9,668 research outputs found
The structure of robust observers
Conventional observers for linear time-invariant systems are shown to be structurally inadequate from a sensitivity standpoint. It is proved that if a linear dynamic system is to provide observer action despite arbitrary small perturbations in a specified subset of its parameters, it must: (1) be a closed loop system, be driven by the observer error, (2) possess redundancy, the observer must be generating, implicitly or explicitly, at least one linear combination of states that is already contained in the measurements, and (3) contain a perturbation-free model of the portion of the system observable from the external input to the observer. The procedure for design of robust observers possessing the above structural features is established and discussed
Comparison of Modules of Wild Type and Mutant Huntingtin and TP53 Protein Interaction Networks: Implications in Biological Processes and Functions
Disease-causing mutations usually change the interacting partners of mutant
proteins. In this article, we propose that the biological consequences of
mutation are directly related to the alteration of corresponding protein
protein interaction networks (PPIN). Mutation of Huntingtin (HTT) which causes
Huntington's disease (HD) and mutations to TP53 which is associated with
different cancers are studied as two example cases. We construct the PPIN of
wild type and mutant proteins separately and identify the structural modules of
each of the networks. The functional role of these modules are then assessed by
Gene Ontology (GO) enrichment analysis for biological processes (BPs). We find
that a large number of significantly enriched (p<0.0001) GO terms in mutant
PPIN were absent in the wild type PPIN indicating the gain of BPs due to
mutation. Similarly some of the GO terms enriched in wild type PPIN cease to
exist in the modules of mutant PPIN, representing the loss. GO terms common in
modules of mutant and wild type networks indicate both loss and gain of BPs. We
further assign relevant biological function(s) to each module by classifying
the enriched GO terms associated with it. It turns out that most of these
biological functions in HTT networks are already known to be altered in HD and
those of TP53 networks are altered in cancers. We argue that gain of BPs, and
the corresponding biological functions, are due to new interacting partners
acquired by mutant proteins. The methodology we adopt here could be applied to
genetic diseases where mutations alter the ability of the protein to interact
with other proteins.Comment: 35 pages, 10 eps figures, (Supplementary material and Datasets are
available on request
Stability margins for multilinear interval systems by way of phase conditions: A unified approach
A simple way of checking the stability with respect to an arbitrary stability region of a family of polynomials containing a vector of parameters varying within prescribed intervals is discussed. It is assumed that the parameters appear affine multilinearly in the characteristic polynomial coefficients. The condition proposed is simply to check the phase difference of the vertex polynomials. This test based on the mapping theorem significantly reduces computational complexity. Mathematical proofs are omitted. The results can be used to determine various stability margins of control systems containing interconnected interval subsystems. These include the gain, phase, time-delay, H(sup infinity), and nonlinear sector bounded stability margins of multilinear interval systems
- …