@inproceedings{8599,
  abstract     = {A graph game is a two-player zero-sum game in which the players move a token throughout a graph to produce an infinite path, which determines the winner or payoff of the game. In bidding games, both players have budgets, and in each turn, we hold an "auction" (bidding) to determine which player moves the token. In this survey, we consider several bidding mechanisms and study their effect on the properties of the game. Specifically, bidding games, and in particular bidding games of infinite duration, have an intriguing equivalence with random-turn games in which in each turn, the player who moves is chosen randomly. We show how minor changes in the bidding mechanism lead to unexpected differences in the equivalence with random-turn games.},
  author       = {Avni, Guy and Henzinger, Thomas A},
  booktitle    = {31st International Conference on Concurrency Theory},
  isbn         = {9783959771603},
  issn         = {18688969},
  location     = {Virtual},
  publisher    = {Schloss Dagstuhl - Leibniz-Zentrum für Informatik},
  title        = {{A survey of bidding games on graphs}},
  doi          = {10.4230/LIPIcs.CONCUR.2020.2},
  volume       = {171},
  year         = {2020},
}

@inproceedings{8600,
  abstract     = {A vector addition system with states (VASS) consists of a finite set of states and counters. A transition changes the current state to the next state, and every counter is either incremented, or decremented, or left unchanged. A state and value for each counter is a configuration; and a computation is an infinite sequence of configurations with transitions between successive configurations. A probabilistic VASS consists of a VASS along with a probability distribution over the transitions for each state. Qualitative properties such as state and configuration reachability have been widely studied for VASS. In this work we consider multi-dimensional long-run average objectives for VASS and probabilistic VASS. For a counter, the cost of a configuration is the value of the counter; and the long-run average value of a computation for the counter is the long-run average of the costs of the configurations in the computation. The multi-dimensional long-run average problem given a VASS and a threshold value for each counter, asks whether there is a computation such that for each counter the long-run average value for the counter does not exceed the respective threshold. For probabilistic VASS, instead of the existence of a computation, we consider whether the expected long-run average value for each counter does not exceed the respective threshold. Our main results are as follows: we show that the multi-dimensional long-run average problem (a) is NP-complete for integer-valued VASS; (b) is undecidable for natural-valued VASS (i.e., nonnegative counters); and (c) can be solved in polynomial time for probabilistic integer-valued VASS, and probabilistic natural-valued VASS when all computations are non-terminating.},
  author       = {Chatterjee, Krishnendu and Henzinger, Thomas A and Otop, Jan},
  booktitle    = {31st International Conference on Concurrency Theory},
  isbn         = {9783959771603},
  issn         = {18688969},
  location     = {Virtual},
  publisher    = {Schloss Dagstuhl - Leibniz-Zentrum für Informatik},
  title        = {{Multi-dimensional long-run average problems for vector addition systems with states}},
  doi          = {10.4230/LIPIcs.CONCUR.2020.23},
  volume       = {171},
  year         = {2020},
}

@article{8607,
  abstract     = {Clathrin-mediated endocytosis (CME) and its core endocytic machinery are evolutionarily conserved across all eukaryotes. In mammals, the heterotetrameric adaptor protein complex-2 (AP-2) sorts plasma membrane (PM) cargoes into vesicles through the recognition of motifs based on tyrosine or di-leucine in their cytoplasmic tails. However, in plants, very little is known on how PM proteins are sorted for CME and whether similar motifs are required. In Arabidopsis thaliana, the brassinosteroid (BR) receptor, BR INSENSITIVE1 (BRI1), undergoes endocytosis that depends on clathrin and AP-2. Here we demonstrate that BRI1 binds directly to the medium AP-2 subunit, AP2M. The cytoplasmic domain of BRI1 contains five putative canonical surface-exposed tyrosine-based endocytic motifs. The tyrosine-to-phenylalanine substitution in Y898KAI reduced BRI1 internalization without affecting its kinase activity. Consistently, plants carrying the BRI1Y898F mutation were hypersensitive to BRs. Our study demonstrates that AP-2-dependent internalization of PM proteins via the recognition of functional tyrosine motifs also operates in plants.},
  author       = {Liu, D and Kumar, R and LAN, Claus and Johnson, Alexander J and Siao, W and Vanhoutte, I and Wang, P and Bender, KW and Yperman, K and Martins, S and Zhao, X and Vert, G and Van Damme, D and Friml, Jiří and Russinova, E},
  issn         = {1532-298x},
  journal      = {Plant Cell},
  number       = {11},
  pages        = {3598--3612},
  publisher    = {American Society of Plant Biologists},
  title        = {{Endocytosis of BRASSINOSTEROID INSENSITIVE1 is partly driven by a canonical tyrosine-based Motif}},
  doi          = {10.1105/tpc.20.00384},
  volume       = {32},
  year         = {2020},
}

@unpublished{8616,
  abstract     = {The brain vasculature supplies neurons with glucose and oxygen, but little is known about how vascular plasticity contributes to brain function. Using longitudinal <jats:italic>in vivo</jats:italic> imaging, we reported that a substantial proportion of blood vessels in the adult brain sporadically occluded and regressed. Their regression proceeded through sequential stages of blood-flow occlusion, endothelial cell collapse, relocation or loss of pericytes, and retraction of glial endfeet. Regressing vessels were found to be widespread in mouse, monkey and human brains. Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion to endothelial cells alleviated LPS-induced vessel regression. We further revealed that blood vessel regression caused a reduction of neuronal activity due to a dysfunction in mitochondrial metabolism and glutamate production. Our results elucidate the mechanism of vessel regression and its role in neuronal function in the adult brain.},
  author       = {Gao, Xiaofei and Li, Jun-Liszt and Chen, Xingjun and Ci, Bo and Chen, Fei and Lu, Nannan and Shen, Bo and Zheng, Lijun and Jia, Jie-Min and Yi, Yating and Zhang, Shiwen and Shi, Ying-Chao and Shi, Kaibin and Propson, Nicholas E and Huang, Yubin and Poinsatte, Katherine and Zhang, Zhaohuan and Yue, Yuanlei and Bosco, Dale B and Lu, Ying-mei and Yang, Shi-bing and Adams, Ralf H. and Lindner, Volkhard and Huang, Fen and Wu, Long-Jun and Zheng, Hui and Han, Feng and Hippenmeyer, Simon and Stowe, Ann M. and Peng, Bo and Margeta, Marta and Wang, Xiaoqun and Liu, Qiang and Körbelin, Jakob and Trepel, Martin and Lu, Hui and Zhou, Bo O. and Zhao, Hu and Su, Wenzhi and Bachoo, Robert M. and Ge, Woo-ping},
  booktitle    = {bioRxiv},
  publisher    = {Cold Spring Harbor Laboratory},
  title        = {{Reduction of neuronal activity mediated by blood-vessel regression in the brain}},
  doi          = {10.1101/2020.09.15.262782},
  year         = {2020},
}

@phdthesis{8620,
  abstract     = {The development of the human brain occurs through a tightly regulated series of dynamic and adaptive processes during prenatal and postnatal life. A disruption of this strictly orchestrated series of events can lead to a number of neurodevelopmental conditions, including Autism Spectrum Disorders (ASDs). ASDs are a very common, etiologically and phenotypically heterogeneous group of disorders sharing the core symptoms of social interaction and communication deficits and restrictive and repetitive interests and behaviors. They are estimated to affect one in 59 individuals in the U.S. and, over the last three decades, mutations in more than a hundred genetic loci have been convincingly linked to ASD pathogenesis. Yet, for the vast majority of these ASD-risk genes their role during brain development and precise molecular function still remain elusive.
De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin 3 (CUL3) lead to ASD. In the study described here, we used Cul3 mouse models to evaluate the consequences of Cul3 mutations in vivo. Our results show that Cul3 heterozygous knockout mice exhibit deficits in motor coordination as well as ASD-relevant social and cognitive impairments. Cul3+/-, Cul3+/fl Emx1-Cre and Cul3fl/fl Emx1-Cre mutant brains display cortical lamination abnormalities due to defective migration of post-mitotic excitatory neurons, as well as reduced numbers of excitatory and inhibitory neurons. In line with the observed abnormal cortical organization, Cul3 heterozygous deletion is associated with decreased spontaneous excitatory and inhibitory activity in the cortex. At the molecular level we show that Cul3 regulates cytoskeletal and adhesion protein abundance in the mouse embryonic cortex. Abnormal regulation of cytoskeletal proteins in Cul3 mutant neural cells results in atypical organization of the actin mesh at the cell leading edge. Of note, heterozygous deletion of Cul3 in adult mice does not induce the majority of the behavioral defects observed in constitutive Cul3 haploinsufficient animals, pointing to a critical time-window for Cul3 deficiency.
In conclusion, our data indicate that Cul3 plays a critical role in the regulation of cytoskeletal proteins and neuronal migration. ASD-associated defects and behavioral abnormalities are primarily due to dosage sensitive Cul3 functions at early brain developmental stages.},
  author       = {Morandell, Jasmin},
  issn         = {2663-337X},
  pages        = {138},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Illuminating the role of Cul3 in autism spectrum disorder pathogenesis}},
  doi          = {10.15479/AT:ISTA:8620},
  year         = {2020},
}

@inproceedings{8623,
  abstract     = {We introduce the monitoring of trace properties under assumptions. An assumption limits the space of possible traces that the monitor may encounter. An assumption may result from knowledge about the system that is being monitored, about the environment, or about another, connected monitor. We define monitorability under assumptions and study its theoretical properties. In particular, we show that for every assumption A, the boolean combinations of properties that are safe or co-safe relative to A are monitorable under A. We give several examples and constructions on how an assumption can make a non-monitorable property monitorable, and how an assumption can make a monitorable property monitorable with fewer resources, such as integer registers.},
  author       = {Henzinger, Thomas A and Sarac, Naci E},
  booktitle    = {Runtime Verification},
  isbn         = {9783030605070},
  issn         = {1611-3349},
  location     = {Los Angeles, CA, United States},
  pages        = {3--18},
  publisher    = {Springer Nature},
  title        = {{Monitorability under assumptions}},
  doi          = {10.1007/978-3-030-60508-7_1},
  volume       = {12399},
  year         = {2020},
}

@article{8634,
  abstract     = {In laboratory studies and numerical simulations, we observe clear signatures of unstable time-periodic solutions in a moderately turbulent quasi-two-dimensional flow. We validate the dynamical relevance of such solutions by demonstrating that turbulent flows in both experiment and numerics transiently display time-periodic dynamics when they shadow unstable periodic orbits (UPOs). We show that UPOs we computed are also statistically significant, with turbulent flows spending a sizable fraction of the total time near these solutions. As a result, the average rates of energy input and dissipation for the turbulent flow and frequently visited UPOs differ only by a few percent.},
  author       = {Suri, Balachandra and Kageorge, Logan and Grigoriev, Roman O. and Schatz, Michael F.},
  issn         = {1079-7114},
  journal      = {Physical Review Letters},
  keywords     = {General Physics and Astronomy},
  number       = {6},
  publisher    = {American Physical Society},
  title        = {{Capturing turbulent dynamics and statistics in experiments with unstable periodic orbits}},
  doi          = {10.1103/physrevlett.125.064501},
  volume       = {125},
  year         = {2020},
}

@article{8643,
  abstract     = {The parabigeminal nucleus (PBG) is the mammalian homologue to the isthmic complex of other vertebrates. Optogenetic stimulation of the PBG induces freezing and escape in mice, a result thought to be caused by a PBG projection to the central nucleus of the amygdala. However, the isthmic complex, including the PBG, has been classically considered satellite nuclei of the Superior Colliculus (SC), which upon stimulation of its medial part also triggers fear and avoidance reactions. As the PBG-SC connectivity is not well characterized, we investigated whether the topology of the PBG projection to the SC could be related to the behavioral consequences of PBG stimulation. To that end, we performed immunohistochemistry, in situ hybridization and neural tracer injections in the SC and PBG in a diurnal rodent, the Octodon degus. We found that all PBG neurons expressed both glutamatergic and cholinergic markers and were distributed in clearly defined anterior (aPBG) and posterior (pPBG) subdivisions. The pPBG is connected reciprocally and topographically to the ipsilateral SC, whereas the aPBG receives afferent axons from the ipsilateral SC and projected exclusively to the contralateral SC. This contralateral projection forms a dense field of terminals that is restricted to the medial SC, in correspondence with the SC representation of the aerial binocular field which, we also found, in O. degus prompted escape reactions upon looming stimulation. Therefore, this specialized topography allows binocular interactions in the SC region controlling responses to aerial predators, suggesting a link between the mechanisms by which the SC and PBG produce defensive behaviors.},
  author       = {Deichler, Alfonso and Carrasco, Denisse and Lopez-Jury, Luciana and Vega Zuniga, Tomas A and Marquez, Natalia and Mpodozis, Jorge and Marin, Gonzalo},
  issn         = {20452322},
  journal      = {Scientific Reports},
  publisher    = {Springer Nature},
  title        = {{A specialized reciprocal connectivity suggests a link between the mechanisms by which the superior colliculus and parabigeminal nucleus produce defensive behaviors in rodents}},
  doi          = {10.1038/s41598-020-72848-0},
  volume       = {10},
  year         = {2020},
}

@article{8644,
  abstract     = {Determining the phase diagram of systems consisting of smaller subsystems 'connected' via a tunable coupling is a challenging task relevant for a variety of physical settings. A general question is whether new phases, not present in the uncoupled limit, may arise. We use machine learning and a suitable quasidistance between different points of the phase diagram to study layered spin models, in which the spin variables constituting each of the uncoupled systems (to which we refer as layers) are coupled to each other via an interlayer coupling. In such systems, in general, composite order parameters involving spins of different layers may emerge as a consequence of the interlayer coupling. We focus on the layered Ising and Ashkin–Teller models as a paradigmatic case study, determining their phase diagram via the application of a machine learning algorithm to the Monte Carlo data. Remarkably our technique is able to correctly characterize all the system phases also in the case of hidden order parameters, i.e. order parameters whose expression in terms of the microscopic configurations would require additional preprocessing of the data fed to the algorithm. We correctly retrieve the three known phases of the Ashkin–Teller model with ferromagnetic couplings, including the phase described by a composite order parameter. For the bilayer and trilayer Ising models the phases we find are only the ferromagnetic and the paramagnetic ones. Within the approach we introduce, owing to the construction of convolutional neural networks, naturally suitable for layered image-like data with arbitrary number of layers, no preprocessing of the Monte Carlo data is needed, also with regard to its spatial structure. The physical meaning of our results is discussed and compared with analytical data, where available. Yet, the method can be used without any a priori knowledge of the phases one seeks to find and can be applied to other models and structures.},
  author       = {Rzadkowski, Wojciech and Defenu, N and Chiacchiera, S and Trombettoni, A and Bighin, Giacomo},
  issn         = {13672630},
  journal      = {New Journal of Physics},
  number       = {9},
  publisher    = {IOP Publishing},
  title        = {{Detecting composite orders in layered models via machine learning}},
  doi          = {10.1088/1367-2630/abae44},
  volume       = {22},
  year         = {2020},
}

@article{8645,
  abstract     = {Epistasis, the context-dependence of the contribution of an amino acid substitution to fitness, is common in evolution. To detect epistasis, fitness must be measured for at least four genotypes: the reference genotype, two different single mutants and a double mutant with both of the single mutations. For higher-order epistasis of the order n, fitness has to be measured for all 2n genotypes of an n-dimensional hypercube in genotype space forming a ‘combinatorially complete dataset’. So far, only a handful of such datasets have been produced by manual curation. Concurrently, random mutagenesis experiments have produced measurements of fitness and other phenotypes in a high-throughput manner, potentially containing a number of combinatorially complete datasets. We present an effective recursive algorithm for finding all hypercube structures in random mutagenesis experimental data. To test the algorithm, we applied it to the data from a recent HIS3 protein dataset and found all 199 847 053 unique combinatorially complete genotype combinations of dimensionality ranging from 2 to 12. The algorithm may be useful for researchers looking for higher-order epistasis in their high-throughput experimental data.},
  author       = {Esteban, Laura A and Lonishin, Lyubov R and Bobrovskiy, Daniil M and Leleytner, Gregory and Bogatyreva, Natalya S and Kondrashov, Fyodor and Ivankov, Dmitry N },
  issn         = {1460-2059},
  journal      = {Bioinformatics},
  number       = {6},
  pages        = {1960--1962},
  publisher    = {Oxford Academic},
  title        = {{HypercubeME: Two hundred million combinatorially complete datasets from a single experiment}},
  doi          = {10.1093/bioinformatics/btz841},
  volume       = {36},
  year         = {2020},
}

@article{8652,
  abstract     = {Nature creates electrons with two values of the spin projection quantum number. In certain applications, it is important to filter electrons with one spin projection from the rest. Such filtering is not trivial, since spin-dependent interactions are often weak, and cannot lead to any substantial effect. Here we propose an efficient spin filter based upon scattering from a two-dimensional crystal, which is made of aligned point magnets. The polarization of the outgoing electron flux is controlled by the crystal, and reaches maximum at specific values of the parameters. In our scheme, polarization increase is accompanied by higher reflectivity of the crystal. High transmission is feasible in scattering from a quantum cavity made of two crystals. Our findings can be used for studies of low-energy spin-dependent scattering from two-dimensional ordered structures made of magnetic atoms or aligned chiral molecules.},
  author       = {Ghazaryan, Areg and Lemeshko, Mikhail and Volosniev, Artem},
  issn         = {2399-3650},
  journal      = {Communications Physics},
  publisher    = {Springer Nature},
  title        = {{Filtering spins by scattering from a lattice of point magnets}},
  doi          = {10.1038/s42005-020-00445-8},
  volume       = {3},
  year         = {2020},
}

@phdthesis{8653,
  abstract     = {Mutations are the raw material of evolution and come in many different flavors. Point mutations change a single letter in the DNA sequence, while copy number mutations like duplications or deletions add or remove many letters of the DNA sequence simultaneously.  Each type of mutation exhibits specific properties like its rate of formation and reversal. 
Gene expression is a fundamental phenotype that can be altered by both, point and copy number mutations. The following thesis is concerned with the dynamics of gene expression evolution and how it is affected by the properties exhibited by point and copy number mutations. Specifically, we are considering i) copy number mutations during adaptation to fluctuating environments and ii) the interaction of copy number and point mutations during adaptation to constant environments.  },
  author       = {Tomanek, Isabella},
  issn         = {2663-337X},
  keywords     = {duplication, amplification, promoter, CNV, AMGET, experimental evolution, Escherichia coli},
  pages        = {117},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{The evolution of gene expression by copy number and point mutations}},
  doi          = {10.15479/AT:ISTA:8653},
  year         = {2020},
}

@phdthesis{8657,
  abstract     = {Synthesis of proteins – translation – is a fundamental process of life. Quantitative studies anchor translation into the context of bacterial physiology and reveal several mathematical relationships, called “growth laws,” which capture physiological feedbacks between protein synthesis and cell growth. Growth laws describe the dependency of the ribosome abundance as a function of growth rate, which can change depending on the growth conditions. Perturbations of translation reveal that bacteria employ a compensatory strategy in which the reduced translation capability results in increased expression of the translation machinery.
Perturbations of translation are achieved in various ways; clinically interesting is the application of translation-targeting antibiotics – translation inhibitors. The antibiotic effects on bacterial physiology are often poorly understood. Bacterial responses to two or more simultaneously applied antibiotics are even more puzzling. The combined antibiotic effect determines the type of drug interaction, which ranges from synergy (the effect is stronger than expected) to antagonism (the effect is weaker) and suppression (one of the drugs loses its potency).
In the first part of this work, we systematically measure the pairwise interaction network for translation inhibitors that interfere with different steps in translation. We find that the interactions are surprisingly diverse and tend to be more antagonistic. To explore the underlying mechanisms, we begin with a minimal biophysical model of combined antibiotic action. We base this model on the kinetics of antibiotic uptake and binding together with the physiological response described by the growth laws. The biophysical model explains some drug interactions, but not all; it specifically fails to predict suppression.
In the second part of this work, we hypothesize that elusive suppressive drug interactions result from the interplay between ribosomes halted in different stages of translation. To elucidate this putative mechanism of drug interactions between translation inhibitors, we generate translation bottlenecks genetically using in- ducible control of translation factors that regulate well-defined translation cycle steps. These perturbations accurately mimic antibiotic action and drug interactions, supporting that the interplay of different translation bottlenecks partially causes these interactions.
We extend this approach by varying two translation bottlenecks simultaneously. This approach reveals the suppression of translocation inhibition by inhibited translation. We rationalize this effect by modeling dense traffic of ribosomes that move on transcripts in a translation factor-mediated manner. This model predicts a dissolution of traffic jams caused by inhibited translocation when the density of ribosome traffic is reduced by lowered initiation. We base this model on the growth laws and quantitative relationships between different translation and growth parameters.
In the final part of this work, we describe a set of tools aimed at quantification of physiological and translation parameters. We further develop a simple model that directly connects the abundance of a translation factor with the growth rate, which allows us to extract physiological parameters describing initiation. We demonstrate the development of tools for measuring translation rate.
This thesis showcases how a combination of high-throughput growth rate mea- surements, genetics, and modeling can reveal mechanisms of drug interactions. Furthermore, by a gradual transition from combinations of antibiotics to precise genetic interventions, we demonstrated the equivalency between genetic and chemi- cal perturbations of translation. These findings tile the path for quantitative studies of antibiotic combinations and illustrate future approaches towards the quantitative description of translation.},
  author       = {Kavcic, Bor},
  isbn         = {978-3-99078-011-4},
  issn         = {2663-337X},
  pages        = {271},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Perturbations of protein synthesis: from antibiotics to genetics and physiology}},
  doi          = {10.15479/AT:ISTA:8657},
  year         = {2020},
}

@article{8669,
  abstract     = {Pancreatic islets play an essential role in regulating blood glucose level. Although the molecular pathways underlying islet cell differentiation are beginning to be resolved, the cellular basis of islet morphogenesis and fate allocation remain unclear. By combining unbiased and targeted lineage tracing, we address the events leading to islet formation in the mouse. From the statistical analysis of clones induced at multiple embryonic timepoints, here we show that, during the secondary transition, islet formation involves the aggregation of multiple equipotent endocrine progenitors that transition from a phase of stochastic amplification by cell division into a phase of sublineage restriction and limited islet fission. Together, these results explain quantitatively the heterogeneous size distribution and degree of polyclonality of maturing islets, as well as dispersion of progenitors within and between islets. Further, our results show that, during the secondary transition, α- and β-cells are generated in a contemporary manner. Together, these findings provide insight into the cellular basis of islet development.},
  author       = {Sznurkowska, Magdalena K. and Hannezo, Edouard B and Azzarelli, Roberta and Chatzeli, Lemonia and Ikeda, Tatsuro and Yoshida, Shosei and Philpott, Anna and Simons, Benjamin D},
  issn         = {20411723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Tracing the cellular basis of islet specification in mouse pancreas}},
  doi          = {10.1038/s41467-020-18837-3},
  volume       = {11},
  year         = {2020},
}

@article{8670,
  abstract     = {The α–z Rényi relative entropies are a two-parameter family of Rényi relative entropies that are quantum generalizations of the classical α-Rényi relative entropies. In the work [Adv. Math. 365, 107053 (2020)], we decided the full range of (α, z) for which the data processing inequality (DPI) is valid. In this paper, we give algebraic conditions for the equality in DPI. For the full range of parameters (α, z), we give necessary conditions and sufficient conditions. For most parameters, we give equivalent conditions. This generalizes and strengthens the results of Leditzky et al. [Lett. Math. Phys. 107, 61–80 (2017)].},
  author       = {Zhang, Haonan},
  issn         = {00222488},
  journal      = {Journal of Mathematical Physics},
  number       = {10},
  publisher    = {AIP Publishing},
  title        = {{Equality conditions of data processing inequality for α-z Rényi relative entropies}},
  doi          = {10.1063/5.0022787},
  volume       = {61},
  year         = {2020},
}

@article{8671,
  abstract     = {We study relations between evidence theory and S-approximation spaces. Both theories have their roots in the analysis of Dempsterchr('39')s multivalued mappings and lower and upper probabilities, and have close relations to rough sets. We show that an S-approximation space, satisfying a monotonicity condition, can induce a natural belief structure which is a fundamental block in evidence theory. We also demonstrate that one can induce a natural belief structure on one set, given a belief structure on another set, if the two sets are related by a partial monotone S-approximation space. },
  author       = {Shakiba, A. and Goharshady, Amir Kafshdar and Hooshmandasl, M.R. and Alambardar Meybodi, M.},
  issn         = {2008-9473},
  journal      = {Iranian Journal of Mathematical Sciences and Informatics},
  number       = {2},
  pages        = {117--128},
  publisher    = {Iranian Academic Center for Education, Culture and Research},
  title        = {{A note on belief structures and s-approximation spaces}},
  doi          = {10.29252/ijmsi.15.2.117},
  volume       = {15},
  year         = {2020},
}

@article{8672,
  abstract     = {Cell fate transitions are key to development and homeostasis. It is thus essential to understand the cellular mechanisms controlling fate transitions. Cell division has been implicated in fate decisions in many stem cell types, including neuronal and epithelial progenitors. In other stem cells, such as embryonic stem (ES) cells, the role of division remains unclear. Here, we show that exit from naive pluripotency in mouse ES cells generally occurs after a division. We further show that exit timing is strongly correlated between sister cells, which remain connected by cytoplasmic bridges long after division, and that bridge abscission progressively accelerates as cells exit naive pluripotency. Finally, interfering with abscission impairs naive pluripotency exit, and artificially inducing abscission accelerates it. Altogether, our data indicate that a switch in the division machinery leading to faster abscission regulates pluripotency exit. Our study identifies abscission as a key cellular process coupling cell division to fate transitions.},
  author       = {Chaigne, Agathe and Labouesse, Céline and White, Ian J. and Agnew, Meghan and Hannezo, Edouard B and Chalut, Kevin J. and Paluch, Ewa K.},
  issn         = {18781551},
  journal      = {Developmental Cell},
  number       = {2},
  pages        = {195--208},
  publisher    = {Elsevier},
  title        = {{Abscission couples cell division to embryonic stem cell fate}},
  doi          = {10.1016/j.devcel.2020.09.001},
  volume       = {55},
  year         = {2020},
}

@article{8674,
  abstract     = {Extrasynaptic actions of glutamate are limited by high-affinity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-to-point transmission in excitatory circuits. Memory formation in the brain is associated with synaptic remodeling, but how this affects PAPs and therefore extrasynaptic glutamate actions is poorly understood. Here, we used advanced imaging methods, in situ and in vivo, to find that a classical synaptic memory mechanism, long-term potentiation (LTP), triggers withdrawal of PAPs from potentiated synapses. Optical glutamate sensors combined with patch-clamp and 3D molecular localization reveal that LTP induction thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate spillover and NMDA-receptor-mediated inter-synaptic cross-talk. The LTP-triggered PAP withdrawal involves NKCC1 transporters and the actin-controlling protein cofilin but does not depend on major Ca2+-dependent cascades in astrocytes. We have therefore uncovered a mechanism by which a memory trace at one synapse could alter signal handling by multiple neighboring connections.},
  author       = {Henneberger, Christian and Bard, Lucie and Panatier, Aude and Reynolds, James P. and Kopach, Olga and Medvedev, Nikolay I. and Minge, Daniel and Herde, Michel K. and Anders, Stefanie and Kraev, Igor and Heller, Janosch P. and Rama, Sylvain and Zheng, Kaiyu and Jensen, Thomas P. and Sanchez-Romero, Inmaculada and Jackson, Colin J. and Janovjak, Harald L and Ottersen, Ole Petter and Nagelhus, Erlend Arnulf and Oliet, Stephane H.R. and Stewart, Michael G. and Nägerl, U. VAlentin and Rusakov, Dmitri A. },
  issn         = {10974199},
  journal      = {Neuron},
  number       = {5},
  pages        = {P919--936.E11},
  publisher    = {Elsevier},
  title        = {{LTP induction boosts glutamate spillover by driving withdrawal of perisynaptic astroglia}},
  doi          = {10.1016/j.neuron.2020.08.030},
  volume       = {108},
  year         = {2020},
}

@article{8679,
  abstract     = {A central goal of artificial intelligence in high-stakes decision-making applications is to design a single algorithm that simultaneously expresses generalizability by learning coherent representations of their world and interpretable explanations of its dynamics. Here, we combine brain-inspired neural computation principles and scalable deep learning architectures to design compact neural controllers for task-specific compartments of a full-stack autonomous vehicle control system. We discover that a single algorithm with 19 control neurons, connecting 32 encapsulated input features to outputs by 253 synapses, learns to map high-dimensional inputs into steering commands. This system shows superior generalizability, interpretability and robustness compared with orders-of-magnitude larger black-box learning systems. The obtained neural agents enable high-fidelity autonomy for task-specific parts of a complex autonomous system.},
  author       = {Lechner, Mathias and Hasani, Ramin and Amini, Alexander and Henzinger, Thomas A and Rus, Daniela and Grosu, Radu},
  issn         = {2522-5839},
  journal      = {Nature Machine Intelligence},
  pages        = {642--652},
  publisher    = {Springer Nature},
  title        = {{Neural circuit policies enabling auditable autonomy}},
  doi          = {10.1038/s42256-020-00237-3},
  volume       = {2},
  year         = {2020},
}

@article{8680,
  abstract     = {Animal development entails the organization of specific cell types in space and time, and spatial patterns must form in a robust manner. In the zebrafish spinal cord, neural progenitors form stereotypic patterns despite noisy morphogen signaling and large-scale cellular rearrangements during morphogenesis and growth. By directly measuring adhesion forces and preferences for three types of endogenous neural progenitors, we provide evidence for the differential adhesion model in which differences in intercellular adhesion mediate cell sorting. Cell type–specific combinatorial expression of different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19) results in homotypic preference ex vivo and patterning robustness in vivo. Furthermore, the differential adhesion code is regulated by the sonic hedgehog morphogen gradient. We propose that robust patterning during tissue morphogenesis results from interplay between adhesion-based self-organization and morphogen-directed patterning.},
  author       = {Tsai, Tony Y.-C. and Sikora, Mateusz K and Xia, Peng and Colak-Champollion, Tugba and Knaut, Holger and Heisenberg, Carl-Philipp J and Megason, Sean G.},
  issn         = {1095-9203},
  journal      = {Science},
  keywords     = {Multidisciplinary},
  number       = {6512},
  pages        = {113--116},
  publisher    = {American Association for the Advancement of Science},
  title        = {{An adhesion code ensures robust pattern formation during tissue morphogenesis}},
  doi          = {10.1126/science.aba6637},
  volume       = {370},
  year         = {2020},
}