Current optical technologies for wireless access

The objective of this paper is to describe recent activities and investigations on free-space optics (FSO) or optical wireless and the excellent results achieved within SatNEx an EU-framework 6th programme and IC 0802 a COST action. In a first part, the FSO technology is briefly discussed. In a second part, we mention some performance evaluation criterions for the FSO. In third part, we briefly discuss some optical signal propagation experiments through the atmosphere by mentioning network architectures for FSO and then discuss the recent investigations in airborne and satellite application experiments for FSO. In part four, we mention some recent investigation results on modelling the FSO channel under fog conditions and atmospheric turbulence. Additionally, some recent major performance improvement results obtained by employing hybrid systems and using some specific modulation and coding schemes are presented

Determining the Surface-To-Bulk Progression in the Normal-State Electronic Structure of Sr2RuO4 by Angle-Resolved Photoemission and Density Functional Theory

In search of the potential realization of novel normal-state phases on the surface of Sr2RuO4 - those stemming from either topological bulk properties or the interplay between spin-orbit coupling (SO) and the broken symmetry of the surface - we revisit the electronic structure of the top-most layers by ARPES with improved data quality as well as ab-initio LDA slab calculations. We find that the current model of a single surface layer (\surd2x\surd2)R45{\deg} reconstruction does not explain all detected features. The observed depth-dependent signal degradation, together with the close quantitative agreement with LDA+SO slab calculations based on the LEED-determined surface crystal structure, reveal that (at a minimum) the sub-surface layer also undergoes a similar although weaker reconstruction. This points to a surface-to-bulk progression of the electronic states driven by structural instabilities, with no evidence for Dirac and Rashba-type states or surface magnetism.Comment: 4 pages, 4 figures, 1 table. Further information and PDF available at: http://www.phas.ubc.ca/~quantmat/ARPES/PUBLICATIONS/articles.htm

Structural, spectroscopic and magnetic investigation of the LiFe1-xMnxPO4 (x = 0 - 0.18) solid solution

Different solid state and sol-gel preparations of undoped and Mn substituted cathode material LiFePO4 are investigated. Li3PO4, Fe2P2O7 and Li4P2O7 are detected and quantified by XRPD only in solid state synthesis. In addition, micro-Raman spectra reveal low amount of different iron oxides clusters. EPR data, combined with the results of magnetization measurements, evidence signals from Fe3+ ions in maghemite nanoclusters, and in Li3Fe2(PO4)3. The sol–gel synthesis, showing the lowest amount of impurity phases, seems the most suitable to obtain a promising cathode material. The structural refinement gives new insights into the cation distribution of the Mn doped triphylite structure: (i) about 85% of Mn2+ ions substitutes Fe2+, the remaining 15% being located on the Li site, thus suggesting a structural disorder also confirmed by EPR and micro-Raman results; (ii) Mn ions on the Li site are responsible for the observed slight cell volume expansion

Intranasal “painless” Human Nerve Growth Factors Slows Amyloid Neurodegeneration and Prevents Memory Deficits in App X PS1 Mice

Nerve Growth Factor (NGF) is being considered as a therapeutic candidate for Alzheimer's disease (AD) treatment but the clinical application is hindered by its potent pro-nociceptive activity. Thus, to reduce systemic exposure that would induce pain, in recent clinical studies NGF was administered through an invasive intracerebral gene-therapy approach. Our group demonstrated the feasibility of a non-invasive intranasal delivery of NGF in a mouse model of neurodegeneration. NGF therapeutic window could be further increased if its nociceptive effects could be avoided altogether. In this study we exploit forms of NGF, mutated at residue R100, inspired by the human genetic disease HSAN V (Hereditary Sensory Autonomic Neuropathy Type V), which would allow increasing the dose of NGF without triggering pain. We show that “painless” hNGF displays full neurotrophic and anti-amyloidogenic activities in neuronal cultures, and a reduced nociceptive activity in vivo. When administered intranasally to APPxPS1 mice ( n = 8), hNGFP61S/R100E prevents the progress of neurodegeneration and of behavioral deficits. These results demonstrate the in vivo neuroprotective and anti-amyloidogenic properties of hNGFR100 mutants and provide a rational basis for the development of “painless” hNGF variants as a new generation of therapeutics for neurodegenerative diseases

Graphene promotes axon elongation through local stall of Nerve Growth Factor signaling endosomes

Several works reported increased differentiation of neuronal cells grown on graphene; however, the molecular mechanism driving axon elongation on this material has remained elusive. Here, we study the axonal transport of nerve growth factor (NGF), the neurotrophin supporting development of peripheral neurons, as a key player in the time course of axonal elongation of dorsal root ganglion neurons on graphene. We find that graphene drastically reduces the number of retrogradely transported NGF vesicles in favor of a stalled population in the first two days of culture, in which the boost of axon elongation is observed. This correlates with a mutual charge redistribution, observed via Raman spectroscopy and electrophysiological recordings. Furthermore, ultrastructural analysis indicates a reduced microtubule distance and an elongated axonal topology. Thus, both electrophysiological and structural effects can account for graphene action on neuron development. Unraveling the molecular players underneath this interplay may open new avenues for axon regeneration applications

Selective Hybridization of a Terpyridine-Based Molecule with a Noble Metal

The electronic properties of metal-molecule interfaces can in principle be controlled by molecular design and self-assembly, yielding great potential for future nano- and optoelectronic technologies. However, the coupling between molecular orbitals and the electronic states of the surface can significantly influence molecular states. In particular, molecules designed to create metal-organic self-assembled networks have functional groups that by necessity are designed to interact strongly with metals. Here, we investigate the adsorption interactions of a terpyridine (tpy)-based molecule on a noble metal, Ag(111), by low-temperature scanning tunneling microscopy (STM) and spectroscopy (STS) together with density functional theory (DFT) calculations. By comparing the local density of states (DOS) information gained from STS for the molecule on the bare Ag(111) surface with that of the molecule decoupled from the underlying metal by a NaCl bilayer, we find that tpy-localized orbitals hybridize strongly with the metal substrate. Meanwhile, those related to the phenyl rings that link the two terminal tpy groups are less influenced by the interaction with the surface. The selective hybridization of the tpy groups provides an example of strong, orbital-specific electronic coupling between a functional group and a noble-metal surface, which may alter the intended balance of interactions and resulting electronic behavior of the molecule-metal interface

Neutralization of nerve growth factor impairs proliferation and differentiation of adult neural progenitors in the subventricular zone

Adult neurogenesis is a multistep process regulated by several extrinsic factors, including neurotrophins. Among them, little is known about the role of nerve growth factor (NGF) in the neurogenic niches of the mouse. Here we analyzed the biology of adult neural stem cells (NSCs) from the subventricular zone (SVZ) of AD11 anti-NGF transgenic mice, in which the expression of the recombinant antibody aD11 leads to a chronic postnatal neutralization of endogenous NGF. We showed that AD11-NSCs proliferate 10-fold less, with respect to their control counterparts, and display a significant impairment in their ability to differentiate into \u3b2-tubulin positive neurons. We found a considerable reduction in the number of SVZ progenitors and neuroblasts also in vivo, which correlates with a lower number of newborn neurons in the olfactory bulbs of AD11 mice and a severe deficit in the ability of these mice to discriminate between different odors. We also demonstrated that, in AD11 mice, the morphology of both SVZ-resident and neurosphere-derived astrocytes is significantly altered. We were able to reproduce the AD11 phenotype in vitro, by acutely treating wild type NSCs with the anti-NGF antibody, further demonstrating that both the proliferation and the differentiation defects are due to the NGF deprivation. Consistently, the proliferative impairment of AD11 progenitors, as well as the atrophic morphology of AD11 astrocytes, can be partly rescued in vitro and in vivo by exogenous NGF addition. Altogether, our results demonstrate a causal link between NGF signaling and proper proliferation and differentiation of neural stem cells from the SVZ.Adult neurogenesis is a multistep process regulated by several extrinsic factors, including neurotrophins. Among them, little is known about the role of nerve growth factor (NGF) in the neurogenic niches of the mouse. Here we analyzed the biology of adult neural stem cells (NSCs) from the subventricular zone (SVZ) of AD11 anti-NGF transgenic mice, in which the expression of the recombinant antibody aD11 leads to a chronic postnatal neutralization of endogenous NGF. We showed that AD11-NSCs proliferate 10-fold less, with respect to their control counterparts, and display a significant impairment in their ability to differentiate into \u3b2-tubulin positive neurons. We found a considerable reduction in the number of SVZ progenitors and neuroblasts also in vivo, which correlates with a lower number of newborn neurons in the olfactory bulbs of AD11 mice and a severe deficit in the ability of these mice to discriminate between different odors. We also demonstrated that, in AD11 mice, the morphology of both SVZ-resident and neurosphere-derived astrocytes is significantly altered. We were able to reproduce the AD11 phenotype in vitro, by acutely treating wild type NSCs with the anti-NGF antibody, further demonstrating that both the proliferation and the differentiation defects are due to the NGF deprivation. Consistently, the proliferative impairment of AD11 progenitors, as well as the atrophic morphology of AD11 astrocytes, can be partly rescued in vitro and in vivo by exogenous NGF addition. Altogether, our results demonstrate a causal link between NGF signaling and proper proliferation and differentiation of neural stem cells from the SVZ

NGF steers microglia toward a neuroprotective phenotype

Microglia are the sentinels of the brain but a clear understanding of the factors that modulate their activation in physiological and pathological conditions is still lacking. Here we demonstrate that Nerve Growth Factor (NGF) acts on microglia by steering them toward a neuroprotective and anti-inflammatory phenotype. We show that microglial cells express functional NGF receptors in vitro and ex vivo. Our transcriptomic analysis reveals how, in primary microglia, NGF treatment leads to a modulation of motility, phagocytosis and degradation pathways. At the functional level, NGF induces an increase in membrane dynamics and macropinocytosis and, in vivo, it activates an outward rectifying current that appears to modulate glutamatergic neurotransmission in nearby neurons. Since microglia are supposed to be a major player in Aβ peptide clearance in the brain, we tested the effects of NGF on its phagocytosis. NGF was shown to promote TrkA-mediated engulfment of Aβ by microglia, and to enhance its degradation. Additionally, the proinflammatory activation induced by Aβ treatment is counteracted by the concomitant administration of NGF. Moreover, by acting specifically on microglia, NGF protects neurons from the Aβ-induced loss of dendritic spines and inhibition of long term potentiation. Finally, in an ex-vivo setup of acute brain slices, we observed a similar increase in Aβ engulfment by microglial cells under the influence of NGF. Our work substantiates a role for NGF in the regulation of microglial homeostatic activities and points toward this neurotrophin as a neuroprotective agent in Aβ accumulation pathologies, via its anti-inflammatory activity on microglia

Prevalence, risk factors and outcomes of patients coming from the community with sepsis due to multidrug resistant bacteria

Background: Although previous studies showed an increasing prevalence of infections due to multi-drug resistant (MDR) bacteria in the community, specific data on sepsis are lacking. We aimed to assess prevalence, risk factors and outcomes of patients with sepsis due to MDR bacteria. Methods: An observational, retrospective study was conducted on consecutive adult patients coming from the community and admitted to the Policlinico Hospital, Milan, Italy, with a diagnosis of sepsis between January 2011 and December 2015. Primary study outcome was in-hospital mortality. Results: Among 518 patients, at least one MDR bacteria was isolated in 88 (17%). ESBL+ Enterobacteriaceae were the most prevalent MDR bacteria (9.7%) followed by MRSA (3.9%). Independent risk factors for sepsis due to MDR bacteria were septic shock (OR: 2.2; p = 0.002) and hospitalization in the previous 90 days (OR: 2.3; p = 0.003). Independent risk factors for sepsis due to ESBL+ bacteria were hospitalization in the previous 90 days (OR: 2.1; p = 0.02) and stroke (OR: 2.1; p = 0.04). A significantly higher mortality was detected among patients with vs. without MDR bacteria (40.2% vs. 23.1% respectively, p = 0.001). Independent risk factors for mortality among patients with sepsis were coagulation dysfunction (OR: 3.2; p = 0.03), septic shock (OR: 3.2; p = 0.003), and isolation of a MDR bacteria (OR: 4.6; p < 0.001). Conclusion: In light of the prevalence and impact of MDR bacteria causing sepsis in patients coming from the community, physicians should consider ESBL coverage when starting an empiric antibiotic therapy in patients with specific risk factors, especially in the presence of septic shock