Localization in underground tunnels

Positioning technologies are becoming ubiquitous and are being used more and more frequently for supporting a large variety of applica- tions. For outdoor applications, global navigation satellite systems (GNSSs), such as the global positioning system (GPS), are the most common and popular choice because of their wide coverage. GPS is also augmented with network-based systems that exploit existing wireless and mobile networks for providing positioning functions where GPS is not available or to save energy in battery-powered devices. Indoors, GNSSs are not a viable solution, but many applications require very accurate, fast, and exible positioning, tracking, and navigation functions. These and other requirements have stim- ulated research activities, in both industry and academia, where a variety of fundamental principles, techniques, and sensors are being integrated to provide positioning functions to many applications. The large majority of positioning technologies is for indoor environments, and most of the existing commercial products have been developed for use in of ce buildings, airports, shopping malls, factory plants, and similar spaces. There are, however, other spaces where positioning, tracking, and navigation systems play a central role in safety and in rescue operations, as well as in supporting speci c activities or for scienti c research activities in other elds. Among those spaces are underground tunnels, mines, and even underwater wells and caves. This chapter describes the research efforts over the past few years that have been put into the development of positioning systems for underground tun- nels, with particular emphasis in the case of the Large Hadron Collider (LHC) at CERN (the European Organization for Nuclear Research), where localiza- tion aims at enabling more automatic and unmanned radiation surveys. Examples of positioning and localization systems that have been devel- oped in the past few years for underground facilities are presented in the fol- lowing section, together with a brief characterization of those spaces’ special conditions and the requirements of some of the most common applications. Section 5.2 provides a short overview of some of the most representative research efforts that are currently being carried out by many research teams around the world. In addition, some of the fundamental principles and tech- niques are identi ed, such as the use of leaky coaxial cables, as used at the LHC. In Section 5.3, we introduce the speci c environment of the LHC and de ne the positioning requirements for the envisaged application. This is followed by a detailed description of our approach and the results that have been achieved so far. Some last comments and remarks are presented in a nal section.

Spectrum-based energy leak localization

Dissertação de Mestrado em Engenharia Informática

Anderson localization of light in disordered superlattices containing graphene layers

We theoretically investigate light propagation and Anderson localization in one-dimensional disordered superlattices composed of dielectric stacks with graphene sheets in between. Disorder is introduced either on graphene material parameters ({\it e.g.} Fermi energy) or on the widths of the dielectric stacks. We derive an analytic expression for the localization length $\xi$, and compare it to numerical simulations using transfer matrix technique; a very good agreement is found. We demonstrate that the presence of graphene may strongly attenuate the anomalously delocalised Breswter modes, and is at the origin of a periodic dependence of $\xi$ on frequency, in contrast to the usual asymptotic decay, $\xi \propto \omega^{-2}$. By unveiling the effects of graphene on Anderson localization of light, we pave the way for new applications of graphene-based, disordered photonic devices in the THz spectral range.

A Gß protein and the TupA Co-Regulator bind to protein kinase A Tpk2 to act as antagonistic molecular switches of fungal morphological changes

A Gß protein and the TupA Co-Regulator Bind to Protein Kinase A Tpk2 to Act as Antagonistic Molecular Switches of Fungal Morphological Changes

Localization of MCT2 at peroxisomes is associated with malignant transformation in prostate cancer

Previous studies on monocarboxylate transporters expression in prostate cancer (PCa) have shown that monocarboxylate transporter 2 (MCT2) was clearly overexpressed in prostate malignant glands, pointing it out as a putative biomarker for PCa. However, its localization and possible role in PCa cells remained unclear. In this study, we demonstrate that MCT2 localizes mainly at peroxisomes in PCa cells and is able to take advantage of the peroxisomal transport machinery by interacting with Pex19. We have also shown an increase in MCT2 expression from non-malignant to malignant cells that was directly correlated with its peroxisomal localization. Upon analysis of the expression of several peroxisomal ß-oxidation proteins in PIN lesions and PCa cells from a large variety of human prostate samples, we suggest that MCT2 presence at peroxisomes is related to an increase in ß -oxidation levels which may be crucial for malignant transformation. Our results present novel evidence that may not only contribute to the study of PCa development mechanisms but also pinpoint novel targets for cancer therapy.

Synthesis, antiangiogenesis evaluation and molecular docking studies of 1-Aryl-3-[(thieno[3,2-b]pyridin-7-ylthio)phenyl]ureas: Discovery of a new substitution pattern for type II VEGFR-2 Tyr kinase inhibitors

The synthesis and biological evaluation of novel 1-aryl-3-[2-, 3- or 4-(thieno[3,2-b]pyridin-7-ylthio)phenyl]ureas 3, 4 and 5 as VEGFR-2 tyrosine kinase inhibitors, are reported. The 1-aryl-3-[3-(thieno[3,2-b]pyridin-7-ylthio)phenyl]ureas 4a-4h, with the arylurea in the meta position to the thioether, showed the lowest IC50 values in enzymatic assays (10-206 nM), the most potent compounds 4d-4h (IC50 10-28 nM) bearing hydrophobic groups (Me, F, CF3 and Cl) in the terminal phenyl ring. A convincing rationalization was achieved for the highest potent compounds 4 as type II VEGFR-2 inhibitors, based on the simultaneous presence of: (1) the thioether linker and (2) the arylurea moiety in the meta position. For compounds 4, significant inhibition of Human Umbilical Vein Endothelial Cells (HUVECs) proliferation (BrdU assay), migration (wound-healing assay) and tube formation were observed at low concentrations. These compounds have also shown to increase apoptosis using the TUNEL assay. Immunostaining for total and phosphorylated (active) VEGFR-2 was performed by Western blotting. The phosphorylation of the receptor was significantly inhibited at 1.0 and 2.5 microM for the most promising compounds. Altogether, these findings point to an antiangiogenic effect in HUVECs.

All over the place localization system

The MAP-i Doctoral Programme in Informatics, of the Universities of Minho, Aveiro and Porto

The role of the mammalian DNA end-processing enzyme polynucleotide kinase 3'-phosphatase in spinocerebellar ataxia Type 3 pathogenesis

DNA strand-breaks (SBs) with non-ligatable ends are generated by ionizing radiation, oxidative stress, various chemotherapeutic agents, and also as base excision repair (BER) intermediates. Several neurological diseases have already been identified as being due to a deficiency in DNA end-processing activities. Two common dirty ends, 3'-P and 5'-OH, are processed by mammalian polynucleotide kinase 3'-phosphatase (PNKP), a bifunctional enzyme with 3'-phosphatase and 5'-kinase activities. We have made the unexpected observation that PNKP stably associates with Ataxin-3 (ATXN3), a polyglutamine repeat-containing protein mutated in spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph Disease (MJD). This disease is one of the most common dominantly inherited ataxias worldwide; the defect in SCA3 is due to CAG repeat expansion (from the normal 14-41 to 55-82 repeats) in the ATXN3 coding region. However, how the expanded form gains its toxic function is still not clearly understood. Here we report that purified wild-type (WT) ATXN3 stimulates, and by contrast the mutant form specifically inhibits, PNKP's 3' phosphatase activity in vitro. ATXN3-deficient cells also show decreased PNKP activity. Furthermore, transgenic mice conditionally expressing the pathological form of human ATXN3 also showed decreased 3'-phosphatase activity of PNKP, mostly in the deep cerebellar nuclei, one of the most affected regions in MJD patients' brain. Finally, long amplicon quantitative PCR analysis of human MJD patients' brain samples showed a significant accumulation of DNA strand breaks. Our results thus indicate that the accumulation of DNA strand breaks due to functional deficiency of PNKP is etiologically linked to the pathogenesis of SCA3/MJD.