University of Nice Sophia Antipolis

About: University of Nice Sophia Antipolis is a education organization based out in Nice, France. It is known for research contribution in the topics: Population & Stars. The organization has 10291 authors who have published 19964 publications receiving 680762 citations. The organization is also known as: UNS & University of Nice-Sophia Antipolis.

Routing for disruption tolerant networks: taxonomy and design

Abstract: Communication networks, whether they are wired or wireless, have traditionally been assumed to be connected at least most of the time. However, emerging applications such as emergency response, special operations, smart environments, VANETs, etc. coupled with node heterogeneity and volatile links (e.g. due to wireless propagation phenomena and node mobility) will likely change the typical conditions under which networks operate. In fact, in such scenarios, networks may be mostly disconnected, i.e., most of the time, end-to-end paths connecting every node pair do not exist. To cope with frequent, long-lived disconnections, opportunistic routing techniques have been proposed in which, at every hop, a node decides whether it should forward or store-and-carry a message. Despite a growing number of such proposals, there still exists little consensus on the most suitable routing algorithm(s) in this context. One of the reasons is the large diversity of emerging wireless applications and networks exhibiting such "episodic" connectivity. These networks often have very different characteristics and requirements, making it very difficult, if not impossible, to design a routing solution that fits all. In this paper, we first break up existing routing strategies into a small number of common and tunable routing modules (e.g. message replication, coding, etc.), and then show how and when a given routing module should be used, depending on the set of network characteristics exhibited by the wireless application. We further attempt to create a taxonomy for intermittently connected networks. We try to identify generic network characteristics that are relevant to the routing process (e.g., network density, node heterogeneity, mobility patterns) and dissect different "challenged" wireless networks or applications based on these characteristics. Our goal is to identify a set of useful design guidelines that will enable one to choose an appropriate routing protocol for the application or network in hand. Finally, to demonstrate the utility of our approach, we take up some case studies of challenged wireless networks, and validate some of our routing design principles using simulations.

The lung amiloride-sensitive Na+ channel: biophysical properties, pharmacology, ontogenesis, and molecular cloning

Abstract: Water balance in the lung is controlled via active Na+ and Cl- transport. Electrophysiological measurements on lung epithelial cells demonstrated the presence of a Na+ channel that is inhibited by amiloride (K0.5 = 90 nM) and some of its derivatives such as phenamil (K0.5 = 19 nM) and benzamil (K0.5 = 14 nM) but not by ethylisopropylamiloride. An amiloride-sensitive Na+ channel of 4 pS was recorded from outside-out patches excised from the apical membrane. This channel is highly selective for Na+ (PNa+/PK+ > or = to 10). Isolation of a human lung cDNA led to the primary structure of the lung Na+ channel. The corresponding protein is 669 residues long and has two large hydrophobic domains. An amiloride-sensitive Na(+)-selective current apparently identical to the one observed in lung epithelial cells was recorded after expression of the cloned channel in oocytes. The level of the mRNA for the Na+ channel was highly increased from fetal to newborn and adult stages. This observation indicates that the increased Na+ reabsorption that occurs at birth as a necessary event to pass to an air-breathing environment is probably associated with control of transcription of this Na+ channel. The human gene for the lung Na+ channel was mapped on chromosome 12p13.

Eprenetapopt (APR-246) and Azacitidine in TP53-Mutant Myelodysplastic Syndromes.

Abstract: PURPOSEApproximately 20% of patients with TP53-mutant myelodysplastic syndromes (MDS) achieve complete remission (CR) with hypomethylating agents. Eprenetapopt (APR-246) is a novel, first-in-class,...

A high-resolution VLT/FLAMES study of individual stars in the centre of the Fornax dwarf spheroidal galaxy

Abstract: For the first time we show the detailed, late-stage, chemical evolution history of a small nearby dwarf spheroidal galaxy in the Local Group. We present the results of a high-resolution (R ~ 20 000, λ = 5340–5620; 6120–6701) FLAMES/GIRAFFE abundance study at ESO/VLT of 81 photometrically selected, red giant branch stars in the central 25 of the Fornax dwarf spheroidal galaxy. We also carried out a detailed comparison of the effects of recent developments in abundance analysis (e.g., spherical models vs. plane-parallel) and the automation that is required to efficiently deal with such large data sets. We present abundances of α-elements (Mg, Si, Ca, and Ti), iron-peak elements (Fe, Ni, and Cr), and heavy elements (Y, Ba, La, Nd, and Eu). Our sample was randomly selected and is clearly dominated by the younger and more metal-rich component of Fornax, which represents the major fraction of stars in the central region. This means that the majority of our stars are 1−4 Gyr old, and thus represent the end phase of chemical evolution in this system. Our sample of stars has unusually low [α/Fe], [Ni/Fe], and [Na/Fe] compared to the Milky Way stellar populations at the same [Fe/H]. The particularly important role of stellar winds from low-metallicity AGB stars in the creation of s-process elements is clearly seen from the high [Ba/Y]. Furthermore, we present evidence of an s-process origin of Eu.

Constitutively active mutants of MAP kinase kinase (MEK1) induce growth factor-relaxation and oncogenicity when expressed in fibroblasts.

Abstract: The Mitogen Activated Protein Kinase (MAPK) module operates downstream of Ras to convey cell surface signals to the nucleus via the nuclear translocation of p42/p44 MAPKs We have previously established that MAPK activation is obligatory and must persist in the G1 phase to allow resting fibroblasts to exit from G0 (Pages et al, Proc Natl Acad Sci1993, 90, 8319-8323) It remained to be established whether MAPK activation was sufficient to trigger cell proliferation To this aim, we generated and expressed in Chinese hamster lung fibroblasts, constitutively active mutants of hamster MAP kinase kinase (MAPKK) Three mutants: S218D, S222D and S218D/S222D in which we substituted the Raf1/MAPKKK-dependent regulatory phosphorylation sites by aspartic acid residues, displayed increased basal activity when expressed in fibroblasts Two of them, S218D and S218D/S222D which have a basal activity higher than serum-stimulated wild type-MAPKK (respectively 2- and 5-fold), induced activation of p42 MAPK in growth factor-deprived cells Interestingly, only these two mutants led to a growth factor-independent state as judged by early gene transcription (activation of the fos promoter), increased sensitivity to growth factors for reinitiation of DNA synthesis, autonomous cell cycling and rapid tumor formation in nude mice Therefore we conclude that the downstream elements of the growth factor signalling cascade, MAPKK-MAPK, are both necessary and sufficient to promote growth factor signals and autonomous cell cycling in fibroblasts