  ista: Milenković I, Petrov T, Kovács G. 2014. Patterns of hippocampal tau pathology
    differentiate neurodegenerative dementias. Dementia and Geriatric Cognitive Disorders.
    38(5–6), 375–388.
  mla: Milenković, Ivan, et al. “Patterns of Hippocampal Tau Pathology Differentiate
    Neurodegenerative Dementias.” <i>Dementia and Geriatric Cognitive Disorders</i>,
    vol. 38, no. 5–6, Karger Publishers, 2014, pp. 375–88, doi:<a href="https://doi.org/10.1159/000365548">10.1159/000365548</a>.
  short: I. Milenković, T. Petrov, G. Kovács, Dementia and Geriatric Cognitive Disorders
    38 (2014) 375–388.
date_created: 2018-12-11T11:54:41Z
date_published: 2014-11-07T00:00:00Z
date_updated: 2023-10-17T10:21:17Z
day: '07'
department:
- _id: CaGu
doi: 10.1159/000365548
external_id:
  pmid:
  - '25195847'
intvolume: '        38'
issue: 5-6
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://kops.uni-konstanz.de/bitstream/123456789/42127/1/Milenkovic_2-17ivylo2up0798.pdf
month: '11'
oa: 1
oa_version: Published Version
page: 375 - 388
pmid: 1
publication: Dementia and Geriatric Cognitive Disorders
publication_identifier:
  issn:
  - 1420-8008
publication_status: published
publisher: Karger Publishers
publist_id: '5181'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Patterns of hippocampal tau pathology differentiate neurodegenerative dementias
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2014'
...
---
_id: '1916'
abstract:
- lang: eng
  text: Hereditary spastic paraplegias (HSPs) are neurodegenerative motor neuron diseases
    characterized by progressive age-dependent loss of corticospinal motor tract function.
    Although the genetic basis is partly understood, only a fraction of cases can
    receive a genetic diagnosis, and a global view of HSP is lacking. By using whole-exome
    sequencing in combination with network analysis, we identified 18 previously unknown
    putative HSP genes and validated nearly all of these genes functionally or genetically.
    The pathways highlighted by these mutations link HSP to cellular transport, nucleotide
    metabolism, and synapse and axon development. Network analysis revealed a host
    of further candidate genes, of which three were mutated in our cohort. Our analysis
    links HSP to other neurodegenerative disorders and can facilitate gene discovery
    and mechanistic understanding of disease.
acknowledgement: Supported by the Deutsche Forschungsgemeinschaft (G.N.)
article_processing_charge: No
article_type: original
author:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
- first_name: Ali
  full_name: Fenstermaker, Ali
  last_name: Fenstermaker
- first_name: Maha
  full_name: Zaki, Maha
  last_name: Zaki
- first_name: Matan
  full_name: Hofree, Matan
  last_name: Hofree
- first_name: Jennifer
  full_name: Silhavy, Jennifer
  last_name: Silhavy
- first_name: Andrew
  full_name: Heiberg, Andrew
  last_name: Heiberg
- first_name: Mostafa
  full_name: Abdellateef, Mostafa
  last_name: Abdellateef
- first_name: Başak
  full_name: Rosti, Başak
  last_name: Rosti
- first_name: Eric
  full_name: Scott, Eric
  last_name: Scott
- first_name: Lobna
  full_name: Mansour, Lobna
  last_name: Mansour
- first_name: Amira
  full_name: Masri, Amira
  last_name: Masri
- first_name: Hülya
  full_name: Kayserili, Hülya
  last_name: Kayserili
- first_name: Jumana
  full_name: Al Aama, Jumana
  last_name: Al Aama
- first_name: Ghada
  full_name: Abdel Salam, Ghada
  last_name: Abdel Salam
- first_name: Ariana
  full_name: Karminejad, Ariana
  last_name: Karminejad
- first_name: Majdi
  full_name: Kara, Majdi
  last_name: Kara
- first_name: Bülent
  full_name: Kara, Bülent
  last_name: Kara
- first_name: Bita
  full_name: Bozorgmehri, Bita
  last_name: Bozorgmehri
- first_name: Tawfeg
  full_name: Ben Omran, Tawfeg
  last_name: Ben Omran
- first_name: Faezeh
  full_name: Mojahedi, Faezeh
  last_name: Mojahedi
- first_name: Iman
  full_name: Mahmoud, Iman
  last_name: Mahmoud
- first_name: Naïma
  full_name: Bouslam, Naïma
  last_name: Bouslam
- first_name: Ahmed
  full_name: Bouhouche, Ahmed
  last_name: Bouhouche
- first_name: Ali
  full_name: Benomar, Ali
  last_name: Benomar
- first_name: Sylvain
  full_name: Hanein, Sylvain
  last_name: Hanein
- first_name: Laure
  full_name: Raymond, Laure
  last_name: Raymond
- first_name: Sylvie
  full_name: Forlani, Sylvie
  last_name: Forlani
- first_name: Massimo
  full_name: Mascaro, Massimo
  last_name: Mascaro
- first_name: Laila
  full_name: Selim, Laila
  last_name: Selim
- first_name: Nabil
  full_name: Shehata, Nabil
  last_name: Shehata
- first_name: Nasir
  full_name: Al Allawi, Nasir
  last_name: Al Allawi
- first_name: Parayil
  full_name: Bindu, Parayil
  last_name: Bindu
- first_name: Matloob
  full_name: Azam, Matloob
  last_name: Azam
- first_name: Murat
  full_name: Günel, Murat
  last_name: Günel
- first_name: Ahmet
  full_name: Caglayan, Ahmet
  last_name: Caglayan
- first_name: Kaya
  full_name: Bilgüvar, Kaya
  last_name: Bilgüvar
- first_name: Aslihan
  full_name: Tolun, Aslihan
  last_name: Tolun
- first_name: Mahmoud
  full_name: Issa, Mahmoud
  last_name: Issa
- first_name: Jana
  full_name: Schroth, Jana
  last_name: Schroth
- first_name: Emily
  full_name: Spencer, Emily
  last_name: Spencer
- first_name: Rasim
  full_name: Rosti, Rasim
  last_name: Rosti
- first_name: Naiara
  full_name: Akizu, Naiara
  last_name: Akizu
- first_name: Keith
  full_name: Vaux, Keith
  last_name: Vaux
- first_name: Anide
  full_name: Johansen, Anide
  last_name: Johansen
- first_name: Alice
  full_name: Koh, Alice
  last_name: Koh
- first_name: Hisham
  full_name: Megahed, Hisham
  last_name: Megahed
- first_name: Alexandra
  full_name: Dürr, Alexandra
  last_name: Dürr
- first_name: Alexis
  full_name: Brice, Alexis
  last_name: Brice
- first_name: Giovanni
  full_name: Stévanin, Giovanni
  last_name: Stévanin
- first_name: Stacy
  full_name: Gabriel, Stacy
  last_name: Gabriel
- first_name: Trey
  full_name: Ideker, Trey
  last_name: Ideker
- first_name: Joseph
  full_name: Gleeson, Joseph
  last_name: Gleeson
citation:
  ama: Novarino G, Fenstermaker A, Zaki M, et al. Exome sequencing links corticospinal
    motor neuron disease to common neurodegenerative disorders. <i>Science</i>. 2014;343(6170):506-511.
    doi:<a href="https://doi.org/10.1126/science.1247363">10.1126/science.1247363</a>
  apa: Novarino, G., Fenstermaker, A., Zaki, M., Hofree, M., Silhavy, J., Heiberg,
    A., … Gleeson, J. (2014). Exome sequencing links corticospinal motor neuron disease
    to common neurodegenerative disorders. <i>Science</i>. American Association for
    the Advancement of Science. <a href="https://doi.org/10.1126/science.1247363">https://doi.org/10.1126/science.1247363</a>
  chicago: Novarino, Gaia, Ali Fenstermaker, Maha Zaki, Matan Hofree, Jennifer Silhavy,
    Andrew Heiberg, Mostafa Abdellateef, et al. “Exome Sequencing Links Corticospinal
    Motor Neuron Disease to Common Neurodegenerative Disorders.” <i>Science</i>. American
    Association for the Advancement of Science, 2014. <a href="https://doi.org/10.1126/science.1247363">https://doi.org/10.1126/science.1247363</a>.
  ieee: G. Novarino <i>et al.</i>, “Exome sequencing links corticospinal motor neuron
    disease to common neurodegenerative disorders,” <i>Science</i>, vol. 343, no.
    6170. American Association for the Advancement of Science, pp. 506–511, 2014.
  ista: Novarino G, Fenstermaker A, Zaki M, Hofree M, Silhavy J, Heiberg A, Abdellateef
    M, Rosti B, Scott E, Mansour L, Masri A, Kayserili H, Al Aama J, Abdel Salam G,
    Karminejad A, Kara M, Kara B, Bozorgmehri B, Ben Omran T, Mojahedi F, Mahmoud
    I, Bouslam N, Bouhouche A, Benomar A, Hanein S, Raymond L, Forlani S, Mascaro
    M, Selim L, Shehata N, Al Allawi N, Bindu P, Azam M, Günel M, Caglayan A, Bilgüvar
    K, Tolun A, Issa M, Schroth J, Spencer E, Rosti R, Akizu N, Vaux K, Johansen A,
    Koh A, Megahed H, Dürr A, Brice A, Stévanin G, Gabriel S, Ideker T, Gleeson J.
    2014. Exome sequencing links corticospinal motor neuron disease to common neurodegenerative
    disorders. Science. 343(6170), 506–511.
  mla: Novarino, Gaia, et al. “Exome Sequencing Links Corticospinal Motor Neuron Disease
    to Common Neurodegenerative Disorders.” <i>Science</i>, vol. 343, no. 6170, American
    Association for the Advancement of Science, 2014, pp. 506–11, doi:<a href="https://doi.org/10.1126/science.1247363">10.1126/science.1247363</a>.
  short: G. Novarino, A. Fenstermaker, M. Zaki, M. Hofree, J. Silhavy, A. Heiberg,
    M. Abdellateef, B. Rosti, E. Scott, L. Mansour, A. Masri, H. Kayserili, J. Al
    Aama, G. Abdel Salam, A. Karminejad, M. Kara, B. Kara, B. Bozorgmehri, T. Ben
    Omran, F. Mojahedi, I. Mahmoud, N. Bouslam, A. Bouhouche, A. Benomar, S. Hanein,
    L. Raymond, S. Forlani, M. Mascaro, L. Selim, N. Shehata, N. Al Allawi, P. Bindu,
    M. Azam, M. Günel, A. Caglayan, K. Bilgüvar, A. Tolun, M. Issa, J. Schroth, E.
    Spencer, R. Rosti, N. Akizu, K. Vaux, A. Johansen, A. Koh, H. Megahed, A. Dürr,
    A. Brice, G. Stévanin, S. Gabriel, T. Ideker, J. Gleeson, Science 343 (2014) 506–511.
date_created: 2018-12-11T11:54:42Z
date_published: 2014-01-31T00:00:00Z
date_updated: 2021-01-12T06:54:03Z
day: '31'
department:
- _id: GaNo
doi: 10.1126/science.1247363
external_id:
  pmid:
  - '24482476'
intvolume: '       343'
issue: '6170'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157572/
month: '01'
oa: 1
oa_version: Submitted Version
page: 506 - 511
pmid: 1
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5178'
quality_controlled: '1'
scopus_import: 1
status: public
title: Exome sequencing links corticospinal motor neuron disease to common neurodegenerative
  disorders
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 343
year: '2014'
...
---
_id: '1917'
abstract:
- lang: eng
  text: Auxin-binding protein 1 (ABP1) was discovered nearly 40 years ago and was
    shown to be essential for plant development and morphogenesis, but its mode of
    action remains unclear. Here, we report that the plasma membrane-localized transmembrane
    kinase (TMK) receptor-like kinases interact with ABP1 and transduce auxin signal
    to activate plasma membrane-associated ROPs [Rho-like guanosine triphosphatases
    (GTPase) from plants], leading to changes in the cytoskeleton and the shape of
    leaf pavement cells in Arabidopsis. The interaction between ABP1 and TMK at the
    cell surface is induced by auxin and requires ABP1 sensing of auxin. These findings
    show that TMK proteins and ABP1 form a cell surface auxin perception complex that
    activates ROP signaling pathways, regulating nontranscriptional cytoplasmic responses
    and associated fundamental processes.
acknowledgement: Supported by the intramural research program of the National Institute
  of Arthritis and Musculoskeletal and Skin Diseases and by its Laboratory Animal
  Care and Use Section and Flow Cytometry Group, Office of Science and Technology
article_processing_charge: No
article_type: original
author:
- first_name: Tongda
  full_name: Xu, Tongda
  last_name: Xu
- first_name: Ning
  full_name: Dai, Ning
  last_name: Dai
- first_name: Jisheng
  full_name: Chen, Jisheng
  last_name: Chen
- first_name: Shingo
  full_name: Nagawa, Shingo
  last_name: Nagawa
- first_name: Min
  full_name: Cao, Min
  last_name: Cao
- first_name: Hongjiang
  full_name: Li, Hongjiang
  id: 33CA54A6-F248-11E8-B48F-1D18A9856A87
  last_name: Li
  orcid: 0000-0001-5039-9660
- first_name: Zimin
  full_name: Zhou, Zimin
  last_name: Zhou
- first_name: Xu
  full_name: Chen, Xu
  id: 4E5ADCAA-F248-11E8-B48F-1D18A9856A87
  last_name: Chen
- first_name: Riet
  full_name: De Rycke, Riet
  last_name: De Rycke
- first_name: Hana
  full_name: Rakusová, Hana
  last_name: Rakusová
- first_name: Wen
  full_name: Wang, Wen
  last_name: Wang
- first_name: Alan
  full_name: Jones, Alan
  last_name: Jones
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
- first_name: Sara
  full_name: Patterson, Sara
  last_name: Patterson
- first_name: Anthony
  full_name: Bleecker, Anthony
  last_name: Bleecker
- first_name: Zhenbiao
  full_name: Yang, Zhenbiao
  last_name: Yang
citation:
  ama: Xu T, Dai N, Chen J, et al. Cell surface ABP1-TMK auxin sensing complex activates
    ROP GTPase signaling. <i>Science</i>. 2014;343(6174):1025-1028. doi:<a href="https://doi.org/10.1126/science.1245125">10.1126/science.1245125</a>
  apa: Xu, T., Dai, N., Chen, J., Nagawa, S., Cao, M., Li, H., … Yang, Z. (2014).
    Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling. <i>Science</i>.
    American Association for the Advancement of Science. <a href="https://doi.org/10.1126/science.1245125">https://doi.org/10.1126/science.1245125</a>
  chicago: Xu, Tongda, Ning Dai, Jisheng Chen, Shingo Nagawa, Min Cao, Hongjiang Li,
    Zimin Zhou, et al. “Cell Surface ABP1-TMK Auxin Sensing Complex Activates ROP
    GTPase Signaling.” <i>Science</i>. American Association for the Advancement of
    Science, 2014. <a href="https://doi.org/10.1126/science.1245125">https://doi.org/10.1126/science.1245125</a>.
  ieee: T. Xu <i>et al.</i>, “Cell surface ABP1-TMK auxin sensing complex activates
    ROP GTPase signaling,” <i>Science</i>, vol. 343, no. 6174. American Association
    for the Advancement of Science, pp. 1025–1028, 2014.
  ista: Xu T, Dai N, Chen J, Nagawa S, Cao M, Li H, Zhou Z, Chen X, De Rycke R, Rakusová
    H, Wang W, Jones A, Friml J, Patterson S, Bleecker A, Yang Z. 2014. Cell surface
    ABP1-TMK auxin sensing complex activates ROP GTPase signaling. Science. 343(6174),
    1025–1028.
  mla: Xu, Tongda, et al. “Cell Surface ABP1-TMK Auxin Sensing Complex Activates ROP
    GTPase Signaling.” <i>Science</i>, vol. 343, no. 6174, American Association for
    the Advancement of Science, 2014, pp. 1025–28, doi:<a href="https://doi.org/10.1126/science.1245125">10.1126/science.1245125</a>.
  short: T. Xu, N. Dai, J. Chen, S. Nagawa, M. Cao, H. Li, Z. Zhou, X. Chen, R. De
    Rycke, H. Rakusová, W. Wang, A. Jones, J. Friml, S. Patterson, A. Bleecker, Z.
    Yang, Science 343 (2014) 1025–1028.
date_created: 2018-12-11T11:54:42Z
date_published: 2014-02-28T00:00:00Z
date_updated: 2021-01-12T06:54:03Z
day: '28'
department:
- _id: JiFr
doi: 10.1126/science.1245125
external_id:
  pmid:
  - '24578577'
intvolume: '       343'
issue: '6174'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166562/
month: '02'
oa: 1
oa_version: Submitted Version
page: 1025 - 1028
pmid: 1
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5177'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 343
year: '2014'
...
---
_id: '1918'
abstract:
- lang: eng
  text: As the nuclear charge Z is continuously decreased an N-electron atom undergoes
    a binding-unbinding transition. We investigate whether the electrons remain bound
    and whether the radius of the system stays finite as the critical value Zc is
    approached. Existence of a ground state at Zc is shown under the condition Zc
    &lt; N-K, where K is the maximal number of electrons that can be removed at Zc
    without changing the energy.
article_number: '1350021'
author:
- first_name: Jacopo
  full_name: Bellazzini, Jacopo
  last_name: Bellazzini
- first_name: Rupert
  full_name: Frank, Rupert
  last_name: Frank
- first_name: Élliott
  full_name: Lieb, Élliott
  last_name: Lieb
- first_name: Robert
  full_name: Seiringer, Robert
  id: 4AFD0470-F248-11E8-B48F-1D18A9856A87
  last_name: Seiringer
  orcid: 0000-0002-6781-0521
citation:
  ama: Bellazzini J, Frank R, Lieb É, Seiringer R. Existence of ground states for
    negative ions at the binding threshold. <i>Reviews in Mathematical Physics</i>.
    2014;26(1). doi:<a href="https://doi.org/10.1142/S0129055X13500219">10.1142/S0129055X13500219</a>
  apa: Bellazzini, J., Frank, R., Lieb, É., &#38; Seiringer, R. (2014). Existence
    of ground states for negative ions at the binding threshold. <i>Reviews in Mathematical
    Physics</i>. World Scientific Publishing. <a href="https://doi.org/10.1142/S0129055X13500219">https://doi.org/10.1142/S0129055X13500219</a>
  chicago: Bellazzini, Jacopo, Rupert Frank, Élliott Lieb, and Robert Seiringer. “Existence
    of Ground States for Negative Ions at the Binding Threshold.” <i>Reviews in Mathematical
    Physics</i>. World Scientific Publishing, 2014. <a href="https://doi.org/10.1142/S0129055X13500219">https://doi.org/10.1142/S0129055X13500219</a>.
  ieee: J. Bellazzini, R. Frank, É. Lieb, and R. Seiringer, “Existence of ground states
    for negative ions at the binding threshold,” <i>Reviews in Mathematical Physics</i>,
    vol. 26, no. 1. World Scientific Publishing, 2014.
  ista: Bellazzini J, Frank R, Lieb É, Seiringer R. 2014. Existence of ground states
    for negative ions at the binding threshold. Reviews in Mathematical Physics. 26(1),
    1350021.
  mla: Bellazzini, Jacopo, et al. “Existence of Ground States for Negative Ions at
    the Binding Threshold.” <i>Reviews in Mathematical Physics</i>, vol. 26, no. 1,
    1350021, World Scientific Publishing, 2014, doi:<a href="https://doi.org/10.1142/S0129055X13500219">10.1142/S0129055X13500219</a>.
  short: J. Bellazzini, R. Frank, É. Lieb, R. Seiringer, Reviews in Mathematical Physics
    26 (2014).
date_created: 2018-12-11T11:54:42Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2021-01-12T06:54:04Z
day: '01'
department:
- _id: RoSe
doi: 10.1142/S0129055X13500219
intvolume: '        26'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://arxiv.org/abs/1301.5370
month: '02'
oa: 1
oa_version: Submitted Version
project:
- _id: 26450934-B435-11E9-9278-68D0E5697425
  name: NSERC Postdoctoral fellowship
publication: Reviews in Mathematical Physics
publication_status: published
publisher: World Scientific Publishing
publist_id: '5176'
quality_controlled: '1'
scopus_import: 1
status: public
title: Existence of ground states for negative ions at the binding threshold
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2014'
...
---
_id: '1919'
abstract:
- lang: eng
  text: Long-lasting memories are formed when the stimulus is temporally distributed
    (spacing effect). However, the synaptic mechanisms underlying this robust phenomenon
    and the precise time course of the synaptic modifications that occur during learning
    remain unclear. Here we examined the adaptation of horizontal optokinetic response
    in mice that underwent 1 h of massed and spaced training at varying intervals.
    Despite similar acquisition by all training protocols, 1 h of spacing produced
    the highest memory retention at 24 h, which lasted for 1 mo. The distinct kinetics
    of memory are strongly correlated with the reduction of floccular parallel fiber-Purkinje
    cell synapses but not with AMPA receptor (AMPAR) number and synapse size. After
    the spaced training, we observed 25%, 23%, and 12% reduction in AMPAR density,
    synapse size, and synapse number, respectively. Four hours after the spaced training,
    half of the synapses and Purkinje cell spines had been eliminated, whereas AMPAR
    density and synapse size were recovered in remaining synapses. Surprisingly, massed
    training also produced long-term memory and halving of synapses; however, this
    occurred slowly over days, and the memory lasted for only 1 wk. This distinct
    kinetics of structural plasticity may serve as a basis for unique temporal profiles
    in the formation and decay of memory with or without intervals.
acknowledgement: his work was supported by Solution Oriented Research for Science
  and Technology (R.S.), Core Research for Evolutional Science and Technology, Japan
  Science and Technology Agency (Y.F.), and Grants-in-Aid for Scientific Research
  on Priority Areas-Molecular Brain Sciences 16300114 (to R.S.) and 18022043 (to Y.F.).
author:
- first_name: Wajeeha
  full_name: Aziz, Wajeeha
  last_name: Aziz
- first_name: Wen
  full_name: Wang, Wen
  last_name: Wang
- first_name: Sebnem
  full_name: Kesaf, Sebnem
  id: 401AB46C-F248-11E8-B48F-1D18A9856A87
  last_name: Kesaf
- first_name: Alsayed
  full_name: Mohamed, Alsayed
  last_name: Mohamed
- first_name: Yugo
  full_name: Fukazawa, Yugo
  last_name: Fukazawa
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
citation:
  ama: Aziz W, Wang W, Kesaf S, Mohamed A, Fukazawa Y, Shigemoto R. Distinct kinetics
    of synaptic structural plasticity, memory formation, and memory decay in massed
    and spaced learning. <i>PNAS</i>. 2014;111(1):E194-E202. doi:<a href="https://doi.org/10.1073/pnas.1303317110">10.1073/pnas.1303317110</a>
  apa: Aziz, W., Wang, W., Kesaf, S., Mohamed, A., Fukazawa, Y., &#38; Shigemoto,
    R. (2014). Distinct kinetics of synaptic structural plasticity, memory formation,
    and memory decay in massed and spaced learning. <i>PNAS</i>. National Academy
    of Sciences. <a href="https://doi.org/10.1073/pnas.1303317110">https://doi.org/10.1073/pnas.1303317110</a>
  chicago: Aziz, Wajeeha, Wen Wang, Sebnem Kesaf, Alsayed Mohamed, Yugo Fukazawa,
    and Ryuichi Shigemoto. “Distinct Kinetics of Synaptic Structural Plasticity, Memory
    Formation, and Memory Decay in Massed and Spaced Learning.” <i>PNAS</i>. National
    Academy of Sciences, 2014. <a href="https://doi.org/10.1073/pnas.1303317110">https://doi.org/10.1073/pnas.1303317110</a>.
  ieee: W. Aziz, W. Wang, S. Kesaf, A. Mohamed, Y. Fukazawa, and R. Shigemoto, “Distinct
    kinetics of synaptic structural plasticity, memory formation, and memory decay
    in massed and spaced learning,” <i>PNAS</i>, vol. 111, no. 1. National Academy
    of Sciences, pp. E194–E202, 2014.
  ista: Aziz W, Wang W, Kesaf S, Mohamed A, Fukazawa Y, Shigemoto R. 2014. Distinct
    kinetics of synaptic structural plasticity, memory formation, and memory decay
    in massed and spaced learning. PNAS. 111(1), E194–E202.
  mla: Aziz, Wajeeha, et al. “Distinct Kinetics of Synaptic Structural Plasticity,
    Memory Formation, and Memory Decay in Massed and Spaced Learning.” <i>PNAS</i>,
    vol. 111, no. 1, National Academy of Sciences, 2014, pp. E194–202, doi:<a href="https://doi.org/10.1073/pnas.1303317110">10.1073/pnas.1303317110</a>.
  short: W. Aziz, W. Wang, S. Kesaf, A. Mohamed, Y. Fukazawa, R. Shigemoto, PNAS 111
    (2014) E194–E202.
date_created: 2018-12-11T11:54:43Z
date_published: 2014-01-07T00:00:00Z
date_updated: 2021-01-12T06:54:04Z
day: '07'
department:
- _id: RySh
doi: 10.1073/pnas.1303317110
intvolume: '       111'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890840/
month: '01'
oa: 1
oa_version: Submitted Version
page: E194 - E202
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5175'
scopus_import: 1
status: public
title: Distinct kinetics of synaptic structural plasticity, memory formation, and
  memory decay in massed and spaced learning
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 111
year: '2014'
...
---
_id: '1920'
abstract:
- lang: eng
  text: Cerebellar motor learning is suggested to be caused by long-term plasticity
    of excitatory parallel fiber-Purkinje cell (PF-PC) synapses associated with changes
    in the number of synaptic AMPA-type glutamate receptors (AMPARs). However, whether
    the AMPARs decrease or increase in individual PF-PC synapses occurs in physiological
    motor learning and accounts for memory that lasts over days remains elusive. We
    combined quantitative SDS-digested freeze-fracture replica labeling for AMPAR
    and physical dissector electron microscopy with a simple model of cerebellar motor
    learning, adaptation of horizontal optokinetic response (HOKR) in mouse. After
    1-h training of HOKR, short-term adaptation (STA) was accompanied with transient
    decrease in AMPARs by 28% in target PF-PC synapses. STA was well correlated with
    AMPAR decrease in individual animals and both STA and AMPAR decrease recovered
    to basal levels within 24 h. Surprisingly, long-termadaptation (LTA) after five
    consecutive daily trainings of 1-h HOKR did not alter the number of AMPARs in
    PF-PC synapses but caused gradual and persistent synapse elimination by 45%, with
    corresponding PC spine loss by the fifth training day. Furthermore, recovery of
    LTA after 2 wk was well correlated with increase of PF-PC synapses to the control
    level. Our findings indicate that the AMPARs decrease in PF-PC synapses and the
    elimination of these synapses are in vivo engrams in short- and long-term motor
    learning, respectively, showing a unique type of synaptic plasticity that may
    contribute to memory consolidation.
acknowledgement: This work was supported by Solution-Oriented Research for Science
  and Technology from the Japan Science and Technology Agency; Ministry of Education,
  Culture, Sports, Science and Technology of Japan Grant 16300114 (to R.S.).
author:
- first_name: Wen
  full_name: Wang, Wen
  last_name: Wang
- first_name: Kazuhiko
  full_name: Nakadate, Kazuhiko
  last_name: Nakadate
- first_name: Miwako
  full_name: Masugi Tokita, Miwako
  last_name: Masugi Tokita
- first_name: Fumihiro
  full_name: Shutoh, Fumihiro
  last_name: Shutoh
- first_name: Wajeeha
  full_name: Aziz, Wajeeha
  last_name: Aziz
- first_name: Etsuko
  full_name: Tarusawa, Etsuko
  last_name: Tarusawa
- first_name: Andrea
  full_name: Lörincz, Andrea
  last_name: Lörincz
- first_name: Elek
  full_name: Molnár, Elek
  last_name: Molnár
- first_name: Sebnem
  full_name: Kesaf, Sebnem
  id: 401AB46C-F248-11E8-B48F-1D18A9856A87
  last_name: Kesaf
- first_name: Yunqing
  full_name: Li, Yunqing
  last_name: Li
- first_name: Yugo
  full_name: Fukazawa, Yugo
  last_name: Fukazawa
- first_name: Soichi
  full_name: Nagao, Soichi
  last_name: Nagao
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
citation:
  ama: Wang W, Nakadate K, Masugi Tokita M, et al. Distinct cerebellar engrams in
    short-term and long-term motor learning. <i>PNAS</i>. 2014;111(1):E188-E193. doi:<a
    href="https://doi.org/10.1073/pnas.1315541111">10.1073/pnas.1315541111</a>
  apa: Wang, W., Nakadate, K., Masugi Tokita, M., Shutoh, F., Aziz, W., Tarusawa,
    E., … Shigemoto, R. (2014). Distinct cerebellar engrams in short-term and long-term
    motor learning. <i>PNAS</i>. National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1315541111">https://doi.org/10.1073/pnas.1315541111</a>
  chicago: Wang, Wen, Kazuhiko Nakadate, Miwako Masugi Tokita, Fumihiro Shutoh, Wajeeha
    Aziz, Etsuko Tarusawa, Andrea Lörincz, et al. “Distinct Cerebellar Engrams in
    Short-Term and Long-Term Motor Learning.” <i>PNAS</i>. National Academy of Sciences,
    2014. <a href="https://doi.org/10.1073/pnas.1315541111">https://doi.org/10.1073/pnas.1315541111</a>.
  ieee: W. Wang <i>et al.</i>, “Distinct cerebellar engrams in short-term and long-term
    motor learning,” <i>PNAS</i>, vol. 111, no. 1. National Academy of Sciences, pp.
    E188–E193, 2014.
  ista: Wang W, Nakadate K, Masugi Tokita M, Shutoh F, Aziz W, Tarusawa E, Lörincz
    A, Molnár E, Kesaf S, Li Y, Fukazawa Y, Nagao S, Shigemoto R. 2014. Distinct cerebellar
    engrams in short-term and long-term motor learning. PNAS. 111(1), E188–E193.
  mla: Wang, Wen, et al. “Distinct Cerebellar Engrams in Short-Term and Long-Term
    Motor Learning.” <i>PNAS</i>, vol. 111, no. 1, National Academy of Sciences, 2014,
    pp. E188–93, doi:<a href="https://doi.org/10.1073/pnas.1315541111">10.1073/pnas.1315541111</a>.
  short: W. Wang, K. Nakadate, M. Masugi Tokita, F. Shutoh, W. Aziz, E. Tarusawa,
    A. Lörincz, E. Molnár, S. Kesaf, Y. Li, Y. Fukazawa, S. Nagao, R. Shigemoto, PNAS
    111 (2014) E188–E193.
date_created: 2018-12-11T11:54:43Z
date_published: 2014-01-07T00:00:00Z
date_updated: 2021-01-12T06:54:05Z
day: '07'
department:
- _id: RySh
doi: 10.1073/pnas.1315541111
intvolume: '       111'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890858/
month: '01'
oa: 1
oa_version: Submitted Version
page: E188 - E193
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5174'
scopus_import: 1
status: public
title: Distinct cerebellar engrams in short-term and long-term motor learning
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 111
year: '2014'
...
---
_id: '1921'
abstract:
- lang: eng
  text: Cell polarity manifested by asymmetric distribution of cargoes, such as receptors
    and transporters, within the plasma membrane (PM) is crucial for essential functions
    in multicellular organisms. In plants, cell polarity (re)establishment is intimately
    linked to patterning processes. Despite the importance of cell polarity, its underlying
    mechanisms are still largely unknown, including the definition and distinctiveness
    of the polar domains within the PM. Here, we show in Arabidopsis thaliana that
    the signaling membrane components, the phosphoinositides phosphatidylinositol
    4-phosphate (PtdIns4P) and phosphatidylinositol 4, 5-bisphosphate [PtdIns(4, 5)P2]
    as well as PtdIns4P 5-kinases mediating their interconversion, are specifically
    enriched at apical and basal polar plasma membrane domains. The PtdIns4P 5-kinases
    PIP5K1 and PIP5K2 are redundantly required for polar localization of specifically
    apical and basal cargoes, such as PIN-FORMED transporters for the plant hormone
    auxin. As a consequence of the polarity defects, instructive auxin gradients as
    well as embryonic and postembryonic patterning are severely compromised. Furthermore,
    auxin itself regulates PIP5K transcription and PtdIns4P and PtdIns(4, 5)P2 levels,
    in particular their association with polar PM domains. Our results provide insight
    into the polar domain-delineating mechanisms in plant cells that depend on apical
    and basal distribution of membrane lipids and are essential for embryonic and
    postembryonic patterning.
acknowledgement: This work was supported by grants from the Odysseus program of the
  Research Foundation-Flanders (to J.F.).
author:
- first_name: Ricardo
  full_name: Tejos, Ricardo
  last_name: Tejos
- first_name: Michael
  full_name: Sauer, Michael
  last_name: Sauer
- first_name: Steffen
  full_name: Vanneste, Steffen
  last_name: Vanneste
- first_name: 'MiriamPalacios '
  full_name: 'Palacios-Gomez, MiriamPalacios '
  last_name: Palacios-Gomez
- first_name: Hongjiang
  full_name: Li, Hongjiang
  id: 33CA54A6-F248-11E8-B48F-1D18A9856A87
  last_name: Li
  orcid: 0000-0001-5039-9660
- first_name: Mareike
  full_name: Heilmann, Mareike
  last_name: Heilmann
- first_name: Ringo
  full_name: Van Wijk, Ringo
  last_name: Van Wijk
- first_name: Joop
  full_name: Vermeer, Joop
  last_name: Vermeer
- first_name: Ingo
  full_name: Heilmann, Ingo
  last_name: Heilmann
- first_name: Teun
  full_name: Munnik, Teun
  last_name: Munnik
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Tejos R, Sauer M, Vanneste S, et al. Bipolar plasma membrane distribution of
    phosphoinositides and their requirement for auxin-mediated cell polarity and patterning
    in Arabidopsis. <i>Plant Cell</i>. 2014;26(5):2114-2128. doi:<a href="https://doi.org/10.1105/tpc.114.126185">10.1105/tpc.114.126185</a>
  apa: Tejos, R., Sauer, M., Vanneste, S., Palacios-Gomez, M., Li, H., Heilmann, M.,
    … Friml, J. (2014). Bipolar plasma membrane distribution of phosphoinositides
    and their requirement for auxin-mediated cell polarity and patterning in Arabidopsis.
    <i>Plant Cell</i>. American Society of Plant Biologists. <a href="https://doi.org/10.1105/tpc.114.126185">https://doi.org/10.1105/tpc.114.126185</a>
  chicago: Tejos, Ricardo, Michael Sauer, Steffen Vanneste, MiriamPalacios  Palacios-Gomez,
    Hongjiang Li, Mareike Heilmann, Ringo Van Wijk, et al. “Bipolar Plasma Membrane
    Distribution of Phosphoinositides and Their Requirement for Auxin-Mediated Cell
    Polarity and Patterning in Arabidopsis.” <i>Plant Cell</i>. American Society of
    Plant Biologists, 2014. <a href="https://doi.org/10.1105/tpc.114.126185">https://doi.org/10.1105/tpc.114.126185</a>.
  ieee: R. Tejos <i>et al.</i>, “Bipolar plasma membrane distribution of phosphoinositides
    and their requirement for auxin-mediated cell polarity and patterning in Arabidopsis,”
    <i>Plant Cell</i>, vol. 26, no. 5. American Society of Plant Biologists, pp. 2114–2128,
    2014.
  ista: Tejos R, Sauer M, Vanneste S, Palacios-Gomez M, Li H, Heilmann M, Van Wijk
    R, Vermeer J, Heilmann I, Munnik T, Friml J. 2014. Bipolar plasma membrane distribution
    of phosphoinositides and their requirement for auxin-mediated cell polarity and
    patterning in Arabidopsis. Plant Cell. 26(5), 2114–2128.
  mla: Tejos, Ricardo, et al. “Bipolar Plasma Membrane Distribution of Phosphoinositides
    and Their Requirement for Auxin-Mediated Cell Polarity and Patterning in Arabidopsis.”
    <i>Plant Cell</i>, vol. 26, no. 5, American Society of Plant Biologists, 2014,
    pp. 2114–28, doi:<a href="https://doi.org/10.1105/tpc.114.126185">10.1105/tpc.114.126185</a>.
  short: R. Tejos, M. Sauer, S. Vanneste, M. Palacios-Gomez, H. Li, M. Heilmann, R.
    Van Wijk, J. Vermeer, I. Heilmann, T. Munnik, J. Friml, Plant Cell 26 (2014) 2114–2128.
date_created: 2018-12-11T11:54:43Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2021-01-12T06:54:05Z
day: '01'
department:
- _id: JiFr
doi: 10.1105/tpc.114.126185
ec_funded: 1
intvolume: '        26'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4079372/
month: '05'
oa: 1
oa_version: Submitted Version
page: 2114 - 2128
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '282300'
  name: Polarity and subcellular dynamics in plants
publication: Plant Cell
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '5173'
scopus_import: 1
status: public
title: Bipolar plasma membrane distribution of phosphoinositides and their requirement
  for auxin-mediated cell polarity and patterning in Arabidopsis
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2014'
...
---
_id: '1923'
abstract:
- lang: eng
  text: We derive the equations for a thin, axisymmetric elastic shell subjected to
    an internal active stress giving rise to active tension and moments within the
    shell. We discuss the stability of a cylindrical elastic shell and its response
    to a localized change in internal active stress. This description is relevant
    to describe the cellular actomyosin cortex, a thin shell at the cell surface behaving
    elastically at a short timescale and subjected to active internal forces arising
    from myosin molecular motor activity. We show that the recent observations of
    cell deformation following detachment of adherent cells (Maître J-L et al 2012
    Science 338 253-6) are well accounted for by this mechanical description. The
    actin cortex elastic and bending moduli can be obtained from a quantitative analysis
    of cell shapes observed in these experiments. Our approach thus provides a non-invasive,
    imaging-based method for the extraction of cellular physical parameters.
article_number: '065005'
author:
- first_name: Hélène
  full_name: Berthoumieux, Hélène
  last_name: Berthoumieux
- first_name: Jean-Léon
  full_name: Maître, Jean-Léon
  id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87
  last_name: Maître
  orcid: 0000-0002-3688-1474
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
- first_name: Ewa
  full_name: Paluch, Ewa
  last_name: Paluch
- first_name: Frank
  full_name: Julicher, Frank
  last_name: Julicher
- first_name: Guillaume
  full_name: Salbreux, Guillaume
  last_name: Salbreux
citation:
  ama: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux
    G. Active elastic thin shell theory for cellular deformations. <i>New Journal
    of Physics</i>. 2014;16. doi:<a href="https://doi.org/10.1088/1367-2630/16/6/065005">10.1088/1367-2630/16/6/065005</a>
  apa: Berthoumieux, H., Maître, J.-L., Heisenberg, C.-P. J., Paluch, E., Julicher,
    F., &#38; Salbreux, G. (2014). Active elastic thin shell theory for cellular deformations.
    <i>New Journal of Physics</i>. IOP Publishing Ltd. <a href="https://doi.org/10.1088/1367-2630/16/6/065005">https://doi.org/10.1088/1367-2630/16/6/065005</a>
  chicago: Berthoumieux, Hélène, Jean-Léon Maître, Carl-Philipp J Heisenberg, Ewa
    Paluch, Frank Julicher, and Guillaume Salbreux. “Active Elastic Thin Shell Theory
    for Cellular Deformations.” <i>New Journal of Physics</i>. IOP Publishing Ltd.,
    2014. <a href="https://doi.org/10.1088/1367-2630/16/6/065005">https://doi.org/10.1088/1367-2630/16/6/065005</a>.
  ieee: H. Berthoumieux, J.-L. Maître, C.-P. J. Heisenberg, E. Paluch, F. Julicher,
    and G. Salbreux, “Active elastic thin shell theory for cellular deformations,”
    <i>New Journal of Physics</i>, vol. 16. IOP Publishing Ltd., 2014.
  ista: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux
    G. 2014. Active elastic thin shell theory for cellular deformations. New Journal
    of Physics. 16, 065005.
  mla: Berthoumieux, Hélène, et al. “Active Elastic Thin Shell Theory for Cellular
    Deformations.” <i>New Journal of Physics</i>, vol. 16, 065005, IOP Publishing
    Ltd., 2014, doi:<a href="https://doi.org/10.1088/1367-2630/16/6/065005">10.1088/1367-2630/16/6/065005</a>.
  short: H. Berthoumieux, J.-L. Maître, C.-P.J. Heisenberg, E. Paluch, F. Julicher,
    G. Salbreux, New Journal of Physics 16 (2014).
date_created: 2018-12-11T11:54:44Z
date_published: 2014-06-01T00:00:00Z
date_updated: 2021-01-12T06:54:06Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1088/1367-2630/16/6/065005
file:
- access_level: open_access
  checksum: 8dbe81ec656bf1264d8889bda9b2b985
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:16:16Z
  date_updated: 2020-07-14T12:45:21Z
  file_id: '5202'
  file_name: IST-2016-429-v1+1_document.pdf
  file_size: 941387
  relation: main_file
file_date_updated: 2020-07-14T12:45:21Z
has_accepted_license: '1'
intvolume: '        16'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: New Journal of Physics
publication_status: published
publisher: IOP Publishing Ltd.
publist_id: '5171'
pubrep_id: '429'
quality_controlled: '1'
scopus_import: 1
status: public
title: Active elastic thin shell theory for cellular deformations
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '1925'
abstract:
- lang: eng
  text: In the past decade carbon nanotubes (CNTs) have been widely studied as a potential
    drug-delivery system, especially with functionality for cellular targeting. Yet,
    little is known about the actual process of docking to cell receptors and transport
    dynamics after internalization. Here we performed single-particle studies of folic
    acid (FA) mediated CNT binding to human carcinoma cells and their transport inside
    the cytosol. In particular, we employed molecular recognition force spectroscopy,
    an atomic force microscopy based method, to visualize and quantify docking of
    FA functionalized CNTs to FA binding receptors in terms of binding probability
    and binding force. We then traced individual fluorescently labeled, FA functionalized
    CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed
    trajectories of directed diffusion and areas of nanotube confinement in the cytosol.
    Our results demonstrate the potential of a single-molecule approach for investigation
    of drug-delivery vehicles and their targeting capacity.
acknowledgement: "This work was supported by EC grant Marie Curie RTN-CT-2006-035616,
  CARBIO 'Carbon nanotubes for biomedical applications' and Austrian FFG grant mnt-era.net
  823980, 'IntelliTip'.\r\n"
article_number: '125704'
article_processing_charge: No
article_type: original
author:
- first_name: Constanze
  full_name: Lamprecht, Constanze
  last_name: Lamprecht
- first_name: Birgit
  full_name: Plochberger, Birgit
  last_name: Plochberger
- first_name: Verena
  full_name: Ruprecht, Verena
  id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
  last_name: Ruprecht
  orcid: 0000-0003-4088-8633
- first_name: Stefan
  full_name: Wieser, Stefan
  id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
  last_name: Wieser
  orcid: 0000-0002-2670-2217
- first_name: Christian
  full_name: Rankl, Christian
  last_name: Rankl
- first_name: Elena
  full_name: Heister, Elena
  last_name: Heister
- first_name: Barbara
  full_name: Unterauer, Barbara
  last_name: Unterauer
- first_name: Mario
  full_name: Brameshuber, Mario
  last_name: Brameshuber
- first_name: Jürgen
  full_name: Danzberger, Jürgen
  last_name: Danzberger
- first_name: Petar
  full_name: Lukanov, Petar
  last_name: Lukanov
- first_name: Emmanuel
  full_name: Flahaut, Emmanuel
  last_name: Flahaut
- first_name: Gerhard
  full_name: Schütz, Gerhard
  last_name: Schütz
- first_name: Peter
  full_name: Hinterdorfer, Peter
  last_name: Hinterdorfer
- first_name: Andreas
  full_name: Ebner, Andreas
  last_name: Ebner
citation:
  ama: Lamprecht C, Plochberger B, Ruprecht V, et al. A single-molecule approach to
    explore binding uptake and transport of cancer cell targeting nanotubes. <i>Nanotechnology</i>.
    2014;25(12). doi:<a href="https://doi.org/10.1088/0957-4484/25/12/125704">10.1088/0957-4484/25/12/125704</a>
  apa: Lamprecht, C., Plochberger, B., Ruprecht, V., Wieser, S., Rankl, C., Heister,
    E., … Ebner, A. (2014). A single-molecule approach to explore binding uptake and
    transport of cancer cell targeting nanotubes. <i>Nanotechnology</i>. IOP Publishing.
    <a href="https://doi.org/10.1088/0957-4484/25/12/125704">https://doi.org/10.1088/0957-4484/25/12/125704</a>
  chicago: Lamprecht, Constanze, Birgit Plochberger, Verena Ruprecht, Stefan Wieser,
    Christian Rankl, Elena Heister, Barbara Unterauer, et al. “A Single-Molecule Approach
    to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” <i>Nanotechnology</i>.
    IOP Publishing, 2014. <a href="https://doi.org/10.1088/0957-4484/25/12/125704">https://doi.org/10.1088/0957-4484/25/12/125704</a>.
  ieee: C. Lamprecht <i>et al.</i>, “A single-molecule approach to explore binding
    uptake and transport of cancer cell targeting nanotubes,” <i>Nanotechnology</i>,
    vol. 25, no. 12. IOP Publishing, 2014.
  ista: Lamprecht C, Plochberger B, Ruprecht V, Wieser S, Rankl C, Heister E, Unterauer
    B, Brameshuber M, Danzberger J, Lukanov P, Flahaut E, Schütz G, Hinterdorfer P,
    Ebner A. 2014. A single-molecule approach to explore binding uptake and transport
    of cancer cell targeting nanotubes. Nanotechnology. 25(12), 125704.
  mla: Lamprecht, Constanze, et al. “A Single-Molecule Approach to Explore Binding
    Uptake and Transport of Cancer Cell Targeting Nanotubes.” <i>Nanotechnology</i>,
    vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:<a href="https://doi.org/10.1088/0957-4484/25/12/125704">10.1088/0957-4484/25/12/125704</a>.
  short: C. Lamprecht, B. Plochberger, V. Ruprecht, S. Wieser, C. Rankl, E. Heister,
    B. Unterauer, M. Brameshuber, J. Danzberger, P. Lukanov, E. Flahaut, G. Schütz,
    P. Hinterdorfer, A. Ebner, Nanotechnology 25 (2014).
date_created: 2018-12-11T11:54:45Z
date_published: 2014-03-28T00:00:00Z
date_updated: 2021-01-12T06:54:07Z
day: '28'
ddc:
- '570'
department:
- _id: CaHe
- _id: MiSi
doi: 10.1088/0957-4484/25/12/125704
file:
- access_level: open_access
  checksum: df4e03d225a19179e7790f6d87a12332
  content_type: application/pdf
  creator: dernst
  date_created: 2020-05-15T09:21:19Z
  date_updated: 2020-07-14T12:45:21Z
  file_id: '7856'
  file_name: 2014_Nanotechnology_Lamprecht.pdf
  file_size: 3804152
  relation: main_file
file_date_updated: 2020-07-14T12:45:21Z
has_accepted_license: '1'
intvolume: '        25'
issue: '12'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Submitted Version
publication: Nanotechnology
publication_status: published
publisher: IOP Publishing
publist_id: '5169'
scopus_import: 1
status: public
title: A single-molecule approach to explore binding uptake and transport of cancer
  cell targeting nanotubes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 25
year: '2014'
...
---
_id: '1926'
abstract:
- lang: eng
  text: We consider cross products of finite graphs with a class of trees that have
    arbitrarily but finitely long line segments, such as the Fibonacci tree. Such
    cross products are called tree-strips. We prove that for small disorder random
    Schrödinger operators on such tree-strips have purely absolutely continuous spectrum
    in a certain set.
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Christian
  full_name: Sadel, Christian
  id: 4760E9F8-F248-11E8-B48F-1D18A9856A87
  last_name: Sadel
  orcid: 0000-0001-8255-3968
citation:
  ama: Sadel C. Absolutely continuous spectrum for random Schrödinger operators on
    the Fibonacci and similar Tree-strips. <i>Mathematical Physics, Analysis and Geometry</i>.
    2014;17(3-4):409-440. doi:<a href="https://doi.org/10.1007/s11040-014-9163-4">10.1007/s11040-014-9163-4</a>
  apa: Sadel, C. (2014). Absolutely continuous spectrum for random Schrödinger operators
    on the Fibonacci and similar Tree-strips. <i>Mathematical Physics, Analysis and
    Geometry</i>. Springer. <a href="https://doi.org/10.1007/s11040-014-9163-4">https://doi.org/10.1007/s11040-014-9163-4</a>
  chicago: Sadel, Christian. “Absolutely Continuous Spectrum for Random Schrödinger
    Operators on the Fibonacci and Similar Tree-Strips.” <i>Mathematical Physics,
    Analysis and Geometry</i>. Springer, 2014. <a href="https://doi.org/10.1007/s11040-014-9163-4">https://doi.org/10.1007/s11040-014-9163-4</a>.
  ieee: C. Sadel, “Absolutely continuous spectrum for random Schrödinger operators
    on the Fibonacci and similar Tree-strips,” <i>Mathematical Physics, Analysis and
    Geometry</i>, vol. 17, no. 3–4. Springer, pp. 409–440, 2014.
  ista: Sadel C. 2014. Absolutely continuous spectrum for random Schrödinger operators
    on the Fibonacci and similar Tree-strips. Mathematical Physics, Analysis and Geometry.
    17(3–4), 409–440.
  mla: Sadel, Christian. “Absolutely Continuous Spectrum for Random Schrödinger Operators
    on the Fibonacci and Similar Tree-Strips.” <i>Mathematical Physics, Analysis and
    Geometry</i>, vol. 17, no. 3–4, Springer, 2014, pp. 409–40, doi:<a href="https://doi.org/10.1007/s11040-014-9163-4">10.1007/s11040-014-9163-4</a>.
  short: C. Sadel, Mathematical Physics, Analysis and Geometry 17 (2014) 409–440.
date_created: 2018-12-11T11:54:45Z
date_published: 2014-12-17T00:00:00Z
date_updated: 2021-01-12T06:54:07Z
day: '17'
department:
- _id: LaEr
doi: 10.1007/s11040-014-9163-4
ec_funded: 1
external_id:
  arxiv:
  - '1304.3862'
intvolume: '        17'
issue: 3-4
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1304.3862
month: '12'
oa: 1
oa_version: Preprint
page: 409 - 440
project:
- _id: 26450934-B435-11E9-9278-68D0E5697425
  name: NSERC Postdoctoral fellowship
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Mathematical Physics, Analysis and Geometry
publication_status: published
publisher: Springer
publist_id: '5168'
quality_controlled: '1'
scopus_import: 1
status: public
title: Absolutely continuous spectrum for random Schrödinger operators on the Fibonacci
  and similar Tree-strips
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2014'
...
