Energy and Cost Analysis of Cellular Networks Under Co-Channel Interference

In this paper we carry out an energy efficiency and economic cost analysis of different cellular network designs. Our system model considers the co-channel interference, different amounts of available bandwidths and also the reuse of frequencies. The energy efficiency analysis employs a realistic power consumption model, while the economic analysis focus on infrastructure, spectrum licenses, and energy costs. Our results show that from an economic point of view the bandwidth cost and the number of employed base stations can be the most relevant factors to be balanced, while from an energy efficiency analysis it is more interesting to employ larger bandwidths and to balance the reuse of frequencies and the number of base stations. Moreover, although the system design under these two different points of view can be rather different, we also look into scenarios when the most energy efficient system design may also lead to the best economic option

Nitric Oxide Released From Luminal S-nitroso-n-acetylcysteine Increases Gastric Mucosal Blood Flow

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Nitric oxide (NO)-mediated vasodilation plays a key role in gastric mucosal defense, and NO-donor drugs may protect against diseases associated with gastric mucosal blood flow (GMBF) deficiencies. In this study, we used the ex vivo gastric chamber method and Laser Doppler Flowmetry to characterize the effects of luminal aqueous NO-donor drug S-nitroso-N-acetylcysteine (SNAC) solution administration compared to aqueous NaNO2 and NaNO3 solutions (pH 7.4) on GMBF in Sprague-Dawley rats. SNAC solutions (600 mu M and 12 mM) led to a rapid threefold increase in GMBF, which was maintained during the incubation of the solutions with the gastric mucosa, while NaNO2 or NaNO3 solutions (12 mM) did not affect GMBF. SNAC solutions (600 mu M and 12 mM) spontaneously released NO at 37 degrees C at a constant rate of 0.3 or 14 nmol center dot mL(-1)center dot min(-1), respectively, while NaNO2 (12 mM) released NO at a rate of 0.06 nmol center dot mL(-1)center dot min(-1) and NaNO3 (12 mM) did not release NO. These results suggest that the SNAC-induced GMBF increase is due to their higher rates of spontaneous NO release compared to equimolar NaNO2 solutions. Taken together, our data indicate that oral SNAC administration is a potential approach for gastric acid-peptic disorder prevention and treatment.20341094123Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [2011/50514-5, 2013/07173-8]CNPq [309390/2011-7]FAPESP [2008/57560-0

Prostaglandin E2-EP1 and EP2 receptor signaling promotes apical junctional complex disassembly of Caco-2 human colorectal cancer cells

<p>Abstract</p> <p>Background</p> <p>The apical junctional complex (AJC) is a dynamic structure responsible to maintain epithelial cell-cell adhesions and it plays important functions such as, polarity, mechanical integrity, and cell signaling. Alteration of this complex during pathological events leads to an impaired epithelial barrier by perturbation of the cell-cell adhesion system. Although clinical and experimental data indicate that prostaglandin E₂(PGE₂) plays a critical function in promoting cell motility and cancer progression, little is known concerning its role in AJC disassembly, an event that takes place at the beginning of colorectal tumorigenesis. Using Caco-2 cells, a cell line derived from human colorectal cancer, we investigated the effects of prostaglandin E₂(PGE₂) treatment on AJC assembly and function.</p> <p>Results</p> <p>Exposition of Caco-2 cells to PGE₂promoted differential alteration of AJC protein distribution, as evidenced by immunofluorescence and immunoblotting analysis and impairs the barrier function, as seen by a decrease in the transepithelial electric resistance and an increase in the permeability to ruthenium red marker. We demonstrated the involvement of EP1 and EP2 prostaglandin E₂receptor subtypes in the modulation of the AJC disassembly caused by prostanoid. Furthermore, pharmacological inhibition of protein kinase-C, but not PKA and p38MAPK significantly prevented the PGE₂effects on the AJC disassembly.</p> <p>Conclusion</p> <p>Our findings strongly suggest a central role of Prostaglandin E2-EP1 and EP2 receptor signaling to mediate AJC disassembly through a mechanism that involves PKC and claudin-1 as important target for the TJ-related effects in human colorectal cancer cells (Caco-2).</p

Effective Action for QED with Fermion Self-Interaction in D=2 and D=3 Dimensions

In this work we discuss the effect of the quartic fermion self-interaction of Thirring type in QED in D=2 and D=3 dimensions. This is done through the computation of the effective action up to quadratic terms in the photon field. We analyze the corresponding nonlocal photon propagators nonperturbatively in % \frac{k}{m}, where k is the photon momentum and m the fermion mass. The poles of the propagators were determined numerically by using the Mathematica software. In D=2 there is always a massless pole whereas for strong enough Thirring coupling a massive pole may appear . For D=3 there are three regions in parameters space. We may have one or two massive poles or even no pole at all. The inter-quark static potential is computed analytically in D=2. We notice that the Thirring interaction contributes with a screening term to the confining linear potential of massive QED_{2}. In D=3 the static potential must be calculated numerically. The screening nature of the massive QED$_{3}$ prevails at any distance, indicating that this is a universal feature of % D=3 electromagnetic interaction. Our results become exact for an infinite number of fermion flavors.Comment: Latex, 13 pages, 3 figure

In vitro determination of extracellular proteins from xylella fastidiosa

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)The phytopathogen Xylella fastidiosa causes economic losses in important agricultural crops. Xylem vessel occlusion caused by biofilm formation is the major mechanism underlying the pathogenicity of distinct strains of X. fastidiosa. Here, we provide a detailed in vitro characterization of the extracellular proteins of X. fastidiosa. Based on the results, we performed a comparison with a strain J1a12, which cannot induce citrus variegated chlorosis symptoms when inoculated into citrus plants. We then extend this approach to analyze the extracellular proteins of X. fastidiosa in media supplemented with calcium. We verified increases in extracellular proteins concomitant with the days of growth and, consequently, biofilm development (330 days). Outer membrane vesicles carrying toxins were identified beginning at 10 days of growth in the 9a5c strain. In addition, a decrease in extracellular proteins in media supplemented with calcium was observed in both strains. Using mass spectrometry, 71 different proteins were identified during 30 days of X. fastidiosa biofilm development, including proteases, quorum-sensing proteins, biofilm formation proteins, hypothetical proteins, phage-related proteins, chaperones, toxins, antitoxins, and extracellular vesicle membrane components.The phytopathogen Xylella fastidiosa causes economic losses in important agricultural crops. Xylem vessel occlusion caused by biofilm formation is the major mechanism underlying the pathogenicity of distinct strains of X. fastidiosa. Here, we provide a de7Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2001/07533-7, 2012/51580-4]Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES, Computational Biology Program)CAPESFAPESP [2011/50268-4]CAPES (Computational Biology Program)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Quadratic Effective Action for QED in D=2,3 Dimensions

We calculate the effective action for Quantum Electrodynamics (QED) in D=2,3 dimensions at the quadratic approximation in the gauge fields. We analyse the analytic structure of the corresponding nonlocal boson propagators nonperturbatively in k/m. In two dimensions for any nonzero fermion mass, we end up with one massless pole for the gauge boson . We also calculate in D=2 the effective potential between two static charges separated by a distance L and find it to be a linearly increasing function of L in agreement with the bosonized theory (massive Sine-Gordon model). In three dimensions we find nonperturbatively in k/m one massive pole in the effective bosonic action leading to screening. Fitting the numerical results we derive a simple expression for the functional dependence of the boson mass upon the dimensionless parameter e^{2}/m .Comment: 10 pages, 2 figure

Climate change will reduce suitable Caatinga dry forest habitat for endemic plants with disproportionate impacts on specialized reproductive strategies

Global climate change alters the dynamic of natural ecosystems and directly affects species distributions, persistence and diversity. The impacts of climate change may lead to dramatic changes in biotic interactions, such as pollination and seed dispersal. Life history traits are extremely important to consider the vulnerability of a species to climate change, producing more robust models than those based primarily on species distributions. Here, we hypothesized that rising temperatures and aridity will reduce suitable habitats for the endemic flora of the Caatinga, the most diverse dry tropical forest on Earth. Specifically, species with specialized reproductive traits (e.g. vertebrate pollination, biotic dispersal, obligatory cross-pollination) should be more affected by climate change than those with generalist traits. We performed two ecological niche models (current and future) to simulate the effects of climate change on the distribution area of endemic species in relation to life-history traits. We used the MIROC-ESM and CCSM4 models for both intermediate (RCP4.5) and highest predicted (RCP8.5) GHG emission scenarios, with a resolution of 30' (~1 km2). Habitat with high occurrence probability (>80%) of endemic species will be reduced (up to ~10% for trees, ~13% for non-arboreous, 10-28% for species with any pollination/reproductive system), with the greatest reductions for species with specialized reproductive traits. In addition, the likely concentration of endemic plants in the extreme northeastern portion of the Caatinga, in more mesic areas, coincides with the currently most human-modified areas of the ecosystem, which combined with climate change will further contract suitable habitats of endemic species. In conclusion, plant species endemic to the Caatinga are highly vulnerable to even conservative scenarios of future climate change and may lose much of their climatic envelopes. New protected areas should be located in the northeastern portion of the Caatinga, which hosts a more favorable climate, but is currently exposed to escalating agricultural intensification