@inproceedings{14862,
  author       = {Rella, Simon and Kulikova, Y and Minnegalieva, Aygul and Kondrashov, Fyodor},
  booktitle    = {European Journal of Public Health},
  issn         = {1464-360X},
  keywords     = {Public Health, Environmental and Occupational Health},
  number       = {Supplement_2},
  publisher    = {Oxford University Press},
  title        = {{Complex vaccination strategies prevent the emergence of vaccine resistance}},
  doi          = {10.1093/eurpub/ckad160.597},
  volume       = {33},
  year         = {2023},
}

@article{14656,
  abstract     = {Although much is known about how single neurons in the hippocampus represent an animal's position, how circuit interactions contribute to spatial coding is less well understood. Using a novel statistical estimator and theoretical modeling, both developed in the framework of maximum entropy models, we reveal highly structured CA1 cell-cell interactions in male rats during open field exploration. The statistics of these interactions depend on whether the animal is in a familiar or novel environment. In both conditions the circuit interactions optimize the encoding of spatial information, but for regimes that differ in the informativeness of their spatial inputs. This structure facilitates linear decodability, making the information easy to read out by downstream circuits. Overall, our findings suggest that the efficient coding hypothesis is not only applicable to individual neuron properties in the sensory periphery, but also to neural interactions in the central brain.},
  author       = {Nardin, Michele and Csicsvari, Jozsef L and Tkačik, Gašper and Savin, Cristina},
  issn         = {1529-2401},
  journal      = {The Journal of Neuroscience},
  number       = {48},
  pages        = {8140--8156},
  publisher    = {Society for Neuroscience},
  title        = {{The structure of hippocampal CA1 interactions optimizes spatial coding across experience}},
  doi          = {10.1523/JNEUROSCI.0194-23.2023},
  volume       = {43},
  year         = {2023},
}

@article{11638,
  abstract     = {Statistical inference is central to many scientific endeavors, yet how it works remains unresolved. Answering this requires a quantitative understanding of the intrinsic interplay between statistical models, inference methods, and the structure in the data. To this end, we characterize the efficacy of direct coupling analysis (DCA)—a highly successful method for analyzing amino acid sequence data—in inferring pairwise interactions from samples of ferromagnetic Ising models on random graphs. Our approach allows for physically motivated exploration of qualitatively distinct data regimes separated by phase transitions. We show that inference quality depends strongly on the nature of data-generating distributions: optimal accuracy occurs at an intermediate temperature where the detrimental effects from macroscopic order and thermal noise are minimal. Importantly our results indicate that DCA does not always outperform its local-statistics-based predecessors; while DCA excels at low temperatures, it becomes inferior to simple correlation thresholding at virtually all temperatures when data are limited. Our findings offer insights into the regime in which DCA operates so successfully, and more broadly, how inference interacts with the structure in the data.},
  author       = {Ngampruetikorn, Vudtiwat and Sachdeva, Vedant and Torrence, Johanna and Humplik, Jan and Schwab, David J. and Palmer, Stephanie E.},
  issn         = {2643-1564},
  journal      = {Physical Review Research},
  number       = {2},
  publisher    = {American Physical Society},
  title        = {{Inferring couplings in networks across order-disorder phase transitions}},
  doi          = {10.1103/PhysRevResearch.4.023240},
  volume       = {4},
  year         = {2022},
}

@article{12156,
  abstract     = {Models of transcriptional regulation that assume equilibrium binding of transcription factors have been less successful at predicting gene expression from sequence in eukaryotes than in bacteria. This could be due to the non-equilibrium nature of eukaryotic regulation. Unfortunately, the space of possible non-equilibrium mechanisms is vast and predominantly uninteresting. The key question is therefore how this space can be navigated efficiently, to focus on mechanisms and models that are biologically relevant. In this review, we advocate for the normative role of theory—theory that prescribes rather than just describes—in providing such a focus. Theory should expand its remit beyond inferring mechanistic models from data, towards identifying non-equilibrium gene regulatory schemes that may have been evolutionarily selected, despite their energy consumption, because they are precise, reliable, fast, or otherwise outperform regulation at equilibrium. We illustrate our reasoning by toy examples for which we provide simulation code.},
  author       = {Zoller, Benjamin and Gregor, Thomas and Tkačik, Gašper},
  issn         = {2452-3100},
  journal      = {Current Opinion in Systems Biology},
  keywords     = {Applied Mathematics, Computer Science Applications, Drug Discovery, General Biochemistry, Genetics and Molecular Biology, Modeling and Simulation},
  number       = {9},
  publisher    = {Elsevier},
  title        = {{Eukaryotic gene regulation at equilibrium, or non?}},
  doi          = {10.1016/j.coisb.2022.100435},
  volume       = {31},
  year         = {2022},
}

@article{12332,
  abstract     = {Activity of sensory neurons is driven not only by external stimuli but also by feedback signals from higher brain areas. Attention is one particularly important internal signal whose presumed role is to modulate sensory representations such that they only encode information currently relevant to the organism at minimal cost. This hypothesis has, however, not yet been expressed in a normative computational framework. Here, by building on normative principles of probabilistic inference and efficient coding, we developed a model of dynamic population coding in the visual cortex. By continuously adapting the sensory code to changing demands of the perceptual observer, an attention-like modulation emerges. This modulation can dramatically reduce the amount of neural activity without deteriorating the accuracy of task-specific inferences. Our results suggest that a range of seemingly disparate cortical phenomena such as intrinsic gain modulation, attention-related tuning modulation, and response variability could be manifestations of the same underlying principles, which combine efficient sensory coding with optimal probabilistic inference in dynamic environments.},
  author       = {Mlynarski, Wiktor F and Tkačik, Gašper},
  issn         = {1545-7885},
  journal      = {PLoS Biology},
  number       = {12},
  pages        = {e3001889},
  publisher    = {Public Library of Science},
  title        = {{Efficient coding theory of dynamic attentional modulation}},
  doi          = {10.1371/journal.pbio.3001889},
  volume       = {20},
  year         = {2022},
}

@article{10530,
  abstract     = {Cell dispersion from a confined area is fundamental in a number of biological processes,
including cancer metastasis. To date, a quantitative understanding of the interplay of single
cell motility, cell proliferation, and intercellular contacts remains elusive. In particular, the role
of E- and N-Cadherin junctions, central components of intercellular contacts, is still
controversial. Combining theoretical modeling with in vitro observations, we investigate the
collective spreading behavior of colonies of human cancer cells (T24). The spreading of these
colonies is driven by stochastic single-cell migration with frequent transient cell-cell contacts.
We find that inhibition of E- and N-Cadherin junctions decreases colony spreading and average
spreading velocities, without affecting the strength of correlations in spreading velocities of
neighboring cells. Based on a biophysical simulation model for cell migration, we show that the
behavioral changes upon disruption of these junctions can be explained by reduced repulsive
excluded volume interactions between cells. This suggests that in cancer cell migration,
cadherin-based intercellular contacts sharpen cell boundaries leading to repulsive rather than
cohesive interactions between cells, thereby promoting efficient cell spreading during collective
migration.
},
  author       = {Zisis, Themistoklis and Brückner, David and Brandstätter, Tom and Siow, Wei Xiong and d’Alessandro, Joseph and Vollmar, Angelika M. and Broedersz, Chase P. and Zahler, Stefan},
  issn         = {0006-3495},
  journal      = {Biophysical Journal},
  keywords     = {Biophysics},
  number       = {1},
  pages        = {P44--60},
  publisher    = {Elsevier},
  title        = {{Disentangling cadherin-mediated cell-cell interactions in collective cancer cell migration}},
  doi          = {10.1016/j.bpj.2021.12.006},
  volume       = {121},
  year         = {2022},
}

@article{10736,
  abstract     = {Predicting function from sequence is a central problem of biology. Currently, this is possible only locally in a narrow mutational neighborhood around a wildtype sequence rather than globally from any sequence. Using random mutant libraries, we developed a biophysical model that accounts for multiple features of σ70 binding bacterial promoters to predict constitutive gene expression levels from any sequence. We experimentally and theoretically estimated that 10–20% of random sequences lead to expression and ~80% of non-expressing sequences are one mutation away from a functional promoter. The potential for generating expression from random sequences is so pervasive that selection acts against σ70-RNA polymerase binding sites even within inter-genic, promoter-containing regions. This pervasiveness of σ70-binding sites implies that emergence of promoters is not the limiting step in gene regulatory evolution. Ultimately, the inclusion of novel features of promoter function into a mechanistic model enabled not only more accurate predictions of gene expression levels, but also identified that promoters evolve more rapidly than previously thought.},
  author       = {Lagator, Mato and Sarikas, Srdjan and Steinrück, Magdalena and Toledo-Aparicio, David and Bollback, Jonathan P and Guet, Calin C and Tkačik, Gašper},
  issn         = {2050-084X},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{Predicting bacterial promoter function and evolution from random sequences}},
  doi          = {10.7554/eLife.64543},
  volume       = {11},
  year         = {2022},
}

@unpublished{10821,
  abstract     = {Rhythmical cortical activity has long been recognized as a pillar in the architecture of brain functions. Yet, the dynamic organization of its underlying neuronal population activity remains elusive. Here we uncover a unique organizational principle regulating collective neural dynamics associated with the alpha rhythm in the awake resting-state. We demonstrate that cascades of neural activity obey attenuation-amplification dynamics (AAD), with a transition from the attenuation regime—within alpha cycles—to the amplification regime—across a few alpha cycles—that correlates with the characteristic frequency of the alpha rhythm. We find that this short-term AAD is part of a large-scale, size-dependent temporal structure of neural cascades that obeys the Omori law: Following large cascades, smaller cascades occur at a rate that decays as a power-law of the time elapsed from such events—a long-term AAD regulating brain activity over the timescale of seconds. We show that such an organization corresponds to the "waxing and waning" of the alpha rhythm. Importantly, we observe that short- and long-term AAD are unique to the awake resting-state, being absent during NREM sleep. These results provide a quantitative, dynamical description of the so-far-qualitative notion of the "waxing and waning" phenomenon, and suggest the AAD as a key principle governing resting-state dynamics across timescales.},
  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},
  booktitle    = {bioRxiv},
  pages        = {25},
  title        = {{Alpha rhythm induces attenuation-amplification dynamics in neural activity cascades}},
  doi          = {10.1101/2022.03.03.482657},
  year         = {2022},
}

@article{12081,
  abstract     = {Selection accumulates information in the genome—it guides stochastically evolving populations toward states (genotype frequencies) that would be unlikely under neutrality. This can be quantified as the Kullback–Leibler (KL) divergence between the actual distribution of genotype frequencies and the corresponding neutral distribution. First, we show that this population-level information sets an upper bound on the information at the level of genotype and phenotype, limiting how precisely they can be specified by selection. Next, we study how the accumulation and maintenance of information is limited by the cost of selection, measured as the genetic load or the relative fitness variance, both of which we connect to the control-theoretic KL cost of control. The information accumulation rate is upper bounded by the population size times the cost of selection. This bound is very general, and applies across models (Wright–Fisher, Moran, diffusion) and to arbitrary forms of selection, mutation, and recombination. Finally, the cost of maintaining information depends on how it is encoded: Specifying a single allele out of two is expensive, but one bit encoded among many weakly specified loci (as in a polygenic trait) is cheap.},
  author       = {Hledik, Michal and Barton, Nicholas H and Tkačik, Gašper},
  issn         = {1091-6490},
  journal      = {Proceedings of the National Academy of Sciences of the United States of America},
  number       = {36},
  publisher    = {National Academy of Sciences},
  title        = {{Accumulation and maintenance of information in evolution}},
  doi          = {10.1073/pnas.2123152119},
  volume       = {119},
  year         = {2022},
}

@article{10535,
  abstract     = {Realistic models of biological processes typically involve interacting components on multiple scales, driven by changing environment and inherent stochasticity. Such models are often analytically and numerically intractable. We revisit a dynamic maximum entropy method that combines a static maximum entropy with a quasi-stationary approximation. This allows us to reduce stochastic non-equilibrium dynamics expressed by the Fokker-Planck equation to a simpler low-dimensional deterministic dynamics, without the need to track microscopic details. Although the method has been previously applied to a few (rather complicated) applications in population genetics, our main goal here is to explain and to better understand how the method works. We demonstrate the usefulness of the method for two widely studied stochastic problems, highlighting its accuracy in capturing important macroscopic quantities even in rapidly changing non-stationary conditions. For the Ornstein-Uhlenbeck process, the method recovers the exact dynamics whilst for a stochastic island model with migration from other habitats, the approximation retains high macroscopic accuracy under a wide range of scenarios in a dynamic environment.},
  author       = {Bod'ová, Katarína and Szep, Eniko and Barton, Nicholas H},
  issn         = {1553-7358},
  journal      = {PLoS Computational Biology},
  number       = {12},
  publisher    = {Public Library of Science},
  title        = {{Dynamic maximum entropy provides accurate approximation of structured population dynamics}},
  doi          = {10.1371/journal.pcbi.1009661},
  volume       = {17},
  year         = {2021},
}

@article{9283,
  abstract     = {Gene expression levels are influenced by multiple coexisting molecular mechanisms. Some of these interactions such as those of transcription factors and promoters have been studied extensively. However, predicting phenotypes of gene regulatory networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic GRN to study in Escherichia coli how network phenotypes depend on local genetic context, i.e. the genetic neighborhood of a transcription factor and its relative position. We show that one GRN with fixed topology can display not only quantitatively but also qualitatively different phenotypes, depending solely on the local genetic context of its components. Transcriptional read-through is the main molecular mechanism that places one transcriptional unit (TU) within two separate regulons without the need for complex regulatory sequences. We propose that relative order of individual TUs, with its potential for combinatorial complexity, plays an important role in shaping phenotypes of GRNs.},
  author       = {Nagy-Staron, Anna A and Tomasek, Kathrin and Caruso Carter, Caroline and Sonnleitner, Elisabeth and Kavcic, Bor and Paixão, Tiago and Guet, Calin C},
  issn         = {2050-084X},
  journal      = {eLife},
  keywords     = {Genetics and Molecular Biology},
  publisher    = {eLife Sciences Publications},
  title        = {{Local genetic context shapes the function of a gene regulatory network}},
  doi          = {10.7554/elife.65993},
  volume       = {10},
  year         = {2021},
}

@article{9362,
  abstract     = {A central goal in systems neuroscience is to understand the functions performed by neural circuits. Previous top-down models addressed this question by comparing the behaviour of an ideal model circuit, optimised to perform a given function, with neural recordings. However, this requires guessing in advance what function is being performed, which may not be possible for many neural systems. To address this, we propose an inverse reinforcement learning (RL) framework for inferring the function performed by a neural network from data. We assume that the responses of each neuron in a network are optimised so as to drive the network towards ‘rewarded’ states, that are desirable for performing a given function. We then show how one can use inverse RL to infer the reward function optimised by the network from observing its responses. This inferred reward function can be used to predict how the neural network should adapt its dynamics to perform the same function when the external environment or network structure changes. This could lead to theoretical predictions about how neural network dynamics adapt to deal with cell death and/or varying sensory stimulus statistics.},
  author       = {Chalk, Matthew J and Tkačik, Gašper and Marre, Olivier},
  issn         = {1932-6203},
  journal      = {PLoS ONE},
  number       = {4},
  publisher    = {Public Library of Science},
  title        = {{Inferring the function performed by a recurrent neural network}},
  doi          = {10.1371/journal.pone.0248940},
  volume       = {16},
  year         = {2021},
}

@article{9439,
  abstract     = {The ability to adapt to changes in stimulus statistics is a hallmark of sensory systems. Here, we developed a theoretical framework that can account for the dynamics of adaptation from an information processing perspective. We use this framework to optimize and analyze adaptive sensory codes, and we show that codes optimized for stationary environments can suffer from prolonged periods of poor performance when the environment changes. To mitigate the adversarial effects of these environmental changes, sensory systems must navigate tradeoffs between the ability to accurately encode incoming stimuli and the ability to rapidly detect and adapt to changes in the distribution of these stimuli. We derive families of codes that balance these objectives, and we demonstrate their close match to experimentally observed neural dynamics during mean and variance adaptation. Our results provide a unifying perspective on adaptation across a range of sensory systems, environments, and sensory tasks.},
  author       = {Mlynarski, Wiktor F and Hermundstad, Ann M.},
  issn         = {1546-1726},
  journal      = {Nature Neuroscience},
  pages        = {998--1009},
  publisher    = {Springer Nature},
  title        = {{Efficient and adaptive sensory codes}},
  doi          = {10.1038/s41593-021-00846-0},
  volume       = {24},
  year         = {2021},
}

@article{9822,
  abstract     = {Attachment of adhesive molecules on cell culture surfaces to restrict cell adhesion to defined areas and shapes has been vital for the progress of in vitro research. In currently existing patterning methods, a combination of pattern properties such as stability, precision, specificity, high-throughput outcome, and spatiotemporal control is highly desirable but challenging to achieve. Here, we introduce a versatile and high-throughput covalent photoimmobilization technique, comprising a light-dose-dependent patterning step and a subsequent functionalization of the pattern via click chemistry. This two-step process is feasible on arbitrary surfaces and allows for generation of sustainable patterns and gradients. The method is validated in different biological systems by patterning adhesive ligands on cell-repellent surfaces, thereby constraining the growth and migration of cells to the designated areas. We then implement a sequential photopatterning approach by adding a second switchable patterning step, allowing for spatiotemporal control over two distinct surface patterns. As a proof of concept, we reconstruct the dynamics of the tip/stalk cell switch during angiogenesis. Our results show that the spatiotemporal control provided by our “sequential photopatterning” system is essential for mimicking dynamic biological processes and that our innovative approach has great potential for further applications in cell science.},
  author       = {Zisis, Themistoklis and Schwarz, Jan and Balles, Miriam and Kretschmer, Maibritt and Nemethova, Maria and Chait, Remy P and Hauschild, Robert and Lange, Janina and Guet, Calin C and Sixt, Michael K and Zahler, Stefan},
  issn         = {1944-8252},
  journal      = {ACS Applied Materials and Interfaces},
  number       = {30},
  pages        = {35545–35560},
  publisher    = {American Chemical Society},
  title        = {{Sequential and switchable patterning for studying cellular processes under spatiotemporal control}},
  doi          = {10.1021/acsami.1c09850},
  volume       = {13},
  year         = {2021},
}

@article{7463,
  abstract     = {Resting-state brain activity is characterized by the presence of neuronal avalanches showing absence of characteristic size. Such evidence has been interpreted in the context of criticality and associated with the normal functioning of the brain. A distinctive attribute of systems at criticality is the presence of long-range correlations. Thus, to verify the hypothesis that the brain operates close to a critical point and consequently assess deviations from criticality for diagnostic purposes, it is of primary importance to robustly and reliably characterize correlations in resting-state brain activity. Recent works focused on the analysis of narrow-band electroencephalography (EEG) and magnetoencephalography (MEG) signal amplitude envelope, showing evidence of long-range temporal correlations (LRTC) in neural oscillations. However, brain activity is a broadband phenomenon, and a significant piece of information useful to precisely discriminate between normal (critical) and pathological behavior (non-critical), may be encoded in the broadband spatio-temporal cortical dynamics. Here we propose to characterize the temporal correlations in the broadband brain activity through the lens of neuronal avalanches. To this end, we consider resting-state EEG and long-term MEG recordings, extract the corresponding neuronal avalanche sequences, and study their temporal correlations. We demonstrate that the broadband resting-state brain activity consistently exhibits long-range power-law correlations in both EEG and MEG recordings, with similar values of the scaling exponents. Importantly, although we observe that the avalanche size distribution depends on scale parameters, scaling exponents characterizing long-range correlations are quite robust. In particular, they are independent of the temporal binning (scale of analysis), indicating that our analysis captures intrinsic characteristics of the underlying dynamics. Because neuronal avalanches constitute a fundamental feature of neural systems with universal characteristics, the proposed approach may serve as a general, systems- and experiment-independent procedure to infer the existence of underlying long-range correlations in extended neural systems, and identify pathological behaviors in the complex spatio-temporal interplay of cortical rhythms.},
  author       = {Lombardi, Fabrizio and Shriki, Oren and Herrmann, Hans J and de Arcangelis, Lucilla},
  issn         = {1872-8286},
  journal      = {Neurocomputing},
  pages        = {657--666},
  publisher    = {Elsevier},
  title        = {{Long-range temporal correlations in the broadband resting state activity of the human brain revealed by neuronal avalanches}},
  doi          = {10.1016/j.neucom.2020.05.126},
  volume       = {461},
  year         = {2021},
}

@article{8997,
  abstract     = {Phenomenological relations such as Ohm’s or Fourier’s law have a venerable history in physics but are still scarce in biology. This situation restrains predictive theory. Here, we build on bacterial “growth laws,” which capture physiological feedback between translation and cell growth, to construct a minimal biophysical model for the combined action of ribosome-targeting antibiotics. Our model predicts drug interactions like antagonism or synergy solely from responses to individual drugs. We provide analytical results for limiting cases, which agree well with numerical results. We systematically refine the model by including direct physical interactions of different antibiotics on the ribosome. In a limiting case, our model provides a mechanistic underpinning for recent predictions of higher-order interactions that were derived using entropy maximization. We further refine the model to include the effects of antibiotics that mimic starvation and the presence of resistance genes. We describe the impact of a starvation-mimicking antibiotic on drug interactions analytically and verify it experimentally. Our extended model suggests a change in the type of drug interaction that depends on the strength of resistance, which challenges established rescaling paradigms. We experimentally show that the presence of unregulated resistance genes can lead to altered drug interaction, which agrees with the prediction of the model. While minimal, the model is readily adaptable and opens the door to predicting interactions of second and higher-order in a broad range of biological systems.},
  author       = {Kavcic, Bor and Tkačik, Gašper and Bollenbach, Tobias},
  issn         = {1553-7358},
  journal      = {PLOS Computational Biology},
  keywords     = {Modelling and Simulation, Genetics, Molecular Biology, Antibiotics, Drug interactions},
  publisher    = {Public Library of Science},
  title        = {{Minimal biophysical model of combined antibiotic action}},
  doi          = {10.1371/journal.pcbi.1008529},
  volume       = {17},
  year         = {2021},
}

@unpublished{10912,
  abstract     = {Brain dynamics display collective phenomena as diverse as neuronal oscillations and avalanches. Oscillations are rhythmic, with fluctuations occurring at a characteristic scale, whereas avalanches are scale-free cascades of neural activity. Here we show that such antithetic features can coexist in a very generic class of adaptive neural networks. In the most simple yet fully microscopic model from this class we make direct contact with human brain resting-state activity recordings via tractable inference of the model's two essential parameters. The inferred model quantitatively captures the dynamics over a broad range of scales, from single sensor fluctuations, collective behaviors of nearly-synchronous extreme events on multiple sensors, to neuronal avalanches unfolding over multiple sensors across multiple time-bins. Importantly, the inferred parameters correlate with model-independent signatures of "closeness to criticality", suggesting that the coexistence of scale-specific (neural oscillations) and scale-free (neuronal avalanches) dynamics in brain activity occurs close to a non-equilibrium critical point at the onset of self-sustained oscillations.},
  author       = {Lombardi, Fabrizio and Pepic, Selver and Shriki, Oren and Tkačik, Gašper and De Martino, Daniele},
  publisher    = {arXiv},
  title        = {{Quantifying the coexistence of neuronal oscillations and avalanches}},
  doi          = {10.48550/ARXIV.2108.06686},
  year         = {2021},
}

@unpublished{10579,
  abstract     = {We consider a totally asymmetric simple exclusion process (TASEP) consisting of particles on a lattice that require binding by a "token" to move. Using a combination of theory and simulations, we address the following questions: (i) How token binding kinetics affects the current-density relation; (ii) How the current-density relation depends on the scarcity of tokens; (iii) How tokens propagate the effects of the locally-imposed disorder (such a slow site) over the entire lattice; (iv) How a shared pool of tokens couples concurrent TASEPs running on multiple lattices; (v) How our results translate to TASEPs with open boundaries that exchange particles with the reservoir. Since real particle motion (including in systems that inspired the standard TASEP model, e.g., protein synthesis or movement of molecular motors) is often catalyzed, regulated, actuated, or otherwise mediated, the token-driven TASEP dynamics analyzed in this paper should allow for a better understanding of real systems and enable a closer match between TASEP theory and experimental observations.},
  author       = {Kavcic, Bor and Tkačik, Gašper},
  booktitle    = {arXiv},
  title        = {{Token-driven totally asymmetric simple exclusion process}},
  doi          = {10.48550/arXiv.2112.13558},
  year         = {2021},
}

@article{9828,
  abstract     = {Amplitude demodulation is a classical operation used in signal processing. For a long time, its effective applications in practice have been limited to narrowband signals. In this work, we generalize amplitude demodulation to wideband signals. We pose demodulation as a recovery problem of an oversampled corrupted signal and introduce special iterative schemes belonging to the family of alternating projection algorithms to solve it. Sensibly chosen structural assumptions on the demodulation outputs allow us to reveal the high inferential accuracy of the method over a rich set of relevant signals. This new approach surpasses current state-of-the-art demodulation techniques apt to wideband signals in computational efficiency by up to many orders of magnitude with no sacrifice in quality. Such performance opens the door for applications of the amplitude demodulation procedure in new contexts. In particular, the new method makes online and large-scale offline data processing feasible, including the calculation of modulator-carrier pairs in higher dimensions and poor sampling conditions, independent of the signal bandwidth. We illustrate the utility and specifics of applications of the new method in practice by using natural speech and synthetic signals.},
  author       = {Gabrielaitis, Mantas},
  issn         = {1941-0476},
  journal      = {IEEE Transactions on Signal Processing},
  pages        = {4039 -- 4054},
  publisher    = {IEEE},
  title        = {{Fast and accurate amplitude demodulation of wideband signals}},
  doi          = {10.1109/TSP.2021.3087899},
  volume       = {69},
  year         = {2021},
}

@article{9226,
  abstract     = {Half a century after Lewis Wolpert's seminal conceptual advance on how cellular fates distribute in space, we provide a brief historical perspective on how the concept of positional information emerged and influenced the field of developmental biology and beyond. We focus on a modern interpretation of this concept in terms of information theory, largely centered on its application to cell specification in the early Drosophila embryo. We argue that a true physical variable (position) is encoded in local concentrations of patterning molecules, that this mapping is stochastic, and that the processes by which positions and corresponding cell fates are determined based on these concentrations need to take such stochasticity into account. With this approach, we shift the focus from biological mechanisms, molecules, genes and pathways to quantitative systems-level questions: where does positional information reside, how it is transformed and accessed during development, and what fundamental limits it is subject to?},
  author       = {Tkačik, Gašper and Gregor, Thomas},
  issn         = {1477-9129},
  journal      = {Development},
  number       = {2},
  publisher    = {Company of Biologists},
  title        = {{The many bits of positional information}},
  doi          = {10.1242/dev.176065},
  volume       = {148},
  year         = {2021},
}