6,238 research outputs found

    Linear and nonlinear theory of cyclotron autoresonance masers with multiple waveguide modes

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    Theory of efficiency enhancement in CARM amplifiers by magnetic field tapering

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    DD-dimensions Dirac fermions BEC-BCS cross-over thermodynamics

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    An effective Proca Lagrangian action is used to address the vector condensation Lorentz violation effects on the equation of state of the strongly interacting fermions system. The interior quantum fluctuation effects are incorporated as an external field approximation indirectly through a fictive generalized Thomson Problem counterterm background. The general analytical formulas for the dd-dimensions thermodynamics are given near the unitary limit region. In the non-relativistic limit for d=3d=3, the universal dimensionless coefficient ξ=4/9\xi ={4}/{9} and energy gap Δ/ϵf=5/18\Delta/\epsilon_f ={5}/{18} are reasonably consistent with the existed theoretical and experimental results. In the unitary limit for d=2d=2 and T=0, the universal coefficient can even approach the extreme occasion ξ=0\xi=0 corresponding to the infinite effective fermion mass m=m^*=\infty which can be mapped to the strongly coupled two-dimensions electrons and is quite similar to the three-dimensions Bose-Einstein Condensation of ideal boson gas. Instead, for d=1d=1, the universal coefficient ξ\xi is negative, implying the non-existence of phase transition from superfluidity to normal state. The solutions manifest the quantum Ising universal class characteristic of the strongly coupled unitary fermions gas.Comment: Improved versio

    Experimental and theoretical studies of a 35 GHz cyclotron autoresonance maser amplifier

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    Large-amplitude traveling electromagnetic waves in collisionless magnetoplasmas

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    Internet of Things over future internet

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    Everyday objects surrounding us including numerous sensors weaved into the daily fabric of life are becoming online, that is, readable and controllable via Internet, these days. By providing a new ecosystem of information, this notion, termed Internet of Things (IoT) will drastically change our ways to interact with real world. Meanwhile, current Internet is facing various challenges such as exponential growth in bandwidth demand. The realization of IoT is also putting current Internet under great pressure due to its unprecedented scale—according to some forecasts, IoT, an integral part of the “future” Internet, will consist of over 50 billion connected things. To cope with such bandwidth demand and complexity as well as to solve other issues, for example, seamless wireless access and mobility support, and security, with current Internet, new architectures for the future Internet have been proposed, for example, information/content centric network architectures and cloud-computing centric network architectures. However, several questions still remain: how IoT will be supported in the future Internet architectures, that is, when deploying large-scale wireless sensor networks do we need to fully integrate embedded sensors with Internet or use dedicated gateways to bridge sensors and Internet similar to state-of-the-art technologies? The aim of this Special Issue is to answer various open questions in realizing IoT over future Internet technologies. The Special Issue includes extended papers forwarded from the seventh International Conference on Ubiquitous and Future Networks (ICUFN 2015) and other contributions from outside the conference highly related to IoT in future Internet. Specifically, 6 high-quality papers out of 18 submitted have been accepted

    JAK2V617F promotes replication fork stalling with disease-restricted impairment of the intra-S checkpoint response

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    Cancers result from the accumulation of genetic lesions, but the cellular consequences of driver mutations remain unclear, especially during the earliest stages of malignancy. The V617F mutation in the JAK2 non-receptor tyrosine kinase (JAK2V617F) is present as an early somatic event in most patients with myeloproliferative neoplasms (MPNs), and the study of these chronic myeloid malignancies provides an experimentally tractable approach to understanding early tumorigenesis. Introduction of exogenous JAK2V617F impairs replication fork progression and is associated with activation of the intra-S checkpoint, with both effects mediated by phosphatidylinositide 3-kinase (PI3K) signaling. Analysis of clonally derived JAK2V617F-positive erythroblasts from MPN patients also demonstrated impaired replication fork progression accompanied by increased levels of replication protein A (RPA)-containing foci. However, the associated intra-S checkpoint response was impaired in erythroblasts from polycythemia vera (PV) patients, but not in those from essential thrombocythemia (ET) patients. Moreover, inhibition of p53 in PV erythroblasts resulted in more gamma-H2Ax (γ-H2Ax)–marked double-stranded breaks compared with in like-treated ET erythroblasts, suggesting the defective intra-S checkpoint function seen in PV increases DNA damage in the context of attenuated p53 signaling. These results demonstrate oncogene-induced impairment of replication fork progression in primary cells from MPN patients, reveal unexpected disease-restricted differences in activation of the intra-S checkpoint, and have potential implications for the clonal evolution of malignancies

    Green tea polyphenols and sulfasalazine have parallel anti-inflammatory properties in colitis models

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    Background: There is no cure for autoimmune chronic inflammatory bowel disease (IBD). IBD patients commonly use complementary and alternative medications of which the safety, efficacy, and interaction with standard-of-care therapies are not fully known. Thus the consequences can become life-threatening. Sulfasalazine commonly used in IBD, potentially has severe adverse effects, including infertility, pulmonary fibrosis, lack of response, and ultimately patients may require intestinal resection. We hypothesized that green tea polyphenols (GrTP, EGCG) and sulfasalazine have similar anti-inflammatory properties. Methods: BALB/c mice received Dextran sodium sulfate (DSS) to induce colitis (ulcerative colitis model). Exposure of IL-10 deficient mice (BALB/c-background) to normal microbiota provoked enterocolitis (mimics Crohn’s disease). Animals were treated with agents incorporated into daily diets. Control animals received sham treatment. Results: DSS-treated animals developed severe bloody diarrhea and colitis (score 0–4, 3.2 ± 0.27). IL-10 deficient mice developed severe enterocolitis as manifested by diarrhea, rectal prolapse, and colonic lesions. Animals tolerated regimens (GrTP, EGCG, sulfasalazine) with no major side effects, and further developed less severe colitis. IL-10 deficient animals became moribund on high dose, while tolerated low and Mid doses with significant improved symptoms of enterocolitis. GrTP, EGCG, and sulfasalazine significantly ameliorated colonic damage and histological scores in treated animals in a similar manner (GrTP vs. DSS p \u3c 0.05; EGCG, sulfasalazine vs. DSS p \u3c 0.01). The inflammatory markers TNFα (3-fold), IL-6 (14-fold), and serum amyloid A (40-fold) increased in colitic animals and significantly decreased with treatment regiments. In contrast, circulatory leptin levels decreased in colitic animals (twofold). EGCG additionally reduced leptin levels (p \u3c 0.01) while GrTP and sulfasalazine had no effect on leptin levels (p \u3c 0.05). Hepatic and colonic antioxidants were significantly depleted in colitic animals and treatment regiments significantly restored antioxidants levels. Conclusion: GrTP and EGCG improved antioxidants levels and attenuated severity of colitis analogous to sulfasalazine. Future studies will reveal whether polyphenols can become an alternative/additive therapy for IBD therapy in humans

    Qubits from Number States and Bell Inequalities for Number Measurements

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    Bell inequalities for number measurements are derived via the observation that the bits of the number indexing a number state are proper qubits. Violations of these inequalities are obtained from the output state of the nondegenerate optical parametric amplifier.Comment: revtex4, 7 pages, v2: results identical but extended presentation, v3: published versio
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