870 research outputs found

    The Case for Liberal Spectrum Licenses: A Technical and Economic Perspective

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    The traditional system of radio spectrum allocation has inefficiently restricted wireless services. Alternatively, liberal licenses ceding de facto spectrum ownership rights yield incentives for operators to maximize airwave value. These authorizations have been widely used for mobile services in the U.S. and internationally, leading to the development of highly productive services and waves of innovation in technology, applications and business models. Serious challenges to the efficacy of such a spectrum regime have arisen, however. Seeing the widespread adoption of such devices as cordless phones and wi-fi radios using bands set aside for unlicensed use, some scholars and policy makers posit that spectrum sharing technologies have become cheap and easy to deploy, mitigating airwave scarcity and, therefore, the utility of exclusive rights. This paper evaluates such claims technically and economically. We demonstrate that spectrum scarcity is alive and well. Costly conflicts over airwave use not only continue, but have intensified with scientific advances that dramatically improve the functionality of wireless devices and so increase demand for spectrum access. Exclusive ownership rights help direct spectrum inputs to where they deliver the highest social gains, making exclusive property rules relatively more socially valuable. Liberal licenses efficiently accommodate rival business models (including those commonly associated with unlicensed spectrum allocations) while mitigating the constraints levied on spectrum use by regulators imposing restrictions in traditional licenses or via use rules and technology standards in unlicensed spectrum allocations.

    酵素の作用(退官記念最終講義)

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    Contains sequential images of Yale logo experimental treatment, replicate

    Avidity maturation of memory CD8 T cells is limited by self-antigen expression

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    Immune tolerance to self-antigens is a complex process that utilizes multiple mechanisms working in concert to maintain homeostasis and prevent autoimmunity. We developed a system that revealed a population of self-specific CD8 T cells within the endogenous T cell repertoire. Immunization of ovalbumin (OVA)-expressing transgenic mice with recombinant viruses expressing OVA-peptide variants induced self-reactive T cells in vivo that matured into memory T cells able to respond to secondary infection. However, whereas the avidity of memory cells in normal mice increased dramatically with repeated immunizations, avidity maturation was limited for self-specific CD8 T cells. Despite decreased avidity, such memory cells afforded protection against infection, but did not induce overt autoimmunity. Further, up-regulation of self-antigen expression in dendritic cells using an inducible system promoted programmed death-1 expression, but not clonal expansion of preexisting memory cells. Thus, the self-reactive T cell repertoire is controlled by overlapping mechanisms influenced by antigen dose

    CD4+ T Cell Regulation of CD25 Expression Controls Development of Short-Lived Effector CD8+ T Cells in Primary and Secondary Responses

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    Both CD4(+) T cell help and IL-2 have been postulated to program activated CD8(+) T cells for memory cell development. However, the linkage between these two signals has not been well elucidated. Here we have studied effector and memory CD8(+) T cell differentiation following infection with three pathogens (Listeria monocytogenes, vesicular stomatitis virus, and vaccinia virus) in the absence of both CD4(+) T cells and IL-2 signaling. We found that expression of CD25 on antigen-specific CD8(+) T cells peaked 3-4 days after initial priming and was dependent on CD4(+) T cell help, likely through a CD28:CD80/86 mediated pathway. CD4(+) T cell or CD25-deficiency led to normal early effector CD8(+) T cell differentiation, but a subsequent lack of accumulation of CD8(+) T cells resulting in overall decreased memory cell generation. Interestingly, in both primary and recall responses KLRG1(high) CD127(low) short-lived effector cells were drastically diminished in the absence of IL-2 signaling, although memory precursors remained intact. In contrast to previous reports, upon secondary antigen encounter CD25-deficient CD8(+) T cells were capable of undergoing robust expansion, but short-lived effector development was again impaired. Thus, these results demonstrated that CD4(+) T cell help and IL-2 signaling were linked via CD25 up-regulation, which controls the expansion and differentiation of antigen-specific effector CD8(+) T cells, rather than programming memory cell traits

    Cell Cycle Phase-Specific Surface Expression of Nerve Growth Factor Receptors TrkA and p75NTR

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    [EN]Expression of the nerve growth factor (NGF) receptors TrkA and p75NTR was found to vary at the surface of PC12 cells in a cell cycle phase-specific manner. This was evidenced by using flow cytometric and microscopic analysis of cell populations labeled with antibodies to the extracellular domains of both receptors. Differential expression of these receptors also was evidenced by biotinylation of surface proteins and Western analysis, using antibodies specific for the extracellular domains of TrkA and p75NTR. TrkA is expressed most strongly at the cell surface in M and early G1 phases, whereas p75NTR is expressed mainly in late G1, S, and G2 phases. This expression reflects the molecular and cellular responses to NGF in specific phases of the cell cycle; in the G1 phase NGF elicits both the anti-mitogenic effect, i.e., inhibition of the G1 to S transition, and the differentiation response whereas a survival effect is provoked elsewhere in the cell cycle. A model is proposed relating these responses to the surface expression of the two receptors. These observations open the way for novel approaches to the investigation of the mechanism of NGF signal transduction

    PHAT Stellar Cluster Survey I. Year 1 Catalog and Integrated Photometry

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    The Panchromatic Hubble Andromeda Treasury (PHAT) survey is an on-going Hubble Space Telescope (HST) multi-cycle program to obtain high spatial resolution imaging of one-third of the M31 disk at ultraviolet through near-infrared wavelengths. In this paper, we present the first installment of the PHAT stellar cluster catalog. When completed, the PHAT cluster catalog will be among the largest and most comprehensive surveys of resolved star clusters in any galaxy. The exquisite spatial resolution achieved with HST has allowed us to identify hundreds of new clusters that were previously inaccessible with existing ground-based surveys. We identify 601 clusters in the Year 1 sample, representing more than a factor of four increase over previous catalogs within the current survey area (390 arcmin^2). This work presents results derived from the first \sim25% of the survey data; we estimate that the final sample will include \sim2500 clusters. For the Year 1 objects, we present a catalog with positions, radii, and six-band integrated photometry. Along with a general characterization of the cluster luminosities and colors, we discuss the cluster luminosity function, the cluster size distributions, and highlight a number of individually interesting clusters found in the Year 1 search.Comment: 26 pages, 22 figures, Accepted by Ap
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