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At least 1,243 records · Page 69Linked to original sources
PubMed2000

Neural systems as nonlinear filters.

Experimental data show that biological synapses behave quite differently from the symbolic synapses in all common artificial neural network models. Biological synapses are dynamic; their "weight" changes on a short timescale by several hundred percent in dependence of the past input to the synapse. In this article we address the question how this inherent synaptic dynamics (which should not be confused with long term learning) affects the computational power of a neural network. In particular, we analyze computations on temporal and spatiotemporal patterns, and we give a complete mathematical characterization of all filters that can be approximated by feedforward neural networks with dynamic synapses. It turns out that even with just a single hidden layer, such networks can approximate a very rich class of nonlinear filters: all filters that can be characterized by Volterra series. This result is robust with regard to various changes in the model for synaptic dynamics. Our characterization result provides for all nonlinear filters that are approximable by Volterra series a new complexity hierarchy related to the cost of implementing such filters in neural systems.

Action Potentials↗
PubMed1999

Endothelial cell apoptosis in capillary network remodeling.

We hypothesized that the regulation of apoptosis is an important determinant of capillary network structure. Using human umbilical vein endothelial cells (HUVEC) in in vitro model systems of capillary tube formation, we initially documented that apoptosis is a prominent feature of network formation. Perturbations of integrin-matrix signaling by the administration of either colchicine or an anti-alpha(v)beta3 antibody resulted in the dissolution of the tubular network in association with increased apoptosis. The activation of the alpha(v)beta3 integrin induced increased expression of the anti-apoptotic gene bcl-2 and conferred resistance to the proapoptotic effect of TGF-beta1. In contrast to the stable networks formed by HUVEC, bovine aortic endothelial cells (BAEC) exhibited a more dynamic process of network formation and spontaneous involution. The inhibition of BAEC apoptosis by stable transfection of bcl-2 prevented the involution of the network. We hypothesized that TGF-beta1 present within the model system mediated network involution by inducing BAEC death. Indeed, blockade of TGF-beta1 with neutralizing antibodies reduced BAEC apoptosis and preserved the network structure. As observed with HUVEC networks, stable BAEC networks formed during blockade of TGF-beta1 were also dependent on the survival-promoting effects of matrixintegrin interactions. This study suggests that capillary network structure is determined by the balance of proapoptotic vs. anti-apoptotic signals mediated by the engagement of cytokine and integrin receptors within the milieu.

Animals↗
PubMed1998

Dynamic rearrangement of the filamentous actin network occurs during zoosporogenesis and encystment in the oomycete phytophthora cinnamomi

The organization of filamentous actin (F-actin) in living cells of the oomycete Phytophthora cinnamomi was determined during zoosporogenesis and zoospore encystment by microinjecting sporangia with fluorescently labeled phalloidin and observing resultant fluorescence by confocal microscopy. In multinucleate sporangia prior to the induction of cleavage, phalloidin labeling took the form of plaques which occurred mainly in the periphery of the sporangia. After induction of cleavage, phalloidin labeling showed that the plaques disappeared and that F-actin began to accumulate along the developing cleavage planes and around nuclei and water expulsion vacuoles. F-actin labeling was also observed near the plasma membrane in zoospores and young cysts but reverted to the plaque form in older cysts. Localization of F-actin close to the developing cleavage planes is consistent with the idea that actin microfilaments function in the positioning and expansion of the cleavage membranes. Observations of plaques of actin in living sporangia provide evidence that plaques are not aldehyde-induced fixation artifacts. Copyright 1998 Academic Press.

Journal Article↗
PubMed2006

Pair-level approximations to the spatio-temporal dynamics of epidemics on asymmetric contact networks.

The process of infection during an epidemic can be envisaged as being transmitted via a network of routes represented by a contact network. Most differential equation models of epidemics are mean-field models. These contain none of the underlying spatial structure of the contact network. By extending the mean-field models to pair-level, some of the spatial structure can be contained in the model. Some networks of transmission such as river or transportation networks are clearly asymmetric, whereas others such as airborne infection can be regarded as symmetric. Pair-level models have been developed to describe symmetric contact networks. Here we report on work to develop a pair-level model that is also applicable to asymmetric contact networks. The procedure for closing the model at the level of pairs is discussed in detail. The model is compared against stochastic simulations of epidemics on asymmetric contact networks and against the predictions of the symmetric model on the same networks.

Communicable Diseases↗
PubMed2023

Profiling of drug resistance in Src kinase at scale uncovers a regulatory network coupling autoinhibition and catalytic domain dynamics.

Kinase inhibitors are effective cancer therapies, but resistance often limits clinical efficacy. Despite the cataloging of numerous resistance mutations, our understanding of kinase inhibitor resistance is still incomplete. Here, we comprehensively profiled the resistance of ∼3,500 Src tyrosine kinase mutants to four different ATP-competitive inhibitors. We found that ATP-competitive inhibitor resistance mutations are distributed throughout Src's catalytic domain. In addition to inhibitor contact residues, residues that participate in regulating Src's phosphotransferase activity were prone to the development of resistance. Unexpectedly, we found that a resistance-prone cluster of residues located on the top face of the N-terminal lobe of Src's catalytic domain contributes to autoinhibition by reducing catalytic domain dynamics, and mutations in this cluster led to resistance by lowering inhibitor affinity and promoting kinase hyperactivation. Together, our studies demonstrate how drug resistance profiling can be used to define potential resistance pathways and uncover new mechanisms of kinase regulation.

src-Family Kinases↗
PubMed2001

Anisotropy of fluctuation dynamics of proteins with an elastic network model.

Fluctuations about the native conformation of proteins have proven to be suitably reproduced with a simple elastic network model, which has shown excellent agreement with a number of different properties for a wide variety of proteins. This scalar model simply investigates the magnitudes of motion of individual residues in the structure. To use the elastic model approach further for developing the details of protein mechanisms, it becomes essential to expand this model to include the added details of the directions of individual residue fluctuations. In this paper a new tool is presented for this purpose and applied to the retinol-binding protein, which indicates enhanced flexibility in the region of entry to the ligand binding site and for the portion of the protein binding to its carrier protein.

Anisotropy↗
PubMed1990

Dynamics of a class of immune networks. I. Global stability of idiotype interactions.

This paper establishes the conditions under which a class of differential equations which appear in the study of immune systems (Varela et al., 1988a, In: Theoretical Immunology Part II. New Jersey: Addison Wesley), are globally stable. This is proved by adapting a Liapunov functional originally proposed by Cohen & Grossberg (1983, IEEE Transac SMC 13, 815-826) for competitive systems. The global stability thus obtained is valid on the fast time scale where only idiotypic interactions are relevant, thus excluding both lymphocyte proliferation processes and repertoire change via recruitment from immature bone marrow B cells.

Animals↗
PubMed1990

Dynamics of a class of immune networks. II. Oscillatory activity of cellular and humoral components.

Simulations show that for a certain range of its free parameters, a model of the immune network including both cellular and humoral components is capable of self-sustained oscillations. The model also possesses a number of fixed points which appear to be unstable. These results, taken together, suggest the hypothesis that the immune network may be able to sustain a non-degenerate diversity of active clones which are actively connected to each other only on condition that the activities of these clones are oscillatory.

Animals↗
PubMedDate not supplied

Actin dynamics: assembly and disassembly of actin networks.

Assembly of branched actin filament networks at the leading edge of migrating cells requires stimulation of the Arp2/3 complex by WASp proteins, in concert with the WASp activators Cdc42, PIP(2) and profilin. Network disassembly and debranching appears to be linked to actin-bound ATP hydrolysis as filaments age.

Actins↗
PubMed2004

Dynamic profiling of the glucose metabolic network in fasted rat hepatocytes using [1,2-13C2]glucose.

Recent studies in metabolic profiling have underscored the importance of the concept of a metabolic network of pathways with special functional characteristics that differ from those of simple reaction sequences. The characterization of metabolic functions requires the simultaneous measurement of substrate fluxes of interconnecting pathways. Here we present a novel stable isotope method by which the forward and reverse fluxes of the futile cycles of the hepatic glucose metabolic network are simultaneously determined. Unlike previous radio-isotope methods, a single tracer [1,2-13C2]D-glucose and mass isotopomer analysis is used. Changes in fluxes of substrate cycles, in response to several gluconeogenic substrates, in isolated fasted hepatocytes from male Wistar rats were measured simultaneously. Incubation with these substrates resulted in a change in glucose-6-phosphatase/glucokinase and glycolytic/gluconeogenic flux ratios. Different net redistributions of intermediates in the glucose network were observed, resulting in distinct metabolic phenotypes of the fasted hepatocytes in response to each substrate condition. Our experimental observations show that the constraints of concentrations of shared intermediates, and enzyme kinetics of intersecting pathways of the metabolic network determine substrate redistribution throughout the network when it is perturbed. These results support the systems-biology notion that network analysis provides an integrated view of the physiological state. Interaction between metabolic intermediates and glycolytic/gluconeogenic pathways is a basic element of cross-talk in hepatocytes, and may explain some of the difficulties in genotype and phenotype correlation.

Animals↗
PubMed1983

Studies on the motility of the foraminifera. II. The dynamic microtubular cytoskeleton of the reticulopodial network of Allogromia laticollaris.

Lamellipodia have been induced to form within the reticulopodial networks of Allogromia laticollaris by being plated on positively charged substrata. Video-enhanced, polarized light, and differential interference contrast microscopy have demonstrated the presence of positively birefringent fibrils within these lamellipodia. The fibrils correspond to the microtubules and bundles of microtubules observed in whole-mount transmission electron micrographs of lamellipodia. Microtubular fibrils exhibit two types of movements within the lamellipodia: lateral and axial translocations. Lateral movements are often accompanied by reversible lateral associations between adjacent fibrils within a lamellipodium. This lateral association-dissociation of adjacent fibrils has been termed 'zipping' and 'unzipping'. Axial translocations are bidirectional. The axial movements of the microtubular fibrils can result in the extension of filopodia by pushing against the plasma membrane of the lamellipodia. Shortening, or complete withdrawal, of such filopodia is accomplished by the reversal of the direction of the axial movement. The bidirectional streaming characteristic of the reticulopodial networks also occurs within the lamellipodia. In these flattened regions the streaming is clearly seen to occur exclusively in association with the intracellular fibrils. Transport of both organelles and bulk hyaline cytoplasm occurs bidirectionally along the fibrils.

Animals↗
PubMedDate not supplied

Zinc dynamics in the myocardial redox signaling network.

Zinc plays a vital role in various cellular functions. Zinc deprivation is associated with severe disorders related to growth, maturation, and stress responses. In the heart, zinc affects differentiation and regeneration of cardiac muscle, cardiac conductance, acute stress responses, and recovery of heart transplants. Recent discoveries of the molecular players in zinc homeostasis revealed that the amount of intracellular free zinc is tightly controlled on the level of uptake, intracellular sequestration, redistribution, storage, and elimination, consequently creating a narrow window of optimal zinc concentration in the cells. Most of intracellular zinc is bound to numerous structural and regulatory proteins, with metabolically active, labile zinc present in picoto nanomolar concentrations. The central position of zinc in the redox signaling network is built on its unique chemical nature. The redox inert zinc creates a redox active environment when it binds to a sulfur ligand. The reversible oxidation of the sulfur ligand is coupled to the reversible zinc release from the protein, thereby executing the task of so-called protein "redox zinc switch." Clearly, the impairment of zinc homeostasis will have far reaching physiological consequences.

Animals↗
PubMed2006

Dynamic modelling and analysis of biochemical networks: mechanism-based models and model-based experiments.

Systems biology applies quantitative, mechanistic modelling to study genetic networks, signal transduction pathways and metabolic networks. Mathematical models of biochemical networks can look very different. An important reason is that the purpose and application of a model are essential for the selection of the best mathematical framework. Fundamental aspects of selecting an appropriate modelling framework and a strategy for model building are discussed. Concepts and methods from system and control theory provide a sound basis for the further development of improved and dedicated computational tools for systems biology. Identification of the network components and rate constants that are most critical to the output behaviour of the system is one of the major problems raised in systems biology. Current approaches and methods of parameter sensitivity analysis and parameter estimation are reviewed. It is shown how these methods can be applied in the design of model-based experiments which iteratively yield models that are decreasingly wrong and increasingly gain predictive power.

Algorithms↗