Manifolds with non-stable fundamental groups at infinity, II

In this paper we continue an earlier study of ends non-compact manifolds. The over-arching goal is to investigate and obtain generalizations of Siebenmann's famous collaring theorem that may be applied to manifolds having non-stable fundamental group systems at infinity. In this paper we show that, for manifolds with compact boundary, the condition of inward tameness has substatial implications for the algebraic topology at infinity. In particular, every inward tame manifold with compact boundary has stable homology (in all dimensions) and semistable fundamental group at each of its ends. In contrast, we also construct examples of this sort which fail to have perfectly semistable fundamental group at infinity. In doing so, we exhibit the first known examples of open manifolds that are inward tame and have vanishing Wall finiteness obstruction at infinity, but are not pseudo-collarable.Comment: Published by Geometry and Topology at http://www.maths.warwick.ac.uk/gt/GTVol7/paper7.abs.htm

Spherical alterations of handles: embedding the manifold plus construction

A key tool in our earlier work on ends of manifolds high-dimensional manifolds was an ability to embed cobordisms provided by the Quillen Plus Construction into those ends. Here we develop a `spherical modification' trick which provides a constructive approach to obtaining such embeddings. More importantly, this approach allows for more general embedding results. In this paper we develop generalizations of the plus construction and show how the corresponding cobordisms can be embedded in manifolds satisfying appropriate fundamental group properties. Results obtained here play an important role in our ongoing study of noncompact manifolds.Comment: This final version will appear in Algebraic & Geometric Topology. Small corrections, including a fix to the statement of Theorem 5.3. 22 pages, 4 figure

Vies moyennes de quelques niveaux du noyau 19F

Les énergies d'excitations et les vies moyennes de 9 niveaux du 19 F d'énergie inférieure à 6 MeV ont été déterminées à l'aide de la réaction 18O(d, nγ) 19F. De ces vies moyennes, mesurées à partir de la méthode du déplacement Doppler, ont été déduites certaines largeurs de transition M1 qui sont comparées aux prédictions de modèles en couches

Byzantine Gathering in Networks

This paper investigates an open problem introduced in [14]. Two or more mobile agents start from different nodes of a network and have to accomplish the task of gathering which consists in getting all together at the same node at the same time. An adversary chooses the initial nodes of the agents and assigns a different positive integer (called label) to each of them. Initially, each agent knows its label but does not know the labels of the other agents or their positions relative to its own. Agents move in synchronous rounds and can communicate with each other only when located at the same node. Up to f of the agents are Byzantine. A Byzantine agent can choose an arbitrary port when it moves, can convey arbitrary information to other agents and can change its label in every round, in particular by forging the label of another agent or by creating a completely new one. What is the minimum number M of good agents that guarantees deterministic gathering of all of them, with termination? We provide exact answers to this open problem by considering the case when the agents initially know the size of the network and the case when they do not. In the former case, we prove M=f+1 while in the latter, we prove M=f+2. More precisely, for networks of known size, we design a deterministic algorithm gathering all good agents in any network provided that the number of good agents is at least f+1. For networks of unknown size, we also design a deterministic algorithm ensuring the gathering of all good agents in any network but provided that the number of good agents is at least f+2. Both of our algorithms are optimal in terms of required number of good agents, as each of them perfectly matches the respective lower bound on M shown in [14], which is of f+1 when the size of the network is known and of f+2 when it is unknown

Anonymous Graph Exploration with Binoculars

International audienceWe investigate the exploration of networks by a mobile agent. It is long known that, without global information about the graph, it is not possible to make the agent halts after the exploration except if the graph is a tree. We therefore endow the agent with binoculars, a sensing device that can show the local structure of the environment at a constant distance of the agent current location.We show that, with binoculars, it is possible to explore and halt in a large class of non-tree networks. We give a complete characterization of the class of networks that can be explored using binoculars using standard notions of discrete topology. This class is much larger than the class of trees: it contains in particular chordal graphs, plane triangulations and triangulations of the projective plane. Our characterization is constructive, we present an Exploration algorithm that is universal; this algorithm explores any network explorable with binoculars, and never halts in non-explorable networks

Estrogen aggravates inflammation in Pseudomonas aeruginosa pneumonia in cystic fibrosis mice

<p>Abstract</p> <p>Background</p> <p>Among patients with cystic fibrosis (CF), females have worse pulmonary function and survival than males, primarily due to chronic lung inflammation and infection with <it>Pseudomonas aeruginosa </it>(<it>P. aeruginosa</it>). A role for gender hormones in the causation of the CF "gender gap" has been proposed. The female gender hormone 17β-estradiol (E2) plays a complex immunomodulatory role in humans and in animal models of disease, suppressing inflammation in some situations while enhancing it in others. Helper T-cells were long thought to belong exclusively to either T helper type 1 (Th1) or type 2 (Th2) lineages. However, a distinct lineage named Th17 is now recognized that is induced by interleukin (IL)-23 to produce IL-17 and other pro-inflammatory Th17 effector molecules. Recent evidence suggests a central role for the IL-23/IL-17 pathway in the pathogenesis of CF lung inflammation. We used a mouse model to test the hypothesis that E2 aggravates the CF lung inflammation that occurs in response to airway infection with <it>P. aeruginosa </it>by a Th17-mediated mechanism.</p> <p>Results</p> <p>Exogenous E2 caused adult male CF mice with pneumonia due to a mucoid CF clinical isolate, the <it>P. aeruginosa </it>strain PA508 (PA508), to develop more severe manifestations of inflammation in both lung tissue and in bronchial alveolar lavage (BAL) fluid, with increased total white blood cell counts and differential and absolute cell counts of polymorphonuclear leukocytes (neutrophils). Inflammatory infiltrates and mucin production were increased on histology. Increased lung tissue mRNA levels for IL-23 and IL-17 were accompanied by elevated protein levels of Th17-associated pro-inflammatory mediators in BAL fluid. The burden of PA508 bacteria was increased in lung tissue homogenate and in BAL fluid, and there was a virtual elimination in lung tissue of mRNA for lactoferrin, an antimicrobial peptide active against <it>P. aeruginosa </it>in vitro.</p> <p>Conclusions</p> <p>Our data show that E2 increases the severity of PA508 pneumonia in adult CF male mice, and suggest two potential mechanisms: enhancement of Th17-regulated inflammation and suppression of innate antibacterial defences. Although this animal model does not recapitulate all aspects of human CF lung disease, our present findings argue for further investigation of the effects of E2 on inflammation and infection with <it>P. aeruginosa </it>in the CF lung.</p