361 research outputs found
Inversion of a block Löwner matrix
AbstractIn this paper, we give a fast algorithm to compute the parameters of an inversion formula for any nonsingular block Löwner matrix. The connection with matrix rational interpolation is given
Matrix interpretation of multiple orthogonality
In this work we give an interpretation of a (s(d + 1) + 1)-term recurrence
relation in terms of type II multiple orthogonal polynomials.We rewrite
this recurrence relation in matrix form and we obtain a three-term recurrence
relation for vector polynomials with matrix coefficients. We present a matrix
interpretation of the type II multi-orthogonality conditions.We state a Favard
type theorem and the expression for the resolvent function associated to the
vector of linear functionals. Finally a reinterpretation of the type II Hermite-
Padé approximation in matrix form is given
A note on the O(n)-storage implementation of the GKO algorithm
We propose a new O(n)-space implementation of the GKO-Cauchy algorithm for
the solution of linear systems with Cauchy-like matrix. Despite its slightly
higher computational cost, this new algorithm makes a more efficient use of the
processor cache memory. Thus, for matrices of size larger than about 500-1000,
it outperforms the existing algorithms.
We present an applicative case of Cauchy-like matrices with
non-reconstructible main diagonal. In this special instance, the O(n) space
algorithms can be adapted nicely to provide an efficient implementation of
basic linear algebra operations in terms of the low displacement-rank
generators
Nucleolin, a Shuttle Protein Promoting Infection of Human Monocytes by Francisella tularensis
International audienceWe herein confirm the importance of nucleolin expression for LVS binding and its specificity as nucleolin is not involved in binding of another intracellular pathogen as L. monocytogenes or an inert particle. Association of nucleolin with F. tularensis during infection continues intracellularly after endocytosis of the bacteria. The present work therefore unravels for the first time the presence of nucleolin in the phagosomal compartment of macrophages
Exploitation of Herpesvirus Immune Evasion Strategies to Modify the Immunogenicity of Human Mesenchymal Stem Cell Transplants
BACKGROUND: Mesenchymal stem cells (MSCs) are multipotent cells residing in the connective tissue of many organs and holding great potential for tissue repair. In culture, human MSCs (hMSCs) are capable of extensive proliferation without showing chromosomal aberrations. Large numbers of hMSCs can thus be acquired from small samples of easily obtainable tissues like fat and bone marrow. MSCs can contribute to regeneration indirectly by secretion of cytokines or directly by differentiation into specialized cell types. The latter mechanism requires their long-term acceptance by the recipient. Although MSCs do not elicit immune responses in vitro, animal studies have revealed that allogeneic and xenogeneic MSCs are rejected. METHODOLOGY/PRINCIPAL FINDINGS: We aim to overcome MSC immune rejection through permanent down-regulation of major histocompatibility complex (MHC) class I proteins on the surface of these MHC class II-negative cells through the use of viral immune evasion proteins. Transduction of hMSCs with a retroviral vector encoding the human cytomegalovirus US11 protein resulted in strong inhibition of MHC class I surface expression. When transplanted into immunocompetent mice, persistence of the US11-expressing and HLA-ABC-negative hMSCs at levels resembling those found in immunodeficient (i.e., NOD/SCID) mice could be attained provided that recipients' natural killer (NK) cells were depleted prior to cell transplantation. CONCLUSIONS/SIGNIFICANCE: Our findings demonstrate the potential utility of herpesviral immunoevasins to prevent rejection of xenogeneic MSCs. The observation that down-regulation of MHC class I surface expression renders hMSCs vulnerable to NK cell recognition and cytolysis implies that multiple viral immune evasion proteins are likely required to make hMSCs non-immunogenic and thereby universally transplantable
A Multilevel Monte Carlo Asymptotic-Preserving Particle Method for Kinetic Equations in the Diffusion Limit
We propose a multilevel Monte Carlo method for a particle-based
asymptotic-preserving scheme for kinetic equations. Kinetic equations model
transport and collision of particles in a position-velocity phase-space. With a
diffusive scaling, the kinetic equation converges to an advection-diffusion
equation in the limit of zero mean free path. Classical particle-based
techniques suffer from a strict time-step restriction to maintain stability in
this limit. Asymptotic-preserving schemes provide a solution to this time step
restriction, but introduce a first-order error in the time step size. We
demonstrate how the multilevel Monte Carlo method can be used as a bias
reduction technique to perform accurate simulations in the diffusive regime,
while leveraging the reduced simulation cost given by the asymptotic-preserving
scheme. We describe how to achieve the necessary correlation between simulation
paths at different levels and demonstrate the potential of the approach via
numerical experiments.Comment: 20 pages, 7 figures, published in Monte Carlo and Quasi-Monte Carlo
Methods 2018, correction of minor typographical error
Signal Peptide-Dependent Inhibition of MHC Class I Heavy Chain Translation by Rhesus Cytomegalovirus
The US2-11 region of human and rhesus cytomegalovirus encodes a conserved family of glycoproteins that inhibit MHC-I assembly with viral peptides, thus preventing cytotoxic T cell recognition. Since HCMV lacking US2-11 is no longer able to block assembly and transport of MHC-I, we examined whether this is also observed for RhCMV lacking the corresponding region. Unexpectedly, recombinant RhCMV lacking US2-11 was still able to inhibit MHC-I expression in infected fibroblasts, suggesting the presence of an additional MHC-I evasion mechanism. Progressive deletion analysis of RhCMV-specific genomic regions revealed that MHC-I expression is fully restored upon additional deletion of rh178. The protein encoded by this RhCMV-specific open reading frame is anchored in the endoplasmic reticulum membrane. In the presence of rh178, RhCMV prevented MHC-I heavy chain (HC) expression, but did not inhibit mRNA transcription or association of HC mRNA with translating ribosomes. Proteasome inhibitors stabilized a HC degradation intermediate in the absence of rh178, but not in its presence, suggesting that rh178 prevents completion of HC translation. This interference was signal sequence-dependent since replacing the signal peptide with that of CD4 or murine HC rendered human HCs resistant to rh178. We have identified an inhibitor of antigen presentation encoded by rhesus cytomegalovirus unique in both its lack of homology to any other known protein and in its mechanism of action. By preventing signal sequence-dependent HC translocation, rh178 acts prior to US2, US3 and US11 which attack MHC-I proteins after protein synthesis is completed. Rh178 is the first viral protein known to interfere at this step of the MHC-I pathway, thus taking advantage of the conserved nature of HC leader peptides, and represents a new mechanism of translational interference
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