Influence of Lorentz-violating terms on a two-level system

The influence of Lorentz- and CPT-violating terms of the extended Standard Model on a semi-classical two-level system is analyzed. It is shown that the Lorentz-violating background (when coupled with the fermion sector in a vector way) is able to induce modifications on the Rabi oscillation pattern, promoting sensitive modulations on the usual oscillations. As for the term involving the coefficient coupled in an axial vector way, it brings about oscillations both on energy states and on the spin states (implied by the background). It is also seen that such backgrounds are able to yield state oscillations even in the absence of the electromagnetic field. The foreseen effects are used to establish upper bounds on the Lorentz-violating coefficients.Comment: 13 pages, 6 figures, revtex style

Features-Aware DDoS Detection in Heterogeneous Smart Environments based on Fog and Cloud Computing

Nowadays, urban environments are deploying smart environments (SEs) to evolve infrastructures, resources, and services. SEs are composed of a huge amount of heterogeneous devices, i.e., the SEs have both personal devices (smartphones, notebooks, tablets, etc) and Internet of Things (IoT) devices (sensors, actuators, and others). One of the existing problems of the SEs is the detection of Distributed Denial of Service (DDoS) attacks, due to the vulnerabilities of IoT devices. In this way, it is necessary to deploy solutions that can detect DDoS in SEs, dealing with issues like scalability, adaptability, and heterogeneity (distinct protocols, hardware capacity, and running applications). Within this context, this article presents an Intelligent System for DDoS detection in SEs, applying Machine Learning (ML), Fog, and Cloud computing approaches. Additionally, the article presents a study about the most important traffic features for detecting DDoS in SEs, as well as a traffic segmentation approach to improve the accuracy of the system. The experiments performed, using real network traffic, suggest that the proposed system reaches 99% of accuracy, while reduces the volume of data exchanged and the detection time

Spironolactone treatment attenuates vascular dysfunction in type 2 diabetic mice by decreasing oxidative stress and restoring NO/GC signaling

Type 2 diabetes (DM2) increases the risk of cardiovascular disease. Aldosterone, which has pro-oxidative and pro-inflammatory effects in the cardiovascular system, is positively regulated in DM2. We assessed whether blockade of mineralocorticoid receptors (MR) with spironolactone decreases reactive oxygen species (ROS)-associated vascular dysfunction and improves vascular nitric oxide (NO) signaling in diabetes. Leptin receptor knockout [LepRdb/LepRdb (db/db)] mice, a model of DM2, and their counterpart controls [LepRdb/LepR+, (db/+) mice] received spironolactone (50 mg/kg body weight/day) or vehicle (ethanol 1%) via oral per gavage for 6 weeks. Spironolactone treatment abolished endothelial dysfunction and increased endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177) in arteries from db/db mice, determined by acetylcholine-induced relaxation and Western Blot analysis, respectively. MR antagonist therapy also abrogated augmented ROS-generation in aorta from diabetic mice, determined by lucigenin luminescence assay. Spironolactone treatment increased superoxide dismutase-1 and catalase expression, improved sodium nitroprusside and BAY 41-2272-induced relaxation, and increased soluble guanylyl cyclase (sGC) β subunit expression in arteries from db/db mice. Our results demonstrate that spironolactone decreases diabetes-associated vascular oxidative stress and prevents vascular dysfunction through processes involving increased expression of antioxidant enzymes and sGC. These findings further elucidate redox-sensitive mechanisms whereby spironolactone protects against vascular injury in diabetes

Chemerin receptor blockade improves vascular function in diabetic obese mice via redox-sensitive- and Akt-dependent pathways

Chemerin and its G protein-coupled receptor [chemerin receptor 23 (ChemR23)] have been associated with endothelial dysfunction, inflammation, and insulin resistance. However, the role of chemerin on insulin signaling in the vasculature is still unknown. We aimed to determine whether chemerin reduces vascular insulin signaling and whether there is interplay between chemerin/ChemR23, insulin resistance, and vascular complications associated with type 2 diabetes (T2D). Molecular and vascular mechanisms were probed in mesenteric arteries and cultured vascular smooth muscle cells (VSMCs) from C57BL/6J, nondiabetic lean db/m, and diabetic obese db/db mice as well as in human microvascular endothelial cells (HMECs). Chemerin decreased insulin-induced vasodilatation in C57BL/6J mice, an effect prevented by CCX832 (ChemR23 antagonist) treatment. In VSMCs, chemerin, via oxidative stress- and ChemR23-dependent mechanisms, decreased insulin-induced Akt phosphorylation, glucose transporter 4 translocation to the membrane, and glucose uptake. In HMECs, chemerin decreased insulin-activated nitric oxide signaling. AMP-activated protein kinase phosphorylation was reduced by chemerin in both HMECs and VSMCs. CCX832 treatment of db/db mice decreased body weight, insulin, and glucose levels as well as vascular oxidative stress. CCX832 also partially restored vascular insulin responses in db/db and high-fat diet-fed mice. Our novel in vivo findings highlight chemerin/ChemR23 as a promising therapeutic target to limit insulin resistance and vascular complications associated with obesity-related diabetes

Fast and efficient method to evaluate the potential of eutectic solvents to dissolve lignocellulosic components

The application of eutectic solvents (ESs) in lignocellulosic biomass fractionation has been demonstrated as a promising approach to accomplish efficient and environmentally friendly biomass valorization. In general, ESs are a combination of two components, a hydrogen-bonding donor and a hydrogen-bonding acceptor, in which the melting point of the mixture is lower than that of the individual components. However, there are plenty of possible combinations to form ESs with the potential to apply in biomass processing. Therefore, the development of fast and effective screening methods to find combinations capable to dissolve the main biomass components—namely cellulose, hemicelluloses, and lignin—is highly required. An accurate and simple technique based on optical microscopy with or without polarized lenses was used in this study to quickly screen and monitor the dissolution of cellulose, xylose (a monomer of hemicelluloses), and lignin in several ESs. The dissolution of these solutes were investigated in different choline-chloride-based ESs (ChCl:UREA, ChCl:PROP, ChCl:EtGLY, ChCl:OXA, ChCl:GLY, ChCl:LAC). Small amounts of solute and solvent with temperature control were applied and the dissolution process was monitored in real time. The results obtained in this study showed that cellulose was insoluble in these ESs, while lignin and xylose were progressively dissolved.publishe

Platelet hyperaggregability in high-fat fed rats: A role for intraplatelet reactive-oxygen species production

<p>Abstract</p> <p>Background</p> <p>Adiposity greatly increases the risk of atherothrombotic events, a pathological condition where a chronic state of oxidative stress is reported to play a major role. This study aimed to investigate the involvement of (NO)-soluble guanylyl cyclase (sGC) signaling pathway in the platelet dysfunction from high fat-fed (HFF) rats.</p> <p>Methods</p> <p>Male Wistar rats were fed for 10 weeks with standard chow (SCD) or high-fat diet (HFD). ADP (10 μM)- and thrombin (100 mU/ml)-induced washed platelet aggregation were evaluated. Measurement of intracellular levels of ROS levels was carried out using flow cytometry. Cyclic GMP levels were evaluated using ELISA kits.</p> <p>Results</p> <p>High-fat fed rats exhibited significant increases in body weight, epididymal fat, fasting glucose levels and glucose intolerance compared with SCD group. Platelet aggregation induced by ADP (<it>n </it>= 8) and thrombin from HFD rats (<it>n </it>= 8) were significantly greater (<it>P </it>< 0.05) compared with SCD group. Platelet activation with ADP increased by 54% the intraplatelet ROS production in HFD group, as measured by flow cytometry (<it>n </it>= 6). N-acetylcysteine (NAC; 1 mM) and PEG-catalase (1000 U/ml) fully prevented the increased ROS production and platelet hyperaggregability in HFD group. The NO donors sodium nitroprusside (SNP; 10 μM) and SNAP (10 μM), as well as the NO-independent soluble guanylyl cyclase stimulator BAY 41-2272 (10 μM) inhibited the platelet aggregation in HFD group with lower efficacy (<it>P </it>< 0.05) compared with SCD group. The cGMP levels in response to these agents were also markedly lower in HFD group (<it>P </it>< 0.05). The prostacyclin analogue iloprost (1 μM) reduced platelet aggregation in HFD and SCD rats in a similar fashion (<it>n </it>= 4).</p> <p>Conclusions</p> <p>Metabolic abnormalities as consequence of HFD cause platelet hyperaggregability involving enhanced intraplatelet ROS production and decreased NO bioavailability that appear to be accompanied by potential defects in the prosthetic haem group of soluble guanylyl cyclase.</p

Semaphorin4A-Plexin D1 Axis Induces Th2 and Th17 While Represses Th1 Skewing in an Autocrine Manner

Semaphorin (Sema)4A is a transmembrane glycoprotein that is elevated in several autoimmune diseases such as systemic sclerosis, rheumatoid arthritis and multiple sclerosis. Sema4A has a key role in the regulation of Thelper Th1 and Th2 differentiation and we recently demonstrated that CD4(+) T cell activation induces the expression of Sema4A. However, the autocrine role of Sema4A on Th cell differentiation remains unknown. Naive Th cells from healthy controls were cell sorted and differentiated into Th1, Th2 and Th17 in the presence or absence of a neutralizing antibody against the Sema4A receptor PlexinD1. Gene expression was determined by quantitative PCR and protein expression by ELISA and flow cytometry. We found that the expression of Sema4A is induced during Th1, Th2 and Th17 differentiation. PlexinD1 neutralization induced the differentiation of Th1 cells, while reduced the Th2 and Th17 skewing. These effects were associated with an upregulation of the transcription factor T-bet by Th1 cells, and to downregulation of GATA3 and RORgammat in Th2 cells and Th17 cells, respectively. Finally, PlexinD1 neutralization regulates the systemic sclerosis patients serum-induced cytokine production by CD4(+) T cells. Therefore, the autocrine Sema4A-PlexinD1 signaling acts as a negative regulator of Th1 skewing but is a key mediator on Th2 and Th17 differentiation, suggesting that dysregulation of this axis might be implicated in the pathogenesis of CD4(+) T cell-mediated diseases

Ecotoxicological Tools to Assess Cytostatic Effects in Freshwater Environments: Aiding Drug Prioritization

Given the growing number of cancer diseases, new cytostatic drugs are approved daily, often with concomitant development, or refinement of some of these drugs aimed at decreasing patient discomfort during the administration period (e.g., prodrugs). Classified as highly toxic, they represent a major environmental problem that may potentiate disease occurrences. For newer cytostatic and prodrugs there are no (or few) reported effects to aquatic organisms; therefore, their prioritization is constrained. In light of the points raised, the IonCytDevice project intended to bridge some of these knowledge gaps and has delivered important benchmarks. Predictions have been obtained on the environmental impacts of three cytostatics (cyclophosphamide: CYP; 5-fluoroucil: 5-FU; and mycophenolic acid: MPA) and one prodrug (capecitabine: CAP) on freshwater biota, with a focus on new species and endpoints likely to be also framed in meta-analysis studies. The results reveal that, for now, CYP, 5-FU, and CAP (prodrug) pose no risk, whilst MPA was flagged as a high environmental risk