A remarkable phenomenon in spatiotemporal dynamical systems is chimera state, where the structurally and dynamically identical oscillators in a coupled networked system spontaneously break into two groups, one exhibiting coherent motion and another incoherent. This phenomenon was typically studied in the setting of non-local coupling configurations. We ask what can happen to chimera states under systematic changes to the network structure when links are removed from the network in an orderly fashion but the local coupling topology remains invariant with respect to an index shift. We find the emergence of multicluster chimera states. Remarkably, as a parameter characterizing the amount of link removal is increased, chimera states of distinct numbers of clusters emerge and persist in different parameter regions. We develop a phenomenological theory, based on enhanced or reduced interactions among oscillators in different spatial groups, to explain why chimera states of certain numbers of clusters occur in certain parameter regions. The theoretical prediction agrees well with numerics.

Autoantibodies refer to antibodies that target self-antigens, which can play pivotal roles in maintaining homeostasis, distinguishing normal from tumor tissue and trigger autoimmune diseases. In the last three decades, tremendous efforts have been devoted to elucidate the generation, evolution and functions of autoantibodies, as well as their target autoantigens. However, reports of these countless previously identified autoantigens are randomly dispersed in the literature. Here, we constructed an AAgAtlas database 1.0 using text-mining and manual curation. We extracted 45 830 autoantigen-related abstracts and 94 313 sentences from PubMed using the keywords of either ‘autoantigen’ or ‘autoantibody’ or their lexical variants, which were further refined to 25 520 abstracts, 43 253 sentences and 3984 candidates by our bio-entity recognizer based on the Protein Ontology. Finally, we identified 1126 genes as human autoantigens and 1071 related human diseases, with which we constructed a human autoantigen database (AAgAtlas database 1.0). The database provides a user-friendly interface to conveniently browse, retrieve and download human autoantigens as well as their associated diseases. The database is freely accessible at http://biokb.ncpsb.org/aagatlas/. We believe this database will be a valuable resource to track and understand human autoantigens as well as to investigate their functions in basic and translational research.

Recently, the phenomenon of quantum-classical correspondence breakdown was uncovered in optomechanics, where in the classical regime the system exhibits chaos but in the corresponding quantum regime the motion is regular - there appears to be no signature of classical chaos whatsoever in the corresponding quantum system, generating a paradox. We find that transient chaos, besides being a physically meaningful phenomenon by itself, provides a resolution. Using the method of quantum state diffusion to simulate the system dynamics subject to continuous homodyne detection, we uncover transient chaos associated with quantum trajectories. The transient behavior is consistent with chaos in the classical limit, while the long term evolution of the quantum system is regular. Transient chaos thus serves as a bridge for the quantum-classical transition (QCT). Strikingly, as the system transitions from the quantum to the classical regime, the average chaotic transient lifetime increases dramatically (faster than the Ehrenfest time characterizing the QCT for isolated quantum systems). We develop a physical theory to explain the scaling law.

Network reconstruction is a fundamental problem for understanding many complex systems with unknown interaction structures. In many complex systems, there are indirect interactions between two individuals without immediate connection but with common neighbors. Despite recent advances in network reconstruction, we continue to lack an approach for reconstructing complex networks with indirect interactions. Here we introduce a two-step strategy to resolve the reconstruction problem, where in the first step, we recover both direct and indirect interactions by employing the Lasso to solve a sparse signal reconstruction problem, and in the second step, we use matrix transformation and optimization to distinguish between direct and indirect interactions. The network structure corresponding to direct interactions can be fully uncovered. We exploit the public goods game occurring on complex networks as a paradigm for characterizing indirect interactions and test our reconstruction approach. We find that high reconstruction accuracy can be achieved for both homogeneous and heterogeneous networks, and a number of empirical networks in spite of insufficient data measurement contaminated by noise. Although a general framework for reconstructing complex networks with arbitrary types of indirect interactions is yet lacking, our approach opens new routes to separate direct and indirect interactions in a representative complex system.

We present a microarray nonlinear calibration (MiNC) method for quantifying antibody binding to the surface of protein microarrays that significantly increases the linear dynamic range and reduces assay variation compared with traditional approaches. A serological analysis of guinea pig Mycobacterium tuberculosis models showed that a larger number of putative antigen targets were identified with MiNC, which is consistent with the improved assay performance of protein microarrays. MiNC has the potential to be employed in biomedical research using multiplex antibody assays that need quantitation, including the discovery of antibody biomarkers, clinical diagnostics with multi-antibody signatures, and construction of immune mathematical models.

Sequential affect dynamics generated during the interaction of intimate dyads, such as married couples, are associated with a cascade of effects - some good and some bad - on each partner, close family members, and other social contacts. Although the effects are well documented, the probabilistic structures associated with micro-social processes connected to the varied outcomes remain enigmatic. Using extant data we developed a method of classifying and subsequently generating couple dynamics using a Hierarchical Dirichlet Process Hidden semi-Markov Model (HDP-HSMM). Our findings indicate that several key aspects of existing models of marital interaction are inadequate: affect state emissions and their durations, along with the expected variability differences between distressed and nondistressed couples are present but highly nuanced; and most surprisingly, heterogeneity among highly satisfied couples necessitate that they be divided into subgroups. We review how this unsupervised learning technique generates plausible dyadic sequences that are sensitive to relationship quality and provide a natural mechanism for computational models of behavioral and affective micro-social processes.

Rho GTPases are frequent targets of virulence factors as they are keystone signaling molecules. Herein, we demonstrate that AMPylation of Rho GTPases by VopS is a multifaceted virulence mechanism that counters several host immunity strategies. Activation of NFκB, Erk, and JNK kinase signaling pathways were inhibited in a VopS-dependent manner during infection with Vibrio parahaemolyticus. Phosphorylation and degradation of IKBα were inhibited in the presence of VopS as was nuclear translocation of the NFκB subunit p65. AMPylation also prevented the generation of superoxide by the phagocytic NADPH oxidase complex, potentially by inhibiting the interaction of Rac and p67. Furthermore, the interaction of GTPases with the E3 ubiquitin ligases cIAP1 and XIAP was hindered, leading to decreased degradation of Rac and RhoA during infection. Finally, we screened for novel Rac1 interactions using a nucleic acid programmable protein array and discovered that Rac1 binds to the protein C1QA, a protein known to promote immune signaling in the cytosol. Interestingly, this interaction was disrupted by AMPylation. We conclude that AMPylation of Rho Family GTPases by VopS results in diverse inhibitory consequences during infection beyond the most obvious phenotype, the collapse of the actin cytoskeleton.

This study extended the findings of Tighe and Schatschneider (2015) by investigating the predictive utility of separate dimensions of morphological awareness as well as vocabulary knowledge to reading comprehension in adult basic education (ABE) students. We competed two- and three-factor structural equation models of reading comprehension. A three-factor model of real word morphological awareness, pseudoword morphological awareness, and vocabulary knowledge emerged as the best fit and accounted for 79% of the reading comprehension variance. The results indicated that the constructs contributed jointly to reading comprehension; however, vocabulary knowledge was the only potentially unique predictor (p = 0.052), accounting for an additional 5.6% of the variance. This study demonstrates the feasibility of applying a latent variable modeling approach to examine individual differences in the reading comprehension skills of ABE students. Further, this study replicates the findings of Tighe and Schatschneider (2015) on the importance of differentiating among dimensions of morphological awareness in this population.

Recent advances in nonequilibrium statistical physics have provided unprecedented insight into the thermodynamics of dynamic processes. The author recently used these advances to extend Landauer’s semi-formal reasoning concerning the thermodynamics of bit erasure, to derive the minimal free energy required to implement an arbitrary computation. Here, I extend this analysis, deriving the minimal free energy required by an organism to run a given (stochastic) map π from its sensor inputs to its actuator outputs. I use this result to calculate the input-output map π of an organism that optimally trades off the free energy needed to run π with the phenotypic fitness that results from implementing π. I end with a general discussion of the limits imposed on the rate of the terrestrial biosphere’s information processing by the flux of sunlight on the Earth.

High proportions of autistic children suffer from gastrointestinal (GI) disorders, implying a link between autism and abnormalities in gut microbial functions. Increasing evidence from recent high-throughput sequencing analyses indicates that disturbances in composition and diversity of gut microbiome are associated with various disease conditions. However, microbiome-level studies on autism are limited and mostly focused on pathogenic bacteria. Therefore, here we aimed to define systemic changes in gut microbiome associated with autism and autism-related GI problems. We recruited 20 neurotypical and 20 autistic children accompanied by a survey of both autistic severity and GI symptoms. By pyrosequencing the V2/V3 regions in bacterial 16S rDNA from fecal DNA samples, we compared gut microbiomes of GI symptom-free neurotypical children with those of autistic children mostly presenting GI symptoms. Unexpectedly, the presence of autistic symptoms, rather than the severity of GI symptoms, was associated with less diverse gut microbiomes. Further, rigorous statistical tests with multiple testing corrections showed significantly lower abundances of the genera Prevotella, Coprococcus, and unclassified Veillonellaceae in autistic samples. These are intriguingly versatile carbohydrate-degrading and/or fermenting bacteria, suggesting a potential influence of unusual diet patterns observed in autistic children. However, multivariate analyses showed that autism-related changes in both overall diversity and individual genus abundances were correlated with the presence of autistic symptoms but not with their diet patterns. Taken together, autism and accompanying GI symptoms were characterized by distinct and less diverse gut microbial compositions with lower levels of Prevotella, Coprococcus, and unclassified Veillonellaceae.