--- _id: '3132' abstract: - lang: eng text: 'Reproductive division of labour is a characteristic trait of social insects. The dominant reproductive individual, often the queen, uses chemical communication and/or behaviour to maintain her social status. Queens of many social insects communicate their fertility status via cuticle-bound substances. As these substances usually possess a low volatility, their range in queen–worker communication is potentially limited. Here, we investigate the range and impact of behavioural and chemical queen signals on workers of the ant Temnothorax longispinosus. We compared the behaviour and ovary development of workers subjected to three different treatments: workers with direct chemical and physical contact to the queen, those solely under the influence of volatile queen substances and those entirely separated from the queen. In addition to short-ranged queen signals preventing ovary development in workers, we discovered a novel secondary pathway influencing worker behaviour. Workers with no physical contact to the queen, but exposed to volatile substances, started to develop their ovaries, but did not change their behaviour compared to workers in direct contact to the queen. In contrast, workers in queen-separated groups showed both increased ovary development and aggressive dominance interactions. We conclude that T. longispinosus queens influence worker ovary development and behaviour via two independent signals, both ensuring social harmony within the colony.' acknowledgement: We like to thank the editor and three anonymous reviewers for their time and constructive criticism and Inon Scharf, Volker Witte and Andreas Modlmeier for helpful comments on earlier versions of the manuscript. The first and second authors appear in alphabetical order and contributed equally to this paper. author: - first_name: Matthias full_name: Konrad, Matthias id: 46528076-F248-11E8-B48F-1D18A9856A87 last_name: Konrad - first_name: Tobias full_name: Pamminger, Tobias last_name: Pamminger - first_name: Susanne full_name: Foitzik, Susanne last_name: Foitzik citation: ama: Konrad M, Pamminger T, Foitzik S. Two pathways ensuring social harmony. Naturwissenschaften. 2012;99(8):627-636. doi:10.1007/s00114-012-0943-z apa: Konrad, M., Pamminger, T., & Foitzik, S. (2012). Two pathways ensuring social harmony. Naturwissenschaften. Springer. https://doi.org/10.1007/s00114-012-0943-z chicago: Konrad, Matthias, Tobias Pamminger, and Susanne Foitzik. “Two Pathways Ensuring Social Harmony.” Naturwissenschaften. Springer, 2012. https://doi.org/10.1007/s00114-012-0943-z. ieee: M. Konrad, T. Pamminger, and S. Foitzik, “Two pathways ensuring social harmony,” Naturwissenschaften, vol. 99, no. 8. Springer, pp. 627–636, 2012. ista: Konrad M, Pamminger T, Foitzik S. 2012. Two pathways ensuring social harmony. Naturwissenschaften. 99(8), 627–636. mla: Konrad, Matthias, et al. “Two Pathways Ensuring Social Harmony.” Naturwissenschaften, vol. 99, no. 8, Springer, 2012, pp. 627–36, doi:10.1007/s00114-012-0943-z. short: M. Konrad, T. Pamminger, S. Foitzik, Naturwissenschaften 99 (2012) 627–636. date_created: 2018-12-11T12:01:34Z date_published: 2012-08-01T00:00:00Z date_updated: 2021-01-12T07:41:17Z day: '01' department: - _id: SyCr doi: 10.1007/s00114-012-0943-z intvolume: ' 99' issue: '8' language: - iso: eng month: '08' oa_version: None page: 627 - 636 publication: Naturwissenschaften publication_status: published publisher: Springer publist_id: '3565' quality_controlled: '1' scopus_import: 1 status: public title: Two pathways ensuring social harmony type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 99 year: '2012' ... --- _id: '3161' abstract: - lang: eng text: 'Some inflammatory stimuli trigger activation of the NLRP3 inflammasome by inducing efflux of cellular potassium. Loss of cellular potassium is known to potently suppress protein synthesis, leading us to test whether the inhibition of protein synthesis itself serves as an activating signal for the NLRP3 inflammasome. Murine bone marrow-derived macrophages, either primed by LPS or unprimed, were exposed to a panel of inhibitors of ribosomal function: ricin, cycloheximide, puromycin, pactamycin, and anisomycin. Macrophages were also exposed to nigericin, ATP, monosodium urate (MSU), and poly I:C. Synthesis of pro-IL-ß and release of IL-1ß from cells in response to these agents was detected by immunoblotting and ELISA. Release of intracellular potassium was measured by mass spectrometry. Inhibition of translation by each of the tested translation inhibitors led to processing of IL-1ß, which was released from cells. Processing and release of IL-1ß was reduced or absent from cells deficient in NLRP3, ASC, or caspase-1, demonstrating the role of the NLRP3 inflammasome. Despite the inability of these inhibitors to trigger efflux of intracellular potassium, the addition of high extracellular potassium suppressed activation of the NLRP3 inflammasome. MSU and double-stranded RNA, which are known to activate the NLRP3 inflammasome, also substantially inhibited protein translation, supporting a close association between inhibition of translation and inflammasome activation. These data demonstrate that translational inhibition itself constitutes a heretofore-unrecognized mechanism underlying IL-1ß dependent inflammatory signaling and that other physical, chemical, or pathogen-associated agents that impair translation may lead to IL-1ß-dependent inflammation through activation of the NLRP3 inflammasome. For agents that inhibit translation through decreased cellular potassium, the application of high extracellular potassium restores protein translation and suppresses activation of the NLRP inflammasome. For agents that inhibit translation through mechanisms that do not involve loss of potassium, high extracellular potassium suppresses IL-1ß processing through a mechanism that remains undefined.' acknowledgement: "Supported by National Institutes of Health grants GM071338 (ML) and AI059355 (BM).\r\nWe acknowledge the expertise of Dr. Martina Ralle in Department of Biochemistry and Molecular Biology at OHSU for measurements of potassium using inductively coupled plasma mass spectrometry." article_number: e36044 author: - first_name: Meghan full_name: Vyleta, Meghan id: 418901AA-F248-11E8-B48F-1D18A9856A87 last_name: Vyleta - first_name: John full_name: Wong, John last_name: Wong - first_name: Bruce full_name: Magun, Bruce last_name: Magun citation: ama: Vyleta M, Wong J, Magun B. Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome. PLoS One. 2012;7(5). doi:10.1371/journal.pone.0036044 apa: Vyleta, M., Wong, J., & Magun, B. (2012). Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0036044 chicago: Vyleta, Meghan, John Wong, and Bruce Magun. “Suppression of Ribosomal Function Triggers Innate Immune Signaling through Activation of the NLRP3 Inflammasome.” PLoS One. Public Library of Science, 2012. https://doi.org/10.1371/journal.pone.0036044. ieee: M. Vyleta, J. Wong, and B. Magun, “Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome,” PLoS One, vol. 7, no. 5. Public Library of Science, 2012. ista: Vyleta M, Wong J, Magun B. 2012. Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome. PLoS One. 7(5), e36044. mla: Vyleta, Meghan, et al. “Suppression of Ribosomal Function Triggers Innate Immune Signaling through Activation of the NLRP3 Inflammasome.” PLoS One, vol. 7, no. 5, e36044, Public Library of Science, 2012, doi:10.1371/journal.pone.0036044. short: M. Vyleta, J. Wong, B. Magun, PLoS One 7 (2012). date_created: 2018-12-11T12:01:45Z date_published: 2012-05-14T00:00:00Z date_updated: 2021-01-12T07:41:29Z day: '14' ddc: - '610' department: - _id: SyCr doi: 10.1371/journal.pone.0036044 file: - access_level: open_access checksum: 30cef37e27eaa467f6571b3640282010 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:30Z date_updated: 2020-07-14T12:46:01Z file_id: '5082' file_name: IST-2012-97-v1+1_journal.pone.0036044.pdf file_size: 2984012 relation: main_file file_date_updated: 2020-07-14T12:46:01Z has_accepted_license: '1' intvolume: ' 7' issue: '5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '3526' pubrep_id: '97' quality_controlled: '1' scopus_import: 1 status: public title: Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome 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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 7 year: '2012' ... --- _id: '3162' abstract: - lang: eng text: Given a dense-time real-valued signal and a parameterized temporal logic formula with both magnitude and timing parameters, we compute the subset of the parameter space that renders the formula satisfied by the trace. We provide two preliminary implementations, one which follows the exact semantics and attempts to compute the validity domain by quantifier elimination in linear arithmetics and one which conducts adaptive search in the parameter space. alternative_title: - LNCS article_processing_charge: No author: - first_name: Eugene full_name: Asarin, Eugene last_name: Asarin - first_name: Alexandre full_name: Donzé, Alexandre last_name: Donzé - first_name: Oded full_name: Maler, Oded last_name: Maler - first_name: Dejan full_name: Nickovic, Dejan id: 41BCEE5C-F248-11E8-B48F-1D18A9856A87 last_name: Nickovic citation: ama: 'Asarin E, Donzé A, Maler O, Nickovic D. Parametric identification of temporal properties. In: Vol 7186. Springer; 2012:147-160. doi:10.1007/978-3-642-29860-8_12' apa: 'Asarin, E., Donzé, A., Maler, O., & Nickovic, D. (2012). Parametric identification of temporal properties (Vol. 7186, pp. 147–160). Presented at the RV: Runtime Verification, San Francisco, CA, United States: Springer. https://doi.org/10.1007/978-3-642-29860-8_12' chicago: Asarin, Eugene, Alexandre Donzé, Oded Maler, and Dejan Nickovic. “Parametric Identification of Temporal Properties,” 7186:147–60. Springer, 2012. https://doi.org/10.1007/978-3-642-29860-8_12. ieee: 'E. Asarin, A. Donzé, O. Maler, and D. Nickovic, “Parametric identification of temporal properties,” presented at the RV: Runtime Verification, San Francisco, CA, United States, 2012, vol. 7186, pp. 147–160.' ista: 'Asarin E, Donzé A, Maler O, Nickovic D. 2012. Parametric identification of temporal properties. RV: Runtime Verification, LNCS, vol. 7186, 147–160.' mla: Asarin, Eugene, et al. Parametric Identification of Temporal Properties. Vol. 7186, Springer, 2012, pp. 147–60, doi:10.1007/978-3-642-29860-8_12. short: E. Asarin, A. Donzé, O. Maler, D. Nickovic, in:, Springer, 2012, pp. 147–160. conference: end_date: 2011-09-30 location: San Francisco, CA, United States name: 'RV: Runtime Verification' start_date: 2011-09-27 date_created: 2018-12-11T12:01:45Z date_published: 2012-01-01T00:00:00Z date_updated: 2021-01-12T07:41:29Z day: '01' ddc: - '000' department: - _id: ToHe doi: 10.1007/978-3-642-29860-8_12 file: - access_level: open_access checksum: ba4a75287008fc64b8fbf78a7476ec32 content_type: application/pdf creator: dernst date_created: 2020-05-15T12:50:15Z date_updated: 2020-07-14T12:46:01Z file_id: '7862' file_name: 2012_RV_Asarin.pdf file_size: 374726 relation: main_file file_date_updated: 2020-07-14T12:46:01Z has_accepted_license: '1' intvolume: ' 7186' language: - iso: eng month: '01' oa: 1 oa_version: Submitted Version page: 147 - 160 publication_status: published publisher: Springer publist_id: '3525' quality_controlled: '1' scopus_import: 1 status: public title: Parametric identification of temporal properties type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 7186 year: '2012' ... --- _id: '3160' abstract: - lang: eng text: There is a long-running controversy about how early cell fate decisions are made in the developing mammalian embryo. 1,2 In particular, it is controversial when the first events that can predict the establishment of the pluripotent and extra-embryonic lineages in the blastocyst of the pre-implantation embryo occur. It has long been proposed that the position and polarity of cells at the 16- to 32-cell stage embryo influence their decision to either give rise to the pluripotent cell lineage that eventually contributes to the inner cell mass (ICM), comprising the primitive endoderm (PE) and the epiblast (EPI), or the extra-embryonic trophectoderm (TE) surrounding the blastocoel. The positioning of cells in the embryo at this developmental stage could largely be the result of random events, making this a stochastic model of cell lineage allocation. Contrary to such a stochastic model, some studies have detected putative differences in the lineage potential of individual blastomeres before compaction, indicating that the first cell fate decisions may occur as early as at the 4-cell stage. Using a non-invasive, quantitative in vivo imaging assay to study the kinetic behavior of Oct4 (also known as POU5F1), a key transcription factor (TF) controlling pre-implantation development in the mouse embryo, 3-5 a recent study identifies Oct4 kinetics as a predictive measure of cell lineage patterning in the early mouse embryo. 6 Here, we discuss the implications of such molecular heterogeneities in early development and offer potential avenues toward a mechanistic understanding of these observations, contributing to the resolution of the controversy of developmental cell lineage allocation. author: - first_name: Periklis full_name: Pantazis, Periklis last_name: Pantazis - first_name: Tobias full_name: Bollenbach, Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X citation: ama: Pantazis P, Bollenbach MT. Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo. Cell Cycle. 2012;11(11):2055-2058. doi:10.4161/cc.20118 apa: Pantazis, P., & Bollenbach, M. T. (2012). Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo. Cell Cycle. Taylor and Francis. https://doi.org/10.4161/cc.20118 chicago: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle. Taylor and Francis, 2012. https://doi.org/10.4161/cc.20118. ieee: P. Pantazis and M. T. Bollenbach, “Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo,” Cell Cycle, vol. 11, no. 11. Taylor and Francis, pp. 2055–2058, 2012. ista: Pantazis P, Bollenbach MT. 2012. Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo. Cell Cycle. 11(11), 2055–2058. mla: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle, vol. 11, no. 11, Taylor and Francis, 2012, pp. 2055–58, doi:10.4161/cc.20118. short: P. Pantazis, M.T. Bollenbach, Cell Cycle 11 (2012) 2055–2058. date_created: 2018-12-11T12:01:44Z date_published: 2012-06-01T00:00:00Z date_updated: 2021-01-12T07:41:28Z day: '01' department: - _id: ToBo doi: 10.4161/cc.20118 intvolume: ' 11' issue: '11' language: - iso: eng month: '06' oa_version: None page: 2055 - 2058 publication: Cell Cycle publication_status: published publisher: Taylor and Francis publist_id: '3531' quality_controlled: '1' scopus_import: 1 status: public title: Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2012' ... --- _id: '3164' abstract: - lang: eng text: Overview of the Special Issue on structured prediction and inference. author: - first_name: Matthew full_name: Blaschko, Matthew last_name: Blaschko - first_name: Christoph full_name: Lampert, Christoph id: 40C20FD2-F248-11E8-B48F-1D18A9856A87 last_name: Lampert orcid: 0000-0001-8622-7887 citation: ama: 'Blaschko M, Lampert C. Guest editorial: Special issue on structured prediction and inference. International Journal of Computer Vision. 2012;99(3):257-258. doi:10.1007/s11263-012-0530-y' apa: 'Blaschko, M., & Lampert, C. (2012). Guest editorial: Special issue on structured prediction and inference. International Journal of Computer Vision. Springer. https://doi.org/10.1007/s11263-012-0530-y' chicago: 'Blaschko, Matthew, and Christoph Lampert. “Guest Editorial: Special Issue on Structured Prediction and Inference.” International Journal of Computer Vision. Springer, 2012. https://doi.org/10.1007/s11263-012-0530-y.' ieee: 'M. Blaschko and C. Lampert, “Guest editorial: Special issue on structured prediction and inference,” International Journal of Computer Vision, vol. 99, no. 3. Springer, pp. 257–258, 2012.' ista: 'Blaschko M, Lampert C. 2012. Guest editorial: Special issue on structured prediction and inference. International Journal of Computer Vision. 99(3), 257–258.' mla: 'Blaschko, Matthew, and Christoph Lampert. “Guest Editorial: Special Issue on Structured Prediction and Inference.” International Journal of Computer Vision, vol. 99, no. 3, Springer, 2012, pp. 257–58, doi:10.1007/s11263-012-0530-y.' short: M. Blaschko, C. Lampert, International Journal of Computer Vision 99 (2012) 257–258. date_created: 2018-12-11T12:01:46Z date_published: 2012-09-01T00:00:00Z date_updated: 2021-01-12T07:41:30Z day: '01' department: - _id: ChLa doi: 10.1007/s11263-012-0530-y intvolume: ' 99' issue: '3' language: - iso: eng month: '09' oa_version: None page: 257 - 258 publication: International Journal of Computer Vision publication_status: published publisher: Springer publist_id: '3521' quality_controlled: '1' scopus_import: 1 status: public title: 'Guest editorial: Special issue on structured prediction and inference' type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 99 year: '2012' ...