@inproceedings{14204,
  abstract     = {Two popular examples of first-order optimization methods over linear spaces are coordinate descent and matching pursuit algorithms, with their randomized variants. While the former targets the optimization by moving along coordinates, the latter considers a generalized notion of directions. Exploiting the connection between the two algorithms, we present a unified analysis of both, providing affine invariant sublinear O(1/t) rates on smooth objectives and linear convergence on strongly convex objectives. As a byproduct of our affine invariant analysis of matching pursuit, our rates for steepest coordinate descent are the tightest known. Furthermore, we show the first accelerated convergence rate O(1/t2) for matching pursuit and steepest coordinate descent on convex objectives.},
  author       = {Locatello, Francesco and Raj, Anant and Karimireddy, Sai Praneeth and Rätsch, Gunnar and Schölkopf, Bernhard and Stich, Sebastian U. and Jaggi, Martin},
  booktitle    = {Proceedings of the 35th International Conference on Machine Learning},
  pages        = {3198--3207},
  publisher    = {ML Research Press},
  title        = {{On matching pursuit and coordinate descent}},
  volume       = {80},
  year         = {2018},
}

@inproceedings{14224,
  abstract     = {Clustering is a cornerstone of unsupervised learning which can be thought as disentangling multiple generative mechanisms underlying the data. In this paper we introduce an algorithmic framework to train mixtures of implicit generative models which we particularize for variational autoencoders. Relying on an additional set of discriminators, we propose a competitive procedure in which the models only need to approximate the portion of the data distribution from which they can produce realistic samples. As a byproduct, each model is simpler to train, and a clustering interpretation arises naturally from the partitioning of the training points among the models. We empirically show that our approach splits the training distribution in a reasonable way and increases the quality of the generated samples.},
  author       = {Locatello, Francesco and Vincent, Damien and Tolstikhin, Ilya and Ratsch, Gunnar and Gelly, Sylvain and Scholkopf, Bernhard},
  booktitle    = {6th International Conference on Learning Representations},
  location     = {Vancouver, Canada},
  title        = {{Clustering meets implicit generative models}},
  year         = {2018},
}

@article{14284,
  abstract     = {Pore-forming toxins (PFT) are virulence factors that transform from soluble to membrane-bound states. The Yersinia YaxAB system represents a family of binary α-PFTs with orthologues in human, insect, and plant pathogens, with unknown structures. YaxAB was shown to be cytotoxic and likely involved in pathogenesis, though the molecular basis for its two-component lytic mechanism remains elusive. Here, we present crystal structures of YaxA and YaxB, together with a cryo-electron microscopy map of the YaxAB complex. Our structures reveal a pore predominantly composed of decamers of YaxA–YaxB heterodimers. Both subunits bear membrane-active moieties, but only YaxA is capable of binding to membranes by itself. YaxB can subsequently be recruited to membrane-associated YaxA and induced to present its lytic transmembrane helices. Pore formation can progress by further oligomerization of YaxA–YaxB dimers. Our results allow for a comparison between pore assemblies belonging to the wider ClyA-like family of α-PFTs, highlighting diverse pore architectures.},
  author       = {Bräuning, Bastian and Bertosin, Eva and Praetorius, Florian M and Ihling, Christian and Schatt, Alexandra and Adler, Agnes and Richter, Klaus and Sinz, Andrea and Dietz, Hendrik and Groll, Michael},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  keywords     = {General Physics and Astronomy, General Biochemistry, Genetics and Molecular Biology, General Chemistry, Multidisciplinary},
  publisher    = {Springer Nature},
  title        = {{Structure and mechanism of the two-component α-helical pore-forming toxin YaxAB}},
  doi          = {10.1038/s41467-018-04139-2},
  volume       = {9},
  year         = {2018},
}

@inproceedings{143,
  abstract     = {Vector Addition Systems with States (VASS) provide a well-known and fundamental model for the analysis of concurrent processes, parameterized systems, and are also used as abstract models of programs in resource bound analysis. In this paper we study the problem of obtaining asymptotic bounds on the termination time of a given VASS. In particular, we focus on the practically important case of obtaining polynomial bounds on termination time. Our main contributions are as follows: First, we present a polynomial-time algorithm for deciding whether a given VASS has a linear asymptotic complexity. We also show that if the complexity of a VASS is not linear, it is at least quadratic. Second, we classify VASS according to quantitative properties of their cycles. We show that certain singularities in these properties are the key reason for non-polynomial asymptotic complexity of VASS. In absence of singularities, we show that the asymptotic complexity is always polynomial and of the form Θ(nk), for some integer k d, where d is the dimension of the VASS. We present a polynomial-time algorithm computing the optimal k. For general VASS, the same algorithm, which is based on a complete technique for the construction of ranking functions in VASS, produces a valid lower bound, i.e., a k such that the termination complexity is (nk). Our results are based on new insights into the geometry of VASS dynamics, which hold the potential for further applicability to VASS analysis.},
  author       = {Brázdil, Tomáš and Chatterjee, Krishnendu and Kučera, Antonín and Novotny, Petr and Velan, Dominik and Zuleger, Florian},
  isbn         = {978-1-4503-5583-4},
  location     = {Oxford, United Kingdom},
  pages        = {185 -- 194},
  publisher    = {IEEE},
  title        = {{Efficient algorithms for asymptotic bounds on termination time in VASS}},
  doi          = {10.1145/3209108.3209191},
  volume       = {F138033},
  year         = {2018},
}

@phdthesis{14306,
  abstract     = {Function and activity of biomolecules often depend on their spatial arrangement. The method introduced here allows genetically encoding the spatial arrangement of proteins and DNA. The approach relies on staple proteins that fold double-stranded DNA into user-defined shapes. This thesis describes the development of staple proteins based on the DNA recognition of TAL effectors and presents experimentally derived rules for designing a variety of self-assembling nanoscale shapes featuring structural motifs such as curvature, vertices, corners, and multilayer helix packing. },
  author       = {Praetorius, Florian M},
  publisher    = {Technische Universität München},
  title        = {{Genetically encoding the spatial arrangement of DNA and proteins in self-assembling nanostructures}},
  year         = {2018},
}

@unpublished{14327,
  abstract     = {A common assumption in causal modeling posits that the data is generated by a
set of independent mechanisms, and algorithms should aim to recover this
structure. Standard unsupervised learning, however, is often concerned with
training a single model to capture the overall distribution or aspects thereof.
Inspired by clustering approaches, we consider mixtures of implicit generative
models that ``disentangle'' the independent generative mechanisms underlying
the data. Relying on an additional set of discriminators, we propose a
competitive training procedure in which the models only need to capture the
portion of the data distribution from which they can produce realistic samples.
As a by-product, each model is simpler and faster to train. We empirically show
that our approach splits the training distribution in a sensible way and
increases the quality of the generated samples.},
  author       = {Locatello, Francesco and Vincent, Damien and Tolstikhin, Ilya and Rätsch, Gunnar and Gelly, Sylvain and Schölkopf, Bernhard},
  booktitle    = {arXiv},
  title        = {{Competitive training of mixtures of independent deep generative models}},
  doi          = {10.48550/arXiv.1804.11130},
  year         = {2018},
}

@inproceedings{144,
  abstract     = {The task of a monitor is to watch, at run-time, the execution of a reactive system, and signal the occurrence of a safety violation in the observed sequence of events. While finite-state monitors have been studied extensively, in practice, monitoring software also makes use of unbounded memory. We define a model of automata equipped with integer-valued registers which can execute only a bounded number of instructions between consecutive events, and thus can form the theoretical basis for the study of infinite-state monitors. We classify these register monitors according to the number k of available registers, and the type of register instructions. In stark contrast to the theory of computability for register machines, we prove that for every k 1, monitors with k + 1 counters (with instruction set 〈+1, =〉) are strictly more expressive than monitors with k counters. We also show that adder monitors (with instruction set 〈1, +, =〉) are strictly more expressive than counter monitors, but are complete for monitoring all computable safety -languages for k = 6. Real-time monitors are further required to signal the occurrence of a safety violation as soon as it occurs. The expressiveness hierarchy for counter monitors carries over to real-time monitors. We then show that 2 adders cannot simulate 3 counters in real-time. Finally, we show that real-time adder monitors with inequalities are as expressive as real-time Turing machines.},
  author       = {Ferrere, Thomas and Henzinger, Thomas A and Saraç, Ege},
  location     = {Oxford, UK},
  pages        = {394 -- 403},
  publisher    = {IEEE},
  title        = {{A theory of register monitors}},
  doi          = {10.1145/3209108.3209194},
  volume       = {Part F138033},
  year         = {2018},
}

@article{145,
  abstract     = {Aged proteins can become hazardous to cellular function, by accumulating molecular damage. This implies that cells should preferentially rely on newly produced ones. We tested this hypothesis in cultured hippocampal neurons, focusing on synaptic transmission. We found that newly synthesized vesicle proteins were incorporated in the actively recycling pool of vesicles responsible for all neurotransmitter release during physiological activity. We observed this for the calcium sensor Synaptotagmin 1, for the neurotransmitter transporter VGAT, and for the fusion protein VAMP2 (Synaptobrevin 2). Metabolic labeling of proteins and visualization by secondary ion mass spectrometry enabled us to query the entire protein makeup of the actively recycling vesicles, which we found to be younger than that of non-recycling vesicles. The young vesicle proteins remained in use for up to ~ 24 h, during which they participated in recycling a few hundred times. They were afterward reluctant to release and were degraded after an additional ~ 24–48 h. We suggest that the recycling pool of synaptic vesicles relies on newly synthesized proteins, while the inactive reserve pool contains older proteins.},
  author       = {Truckenbrodt, Sven M and Viplav, Abhiyan and Jähne, Sebsatian and Vogts, Angela and Denker, Annette and Wildhagen, Hanna and Fornasiero, Eugenio and Rizzoli, Silvio},
  issn         = {0261-4189},
  journal      = {The EMBO Journal},
  number       = {15},
  publisher    = {Wiley},
  title        = {{Newly produced synaptic vesicle proteins are preferentially used in synaptic transmission}},
  doi          = {10.15252/embj.201798044},
  volume       = {37},
  year         = {2018},
}

@article{146,
  abstract     = {The root cap protects the stem cell niche of angiosperm roots from damage. In Arabidopsis, lateral root cap (LRC) cells covering the meristematic zone are regularly lost through programmed cell death, while the outermost layer of the root cap covering the tip is repeatedly sloughed. Efficient coordination with stem cells producing new layers is needed to maintain a constant size of the cap. We present a signalling pair, the peptide IDA-LIKE1 (IDL1) and its receptor HAESA-LIKE2 (HSL2), mediating such communication. Live imaging over several days characterized this process from initial fractures in LRC cell files to full separation of a layer. Enhanced expression of IDL1 in the separating root cap layers resulted in increased frequency of sloughing, balanced with generation of new layers in a HSL2-dependent manner. Transcriptome analyses linked IDL1-HSL2 signalling to the transcription factors BEARSKIN1/2 and genes associated with programmed cell death. Mutations in either IDL1 or HSL2 slowed down cell division, maturation and separation. Thus, IDL1-HSL2 signalling potentiates dynamic regulation of the homeostatic balance between stem cell division and sloughing activity.},
  author       = {Shi, Chun Lin and Von Wangenheim, Daniel and Herrmann, Ullrich and Wildhagen, Mari and Kulik, Ivan and Kopf, Andreas and Ishida, Takashi and Olsson, Vilde and Anker, Mari Kristine and Albert, Markus and Butenko, Melinka A and Felix, Georg and Sawa, Shinichiro and Claassen, Manfred and Friml, Jirí and Aalen, Reidunn B},
  journal      = {Nature Plants},
  number       = {8},
  pages        = {596 -- 604},
  publisher    = {Nature Publishing Group},
  title        = {{The dynamics of root cap sloughing in Arabidopsis is regulated by peptide signalling}},
  doi          = {10.1038/s41477-018-0212-z},
  volume       = {4},
  year         = {2018},
}

@article{147,
  abstract     = {The trafficking of subcellular cargos in eukaryotic cells crucially depends on vesicle budding, a process mediated by ARF-GEFs (ADP-ribosylation factor guanine nucleotide exchange factors). In plants, ARF-GEFs play essential roles in endocytosis, vacuolar trafficking, recycling, secretion, and polar trafficking. Moreover, they are important for plant development, mainly through controlling the polar subcellular localization of PIN-FORMED (PIN) transporters of the plant hormone auxin. Here, using a chemical genetics screen in Arabidopsis thaliana, we identified Endosidin 4 (ES4), an inhibitor of eukaryotic ARF-GEFs. ES4 acts similarly to and synergistically with the established ARF-GEF inhibitor Brefeldin A and has broad effects on intracellular trafficking, including endocytosis, exocytosis, and vacuolar targeting. Additionally, Arabidopsis and yeast (Sacharomyces cerevisiae) mutants defective in ARF-GEF show altered sensitivity to ES4. ES4 interferes with the activation-based membrane association of the ARF1 GTPases, but not of their mutant variants that are activated independently of ARF-GEF activity. Biochemical approaches and docking simulations confirmed that ES4 specifically targets the SEC7 domain-containing ARF-GEFs. These observations collectively identify ES4 as a chemical tool enabling the study of ARF-GEF-mediated processes, including ARF-GEF-mediated plant development.},
  author       = {Kania, Urszula and Nodzyński, Tomasz and Lu, Qing and Hicks, Glenn R and Nerinckx, Wim and Mishev, Kiril and Peurois, Francois and Cherfils, Jacqueline and De, Rycke Riet Maria and Grones, Peter and Robert, Stéphanie and Russinova, Eugenia and Friml, Jirí},
  issn         = {1040-4651},
  journal      = {The Plant Cell},
  number       = {10},
  pages        = {2553 -- 2572},
  publisher    = {Oxford University Press},
  title        = {{The inhibitor Endosidin 4 targets SEC7 domain-type ARF GTPase exchange factors and interferes with sub cellular trafficking in eukaryotes}},
  doi          = {10.1105/tpc.18.00127},
  volume       = {30},
  year         = {2018},
}

@phdthesis{539,
  abstract     = {The whole life cycle of plants as well as their responses to environmental stimuli is governed by a complex network of hormonal regulations. A number of studies have demonstrated an essential role of both auxin and cytokinin in the regulation of many aspects of plant growth and development including embryogenesis, postembryonic organogenic processes such as root, and shoot branching, root and shoot apical meristem activity and phyllotaxis. Over the last decades essential knowledge on the key molecular factors and pathways that spatio-temporally define auxin and cytokinin activities in the plant body has accumulated. However, how both hormonal pathways are interconnected by a complex network of interactions and feedback circuits that determines the final outcome of the individual hormone actions is still largely unknown. Root system architecture establishment and in particular formation of lateral organs is prime example of developmental process at whose regulation both auxin and cytokinin pathways converge. To dissect convergence points and pathways that tightly balance auxin - cytokinin antagonistic activities that determine the root branching pattern transcriptome profiling was applied. Genome wide expression analyses of the xylem pole pericycle, a tissue giving rise to lateral roots, led to identification of genes that are highly responsive to combinatorial auxin and cytokinin treatments and play an essential function in the auxin-cytokinin regulated root branching. SYNERGISTIC AUXIN CYTOKININ 1 (SYAC1) gene, which encodes for a protein of unknown function, was detected among the top candidate genes of which expression was synergistically up-regulated by simultaneous hormonal treatment. Plants with modulated SYAC1 activity exhibit severe defects in the root system establishment and attenuate developmental responses to both auxin and cytokinin. To explore the biological function of the SYAC1, we employed different strategies including expression pattern analysis, subcellular localization and phenotypic analyses of the syac1 loss-of-function and gain-of-function transgenic lines along with the identification of the SYAC1 interaction partners. Detailed functional characterization revealed that SYAC1 acts as a developmentally specific regulator of the secretory pathway to control deposition of cell wall components and thereby rapidly fine tune elongation growth.},
  author       = {Hurny, Andrej},
  issn         = {2663-337X},
  pages        = {147},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Identification and characterization of novel auxin-cytokinin cross-talk components}},
  doi          = {10.15479/AT:ISTA:th_930},
  year         = {2018},
}

@article{54,
  abstract     = {During epithelial tissue development, repair, and homeostasis, adherens junctions (AJs) ensure intercellular adhesion and tissue integrity while allowing for cell and tissue dynamics. Mechanical forces play critical roles in AJs’ composition and dynamics. Recent findings highlight that beyond a well-established role in reinforcing cell-cell adhesion, AJ mechanosensitivity promotes junctional remodeling and polarization, thereby regulating critical processes such as cell intercalation, division, and collective migration. Here, we provide an integrated view of mechanosensing mechanisms that regulate cell-cell contact composition, geometry, and integrity under tension and highlight pivotal roles for mechanosensitive AJ remodeling in preserving epithelial integrity and sustaining tissue dynamics.},
  author       = {Nunes Pinheiro, Diana C and Bellaïche, Yohanns},
  journal      = {Developmental Cell},
  number       = {1},
  pages        = {3 -- 19},
  publisher    = {Cell Press},
  title        = {{Mechanical force-driven adherents junction remodeling and epithelial dynamics}},
  doi          = {10.1016/j.devcel.2018.09.014},
  volume       = {47},
  year         = {2018},
}

@article{542,
  abstract     = {The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a model for autosomal segregation distortion for close to a century, but several questions remain regarding its biology and evolutionary history. A recently published set of population genomics resources for wild mice includes several individuals heterozygous for the t-haplotype, which we use to characterize this selfish element at the genomic and transcriptomic level. Our results show that large sections of the t-haplotype have been replaced by standard homologous sequences, possibly due to occasional events of recombination, and that this complicates the inference of its history. As expected for a long genomic segment of very low recombination, the t-haplotype carries an excess of fixed nonsynonymous mutations compared to the standard chromosome. This excess is stronger for regions that have not undergone recent recombination, suggesting that occasional gene flow between the t and the standard chromosome may provide a mechanism to regenerate coding sequences that have accumulated deleterious mutations. Finally, we find that t-complex genes with altered expression largely overlap with deleted or amplified regions, and that carrying a t-haplotype alters the testis expression of genes outside of the t-complex, providing new leads into the pathways involved in the biology of this segregation distorter.},
  author       = {Kelemen, Réka K and Vicoso, Beatriz},
  journal      = {Genetics},
  number       = {1},
  pages        = {365 -- 375},
  publisher    = {Genetics Society of America},
  title        = {{Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver}},
  doi          = {10.1534/genetics.117.300513},
  volume       = {208},
  year         = {2018},
}

@article{543,
  abstract     = {A central goal in theoretical neuroscience is to predict the response properties of sensory neurons from first principles. To this end, “efficient coding” posits that sensory neurons encode maximal information about their inputs given internal constraints. There exist, however, many variants of efficient coding (e.g., redundancy reduction, different formulations of predictive coding, robust coding, sparse coding, etc.), differing in their regimes of applicability, in the relevance of signals to be encoded, and in the choice of constraints. It is unclear how these types of efficient coding relate or what is expected when different coding objectives are combined. Here we present a unified framework that encompasses previously proposed efficient coding models and extends to unique regimes. We show that optimizing neural responses to encode predictive information can lead them to either correlate or decorrelate their inputs, depending on the stimulus statistics; in contrast, at low noise, efficiently encoding the past always predicts decorrelation. Later, we investigate coding of naturalistic movies and show that qualitatively different types of visual motion tuning and levels of response sparsity are predicted, depending on whether the objective is to recover the past or predict the future. Our approach promises a way to explain the observed diversity of sensory neural responses, as due to multiple functional goals and constraints fulfilled by different cell types and/or circuits.},
  author       = {Chalk, Matthew J and Marre, Olivier and Tkacik, Gasper},
  journal      = {PNAS},
  number       = {1},
  pages        = {186 -- 191},
  publisher    = {National Academy of Sciences},
  title        = {{Toward a unified theory of efficient, predictive, and sparse coding}},
  doi          = {10.1073/pnas.1711114115},
  volume       = {115},
  year         = {2018},
}

@article{544,
  abstract     = {Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes, are essential for immune responses, but also play key roles from early development to death through their interactions with other cell types. They regulate homeostasis and signaling during development, stem cell proliferation, metabolism, cancer, wound responses and aging, displaying intriguing molecular and functional conservation with vertebrate macrophages. Given the relative ease of genetics in Drosophila compared to vertebrates, tools permitting visualization and genetic manipulation of plasmatocytes and surrounding tissues independently at all stages would greatly aid in fully understanding these processes, but are lacking. Here we describe a comprehensive set of transgenic lines that allow this. These include extremely brightly fluorescing mCherry-based lines that allow GAL4-independent visualization of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8 through adulthood in both live and fixed samples even as heterozygotes, greatly facilitating screening. These lines allow live visualization and tracking of embryonic plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes and inner tissues can be seen in live or fixed embryos, larvae and adults. They permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout life. To facilitate genetic analysis of reciprocal signaling, we have also made a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers allows independent genetic manipulation of both plasmatocytes and surrounding tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes, both of which function from the early embryo to the adult.},
  author       = {György, Attila and Roblek, Marko and Ratheesh, Aparna and Valosková, Katarina and Belyaeva, Vera and Wachner, Stephanie and Matsubayashi, Yutaka and Sanchez Sanchez, Besaiz and Stramer, Brian and Siekhaus, Daria E},
  journal      = {G3: Genes, Genomes, Genetics},
  number       = {3},
  pages        = {845 -- 857},
  publisher    = {Genetics Society of America},
  title        = {{Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues}},
  doi          = {10.1534/g3.117.300452},
  volume       = {8},
  year         = {2018},
}

@misc{5457,
  abstract     = {We consider the problem of expected cost analysis over nondeterministic probabilistic programs, which aims at automated methods for analyzing the resource-usage of such programs. Previous approaches for this problem could only handle nonnegative bounded costs. However, in many scenarios, such as queuing networks or analysis of cryptocurrency protocols, both positive and negative costs are necessary and the costs are unbounded as well.

In this work, we present a sound and efficient approach to obtain polynomial bounds on the expected accumulated cost of nondeterministic probabilistic programs. Our approach can handle (a) general positive and negative costs with bounded updates in variables; and (b) nonnegative costs with general updates to variables. We show that several natural examples which could not be handled by previous approaches are captured in our framework.

Moreover, our approach leads to an efficient polynomial-time algorithm, while no previous approach for cost analysis of probabilistic programs could guarantee polynomial runtime. Finally, we show the effectiveness of our approach by presenting experimental results on a variety of programs, motivated by real-world applications, for which we efficiently synthesize tight resource-usage bounds.},
  author       = {Anonymous, 1 and Anonymous, 2 and Anonymous, 3 and Anonymous, 4 and Anonymous, 5 and Anonymous, 6},
  issn         = {2664-1690},
  pages        = {27},
  publisher    = {IST Austria},
  title        = {{Cost analysis of nondeterministic probabilistic programs}},
  year         = {2018},
}

@article{546,
  abstract     = {The precise control of neural stem cell (NSC) proliferation and differentiation is crucial for the development and function of the human brain. Here, we review the emerging links between the alteration of embryonic and adult neurogenesis and the etiology of neuropsychiatric disorders (NPDs) such as autism spectrum disorders (ASDs) and schizophrenia (SCZ), as well as the advances in stem cell-based modeling and the novel therapeutic targets derived from these studies.},
  author       = {Sacco, Roberto and Cacci, Emanuele and Novarino, Gaia},
  journal      = {Current Opinion in Neurobiology},
  number       = {2},
  pages        = {131 -- 138},
  publisher    = {Elsevier},
  title        = {{Neural stem cells in neuropsychiatric disorders}},
  doi          = {10.1016/j.conb.2017.12.005},
  volume       = {48},
  year         = {2018},
}

@article{547,
  abstract     = {The formation of the vertebrate brain requires the generation, migration, differentiation and survival of neurons. Genetic mutations that perturb these critical cellular events can result in malformations of the telencephalon, providing a molecular window into brain development. Here we report the identification of an N-ethyl-N-nitrosourea-induced mouse mutant characterized by a fractured hippocampal pyramidal cell layer, attributable to defects in neuronal migration. We show that this is caused by a hypomorphic mutation in Vps15 that perturbs endosomal-lysosomal trafficking and autophagy, resulting in an upregulation of Nischarin, which inhibits Pak1 signaling. The complete ablation of Vps15 results in the accumulation of autophagic substrates, the induction of apoptosis and severe cortical atrophy. Finally, we report that mutations in VPS15 are associated with cortical atrophy and epilepsy in humans. These data highlight the importance of the Vps15-Vps34 complex and the Nischarin-Pak1 signaling hub in the development of the telencephalon.},
  author       = {Gstrein, Thomas and Edwards, Andrew and Přistoupilová, Anna and Leca, Ines and Breuss, Martin and Pilat Carotta, Sandra and Hansen, Andi H and Tripathy, Ratna and Traunbauer, Anna and Hochstoeger, Tobias and Rosoklija, Gavril and Repic, Marco and Landler, Lukas and Stránecký, Viktor and Dürnberger, Gerhard and Keane, Thomas and Zuber, Johannes and Adams, David and Flint, Jonathan and Honzik, Tomas and Gut, Marta and Beltran, Sergi and Mechtler, Karl and Sherr, Elliott and Kmoch, Stanislav and Gut, Ivo and Keays, David},
  journal      = {Nature Neuroscience},
  number       = {2},
  pages        = {207 -- 217},
  publisher    = {Nature Publishing Group},
  title        = {{Mutations in Vps15 perturb neuronal migration in mice and are associated with neurodevelopmental disease in humans}},
  doi          = {10.1038/s41593-017-0053-5},
  volume       = {21},
  year         = {2018},
}

@article{55,
  abstract     = {Many animals use antimicrobials to prevent or cure disease [1,2]. For example, some animals will ingest plants with medicinal properties, both prophylactically to prevent infection and therapeutically to self-medicate when sick. Antimicrobial substances are also used as topical disinfectants, to prevent infection, protect offspring and to sanitise their surroundings [1,2]. Social insects (ants, bees, wasps and termites) build nests in environments with a high abundance and diversity of pathogenic microorganisms — such as soil and rotting wood — and colonies are often densely crowded, creating conditions that favour disease outbreaks. Consequently, social insects have evolved collective disease defences to protect their colonies from epidemics. These traits can be seen as functionally analogous to the immune system of individual organisms [3,4]. This ‘social immunity’ utilises antimicrobials to prevent and eradicate infections, and to keep the brood and nest clean. However, these antimicrobial compounds can be harmful to the insects themselves, and it is unknown how colonies prevent collateral damage when using them. Here, we demonstrate that antimicrobial acids, produced by workers to disinfect the colony, are harmful to the delicate pupal brood stage, but that the pupae are protected from the acids by the presence of a silk cocoon. Garden ants spray their nests with an antimicrobial poison to sanitize contaminated nestmates and brood. Here, Pull et al show that they also prophylactically sanitise their colonies, and that the silk cocoon serves as a barrier to protect developing pupae, thus preventing collateral damage during nest sanitation.},
  author       = {Pull, Christopher and Metzler, Sina and Naderlinger, Elisabeth and Cremer, Sylvia},
  journal      = {Current Biology},
  number       = {19},
  pages        = {R1139 -- R1140},
  publisher    = {Cell Press},
  title        = {{Protection against the lethal side effects of social immunity in ants}},
  doi          = {10.1016/j.cub.2018.08.063},
  volume       = {28},
  year         = {2018},
}

@article{554,
  abstract     = {We analyse the canonical Bogoliubov free energy functional in three dimensions at low temperatures in the dilute limit. We prove existence of a first-order phase transition and, in the limit (Formula presented.), we determine the critical temperature to be (Formula presented.) to leading order. Here, (Formula presented.) is the critical temperature of the free Bose gas, ρ is the density of the gas and a is the scattering length of the pair-interaction potential V. We also prove asymptotic expansions for the free energy. In particular, we recover the Lee–Huang–Yang formula in the limit (Formula presented.).},
  author       = {Napiórkowski, Marcin M and Reuvers, Robin and Solovej, Jan},
  issn         = {00103616},
  journal      = {Communications in Mathematical Physics},
  number       = {1},
  pages        = {347--403},
  publisher    = {Springer},
  title        = {{The Bogoliubov free energy functional II: The dilute Limit}},
  doi          = {10.1007/s00220-017-3064-x},
  volume       = {360},
  year         = {2018},
}

