Low noise single aperture multimode monopulse antenna feed system Patent

Development and characteristics of low-noise multimode monopulse antenna feed system for use with microwave communication equipmen

Mammalian telomeres and their partnership with lamins

Chromosome ends are complex structures, which require a panel of factors for their elongation, replication, and protection. We describe here the mechanics of mammalian telomeres, dynamics and maintainance in relation to lamins. Multiple biochemical connections, including association of telomeres to the nuclear envelope and matrix, of telomeric proteins to lamins, and of lamin-associated proteins to chromosome ends, underline the interplay between lamins and telomeres. Paths toward senescence, such as defective telomere replication, altered heterochromatin organization, and impaired DNA repair, are common to lamins' and telomeres' dysfunction. The convergence of phenotypes can be interpreted through a model of dynamic, lamin-controlled functional platforms dedicated to the function of telomeres as fragile sites. The features of telomeropathies and laminopathies, and of animal models underline further overlapping aspects, including the alteration of stem cell compartments. We expect that future studies of basic biology and on aging will benefit from the analysis of this telomere-lamina interplay

Emerging roles of telomeric chromatin alterations in cancer

Telomeres, the nucleoprotein structures that cap the ends of eukaryotic chromosomes, play important and multiple roles in tumorigenesis. Functional telomeres need the establishment of a protective chromatin structure based on the interplay between the specific complex named shelterin and a tight nucleosomal organization. Telomere shortening in duplicating somatic cells leads eventually to the destabilization of the telomere capping structure and to the activation of a DNA damage response (DDR) signaling. The final outcome of this process is cell replicative senescence, which constitute a protective barrier against unlimited proliferation. Cells that can bypass senescence checkpoint continue to divide until a second replicative checkpoint, crisis, characterized by chromosome fusions and rearrangements leading to massive cell death by apoptosis. During crisis telomere dysfunctions can either inhibit cell replication or favor tumorigenesis by the accumulation of chromosomal rearrangements and neoplastic mutations. The acquirement of a telomere maintenance mechanism allows fixing the aberrant phenotype, and gives the neoplastic cell unlimited replicative potential, one of the main hallmarks of cancer. Despite the crucial role that telomeres play in cancer development, little is known about the epigenetic alterations of telomeric chromatin that affect telomere protection and are associated with tumorigenesis. Here we discuss the current knowledge on the role of telomeric chromatin in neoplastic transformation, with a particular focus on H3.3 mutations in alternative lengthening of telomeres (ALT) cancers and sirtuin deacetylases dysfunctions

Histone H3 lysine 56 acetylation by Rtt109 is crucial for chromosome positioning

Peer reviewedPublisher PD

Pair Approximation Models for Disease Spread

We consider a Susceptible-Infective-Recovered (SIR) model, where the mechanism for the renewal of susceptibles is demographic, on a ring with next nearest neighbour interactions, and a family of correlated pair approximations (CPA), parametrized by a measure of the relative contributions of loops and open triplets of the sites involved in the infection process. We have found that the phase diagram of the CPA, at fixed coordination number, changes qualitatively as the relative weight of the loops increases, from the phase diagram of the uncorrelated pair approximation to phase diagrams typical of one-dimensional systems. In addition, we have performed computer simulations of the same model and shown that while the CPA with a constant correlation parameter cannot describe the global behaviour of the model, a reasonable description of the endemic equilibria as well as of the phase diagram may be obtained by allowing the parameter to depend on the demographic rate.Comment: 6 pages, 3 figures, LaTeX2e+SVJour+AmSLaTeX, NEXTSigmaPhi 2005; metadata title corrected wrt paper titl

Nonequilibrium adsorption of 2AnB patchy colloids on substrates

We study the irreversible adsorption of spherical $2AnB$ patchy colloids (with two $A$-patches on the poles and $n$ $B$-patches along the equator) on a substrate. In particular, we consider dissimilar $AA$, $AB$, and $BB$ binding probabilities. We characterize the patch-colloid network and its dependence on $n$ and on the binding probabilities. Two growth regimes are identified with different density profiles and we calculate a growth mode diagram as a function of the colloid parameters. We also find that, close to the substrate, the density of the network, which depends on the colloid parameters, is characterized by a depletion zone