---
_id: '1804'
abstract:
- lang: eng
text: It is known that in classical fluids turbulence typically occurs at high Reynolds
numbers. But can turbulence occur at low Reynolds numbers? Here we investigate
the transition to turbulence in the classic Taylor-Couette system in which the
rotating fluids are manufactured ferrofluids with magnetized nanoparticles embedded
in liquid carriers. We find that, in the presence of a magnetic field transverse
to the symmetry axis of the system, turbulence can occur at Reynolds numbers that
are at least one order of magnitude smaller than those in conventional fluids.
This is established by extensive computational ferrohydrodynamics through a detailed
investigation of transitions in the flow structure, and characterization of behaviors
of physical quantities such as the energy, the wave number, and the angular momentum
through the bifurcations. A finding is that, as the magnetic field is increased,
onset of turbulence can be determined accurately and reliably. Our results imply
that experimental investigation of turbulence may be feasible by using ferrofluids.
Our study of transition to and evolution of turbulence in the Taylor-Couette ferrofluidic
flow system provides insights into the challenging problem of turbulence control.
article_number: '10781'
author:
- first_name: Sebastian
full_name: Altmeyer, Sebastian
id: 2EE67FDC-F248-11E8-B48F-1D18A9856A87
last_name: Altmeyer
orcid: 0000-0001-5964-0203
- first_name: Younghae
full_name: Do, Younghae
last_name: Do
- first_name: Ying
full_name: Lai, Ying
last_name: Lai
citation:
ama: Altmeyer S, Do Y, Lai Y. Transition to turbulence in Taylor-Couette ferrofluidic
flow. Scientific Reports. 2015;5. doi:10.1038/srep10781
apa: Altmeyer, S., Do, Y., & Lai, Y. (2015). Transition to turbulence in Taylor-Couette
ferrofluidic flow. Scientific Reports. Nature Publishing Group. https://doi.org/10.1038/srep10781
chicago: Altmeyer, Sebastian, Younghae Do, and Ying Lai. “Transition to Turbulence
in Taylor-Couette Ferrofluidic Flow.” Scientific Reports. Nature Publishing
Group, 2015. https://doi.org/10.1038/srep10781.
ieee: S. Altmeyer, Y. Do, and Y. Lai, “Transition to turbulence in Taylor-Couette
ferrofluidic flow,” Scientific Reports, vol. 5. Nature Publishing Group,
2015.
ista: Altmeyer S, Do Y, Lai Y. 2015. Transition to turbulence in Taylor-Couette
ferrofluidic flow. Scientific Reports. 5, 10781.
mla: Altmeyer, Sebastian, et al. “Transition to Turbulence in Taylor-Couette Ferrofluidic
Flow.” Scientific Reports, vol. 5, 10781, Nature Publishing Group, 2015,
doi:10.1038/srep10781.
short: S. Altmeyer, Y. Do, Y. Lai, Scientific Reports 5 (2015).
date_created: 2018-12-11T11:54:06Z
date_published: 2015-06-12T00:00:00Z
date_updated: 2021-01-12T06:53:18Z
day: '12'
ddc:
- '530'
department:
- _id: BjHo
doi: 10.1038/srep10781
file:
- access_level: open_access
checksum: 7716f582f8c9d82d8f2bf80bf896b440
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:26Z
date_updated: 2020-07-14T12:45:16Z
file_id: '5280'
file_name: IST-2016-450-v1+1_srep10781.pdf
file_size: 2449723
relation: main_file
file_date_updated: 2020-07-14T12:45:16Z
has_accepted_license: '1'
intvolume: ' 5'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '5306'
pubrep_id: '450'
quality_controlled: '1'
scopus_import: 1
status: public
title: Transition to turbulence in Taylor-Couette ferrofluidic flow
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2015'
...
---
_id: '1803'
abstract:
- lang: eng
text: Repeated stress has been suggested to underlie learning and memory deficits
via the basolateral amygdala (BLA) and the hippocampus; however, the functional
contribution of BLA inputs to the hippocampus and their molecular repercussions
are not well understood. Here we show that repeated stress is accompanied by generation
of the Cdk5 (cyclin-dependent kinase 5)-activator p25, up-regulation and phosphorylation
of glucocorticoid receptors, increased HDAC2 expression, and reduced expression
of memoryrelated genes in the hippocampus. A combination of optogenetic and pharmacosynthetic
approaches shows that BLA activation is both necessary and sufficient for stress-associated
molecular changes and memory impairments. Furthermore, we show that this effect
relies on direct glutamatergic projections from the BLA to the dorsal hippocampus.
Finally, we show that p25 generation is necessary for the stress-induced memory
dysfunction. Taken together, our data provide a neural circuit model for stress-induced
hippocampal memory deficits through BLA activity-dependent p25 generation.
acknowledgement: |-
AG047661; NIH; Schweizerische Nationalfonds zur Förderung der Wissenschaftlichen Forschung
NS051874; NIH; Schweizerische Nationalfonds zur Förderung der Wissenschaftlichen Forschung
SNSF; Schweizerische Nationalfonds zur Förderung der Wissenschaftlichen Forschung
author:
- first_name: Damien
full_name: Rei, Damien
last_name: Rei
- first_name: Xenos
full_name: Mason, Xenos
last_name: Mason
- first_name: Jinsoo
full_name: Seo, Jinsoo
last_name: Seo
- first_name: Johannes
full_name: Gräff, Johannes
last_name: Gräff
- first_name: Andrii
full_name: Rudenko, Andrii
last_name: Rudenko
- first_name: Jùn
full_name: Wang, Jùn
last_name: Wang
- first_name: Richard
full_name: Rueda, Richard
last_name: Rueda
- first_name: Sandra
full_name: Sandra Siegert
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
- first_name: Sukhee
full_name: Cho, Sukhee
last_name: Cho
- first_name: Rebecca
full_name: Canter, Rebecca G
last_name: Canter
- first_name: Alison
full_name: Mungenast, Alison E
last_name: Mungenast
- first_name: Karl
full_name: Deisseroth, Karl A
last_name: Deisseroth
- first_name: Lihuei
full_name: Tsai, Lihuei
last_name: Tsai
citation:
ama: Rei D, Mason X, Seo J, et al. Basolateral amygdala bidirectionally modulates
stress induced hippocampal learning and memory deficits through a p25/Cdk5-dependent
pathway. PNAS. 2015;112(23):7291-7296. doi:10.1073/pnas.1415845112
apa: Rei, D., Mason, X., Seo, J., Gräff, J., Rudenko, A., Wang, J., … Tsai, L. (2015).
Basolateral amygdala bidirectionally modulates stress induced hippocampal learning
and memory deficits through a p25/Cdk5-dependent pathway. PNAS. National
Academy of Sciences. https://doi.org/10.1073/pnas.1415845112
chicago: Rei, Damien, Xenos Mason, Jinsoo Seo, Johannes Gräff, Andrii Rudenko, Jùn
Wang, Richard Rueda, et al. “Basolateral Amygdala Bidirectionally Modulates Stress
Induced Hippocampal Learning and Memory Deficits through a P25/Cdk5-Dependent
Pathway.” PNAS. National Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1415845112.
ieee: D. Rei et al., “Basolateral amygdala bidirectionally modulates stress
induced hippocampal learning and memory deficits through a p25/Cdk5-dependent
pathway,” PNAS, vol. 112, no. 23. National Academy of Sciences, pp. 7291–7296,
2015.
ista: Rei D, Mason X, Seo J, Gräff J, Rudenko A, Wang J, Rueda R, Siegert S, Cho
S, Canter R, Mungenast A, Deisseroth K, Tsai L. 2015. Basolateral amygdala bidirectionally
modulates stress induced hippocampal learning and memory deficits through a p25/Cdk5-dependent
pathway. PNAS. 112(23), 7291–7296.
mla: Rei, Damien, et al. “Basolateral Amygdala Bidirectionally Modulates Stress
Induced Hippocampal Learning and Memory Deficits through a P25/Cdk5-Dependent
Pathway.” PNAS, vol. 112, no. 23, National Academy of Sciences, 2015, pp.
7291–96, doi:10.1073/pnas.1415845112.
short: D. Rei, X. Mason, J. Seo, J. Gräff, A. Rudenko, J. Wang, R. Rueda, S. Siegert,
S. Cho, R. Canter, A. Mungenast, K. Deisseroth, L. Tsai, PNAS 112 (2015) 7291–7296.
date_created: 2018-12-11T11:54:06Z
date_published: 2015-06-09T00:00:00Z
date_updated: 2021-01-12T06:53:18Z
day: '09'
doi: 10.1073/pnas.1415845112
extern: 1
intvolume: ' 112'
issue: '23'
month: '06'
page: 7291 - 7296
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5307'
quality_controlled: 0
status: public
title: Basolateral amygdala bidirectionally modulates stress induced hippocampal learning
and memory deficits through a p25/Cdk5-dependent pathway
type: journal_article
volume: 112
year: '2015'
...
---
_id: '1807'
abstract:
- lang: eng
text: We study a double Cahn-Hilliard type functional related to the Gross-Pitaevskii
energy of two-components Bose-Einstein condensates. In the case of large but same
order intercomponent and intracomponent coupling strengths, we prove Γ-convergence
to a perimeter minimisation functional with an inhomogeneous surface tension.
We study the asymptotic behavior of the surface tension as the ratio between the
intercomponent and intracomponent coupling strengths becomes very small or very
large and obtain good agreement with the physical literature. We obtain as a consequence,
symmetry breaking of the minimisers for the harmonic potential.
author:
- first_name: Michael
full_name: Goldman, Michael
last_name: Goldman
- first_name: Jimena
full_name: Royo-Letelier, Jimena
id: 4D3BED28-F248-11E8-B48F-1D18A9856A87
last_name: Royo-Letelier
citation:
ama: Goldman M, Royo-Letelier J. Sharp interface limit for two components Bose-Einstein
condensates. ESAIM - Control, Optimisation and Calculus of Variations.
2015;21(3):603-624. doi:10.1051/cocv/2014040
apa: Goldman, M., & Royo-Letelier, J. (2015). Sharp interface limit for two
components Bose-Einstein condensates. ESAIM - Control, Optimisation and Calculus
of Variations. EDP Sciences. https://doi.org/10.1051/cocv/2014040
chicago: Goldman, Michael, and Jimena Royo-Letelier. “Sharp Interface Limit for
Two Components Bose-Einstein Condensates.” ESAIM - Control, Optimisation and
Calculus of Variations. EDP Sciences, 2015. https://doi.org/10.1051/cocv/2014040.
ieee: M. Goldman and J. Royo-Letelier, “Sharp interface limit for two components
Bose-Einstein condensates,” ESAIM - Control, Optimisation and Calculus of Variations,
vol. 21, no. 3. EDP Sciences, pp. 603–624, 2015.
ista: Goldman M, Royo-Letelier J. 2015. Sharp interface limit for two components
Bose-Einstein condensates. ESAIM - Control, Optimisation and Calculus of Variations.
21(3), 603–624.
mla: Goldman, Michael, and Jimena Royo-Letelier. “Sharp Interface Limit for Two
Components Bose-Einstein Condensates.” ESAIM - Control, Optimisation and Calculus
of Variations, vol. 21, no. 3, EDP Sciences, 2015, pp. 603–24, doi:10.1051/cocv/2014040.
short: M. Goldman, J. Royo-Letelier, ESAIM - Control, Optimisation and Calculus
of Variations 21 (2015) 603–624.
date_created: 2018-12-11T11:54:07Z
date_published: 2015-05-01T00:00:00Z
date_updated: 2021-01-12T06:53:20Z
day: '01'
department:
- _id: RoSe
doi: 10.1051/cocv/2014040
intvolume: ' 21'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://arxiv.org/abs/1401.1727
month: '05'
oa: 1
oa_version: Preprint
page: 603 - 624
publication: ESAIM - Control, Optimisation and Calculus of Variations
publication_status: published
publisher: EDP Sciences
publist_id: '5303'
quality_controlled: '1'
scopus_import: 1
status: public
title: Sharp interface limit for two components Bose-Einstein condensates
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 21
year: '2015'
...
---
_id: '1802'
abstract:
- lang: eng
text: Noncoding variants in the human MIR137 gene locus increase schizophrenia risk
with genome-wide significance. However, the functional consequence of these risk
alleles is unknown. Here we examined induced human neurons harboring the minor
alleles of four disease-associated single nucleotide polymorphisms in MIR137.
We observed increased MIR137 levels compared to those in major allele–carrying
cells. microRNA-137 gain of function caused downregulation of the presynaptic
target genes complexin-1 (Cplx1), Nsf and synaptotagmin-1 (Syt1), leading to impaired
vesicle release. In vivo, miR-137 gain of function resulted in changes in synaptic
vesicle pool distribution, impaired induction of mossy fiber long-term potentiation
and deficits in hippocampus-dependent learning and memory. By sequestering endogenous
miR-137, we were able to ameliorate the synaptic phenotypes. Moreover, reinstatement
of Syt1 expression partially restored synaptic plasticity, demonstrating the importance
of Syt1 as a miR-137 target. Our data provide new insight into the mechanism by
which miR-137 dysregulation can impair synaptic plasticity in the hippocampus.
acknowledgement: S.S. was supported by a Human Frontier Science Program (HFSP) long-term
postdoctoral fellowship and a Swiss National Science Foundation fellowship for prospective
researchers. E.J.K. was supported by a Simons Foundation Postdoctoral Fellowship.
A.R. was supported by a NARSAD Young Investigator Award. This work was supported
by a Seed Grant from the Simons Center for the Social Brain and US National Institutes
of Health grant RO1 MH 091115 to L.-H.T.
author:
- first_name: Sandra
full_name: Sandra Siegert
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
- first_name: Jinsoo
full_name: Seo, Jinsoo
last_name: Seo
- first_name: Ester
full_name: Kwon, Ester J
last_name: Kwon
- first_name: Andrii
full_name: Rudenko, Andrii
last_name: Rudenko
- first_name: Sukhee
full_name: Cho, Sukhee
last_name: Cho
- first_name: Wenyuan
full_name: Wang, Wenyuan
last_name: Wang
- first_name: Zachary
full_name: Flood, Zachary C
last_name: Flood
- first_name: Anthony
full_name: Martorell, Anthony J
last_name: Martorell
- first_name: Maria
full_name: Ericsson, Maria
last_name: Ericsson
- first_name: Alison
full_name: Mungenast, Alison E
last_name: Mungenast
- first_name: Lihuei
full_name: Tsai, Lihuei
last_name: Tsai
citation:
ama: Siegert S, Seo J, Kwon E, et al. The schizophrenia risk gene product miR-137
alters presynaptic plasticity. Nature Neuroscience. 2015;18:1008-1016.
doi:10.1038/nn.4023
apa: Siegert, S., Seo, J., Kwon, E., Rudenko, A., Cho, S., Wang, W., … Tsai, L.
(2015). The schizophrenia risk gene product miR-137 alters presynaptic plasticity.
Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.4023
chicago: Siegert, Sandra, Jinsoo Seo, Ester Kwon, Andrii Rudenko, Sukhee Cho, Wenyuan
Wang, Zachary Flood, et al. “The Schizophrenia Risk Gene Product MiR-137 Alters
Presynaptic Plasticity.” Nature Neuroscience. Nature Publishing Group,
2015. https://doi.org/10.1038/nn.4023.
ieee: S. Siegert et al., “The schizophrenia risk gene product miR-137 alters
presynaptic plasticity,” Nature Neuroscience, vol. 18. Nature Publishing
Group, pp. 1008–1016, 2015.
ista: Siegert S, Seo J, Kwon E, Rudenko A, Cho S, Wang W, Flood Z, Martorell A,
Ericsson M, Mungenast A, Tsai L. 2015. The schizophrenia risk gene product miR-137
alters presynaptic plasticity. Nature Neuroscience. 18, 1008–1016.
mla: Siegert, Sandra, et al. “The Schizophrenia Risk Gene Product MiR-137 Alters
Presynaptic Plasticity.” Nature Neuroscience, vol. 18, Nature Publishing
Group, 2015, pp. 1008–16, doi:10.1038/nn.4023.
short: S. Siegert, J. Seo, E. Kwon, A. Rudenko, S. Cho, W. Wang, Z. Flood, A. Martorell,
M. Ericsson, A. Mungenast, L. Tsai, Nature Neuroscience 18 (2015) 1008–1016.
date_created: 2018-12-11T11:54:05Z
date_published: 2015-07-01T00:00:00Z
date_updated: 2021-01-12T06:53:18Z
day: '01'
doi: 10.1038/nn.4023
extern: 1
intvolume: ' 18'
month: '07'
page: 1008 - 1016
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '5308'
quality_controlled: 0
status: public
title: The schizophrenia risk gene product miR-137 alters presynaptic plasticity
type: journal_article
volume: 18
year: '2015'
...
---
_id: '1810'
abstract:
- lang: eng
text: Combining antibiotics is a promising strategy for increasing treatment efficacy
and for controlling resistance evolution. When drugs are combined, their effects
on cells may be amplified or weakened, that is the drugs may show synergistic
or antagonistic interactions. Recent work revealed the underlying mechanisms of
such drug interactions by elucidating the drugs'; joint effects on cell physiology.
Moreover, new treatment strategies that use drug combinations to exploit evolutionary
tradeoffs were shown to affect the rate of resistance evolution in predictable
ways. High throughput studies have further identified drug candidates based on
their interactions with established antibiotics and general principles that enable
the prediction of drug interactions were suggested. Overall, the conceptual and
technical foundation for the rational design of potent drug combinations is rapidly
developing.
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: 'Bollenbach MT. Antimicrobial interactions: Mechanisms and implications for
drug discovery and resistance evolution. Current Opinion in Microbiology.
2015;27:1-9. doi:10.1016/j.mib.2015.05.008'
apa: 'Bollenbach, M. T. (2015). Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution. Current Opinion in Microbiology.
Elsevier. https://doi.org/10.1016/j.mib.2015.05.008'
chicago: 'Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications
for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology.
Elsevier, 2015. https://doi.org/10.1016/j.mib.2015.05.008.'
ieee: 'M. T. Bollenbach, “Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution,” Current Opinion in Microbiology,
vol. 27. Elsevier, pp. 1–9, 2015.'
ista: 'Bollenbach MT. 2015. Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution. Current Opinion in Microbiology.
27, 1–9.'
mla: 'Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications
for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology,
vol. 27, Elsevier, 2015, pp. 1–9, doi:10.1016/j.mib.2015.05.008.'
short: M.T. Bollenbach, Current Opinion in Microbiology 27 (2015) 1–9.
date_created: 2018-12-11T11:54:08Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2021-01-12T06:53:21Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1016/j.mib.2015.05.008
ec_funded: 1
file:
- access_level: open_access
checksum: 1683bb0f42ef892a5b3b71a050d65d25
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:23Z
date_updated: 2020-07-14T12:45:17Z
file_id: '5277'
file_name: IST-2016-493-v1+1_1-s2.0-S1369527415000594-main.pdf
file_size: 1047255
relation: main_file
file_date_updated: 2020-07-14T12:45:17Z
has_accepted_license: '1'
intvolume: ' 27'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 1 - 9
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
publication: Current Opinion in Microbiology
publication_status: published
publisher: Elsevier
publist_id: '5298'
pubrep_id: '493'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Antimicrobial interactions: Mechanisms and implications for drug discovery
and resistance evolution'
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2015'
...