16 research outputs found
de Branges-Rovnyak spaces: basics and theory
For a contractive analytic operator-valued function on the unit disk
, de Branges and Rovnyak associate a Hilbert space of analytic
functions and related extension space
consisting of pairs of analytic functions on the unit disk . This
survey describes three equivalent formulations (the original geometric de
Branges-Rovnyak definition, the Toeplitz operator characterization, and the
characterization as a reproducing kernel Hilbert space) of the de
Branges-Rovnyak space , as well as its role as the underlying
Hilbert space for the modeling of completely non-isometric Hilbert-space
contraction operators. Also examined is the extension of these ideas to handle
the modeling of the more general class of completely nonunitary contraction
operators, where the more general two-component de Branges-Rovnyak model space
and associated overlapping spaces play key roles. Connections
with other function theory problems and applications are also discussed. More
recent applications to a variety of subsequent applications are given in a
companion survey article
Rule-Based Cell Systems Model of Aging using Feedback Loop Motifs Mediated by Stress Responses
Investigating the complex systems dynamics of the aging process requires integration of a broad range of cellular processes describing damage and functional decline co-existing with adaptive and protective regulatory mechanisms. We evolve an integrated generic cell network to represent the connectivity of key cellular mechanisms structured into positive and negative feedback loop motifs centrally important for aging. The conceptual network is casted into a fuzzy-logic, hybrid-intelligent framework based on interaction rules assembled from a priori knowledge. Based upon a classical homeostatic representation of cellular energy metabolism, we first demonstrate how positive-feedback loops accelerate damage and decline consistent with a vicious cycle. This model is iteratively extended towards an adaptive response model by incorporating protective negative-feedback loop circuits. Time-lapse simulations of the adaptive response model uncover how transcriptional and translational changes, mediated by stress sensors NF-κB and mTOR, counteract accumulating damage and dysfunction by modulating mitochondrial respiration, metabolic fluxes, biosynthesis, and autophagy, crucial for cellular survival. The model allows consideration of lifespan optimization scenarios with respect to fitness criteria using a sensitivity analysis. Our work establishes a novel extendable and scalable computational approach capable to connect tractable molecular mechanisms with cellular network dynamics underlying the emerging aging phenotype