@article{3160,
abstract = {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 = {Pantazis, Periklis and Bollenbach, Tobias},
journal = {Cell Cycle},
number = {11},
pages = {2055 -- 2058},
publisher = {Taylor and Francis},
title = {{Transcription factor kinetics and the emerging asymmetry in the early mammalian embryo}},
doi = {10.4161/cc.20118},
volume = {11},
year = {2012},
}
@article{3161,
abstract = {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.},
author = {Vyleta, Meghan and Wong, John and Magun, Bruce},
journal = {PLoS One},
number = {5},
publisher = {Public Library of Science},
title = {{Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome}},
doi = {10.1371/journal.pone.0036044},
volume = {7},
year = {2012},
}
@inproceedings{3162,
abstract = {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.},
author = {Asarin, Eugene and Donzé, Alexandre and Maler, Oded and Nickovic, Dejan},
location = {San Francisco, CA, United States},
pages = {147 -- 160},
publisher = {Springer},
title = {{Parametric identification of temporal properties}},
doi = {10.1007/978-3-642-29860-8_12},
volume = {7186},
year = {2012},
}
@article{3164,
abstract = {Overview of the Special Issue on structured prediction and inference.},
author = {Blaschko, Matthew and Lampert, Christoph},
journal = {International Journal of Computer Vision},
number = {3},
pages = {257 -- 258},
publisher = {Springer},
title = {{Guest editorial: Special issue on structured prediction and inference}},
doi = {10.1007/s11263-012-0530-y},
volume = {99},
year = {2012},
}
@inproceedings{3165,
abstract = {Computing the winning set for Büchi objectives in alternating games on graphs is a central problem in computer aided verification with a large number of applications. The long standing best known upper bound for solving the problem is Õ(n·m), where n is the number of vertices and m is the number of edges in the graph. We are the first to break the Õ(n·m) boundary by presenting a new technique that reduces the running time to O(n 2). This bound also leads to O(n 2) time algorithms for computing the set of almost-sure winning vertices for Büchi objectives (1) in alternating games with probabilistic transitions (improving an earlier bound of Õ(n·m)), (2) in concurrent graph games with constant actions (improving an earlier bound of O(n 3)), and (3) in Markov decision processes (improving for m > n 4/3 an earlier bound of O(min(m 1.5, m·n 2/3)). We also show that the same technique can be used to compute the maximal end-component decomposition of a graph in time O(n 2), which is an improvement over earlier bounds for m > n 4/3. Finally, we show how to maintain the winning set for Büchi objectives in alternating games under a sequence of edge insertions or a sequence of edge deletions in O(n) amortized time per operation. This is the first dynamic algorithm for this problem.},
author = {Chatterjee, Krishnendu and Henzinger, Monika},
booktitle = {Proceedings of the Annual ACM-SIAM Symposium on Discrete Algorithms},
location = {Kyoto, Japan},
pages = {1386 -- 1399},
publisher = {SIAM},
title = {{An O(n2) time algorithm for alternating Büchi games}},
doi = {10.1137/1.9781611973099.109},
year = {2012},
}