--- _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' ...