@inproceedings{3843,
  abstract     = {Within systems biology there is an increasing interest in the stochastic behavior of biochemical reaction networks. An appropriate stochastic description is provided by the chemical master equation, which represents a continuous- time Markov chain (CTMC).
Standard Uniformization (SU) is an efficient method for the transient analysis of CTMCs. For systems with very different time scales, such as biochemical reaction networks, SU is computationally expensive. In these cases, a variant of SU, called adaptive uniformization (AU), is known to reduce the large number of iterations needed by SU. The additional difficulty of AU is that it requires the solution of a birth process.
In this paper we present an on-the-fly variant of AU, where we improve the original algorithm for AU at the cost of a small approximation error. By means of several examples, we show that our approach is particularly well-suited for biochemical reaction networks.},
  author       = {Didier, Frédéric and Henzinger, Thomas A and Mateescu, Maria and Wolf, Verena},
  location     = {Trento, Italy},
  number       = {6},
  pages        = {118 -- 127},
  publisher    = {IEEE},
  title        = {{Fast adaptive uniformization of the chemical master equation}},
  doi          = {10.1109/HiBi.2009.23},
  volume       = {4},
  year         = {2009},
}

@inproceedings{3844,
  abstract     = {The Hierarchical Timing Language (HTL) is a real-time coordination language for distributed control systems. HTL programs must be checked for well-formedness, race freedom, transmission safety (schedulability of inter-host communication), and time safety (schedulability of host computation). We present a modular abstract syntax and semantics for HTL, modular checks of well-formedness, race freedom, and transmission safety, and modular code distribution. Our contributions here complement previous results on HTL time safety and modular code generation. Modularity in HTL can be utilized in easy program composition as well as fast program analysis and code generation, but also in so-called runtime patching, where program components may be modified at runtime.},
  author       = {Henzinger, Thomas A and Kirsch, Christoph and Marques, Eduardo and Sokolova, Ana},
  location     = {Washington, DC, United States},
  pages        = {171 -- 180},
  publisher    = {IEEE},
  title        = {{Distributed, modular HTL}},
  doi          = {10.1109/RTSS.2009.9},
  year         = {2009},
}

@article{3869,
  abstract     = {We investigate logics and equivalence relations that capture the qualitative behavior of Markov Decision Processes (MDPs). We present Qualitative Randomized CTL (QRCTL): formulas of this logic can express the fact that certain temporal properties hold over all paths, or with probability 0 or 1, but they do not distinguish among intermediate probability values. We present a symbolic, polynomial time model-checking algorithm for QRCTL on MDPs. The logic QRCTL induces an equivalence relation over states of an MDP that we call qualitative equivalence: informally, two states are qualitatively equivalent if the sets of formulas that hold with probability 0 or 1 at the two states are the same. We show that for finite alternating MDPs, where nondeterministic and probabilistic choices occur in different states, qualitative equivalence coincides with alternating bisimulation, and can thus be computed via efficient partition-refinement algorithms. On the other hand, in non-alternating MDPs the equivalence relations cannot be computed via partition-refinement algorithms, but rather, they require non-local computation. Finally, we consider QRCTL*, that extends QRCTL with nested temporal operators in the same manner in which CTL* extends CTL. We show that QRCTL and QRCTL* induce the same qualitative equivalence on alternating MDPs, while on non-alternating MDPs, the equivalence arising from QRCTL* can be strictly finer. We also provide a full characterization of the relation between qualitative equivalence, bisimulation, and alternating bisimulation, according to whether the MDPs are finite, and to whether their transition relations are finitely-branching.},
  author       = {Krishnendu Chatterjee and de Alfaro, Luca and Faella, Marco and Legay, Axel},
  journal      = {Logical Methods in Computer Science},
  number       = {2},
  publisher    = {International Federation of Computational Logic},
  title        = {{Qualitative logics and equivalences for probabilistic systems}},
  doi          = {10.2168/LMCS-5(2:7)2009},
  volume       = {5},
  year         = {2009},
}

@article{3870,
  abstract     = {Games on graphs with omega-regular objectives provide a model for the control and synthesis of reactive systems. Every omega-regular objective can be decomposed into a safety part and a liveness part. The liveness part ensures that something good happens “eventually.” Two main strengths of the classical, infinite-limit formulation of liveness are robustness (independence from the granularity of transitions) and simplicity (abstraction of complicated time bounds). However, the classical liveness formulation suffers from the drawback that the time until something good happens may be unbounded. A stronger formulation of liveness, so-called finitary liveness, overcomes this drawback, while still retaining robustness and simplicity. Finitary liveness requires that there exists an unknown, fixed bound b such that something good happens within b transitions. While for one-shot liveness (reachability) objectives, classical and finitary liveness coincide, for repeated liveness (Buchi) objectives, the finitary formulation is strictly stronger. In this work we study games with finitary parity and Streett objectives. We prove the determinacy of these games, present algorithms for solving these games, and characterize the memory requirements of winning strategies. We show that finitary parity games can be solved in polynomial time, which is not known for infinitary parity games. For finitary Streett games, we give an EXPTIME algorithm and show that the problem is NP-hard. Our algorithms can be used, for example, for synthesizing controllers that do not let the response time of a system increase without bound.},
  author       = {Chatterjee, Krishnendu and Henzinger, Thomas A and Horn, Florian},
  journal      = {ACM Transactions on Computational Logic (TOCL)},
  number       = {1},
  publisher    = {ACM},
  title        = {{Finitary winning in omega-regular games}},
  doi          = {10.1145/1614431.1614432},
  volume       = {11},
  year         = {2009},
}

@inproceedings{3871,
  abstract     = {Nondeterministic weighted automata are finite automata with numerical weights oil transitions. They define quantitative languages 1, that assign to each word v; a real number L(w). The value of ail infinite word w is computed as the maximal value of all runs over w, and the value of a run as the supremum, limsup liminf, limit average, or discounted sum of the transition weights. We introduce probabilistic weighted antomata, in which the transitions are chosen in a randomized (rather than nondeterministic) fashion. Under almost-sure semantics (resp. positive semantics), the value of a word v) is the largest real v such that the runs over w have value at least v with probability I (resp. positive probability). We study the classical questions of automata theory for probabilistic weighted automata: emptiness and universality, expressiveness, and closure under various operations oil languages. For quantitative languages, emptiness university axe defined as whether the value of some (resp. every) word exceeds a given threshold. We prove some, of these questions to he decidable, and others undecidable. Regarding expressive power, we show that probabilities allow its to define a wide variety of new classes of quantitative languages except for discounted-sum automata, where probabilistic choice is no more expressive than nondeterminism. Finally we live ail almost complete picture of the closure of various classes of probabilistic weighted automata for the following, provide, is operations oil quantitative languages: maximum, sum. and numerical complement.},
  author       = {Chatterjee, Krishnendu and Doyen, Laurent and Henzinger, Thomas A},
  location     = {Bologna, Italy},
  pages        = {244 -- 258},
  publisher    = {Springer},
  title        = {{Probabilistic weighted automata}},
  doi          = {10.1007/978-3-642-04081-8_17},
  volume       = {5710},
  year         = {2009},
}

@article{3946,
  abstract     = {We compare anti-parasite defences at the level of multicellular organisms and insect societies, and find that selection by parasites at these two organisational levels is often very similar and has created a number of parallel evolutionary solutions in the host's immune response. The defence mechanisms of both individuals and insect colonies start with border defences to prevent parasite intake and are followed by soma defences that prevent the establishment and spread of the parasite between the body's cells or the social insect workers. Lastly, germ line defences are employed to inhibit infection of the reproductive tissue of organisms or the reproductive individuals in colonies. We further find sophisticated self/non-self-recognition systems operating at both levels, which appear to be vital in maintaining the integrity of the body or colony as a reproductive entity. We then expand on the regulation of immune responses and end with a contemplation of how evolution may shape the different immune components, both within and between levels. The aim of this review is to highlight common evolutionary principles acting in disease defence at the level of both individual organisms and societies, thereby linking the fields of physiological and ecological immunology.},
  author       = {Cremer, Sylvia and Sixt, Michael K},
  journal      = {Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences},
  number       = {1513},
  pages        = {129 -- 142},
  publisher    = {Royal Society, The},
  title        = {{Analogies in the evolution of individual and social immunity}},
  doi          = {10.1098/rstb.2008.0166},
  volume       = {364},
  year         = {2009},
}

@article{3947,
  abstract     = {Mature dendritic cells (DCs) moving from the skin to the lymph node are a prototypic example of rapidly migrating amoeboid leukocytes. Interstitial DC migration is directionally guided by chemokines, but independent of specific adhesive interactions with the tissue as well as pericellular proteolysis. Instead, the protrusive flow of the actin cytoskeleton directly drives a basal mode of locomotion that is occasionally supported by actomyosin contractions at the trailing edge to propel the cell's rigid nucleus. We here delete the small GTPase Cdc42 in DCs and find that actin flow and actomyosin contraction are still initiated in response to chemotactic cues. Accordingly, the cells are able to polarize and form protrusions. However, in the absence of Cdc42 the protrusions are temporally and spatially dysregulated, which leads to impaired leading edge coordination. Although this defect still allows the cells to move on 2-dimensional surfaces, their in vivo motility is completely abrogated. We show that this difference is entirely caused by the geometric complexity of the environment, as multiple competing protrusions lead to instantaneous entanglement within 3-dimensional extracellular matrix scaffolds. This demonstrates that the decisive factor for migrating DCs is not specific interaction with the extracellular environment, but adequate coordination of cytoskeletal flow.},
  author       = {Lämmermann, Tim and Jörg Renkawitz and Wu, Xunwei and Hirsch, Karin and Brakebusch, Cord and Michael Sixt},
  journal      = {Blood},
  number       = {23},
  pages        = {5703 -- 5710},
  publisher    = {American Society of Hematology},
  title        = {{Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper)}},
  doi          = {10.1182/blood-2008-11-191882},
  volume       = {113},
  year         = {2009},
}

@article{3948,
  abstract     = {Inhibiting the alpha(4) subunit of the integrin heterodimers alpha(4)beta(1) and alpha(4)beta(7) with the monoclonal antibody natalizumab is an effective treatment for multiple sclerosis (MS). However, the pharmacological action of natalizumab is not understood conclusively. Previous studies suggested that natalizumab inhibits activation, proliferation, or extravasation of inflammatory cells. To specify which mechanisms, cell types, and alpha(4) heterodimers are affected by the antibody treatment, we studied MS-like experimental autoimmune encephalomyelitis (EAE) in mice lacking the beta(1)-integrin gene either in all hematopoietic cells or selectively in T lymphocytes. Our results show that T cells critically rely on beta(1) integrins to accumulate in the central nervous system (CNS) during EAE, whereas CNS infiltration of beta(1)-deficient myeloid cells remains unaffected, suggesting that T cells are the main target of anti-alpha(4)-antibody blockade. We demonstrate that beta(1)-integrin expression on encephalitogenic T cells is critical for EAE development, and we therefore exclude alpha(4)beta(7) as a target integrin of the antibody treatment. T cells lacking beta(1) integrin are unable to firmly adhere to CNS endothelium in vivo, whereas their priming and expansion remain unaffected. Collectively, these results suggest that the primary action of natalizumab is interference with T cell extravasation via inhibition of alpha(4)beta(1) integrins.},
  author       = {Bauer, Martina and Brakebusch, Cord and Coisne, Caroline and Michael Sixt and Wekerle, Hartmut and Engelhardt, Britta and Fässler, Reinhard},
  journal      = {PNAS},
  number       = {6},
  pages        = {1920 -- 1925},
  publisher    = {National Academy of Sciences},
  title        = {{β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity}},
  doi          = {10.1073/pnas.0808909106},
  volume       = {106},
  year         = {2009},
}

@article{3949,
  abstract     = {Adhesion and motility of mammalian leukocytes are essential requirements for innate and adaptive immune defense mechanisms. We show here that the guanine nucleotide exchange factor cytohesin-1, which had previously been demonstrated to be an important component of beta-2 integrin activation in lymphocytes, regulates the activation of the small GTPase RhoA in primary dendritic cells (DCs). Cytohesin-1 and RhoA are both required for the induction of chemokine-dependent conformational changes of the integrin beta-2 subunit of DCs during adhesion under physiological flow conditions. Furthermore, use of RNAi in murine bone marrow DCs (BM-DCs) revealed that interference with cytohesin-1 signaling impairs migration of wild-type dendritic cells in complex 3D environments and in vivo. This phenotype was not observed in the complete absence of integrins. We thus demonstrate an essential role of cytohesin-1/RhoA during ameboid migration in the presence of integrins and further suggest that DCs without integrins switch to a different migration mode.},
  author       = {Quast, Thomas and Tappertzhofen, Barbara and Schild, Cora and Grell, Jessica and Czeloth, Niklas and Förster, Reinhold and Alon, Ronen and Fraemohs, Line and Dreck, Katrin and Weber, Christian and Lämmermann, Tim and Michael Sixt and Kolanus, Waldemar},
  journal      = {Blood},
  number       = {23},
  pages        = {5801 -- 5810},
  publisher    = {American Society of Hematology},
  title        = {{Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells}},
  doi          = {10.1182/blood-2008-08-176123},
  volume       = {113},
  year         = {2009},
}

@article{3950,
  abstract     = {Integrin activation is essential for the function of all blood cells, including platelets and leukocytes. The blood cell-specific FERM domain protein Kindlin-3 is required for the activation of the beta1 and beta3 integrins on platelets. Impaired activation of beta1, beta2 and beta3 integrins on platelets and leukocytes is the hallmark of a rare autosomal recessive leukocyte adhesion deficiency syndrome in humans called LAD-III, characterized by severe bleeding and impaired adhesion of leukocytes to inflamed endothelia. Here we show that Kindlin-3 also binds the beta2 integrin cytoplasmic domain and is essential for neutrophil binding and spreading on beta2 integrin-dependent ligands such as intercellular adhesion molecule-1 and the complement C3 activation product iC3b. Moreover, loss of Kindlin-3 expression abolished firm adhesion and arrest of neutrophils on activated endothelial cells in vitro and in vivo, whereas selectin-mediated rolling was unaffected. Thus, Kindlin-3 is essential to activate the beta1, beta2 and beta3 integrin classes, and loss of Kindlin-3 function is sufficient to cause a LAD-III-like phenotype in mice.},
  author       = {Moser, Markus and Bauer, Martina and Schmid, Stephan and Ruppert, Raphael and Schmidt, Sarah and Michael Sixt and Wang, Hao-Ven and Sperandio, Markus and Fässler, Reinhard},
  journal      = {Nature Medicine},
  number       = {3},
  pages        = {300 -- 305},
  publisher    = {Nature Publishing Group},
  title        = {{Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells}},
  doi          = {10.1038/nm.1921},
  volume       = {15},
  year         = {2009},
}

@article{3951,
  abstract     = {The morphological term 'amoeboid' migration subsumes a number of rather distinct biophysical modes of cellular locomotion that range from blebbing motility to entirely actin-polymerization-based gliding. Here, we discuss the diverse principles of force generation and force transduction that lead to the distinct amoeboid phenotypes. We argue that shifting the balance between actin protrusion, actomyosin contraction, and adhesion to the extracellular substrate can explain the different modes of amoeboid movement and that blebbing and gliding are barely extreme variants of one common migration strategy. Depending on the cell type, physiological conditions or experimental manipulation, amoeboid cells can adopt the distinct mechanical modes of amoeboid migration.},
  author       = {Lämmermann, Tim and Michael Sixt},
  journal      = {Current Opinion in Cell Biology},
  number       = {5},
  pages        = {636 -- 644},
  publisher    = {Elsevier},
  title        = {{Mechanical modes of 'amoeboid' cell migration}},
  doi          = {10.1016/j.ceb.2009.05.003},
  volume       = {21},
  year         = {2009},
}

@article{3952,
  abstract     = {The mammalian actin-binding protein 1 (mAbp1, Hip-55, SH3P7) is phosphorylated by the nonreceptor tyrosine kinase Syk that has a fundamental effect for several beta(2) integrin (CD11/CD18)-mediated neutrophil functions. Live cell imaging showed a dynamic enrichment of enhanced green fluorescence protein-tagged mAbp1 at the phagocytic cup of neutrophil-like differentiated HL-60 cells during beta(2) integrin-mediated phagocytosis of serum-opsonized Escherichia coli. The genetic absence of Syk or its pharmacologic inhibition using piceatannol abrogated the proper localization of mAbp1 at the phagocytic cup. The genetic absence or down-regulation of mAbp1 using the RNA interference technique significantly compromised beta(2) integrin-mediated phagocytosis of serum-opsonized E coli or Salmonella typhimurium in vitro as well as clearance of S typhimurium infection in vivo. Moreover, the genetic absence of mAbp1 almost completely abrogated firm neutrophil adhesion under physiologic shear stress conditions in vitro as well as leukocyte adhesion and extravasation in inflamed cremaster muscle venules of mice treated with tumor-necrosis factor alpha. Functional analysis showed that the down-regulation of mAbp1 diminished the number of beta(2) integrin clusters in the high-affinity conformation under flow conditions. These unanticipated results define mAbp1 as a novel molecular player in integrin biology that is critical for phagocytosis and firm neutrophil adhesion under flow conditions.},
  author       = {Schymeinsky, Jürgen and Gerstl, Ronald and Mannigel, Ingrid and Niedung, Katy and Frommhold, David and Panthel, Klaus and Heesemann, Jürgen and Michael Sixt and Quast, Thomas and Kolanus, Waldemar and Mocsai, Attila and Wienands, Jürgen and Sperandio, Markus and Walzog, Barbara},
  journal      = {Blood},
  number       = {19},
  pages        = {4209 -- 4220},
  publisher    = {American Society of Hematology},
  title        = {{A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo}},
  doi          = {10.1182/blood-2009-02-206169},
  volume       = {114},
  year         = {2009},
}

@article{3953,
  abstract     = {CD4(+)CD25(+) regulatory T cell (Treg) entry into secondary lymphoid organs and local expansion is critical for their immunosuppressive function. Long-term application of the sphingosine-1 phosphate receptor agonist FTY720 exerts pleiotropic anti-inflammatory effects, whereas short-term FTY720 boosts antiviral immunity. In this study, we provide evidence that FTY720 potently inhibits Treg proliferation in vitro and in vivo without affecting their viability, phenotype, or in vitro immunosuppression. In contrast, adoptively transferred Treg exposed ex vivo to FTY720 lost their protective effects in murine models of acute glomerulonephritis and acute graft-vs-host disease. On a cellular level, FTY720 inhibits IL-2-induced STAT-5 phosphorylation, paralleled by a loss of FoxP3 expression during Treg expansion in vitro. Notably, loss of in vivo immunosuppression is not due to impaired migration to or localization within secondary lymphoid organs. We could even show a selective trapping of adoptively transferred Treg in inflammatory lymph nodes by FTY720. Finally, Treg isolated from animals systemically exposed to FTY720 also exhibit a significantly impaired proliferative response upon restimulation when compared with Treg isolated from solvent-treated animals. In summary, our data suggest that sphingosine-1 phosphate receptor-mediated signals induced by FTY720 abrogate their in vivo immunosuppressive potential by blocking IL-2 induced expansion, which is indispensable for their in vivo immunosuppressive activity.},
  author       = {Wolf, Anna Maria and Eller, Kathrin and Zeiser, Robert and Dürr, Christoph and Gerlach, Ulrike V and Michael Sixt and Markut, Lydia and Gastl, Guenther and Rosenkranz, Alexander R and Wolf, Dominik},
  journal      = {Journal of Immunology},
  number       = {6},
  pages        = {3751 -- 3760},
  publisher    = {American Association of Immunologists},
  title        = {{The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo}},
  doi          = {10.4049/jimmunol.0901011},
  volume       = {183},
  year         = {2009},
}

@article{3954,
  abstract     = {The leading front of a cell can either protrude as an actin-free membrane bleb that is inflated by actomyosin-driven contractile forces, or as an actin-rich pseudopodium, a site where polymerizing actin filaments push out the membrane. Pushing filaments can only cause the membrane to protrude if the expanding actin network experiences a retrograde counter-force, which is usually provided by transmembrane receptors of the integrin family. Here we show that chemotactic dendritic cells mechanically adapt to the adhesive properties of their substrate by switching between integrin-mediated and integrin-independent locomotion. We found that on engaging the integrin-actin clutch, actin polymerization was entirely turned into protrusion, whereas on disengagement actin underwent slippage and retrograde flow. Remarkably, accelerated retrograde flow was balanced by an increased actin polymerization rate; therefore, cell shape and protrusion velocity remained constant on alternating substrates. Due to this adaptive response in polymerization dynamics, tracks of adhesive substrate did not dictate the path of the cells. Instead, directional guidance was exclusively provided by a soluble gradient of chemoattractant, which endowed these 'amoeboid' cells with extraordinary flexibility, enabling them to traverse almost every type of tissue.},
  author       = {Renkawitz, Jörg and Schumann, Kathrin and Weber, Michele and Lämmermann, Tim and Pflicke, Holger and Piel, Matthieu and Polleux, Julien and Spatz, Joachim and Sixt, Michael K},
  journal      = {Nature Cell Biology},
  number       = {12},
  pages        = {1438 -- 1443},
  publisher    = {Nature Publishing Group},
  title        = {{Adaptive force transmission in amoeboid cell migration}},
  doi          = {10.1038/ncb1992},
  volume       = {11},
  year         = {2009},
}

@article{3955,
  abstract     = {Although both processes occur at similar rates, leukocyte extravasation from the blood circulation is well investigated, whereas intravasation into lymphatic vessels has hardly been studied. In contrast to a common assumption-that intra- and extravasation follow similar molecular principles-we previously showed that lymphatic entry of dendritic cells (DCs) does not require integrin-mediated adhesive interactions. In this study, we demonstrate that DC-entry is also independent of pericellular proteolysis, raising the question of whether lymphatic vessels offer preexisting entry routes. We find that the perilymphatic basement membrane of initial lymphatic vessels is discontinuous and therefore leaves gaps for entering cells. Using a newly developed in situ live cell imaging approach that allows us to dynamically visualize the cells and their extracellular environment, we demonstrate that DCs enter through these discontinuities, which are transiently mechanically dilated by the passaging cells. We further show that penetration of the underlying lymphatic endothelial layer occurs through flap valves lacking continuous intercellular junctions. Together, we demonstrate free cellular communication between interstitium and lymphatic lumen.},
  author       = {Pflicke, Holger and Michael Sixt},
  journal      = {The Journal of Experimental Medicine},
  number       = {13},
  pages        = {2925 -- 2935},
  publisher    = {Rockefeller University Press},
  title        = {{Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels}},
  doi          = {10.1084/jem.20091739},
  volume       = {206},
  year         = {2009},
}

@article{3966,
  abstract     = {Persistent homology has proven to be a useful tool in a variety of contexts, including the recognition and measurement of shape characteristics of surfaces in ℝ3. Persistence pairs homology classes that are born and die in a filtration of a topological space, but does not pair its actual homology classes. For the sublevelset filtration of a surface in ℝ3, persistence has been extended to a pairing of essential classes using Reeb graphs. In this paper, we give an algebraic formulation that extends persistence to essential homology for any filtered space, present an algorithm to calculate it, and describe how it aids our ability to recognize shape features for codimension 1 submanifolds of Euclidean space. The extension derives from Poincaré duality but generalizes to nonmanifold spaces. We prove stability for general triangulated spaces and duality as well as symmetry for triangulated manifolds. },
  author       = {Cohen-Steiner, David and Herbert Edelsbrunner and Harer, John},
  journal      = {Foundations of Computational Mathematics},
  number       = {1},
  pages        = {79 -- 103},
  publisher    = {Springer},
  title        = {{Extending persistence using Poincare and Lefschetz duality}},
  doi          = {10.1007/s10208-008-9027-z},
  volume       = {9},
  year         = {2009},
}

@inproceedings{3967,
  abstract     = {Motivated by the measurement of local homology and of functions on noisy domains, we extend the notion of persistent homology to sequences of kernels, images, and cokernels of maps induced by inclusions in a filtration of pairs of spaces. Specifically, we note that persistence in this context is well defined, we prove that the persistence diagrams are stable, and we explain how to compute them.},
  author       = {Cohen-Steiner, David and Herbert Edelsbrunner and Harer, John and Morozov, Dmitriy},
  pages        = {1011 -- 1020},
  publisher    = {SIAM},
  title        = {{Persistent homology for kernels, images, and cokernels}},
  year         = {2009},
}

@inproceedings{3968,
  abstract     = {We describe an algorithm for segmenting three-dimensional medical imaging data modeled as a continuous function on a 3-manifold. It is related to watershed algorithms developed in image processing but is closer to its mathematical roots, which are Morse theory and homological algebra. It allows for the implicit treatment of an underlying mesh, thus combining the structural integrity of its mathematical foundations with the computational efficiency of image processing.},
  author       = {Edelsbrunner, Herbert and Harer, John},
  location     = {Zermatt, Switzerland},
  pages        = {36 -- 50},
  publisher    = {Springer},
  title        = {{The persistent Morse complex segmentation of a 3-manifold}},
  doi          = {10.1007/978-3-642-10470-1_4},
  volume       = {5903},
  year         = {2009},
}

@article{4136,
  abstract     = {Populations living in a spatially and temporally changing environment can adapt to the changing optimum and/or migrate toward favorable habitats. Here we extend previous analyses with a static optimum to allow the environment to vary in time as well as in space. The model follows both population dynamics and the trait mean under stabilizing selection, and the outcomes can be understood by comparing the loads due to genetic variance, dispersal, and temporal change. With fixed genetic variance, we obtain two regimes: (1) adaptation that is uniform along the environmental gradient and that responds to the moving optimum as expected for panmictic populations and when the spatial gradient is sufficiently steep, and (2) a population with limited range that adapts more slowly than the environmental optimum changes in both time and space; the population therefore becomes locally extinct and migrates toward suitable habitat. We also use a population‐genetic model with many loci to allow genetic variance to evolve, and we show that the only solution now has uniform adaptation.},
  author       = {Polechova, Jitka and Barton, Nicholas H and Marion, Glenn},
  journal      = {American Naturalist},
  number       = {5},
  pages        = {E186 -- E204},
  publisher    = {University of Chicago Press},
  title        = {{Species' range: Adaptation in space and time}},
  doi          = {10.1086/605958},
  volume       = {174},
  year         = {2009},
}

@article{4143,
  abstract     = {The migration of single cells and epithelial sheets is of great importance for gastrulation and organ formation in developing embryos and, if misregulated, can have dire consequences e.g. during cancer metastasis. A keystone of cell migration is the regulation of adhesive contacts, which are dynamically assembled and disassembled via endocytosis. Here, we discuss some of the basic concepts about the function of endocytic trafficking during cell migration: transport of integrins from the cell rear to the leading edge in fibroblasts; confinement of signalling to the front of single cells by endocytic transport of growth factors; regulation of movement coherence in multicellular sheets by cadherin turnover; and shaping of extracellular chemokine gradients. Taken together, endocytosis enables migrating cells and tissues to dynamically modulate their adhesion and signalling, allowing them to efficiently migrate through their extracellular environment.},
  author       = {Ulrich, Florian and Heisenberg, Carl-Philipp J},
  journal      = {Traffic},
  number       = {7},
  pages        = {811 -- 818},
  publisher    = {Wiley-Blackwell},
  title        = {{Trafficking and cell migration}},
  doi          = {10.1111/j.1600-0854.2009.00929.x},
  volume       = {10},
  year         = {2009},
}