Another algorithm for reducing bandwidth and profile of a sparse matrix

The paper describes a new bandwidth reduction method for sparse matrices which promises to be both fast and effective in comparison with known methods. The algorithm operates on the undirected graph corresponding to the incidence matrix induced by the original sparse matrix, and separates into three distinct phases: (1) determination of a spanning tree of maximum length, (2) modification of the spanning tree into a free level structure of small width, (3) level-by-level numbering of the level structure. The final numbering produced corresponds to a renumbering of the rows and columns of a sparse matrix so as to concentrate non-zero elements of the matrix in a band about the main diagonal

The age of the Galactic thin disk from Th/Eu nucleocosmochronology II. Chronological analysis

The purpose of this work is to resume investigation of Galactic thin disk dating using nucleocosmochronology with Th/Eu stellar abundance ratios, a theme absent from the literature since 1990. [Th/Eu] abundance ratios for a sample of 20 disk dwarfs/subgiants of F5 to G8 spectral type with -0.8 <= [Fe/H] <= +0.3, determined in the first paper of this series, were adopted for this analysis. We developed a Galactic chemical evolution model that includes the effect of refuses, which are composed of stellar remnants (white dwarfs, neutron stars and black holes) and low-mass stellar formation residues (terrestrial planets, comets, etc.), contributing to a better fit to observational constraints. Two Galactic disk ages were estimated, by comparing literature data on Th/Eu production and solar abundance ratios to the model ((8.7 +5.8-4.1) Gyr), and by comparing [Th/Eu] vs. [Fe/H] curves from the model to our stellar abundance ratio data ((8.2 +/- 1.9) Gyr), yielding the final, average value (8.3 +/- 1.8) Gyr. This is the first Galactic disk age determined via Th/Eu nucleocosmochronology, and corroborates the most recent white dwarf ages determined via cooling sequence calculations, which indicate a low age (<~ 10 Gyr) for the disk.Comment: 9 pages, 7 Postscript figures, accepted for publication in Astronomy & Astrophysics, final versio

30 anos do curso de graduação em astronomia da UFRJ: uma análise crítica

Neste trabalho, fazemos um histórico dos 30 anos do Curso de Graduação em Astronomia da UFRJ. Seu padrão vem evoluindo, passando a constar, a partir de 1993, da lista de instituições de ensino de Astronomia no Brasil, junto à International Astronomical Union (IAU). Mostramos a evolução da qualificação docente e de ex-alunos. Analisamos a evolução do número de alunos formados e ingressos, e a influência da reforma curricular de 1984 sobre a produção discente: Projetos de Final de Curso e trabalhos apresentados nas Jornadas de Iniciação Científica da UFRJ e nas Reuniões da Sociedade Astronômica Brasileira (SAB). Verificamos que houve mudança no perfil do aluno formado, na direção do maior interesse pelas áreas da Astrofísica. Fazemos um esboço dos objetivos de nova reforma curricular

Long-term cerebral thromboembolic complications of transapical endocardial resynchronization therapy

Purpose: Cardiac resynchronization therapy (CRT) is an established therapeutic option in selected heart failure patients (pts). However, the transvenous left ventricular (LV) lead implantation remains ineffectual in a considerable number of pts. Transapical LV (TALV) lead implantation is an alternative minimally invasive, surgical, endocardial implantation technique. The aim of the present prospective study is to determine the long-term outcome, including the cerebral thromboembolic complications, of pts

Fibroblast growth factor receptor 5 (FGFR5) is a co-receptor for FGFR1 that is up-regulated in beta-cells by cytokine-induced inflammation

Fibroblast growth factor receptor-1 (FGFR1) activity at the plasma membrane is tightly controlled by the availability of co-receptors and competing receptor isoforms. We have previously shown that FGFR1 activity in pancreatic beta-cells modulates a wide range of processes, including lipid metabolism, insulin processing, and cell survival. More recently, we have revealed that co-expression of FGFR5, a receptor isoform that lacks a tyrosine-kinase domain, influences FGFR1 responses. We therefore hypothesized that FGFR5 is a co-receptor to FGFR1 that modulates responses to ligands by forming a receptor heterocomplex with FGFR1. We first show here increased FGFR5 expression in the pancreatic islets of nonobese diabetic (NOD) mice and also in mouse and human islets treated with proinflammatory cytokines. Using siRNA knockdown, we further report that FGFR5 and FGFR1 expression improves beta-cell survival. Co-immunoprecipitation and quantitative live-cell imaging to measure the molecular interaction between FGFR5 and FGFR1 revealed that FGFR5 forms a mixture of ligand-independent homodimers (25%) and homotrimers (75%) at the plasma membrane. Interestingly, co-expressed FGFR5 and FGFR1 formed heterocomplexes with a 2:1 ratio and subsequently responded to FGF2 by forming FGFR5/FGFR1 signaling complexes with a 4:2 ratio. Taken together, our findings identify FGFR5 as a co-receptor that is up-regulated by inflammation and promotes FGFR1-induced survival, insights that reveal a potential target for intervention during beta-cell pathogenesis

Long-term cerebral thromboembolic complications of transapical endocardial resynchronization therapy

Purpose: Cardiac resynchronization therapy (CRT) is an established therapeutic option in selected heart failure patients (pts). However, the transvenous left ventricular (LV) lead implantation remains ineffectual in a considerable number of pts. Transapical LV (TALV) lead implantation is an alternative minimally invasive, surgical, endocardial implantation technique. The aim of the present prospective study is to determine the long-term outcome, including the cerebral thromboembolic complications, of pts

Susceptibility to fatty acid-induced β-cell dysfunction is enhanced in prediabetic diabetes-prone biobreeding rats: A potential link between β-cell lipotoxicity and islet inflammation

β-Cell lipotoxicity is thought to play an important role in the development of type 2 diabetes. However, no study has examined its role in type 1 diabetes, which could be clinically relevant for slow-onset type 1 diabetes. Reports of enhanced cytokine toxicity in fat-laden islets are consistent with the hypothesis that lipid and cytokine toxicity maybe synergistic. Thus, β-cell lipotoxicity could be enhanced in models of autoimmune diabetes. To determine this, we examined the effects of prolonged free fatty acids elevation on β-cell secretory function in the prediabetic diabetes-prone BioBreeding (dp-BB) rat, its diabetes-resistant BioBreeding (dr-BB) control, and normal Wistar-Furth (WF) rats. Rats received a 48-h iv infusion of saline or Intralipid plus heparin (IH) (to elevate free fatty acid levels ∼2-fold) followed by hyperglycemic clamp or islet secretion studies ex vivo. IH significantly decreased β-cell function, assessed both by the disposition index (insulin secretion corrected for IH-induced insulin resistance) and in isolated islets, in dp-BB, but not in dr-BB or WF, rats, and the effect of IH was inhibited by the antioxidant N-acetylcysteine. Furthermore, IH significantly increased islet cytokine mRNA and plasma cytokine levels (monocyte chemoattractant protein-1 and IL-10) in dp-BB, but not in dr-BB or WF, rats. All dp-BB rats had mononuclear infiltration of islets, which was absent in dr-BB and WF rats. In conclusion, the presence of insulitis was permissive for IH-induced β-cell dysfunction in the BB rat, which suggests a link between β-cell lipotoxicity and islet inflammation. Copyright © 2013 by The Endocrine Society

Exploring hypotheses of the actions of TGF-beta 1 in epidermal wound healing using a 3D computational multiscale model of the human epidermis

In vivo and in vitro studies give a paradoxical picture of the actions of the key regulatory factor TGF-beta 1 in epidermal wound healing with it stimulating migration of keratinocytes but also inhibiting their proliferation. To try to reconcile these into an easily visualized 3D model of wound healing amenable for experimentation by cell biologists, a multiscale model of the formation of a 3D skin epithelium was established with TGF-beta 1 literature-derived rule sets and equations embedded within it. At the cellular level, an agent-based bottom-up model that focuses on individual interacting units ( keratinocytes) was used. This was based on literature-derived rules governing keratinocyte behavior and keratinocyte/ECM interactions. The selection of these rule sets is described in detail in this paper. The agent-based model was then linked with a subcellular model of TGF-beta 1 production and its action on keratinocytes simulated with a complex pathway simulator. This multiscale model can be run at a cellular level only or at a combined cellular/subcellular level. It was then initially challenged ( by wounding) to investigate the behavior of keratinocytes in wound healing at the cellular level. To investigate the possible actions of TGF-beta 1, several hypotheses were then explored by deliberately manipulating some of these rule sets at subcellular levels. This exercise readily eliminated some hypotheses and identified a sequence of spatial-temporal actions of TGF-beta 1 for normal successful wound healing in an easy-to-follow 3D model. We suggest this multiscale model offers a valuable, easy-to-visualize aid to our understanding of the actions of this key regulator in wound healing, and provides a model that can now be used to explore pathologies of wound healing

The age of the Galactic thin disk from Th/Eu nucleocosmochronology III. Extended sample

The first determination of the age of the Galactic thin disk from Th/Eu nucleocosmochronology was accomplished by us in Papers I and II. The present work aimed at reducing the age uncertainty by expanding the stellar sample with the inclusion of seven new objects - an increase by 37%. A set of [Th/Eu] abundance ratios was determined from spectral synthesis and merged with the results from Paper I. Abundances for the new, extended sample were analyzed with the aid of a Galactic disk chemical evolution (GDCE) model developed by us is Paper II. The result was averaged with an estimate obtained in Paper II from a conjunction of literature data and our GDCE model, providing our final, adopted disk age T_G = (8.8 +/- 1.7) Gyr with a reduction of 0.1 Gyr (6%) in the uncertainty. This value is compatible with the most up-to-date white dwarf age determinations (<~ 10 Gyr). Considering that the halo is currently presumed to be (13.5 +/- 0.7) Gyr old, our result prompts groups developing Galactic formation models to include an hiatus of (4.7 +/- 1.8) Gyr between the formation of halo and disk.Comment: 7 pages, 5 Postscript figures, accepted for publication in Astronomy & Astrophysic