@unpublished{14333,
  abstract     = {As causal ground truth is incredibly rare, causal discovery algorithms are
commonly only evaluated on simulated data. This is concerning, given that
simulations reflect common preconceptions about generating processes regarding
noise distributions, model classes, and more. In this work, we propose a novel
method for falsifying the output of a causal discovery algorithm in the absence
of ground truth. Our key insight is that while statistical learning seeks
stability across subsets of data points, causal learning should seek stability
across subsets of variables. Motivated by this insight, our method relies on a
notion of compatibility between causal graphs learned on different subsets of
variables. We prove that detecting incompatibilities can falsify wrongly
inferred causal relations due to violation of assumptions or errors from finite
sample effects. Although passing such compatibility tests is only a necessary
criterion for good performance, we argue that it provides strong evidence for
the causal models whenever compatibility entails strong implications for the
joint distribution. We also demonstrate experimentally that detection of
incompatibilities can aid in causal model selection.},
  author       = {Faller, Philipp M. and Vankadara, Leena Chennuru and Mastakouri, Atalanti A. and Locatello, Francesco and Janzing, Dominik},
  booktitle    = {arXiv},
  title        = {{Self-compatibility: Evaluating causal discovery without ground truth}},
  doi          = {10.48550/arXiv.2307.09552},
  year         = {2023},
}

@article{14334,
  abstract     = {Quantum kinetically constrained models have recently attracted significant attention due to their anomalous dynamics and thermalization. In this work, we introduce a hitherto unexplored family of kinetically constrained models featuring conserved particle number and strong inversion-symmetry breaking due to facilitated hopping. We demonstrate that these models provide a generic example of so-called quantum Hilbert space fragmentation, that is manifested in disconnected sectors in the Hilbert space that are not apparent in the computational basis. Quantum Hilbert space fragmentation leads to an exponential in system size number of eigenstates with exactly zero entanglement entropy across several bipartite cuts. These eigenstates can be probed dynamically using quenches from simple initial product states. In addition, we study the particle spreading under unitary dynamics launched from the domain wall state, and find faster than diffusive dynamics at high particle densities, that crosses over into logarithmically slow relaxation at smaller densities. Using a classically simulable cellular automaton, we reproduce the logarithmic dynamics observed in the quantum case. Our work suggests that particle conserving constrained models with inversion symmetry breaking realize so far unexplored dynamical behavior and invite their further theoretical and experimental studies.},
  author       = {Brighi, Pietro and Ljubotina, Marko and Serbyn, Maksym},
  issn         = {2542-4653},
  journal      = {SciPost Physics},
  keywords     = {General Physics and Astronomy},
  number       = {3},
  publisher    = {SciPost Foundation},
  title        = {{Hilbert space fragmentation and slow dynamics in particle-conserving quantum East models}},
  doi          = {10.21468/scipostphys.15.3.093},
  volume       = {15},
  year         = {2023},
}

@article{14339,
  abstract     = {Lateral roots are typically maintained at non-vertical angles with respect to gravity. These gravitropic setpoint angles are intriguing because their maintenance requires that roots are able to effect growth response both with and against the gravity vector, a phenomenon previously attributed to gravitropism acting against an antigravitropic offset mechanism. Here we show how the components mediating gravitropism in the vertical primary root—PINs and phosphatases acting upon them—are reconfigured in their regulation such that lateral root growth at a range of angles can be maintained. We show that the ability of Arabidopsis lateral roots to bend both downward and upward requires the generation of auxin asymmetries and is driven by angle-dependent variation in downward gravitropic auxin flux acting against angle-independent upward, antigravitropic flux. Further, we demonstrate a symmetry in auxin distribution in lateral roots at gravitropic setpoint angle that can be traced back to a net, balanced polarization of PIN3 and PIN7 auxin transporters in the columella. These auxin fluxes are shifted by altering PIN protein phosphoregulation in the columella, either by introducing PIN3 phosphovariant versions or via manipulation of levels of the phosphatase subunit PP2A/RCN1. Finally, we show that auxin, in addition to driving lateral root directional growth, acts within the lateral root columella to induce more vertical growth by increasing RCN1 levels, causing a downward shift in PIN3 localization, thereby diminishing the magnitude of the upward, antigravitropic auxin flux.},
  author       = {Roychoudhry, S and Sageman-Furnas, K and Wolverton, C and Grones, Peter and Tan, Shutang and Molnar, Gergely and De Angelis, M and Goodman, HL and Capstaff, N and JPB, Lloyd and Mullen, J and Hangarter, R and Friml, Jiří and Kepinski, S},
  issn         = {2055-0278},
  journal      = {Nature Plants},
  pages        = {1500--1513},
  publisher    = {Springer Nature},
  title        = {{Antigravitropic PIN polarization maintains non-vertical growth in lateral roots}},
  doi          = {10.1038/s41477-023-01478-x},
  volume       = {9},
  year         = {2023},
}

@article{14341,
  abstract     = {Flows through pipes and channels are, in practice, almost always turbulent, and the multiscale eddying motion is responsible for a major part of the encountered friction losses and pumping costs1. Conversely, for pulsatile flows, in particular for aortic blood flow, turbulence levels remain low despite relatively large peak velocities. For aortic blood flow, high turbulence levels are intolerable as they would damage the shear-sensitive endothelial cell layer2,3,4,5. Here we show that turbulence in ordinary pipe flow is diminished if the flow is driven in a pulsatile mode that incorporates all the key features of the cardiac waveform. At Reynolds numbers comparable to those of aortic blood flow, turbulence is largely inhibited, whereas at much higher speeds, the turbulent drag is reduced by more than 25%. This specific operation mode is more efficient when compared with steady driving, which is the present situation for virtually all fluid transport processes ranging from heating circuits to water, gas and oil pipelines.},
  author       = {Scarselli, Davide and Lopez Alonso, Jose M and Varshney, Atul and Hof, Björn},
  issn         = {1476-4687},
  journal      = {Nature},
  number       = {7977},
  pages        = {71--74},
  publisher    = {Springer Nature},
  title        = {{Turbulence suppression by cardiac-cycle-inspired driving of pipe flow}},
  doi          = {10.1038/s41586-023-06399-5},
  volume       = {621},
  year         = {2023},
}

@article{14342,
  abstract     = {We propose a simple method to measure nonlinear Kerr refractive index in mid-infrared frequency range that avoids using sophisticated infrared detectors. Our approach is based on using a near-infrared probe beam which interacts with a mid-IR beam via wavelength-non-degenerate cross-phase modulation (XPM). By carefully measuring XPM-induced spectral modifications in the probe beam and comparing the experimental data with simulation results, we extract the value for the non-degenerate Kerr index. Finally, in order to obtain the value of degenerate mid-IR Kerr index, we use the well-established two-band formalism of Sheik-Bahae et al., which is shown to become particularly simple in the limit of low frequencies. The proposed technique is complementary to the conventional techniques, such as z-scan, and has the advantage of not requiring any mid-infrared detectors.},
  author       = {Lorenc, Dusan and Alpichshev, Zhanybek},
  issn         = {0003-6951},
  journal      = {Applied Physics Letters},
  number       = {9},
  publisher    = {AIP Publishing},
  title        = {{Mid-infrared Kerr index evaluation via cross-phase modulation with a near-infrared probe beam}},
  doi          = {10.1063/5.0161713},
  volume       = {123},
  year         = {2023},
}

@inproceedings{14344,
  abstract     = {We study the Hamilton cycle problem with input a random graph G ~ G(n,p) in two different settings. In the first one, G is given to us in the form of randomly ordered adjacency lists while in the second one, we are given the adjacency matrix of G. In each of the two settings we derive a deterministic algorithm that w.h.p. either finds a Hamilton cycle or returns a certificate that such a cycle does not exist for p = p(n) ≥ 0. The running times of our algorithms are O(n) and  respectively, each being best possible in its own setting.},
  author       = {Anastos, Michael},
  booktitle    = {Proceedings of the Annual ACM-SIAM Symposium on Discrete Algorithms},
  isbn         = {9781611977554},
  location     = {Florence, Italy},
  pages        = {2286--2323},
  publisher    = {Society for Industrial and Applied Mathematics},
  title        = {{Fast algorithms for solving the Hamilton cycle problem with high probability}},
  doi          = {10.1137/1.9781611977554.ch88},
  volume       = {2023},
  year         = {2023},
}

@article{14361,
  abstract     = {Whether one considers swarming insects, flocking birds, or bacterial colonies, collective motion arises from the coordination of individuals and entails the adjustment of their respective velocities. In particular, in close confinements, such as those encountered by dense cell populations during development or regeneration, collective migration can only arise coordinately. Yet, how individuals unify their velocities is often not understood. Focusing on a finite number of cells in circular confinements, we identify waves of polymerizing actin that function as a pacemaker governing the speed of individual cells. We show that the onset of collective motion coincides with the synchronization of the wave nucleation frequencies across the population. Employing a simpler and more readily accessible mechanical model system of active spheres, we identify the synchronization of the individuals’ internal oscillators as one of the essential requirements to reach the corresponding collective state. The mechanical ‘toy’ experiment illustrates that the global synchronous state is achieved by nearest neighbor coupling. We suggest by analogy that local coupling and the synchronization of actin waves are essential for the emergent, self-organized motion of cell collectives.},
  author       = {Riedl, Michael and Mayer, Isabelle D and Merrin, Jack and Sixt, Michael K and Hof, Björn},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Synchronization in collectively moving inanimate and living active matter}},
  doi          = {10.1038/s41467-023-41432-1},
  volume       = {14},
  year         = {2023},
}

@article{14362,
  abstract     = {Motivated by recent applications to entropy theory in dynamical systems, we generalise notions introduced by Matthews and define weakly weighted and componentwise weakly weighted (generalised) quasi-metrics. We then systematise and extend to full generality the correspondences between these objects and other structures arising in theoretical computer science and dynamics. In particular, we study the correspondences with weak partial metrics and, if the underlying space is a semilattice, with invariant (generalised) quasi-metrics satisfying the descending path condition, and with strictly monotone semi(-co-)valuations.
We conclude discussing, for endomorphisms of generalised quasi-metric semilattices, a generalisation of both the known intrinsic semilattice entropy and the semigroup entropy.},
  author       = {Castellano, Ilaria and Giordano Bruno, Anna and Zava, Nicolò},
  issn         = {0304-3975},
  journal      = {Theoretical Computer Science},
  publisher    = {Elsevier},
  title        = {{Weakly weighted generalised quasi-metric spaces and semilattices}},
  doi          = {10.1016/j.tcs.2023.114129},
  volume       = {977},
  year         = {2023},
}

@article{14363,
  abstract     = {Mitochondrial networks remodel their connectivity, content, and subcellular localization to support optimized energy production in conditions of increased environmental or cellular stress. Microglia rely on mitochondria to respond to these stressors, however our knowledge about mitochondrial networks and their adaptations in microglia in vivo is limited. Here, we generate a mouse model that selectively labels mitochondria in microglia. We identify that mitochondrial networks are more fragmented with increased content and perinuclear localization in vitro vs. in vivo. Mitochondrial networks adapt similarly in microglia closest to the injury site after optic nerve crush. Preventing microglial UCP2 increase after injury by selective knockout induces cellular stress. This results in mitochondrial hyperfusion in male microglia, a phenotype absent in females due to circulating estrogens. Our results establish the foundation for mitochondrial network analysis of microglia in vivo, emphasizing the importance of mitochondrial-based sex effects of microglia in other pathologies.},
  author       = {Maes, Margaret E and Colombo, Gloria and Schoot Uiterkamp, Florianne E and Sternberg, Felix and Venturino, Alessandro and Pohl, Elena E. and Siegert, Sandra},
  issn         = {2589-0042},
  journal      = {iScience},
  number       = {10},
  publisher    = {Elsevier},
  title        = {{Mitochondrial network adaptations of microglia reveal sex-specific stress response after injury and UCP2 knockout}},
  doi          = {10.1016/j.isci.2023.107780},
  volume       = {26},
  year         = {2023},
}

@article{14364,
  abstract     = {We introduce extension-based proofs, a class of impossibility proofs that includes valency arguments. They are modelled as an interaction between a prover and a protocol. Using proofs based on combinatorial topology, it has been shown that it is impossible to deterministically solve -set agreement among  processes or approximate agreement on a cycle of length 4 among  processes in a wait-free manner in asynchronous models where processes communicate using objects that can be constructed from shared registers. However, it was unknown whether proofs based on simpler techniques were possible. We show that these impossibility results cannot be obtained by extension-based proofs in the iterated snapshot model and, hence, extension-based proofs are limited in power.},
  author       = {Alistarh, Dan-Adrian and Aspnes, James and Ellen, Faith and Gelashvili, Rati and Zhu, Leqi},
  issn         = {1095-7111},
  journal      = {SIAM Journal on Computing},
  number       = {4},
  pages        = {913--944},
  publisher    = {Society for Industrial and Applied Mathematics},
  title        = {{Why extension-based proofs fail}},
  doi          = {10.1137/20M1375851},
  volume       = {52},
  year         = {2023},
}

@article{14368,
  abstract     = {Purpose: 
Biallelic variants in TARS2, encoding the mitochondrial threonyl-tRNA-synthetase, have been reported in a small group of individuals displaying a neurodevelopmental phenotype but with limited neuroradiological data and insufficient evidence for causality of the variants.
Methods:
Exome or genome sequencing was carried out in 15 families. Clinical and neuroradiological evaluation was performed for all affected individuals, including review of 10 previously reported individuals. The pathogenicity of TARS2 variants was evaluated using in vitro assays and a zebrafish model.
Results:
We report 18 new individuals harboring biallelic TARS2 variants. Phenotypically, these individuals show developmental delay/intellectual disability, regression, cerebellar and cerebral atrophy, basal ganglia signal alterations, hypotonia, cerebellar signs, and increased blood lactate. In vitro studies showed that variants within the TARS2301-381 region had decreased binding to Rag GTPases, likely impairing mTORC1 activity. The zebrafish model recapitulated key features of the human phenotype and unraveled dysregulation of downstream targets of mTORC1 signaling. Functional testing of the variants confirmed the pathogenicity in a zebrafish model.
Conclusion:
We define the clinico-radiological spectrum of TARS2-related mitochondrial disease, unveil the likely involvement of the mTORC1 signaling pathway as a distinct molecular mechanism, and establish a TARS2 zebrafish model as an important tool to study variant pathogenicity.},
  author       = {Accogli, Andrea and Lin, Sheng-Jia and Severino, Mariasavina and Kim, Sung-Hoon and Huang, Kevin and Rocca, Clarissa and Landsverk, Megan and Zaki, Maha S. and Al-Maawali, Almundher and Srinivasan, Varunvenkat M. and Al-Thihli, Khalid and Schaefer, G. Bradly and Davis, Monica and Tonduti, Davide and Doneda, Chiara and Marten, Lara M. and Mühlhausen, Chris and Gomez, Maria and Lamantea, Eleonora and Mena, Rafael and Nizon, Mathilde and Procaccio, Vincent and Begtrup, Amber and Telegrafi, Aida and Cui, Hong and Schulz, Heidi L. and Mohr, Julia and Biskup, Saskia and Loos, Mariana Amina and Aráoz, Hilda Verónica and Salpietro, Vincenzo and Keppen, Laura Davis and Chitre, Manali and Petree, Cassidy and Raymond, Lucy and Vogt, Julie and Sawyer, Lindsey B. and Basinger, Alice A. and Pedersen, Signe Vandal and Pearson, Toni S. and Grange, Dorothy K. and Lingappa, Lokesh and McDunnah, Paige and Horvath, Rita and Cognè, Benjamin and Isidor, Bertrand and Hahn, Andreas and Gripp, Karen W. and Jafarnejad, Seyed Mehdi and Østergaard, Elsebet and Prada, Carlos E. and Ghezzi, Daniele and Gowda, Vykuntaraju K. and Taylor, Robert W. and Sonenberg, Nahum and Houlden, Henry and Sissler, Marie and Varshney, Gaurav K. and Maroofian, Reza},
  issn         = {1098-3600},
  journal      = {Genetics in Medicine},
  keywords     = {Genetics (clinical)},
  number       = {11},
  publisher    = {Elsevier},
  title        = {{Clinical, neuroradiological, and molecular characterization of mitochondrial threonyl-tRNA-synthetase (TARS2)-related disorder}},
  doi          = {10.1016/j.gim.2023.100938},
  volume       = {25},
  year         = {2023},
}

@article{14377,
  abstract     = {Coherent flows of self-propelled particles are characterized by vortices and jets that sustain chaotic flows, referred to as active turbulence. Here, we reveal a crossover between defect-free active turbulence and active turbulence laden with topological defects. Interestingly, we show that concurrent to the crossover from defect-free to defect-laden active turbulence is the restoration of the previously broken SO(2) symmetry signaled by the fast decay of the two-point correlations. By stability analyses of the topological charge density field, we provide theoretical insights on the criterion for the crossover to the defect-laden active turbulent state. Despite the distinct symmetry features between these two active turbulence regimes, the flow fluctuations exhibit universal statistical scaling behaviors at large scales, while the spectrum of polarity fluctuations decays exponentially at small length scales compared to the active energy injection length. These findings reveal a dynamical crossover between distinct spatiotemporal organization patterns in polar active matter.},
  author       = {Andersen, Benjamin H. and Renaud, Julian B and Rønning, Jonas and Angheluta, Luiza and Doostmohammadi, Amin},
  issn         = {2469-990X},
  journal      = {Physical Review Fluids},
  keywords     = {Fluid Flow and Transfer Processes, Modeling and Simulation, Computational Mechanics},
  number       = {6},
  publisher    = {American Physical Society},
  title        = {{Symmetry-restoring crossover from defect-free to defect-laden turbulence in polar active matter}},
  doi          = {10.1103/physrevfluids.8.063101},
  volume       = {8},
  year         = {2023},
}

@article{14378,
  abstract     = {Branching morphogenesis is a ubiquitous process that gives rise to high exchange surfaces in the vasculature and epithelial organs. Lymphatic capillaries form branched networks, which play a key role in the circulation of tissue fluid and immune cells. Although mouse models and correlative patient data indicate that the lymphatic capillary density directly correlates with functional output, i.e., tissue fluid drainage and trafficking efficiency of dendritic cells, the mechanisms ensuring efficient tissue coverage remain poorly understood. Here, we use the mouse ear pinna lymphatic vessel network as a model system and combine lineage-tracing, genetic perturbations, whole-organ reconstructions and theoretical modeling to show that the dermal lymphatic capillaries tile space in an optimal, space-filling manner. This coverage is achieved by two complementary mechanisms: initial tissue invasion provides a non-optimal global scaffold via self-organized branching morphogenesis, while VEGF-C dependent side-branching from existing capillaries rapidly optimizes local coverage by directionally targeting low-density regions. With these two ingredients, we show that a minimal biophysical model can reproduce quantitatively whole-network reconstructions, across development and perturbations. Our results show that lymphatic capillary networks can exploit local self-organizing mechanisms to achieve tissue-scale optimization.},
  author       = {Ucar, Mehmet C and Hannezo, Edouard B and Tiilikainen, Emmi and Liaqat, Inam and Jakobsson, Emma and Nurmi, Harri and Vaahtomeri, Kari},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Self-organized and directed branching results in optimal coverage in developing dermal lymphatic networks}},
  doi          = {10.1038/s41467-023-41456-7},
  volume       = {14},
  year         = {2023},
}

@article{14401,
  abstract     = {Background: 
Pro-apoptotic BAX is a central mediator of retinal ganglion cell (RGC) death after optic nerve damage. BAX activation occurs in two stages including translocation of latent BAX to the mitochondrial outer membrane (MOM) and then permeabilization of the MOM to facilitate the release of apoptotic signaling molecules. As a critical component of RGC death, BAX is an attractive target for neuroprotective therapies and an understanding of the kinetics of BAX activation and the mechanisms controlling the two stages of this process in RGCs is potentially valuable in informing the development of a neuroprotective strategy.
Methods:
The kinetics of BAX translocation were assessed by both static and live-cell imaging of a GFP-BAX fusion protein introduced into RGCs using AAV2-mediated gene transfer in mice. Activation of BAX was achieved using an acute optic nerve crush (ONC) protocol. Live-cell imaging of GFP-BAX was achieved using explants of mouse retina harvested 7 days after ONC. Kinetics of translocation in RGCs were compared to GFP-BAX translocation in 661W tissue culture cells. Permeabilization of GFP-BAX was assessed by staining with the 6A7 monoclonal antibody, which recognizes a conformational change in this protein after MOM insertion. Assessment of individual kinases associated with both stages of activation was made using small molecule inhibitors injected into the vitreous either independently or in concert with ONC surgery. The contribution of the Dual Leucine Zipper-JUN-N-Terminal Kinase cascade was evaluated using mice with a double conditional knock-out of both Mkk4 and Mkk7.
Results:
ONC induces the translocation of GFP-BAX in RGCs at a slower rate and with less intracellular synchronicity than 661W cells, but exhibits less variability among mitochondrial foci within a single cell. GFP-BAX was also found to translocate in all compartments of an RGC including the dendritic arbor and axon. Approximately 6% of translocating RGCs exhibited retrotranslocation of BAX immediately following translocation. Unlike tissue culture cells, which exhibit simultaneous translocation and permeabilization, RGCs exhibited a significant delay between these two stages, similar to detached cells undergoing anoikis. Translocation, with minimal permeabilization could be induced in a subset of RGCs using an inhibitor of Focal Adhesion Kinase (PF573228). Permeabilization after ONC, in a majority of RGCs, could be inhibited with a broad spectrum kinase inhibitor (sunitinib) or a selective inhibitor for p38/MAPK14 (SB203580). Intervention of DLK-JNK axis signaling abrogated GFP-BAX translocation after ONC.
Conclusions:
A comparison between BAX activation kinetics in tissue culture cells and in cells of a complex tissue environment shows distinct differences indicating that caution should be used when translating findings from one condition to the other. RGCs exhibit both a delay between translocation and permeabilization and the ability for translocated BAX to be retrotranslocated, suggesting several stages at which intervention of the activation process could be exploited in the design of a therapeutic strategy.},
  author       = {Maes, Margaret E and Donahue, Ryan J. and Schlamp, Cassandra L. and Marola, Olivia J. and Libby, Richard T. and Nickells, Robert W.},
  issn         = {1750-1326},
  journal      = {Molecular Neurodegeneration},
  publisher    = {Springer Nature},
  title        = {{BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps}},
  doi          = {10.1186/s13024-023-00659-8},
  volume       = {18},
  year         = {2023},
}

@article{14402,
  abstract     = {Alpha oscillations are a distinctive feature of the awake resting state of the human brain. However, their functional role in resting-state neuronal dynamics remains poorly understood. Here we show that, during resting wakefulness, alpha oscillations drive an alternation of attenuation and amplification bouts in neural activity. Our analysis indicates that inhibition is activated in pulses that last for a single alpha cycle and gradually suppress neural activity, while excitation is successively enhanced over a few alpha cycles to amplify neural activity. Furthermore, we show that long-term alpha amplitude fluctuations—the “waxing and waning” phenomenon—are an attenuation-amplification mechanism described by a power-law decay of the activity rate in the “waning” phase. Importantly, we do not observe such dynamics during non-rapid eye movement (NREM) sleep with marginal alpha oscillations. The results suggest that alpha oscillations modulate neural activity not only through pulses of inhibition (pulsed inhibition hypothesis) but also by timely enhancement of excitation (or disinhibition).},
  author       = {Lombardi, Fabrizio and Herrmann, Hans J. and Parrino, Liborio and Plenz, Dietmar and Scarpetta, Silvia and Vaudano, Anna Elisabetta and De Arcangelis, Lucilla and Shriki, Oren},
  issn         = {2211-1247},
  journal      = {Cell Reports},
  number       = {10},
  publisher    = {Elsevier},
  title        = {{Beyond pulsed inhibition: Alpha oscillations modulate attenuation and amplification of neural activity in the awake resting state}},
  doi          = {10.1016/j.celrep.2023.113162},
  volume       = {42},
  year         = {2023},
}

@inproceedings{14405,
  abstract     = {We introduce hypernode automata as a new specification formalism for hyperproperties of concurrent systems. They are finite automata with nodes labeled with hypernode logic formulas and transitions labeled with actions. A hypernode logic formula specifies relations between sequences of variable values in different system executions. Unlike HyperLTL, hypernode logic takes an asynchronous view on execution traces by constraining the values and the order of value changes of each variable without correlating the timing of the changes. Different execution traces are synchronized solely through the transitions of hypernode automata. Hypernode automata naturally combine asynchronicity at the node level with synchronicity at the transition level. We show that the model-checking problem for hypernode automata is decidable over action-labeled Kripke structures, whose actions induce transitions of the specification automata. For this reason, hypernode automaton is a suitable formalism for specifying and verifying asynchronous hyperproperties, such as declassifying observational determinism in multi-threaded programs.},
  author       = {Bartocci, Ezio and Henzinger, Thomas A and Nickovic, Dejan and Oliveira da Costa, Ana},
  booktitle    = {34th International Conference on Concurrency Theory},
  isbn         = {9783959772990},
  issn         = {1868-8969},
  location     = {Antwerp, Belgium},
  publisher    = {Schloss Dagstuhl - Leibniz-Zentrum für Informatik},
  title        = {{Hypernode automata}},
  doi          = {10.4230/LIPIcs.CONCUR.2023.21},
  volume       = {279},
  year         = {2023},
}

@article{14406,
  abstract     = {Recently, a concept of generalized multifractality, which characterizes fluctuations and correlations of critical eigenstates, was introduced and explored for all 10 symmetry classes of disordered systems. Here, by using the nonlinear sigma-model (
NL
σ
M
) field theory, we extend the theory of generalized multifractality to boundaries of systems at criticality. Our numerical simulations on two-dimensional systems of symmetry classes A, C, and AII fully confirm the analytical predictions of pure-scaling observables and Weyl symmetry relations between critical exponents of surface generalized multifractality. This demonstrates the validity of the 
NL
σ
M
 for the description of Anderson-localization critical phenomena, not only in the bulk but also on the boundary. The critical exponents strongly violate generalized parabolicity, in analogy with earlier results for the bulk, corroborating the conclusion that the considered Anderson-localization critical points are not described by conformal field theories. We further derive relations between generalized surface multifractal spectra and linear combinations of Lyapunov exponents of a strip in quasi-one-dimensional geometry, which hold under the assumption of invariance with respect to a logarithmic conformal map. Our numerics demonstrate that these relations hold with an excellent accuracy. Taken together, our results indicate an intriguing situation: the conformal invariance is broken but holds partially at critical points of Anderson localization.},
  author       = {Babkin, Serafim and Karcher, Jonas F. and Burmistrov, Igor S. and Mirlin, Alexander D.},
  issn         = {2469-9969},
  journal      = {Physical Review B},
  number       = {10},
  publisher    = {American Physical Society},
  title        = {{Generalized surface multifractality in two-dimensional disordered systems}},
  doi          = {10.1103/PhysRevB.108.104205},
  volume       = {108},
  year         = {2023},
}

@article{14409,
  abstract     = {We present a photon- and metal-free approach for the radical fluorination of aliphatic oxalate-activated alcohols. The method relies on the spontaneous generation of the N-(chloromethyl)triethylenediamine radical dication, a potent single electron oxidant, from Selectfluor and 4-(dimethylamino)pyridine. The protocol is easily scalable and provides the desired fluorinated products within only a few minutes reaction time.},
  author       = {Baunis, Haralds and Pieber, Bartholomäus},
  issn         = {1099-0690},
  journal      = {European Journal of Organic Chemistry},
  number       = {42},
  publisher    = {Wiley},
  title        = {{Formal radical deoxyfluorination of oxalate-activated alcohols triggered by the selectfluor-DMAP charge-transfer complex}},
  doi          = {10.1002/ejoc.202300769},
  volume       = {26},
  year         = {2023},
}

@inproceedings{14411,
  abstract     = {Partially specified Boolean networks (PSBNs) represent a promising framework for the qualitative modelling of biological systems in which the logic of interactions is not completely known. Phenotype control aims to stabilise the network in states exhibiting specific traits.
In this paper, we define the phenotype control problem in the context of asynchronous PSBNs and propose a novel semi-symbolic algorithm for solving this problem with permanent variable perturbations.},
  author       = {Beneš, Nikola and Brim, Luboš and Pastva, Samuel and Šafránek, David and Šmijáková, Eva},
  booktitle    = {21st International Conference on Computational Methods in Systems Biology},
  isbn         = {9783031426964},
  issn         = {1611-3349},
  location     = {Luxembourg City, Luxembourg},
  pages        = {18--35},
  publisher    = {Springer Nature},
  title        = {{Phenotype control of partially specified boolean networks}},
  doi          = {10.1007/978-3-031-42697-1_2},
  volume       = {14137},
  year         = {2023},
}

@inproceedings{14417,
  abstract     = {Entropic risk (ERisk) is an established risk measure in finance, quantifying risk by an exponential re-weighting of rewards. We study ERisk for the first time in the context of turn-based stochastic games with the total reward objective. This gives rise to an objective function that demands the control of systems in a risk-averse manner. We show that the resulting games are determined and, in particular, admit optimal memoryless deterministic strategies. This contrasts risk measures that previously have been considered in the special case of Markov decision processes and that require randomization and/or memory. We provide several results on the decidability and the computational complexity of the threshold problem, i.e. whether the optimal value of ERisk exceeds a given threshold. In the most general case, the problem is decidable subject to Shanuel’s conjecture. If all inputs are rational, the resulting threshold problem can be solved using algebraic numbers, leading to decidability via a polynomial-time reduction to the existential theory of the reals. Further restrictions on the encoding of the input allow the solution of the threshold problem in NP∩coNP. Finally, an approximation algorithm for the optimal value of ERisk is provided.},
  author       = {Baier, Christel and Chatterjee, Krishnendu and Meggendorfer, Tobias and Piribauer, Jakob},
  booktitle    = {48th International Symposium on Mathematical Foundations of Computer Science},
  isbn         = {9783959772921},
  issn         = {1868-8969},
  location     = {Bordeaux, France},
  publisher    = {Schloss Dagstuhl - Leibniz-Zentrum für Informatik},
  title        = {{Entropic risk for turn-based stochastic games}},
  doi          = {10.4230/LIPIcs.MFCS.2023.15},
  volume       = {272},
  year         = {2023},
}

