Digital homotopy with obstacles

AbstractIn (Ayala et al. (Discrete Appl. Math. 125 (1) (2003) 3) it was introduced the notion of a digital fundamental group π1d(O/S;σ) for a set of pixels O in relation to another set S which plays the role of an “obstacle”. This notion intends to be a generalization of the digital fundamental groups of both digital objects and their complements in a digital space. However, the suitability of this group was only checked for digital objects in that paper. As a sequel, we extend here the results in Ayala et al. (2003) for complements of objects. More precisely, we prove that for arbitrary digital spaces the group π1d(O/S;σ) maps onto the usual fundamental group of the difference of continuous analogues |AO∪S|−|AS|. Moreover, this epimorphism turns to be an isomorphism for a large class of digital spaces including most of the examples in digital topology

Weak lighting functions and strong 26-surfaces

AbstractThe goal of this paper is to introduce the notion of weak lighting function in order to replicate the “continuous perception” associated with strong 26-surfaces. As a consequence, the continuous analogue defined ad hoc by Malgouyres and Bertrand only for these surfaces is extended for arbitrary objects, and the local characterization of finite strong 26-surfaces given in (Malgouyres and Bertrand, Int. J. Pattern Recognition Art. Intell. 13(4) (1999) 465–484) is generalized to possibly infinite surfaces. Moreover, weak lighting functions also replicate the “continuous perception” associated with (α,β)-surfaces, (α,β)≠(6,6), since they are generalizing the lighting functions previously defined by the authors

Plastic deformation at high temperatures of pure and Mn-doped GaSb

In this work the plastic behavior of GaSb and Mn-doped GaSb at high temperature has been analyzed. Several experiments at different constant load and temperatures around 500 °C were carried out. The parameters used in the Haasen model have been obtained experimentally and compared with the ones obtained from simulations

DNA polymerase λ, a novel DNA repair enzyme in human cells

DNA polymerase lambda (pol λ) is a novel family X DNA polymerase that has been suggested to play a role in meiotic recombination and DNA repair. The recent demonstration of an intrinsic 5′-deoxyribose-5-phosphate lyase activity in pol λ supports a function of this enzyme in base excision repair. However, the biochemical properties of the polymerization activity of this enzyme are still largely unknown. We have cloned and purified human pol λ to homogeneity in a soluble and active form, and we present here a biochemical description of its polymerization features. In support of a role in DNA repair, pol λ inserts nucleotides in a DNA template-dependent manner and is processive in small gaps containing a 5′-phosphate group. These properties, together with its nucleotide insertion fidelity parameters and lack of proofreading activity, indicate that pol λ is a novel β-like DNA polymerase. However, the high affinity of pol λ for dNTPs (37-fold over pol β) is consistent with its possible involvement in DNA transactions occurring under low cellular levels of dNTPs. This suggests that, despite their similarities, pol β and pol λ have nonredundant in vivo functions.This work was supported by Ministerio de Ciencia y Tecnologı´a Grant BMC2000-1138, Comunidad Auto´noma de Madrid Grant 08.5/0063/2000 (to L. B.) and by an institutional grant from Fundacio´n Ramo´n Areces

DNA polymerase lambda (Pol λ), a novel eukaryotic DNA polymerase with a potential role in meiosis

A new gene (POLL) encoding a novel DNA polymerase (Pol λ) has been identified at mouse chromosome 19. Murine Pol λ, consisting of 573 amino acid residues, has a 32 % identity to Pol β, involved in nuclear DNA repair in eukaryotic cells. It is interesting that Pol λ contains all the critical residues involved in DNA binding, nucleotide binding and selection, and catalysis of DNA polymerization, that are conserved in Pol β and other DNA polymerases belonging to family X. Murine Pol λ, overproduced in Escherichia coli, displayed intrinsic DNA polymerase activity when assessed by in situ gel analysis. Pol λ also conserves the critical residues of Pol β required for its intrinsic deoxyribose phosphate lyase (dRPase) activity. The first 230 amino acid residues of Pol λ, that have no counterpart in Pol β, contain a BRCT domain, present in a variety of cell-cycle check-point control proteins responsive to DNA damage and proteins involved in DNA repair. Northern blotting, in situ hybridization analysis and immunostaining showed high levels of Pol λ specifically expressed in testis, being developmentally regulated and mainly associated to pachytene spermatocytes. These first evidences, although indirect, suggest a potential role of Pol λ in DNA repair synthesis associated with meiosis.This work has been granted by DGES (PB97-1192) and CAM (08.1/0044/98) to LB; CAM(08.1/0044.2/98) to AB; DGICYT (PB 95-0119), EC PL96-0183 and CAM (07/0022) to JM, and by an institutional grant from Fundación Ramón Areces

Listeria pathogenesis and molecular virulence determinants

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

Model for crystallization kinetics: Deviations from Kolmogorov-Johnson-Mehl-Avrami kinetics

We propose a simple and versatile model to understand the deviations from the well-known Kolmogorov-Johnson-Mehl-Avrami kinetics theory found in metal recrystallization and amorphous semiconductor crystallization. We analyze the kinetics of the transformation and the grain-size distribution of the product material, finding a good overall agreement between our model and available experimental data. The information so obtained could help to relate the mentioned experimental deviations due to preexisting anisotropy along some regions, to a certain degree of crystallinity of the amorphous phases during deposition, or more generally, to impurities or roughness of the substrate