82 research outputs found

    Profiling the temperature distribution in AlGaN/GaN HEMTs with nanocrystalline diamond heat spreading layers

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    Reduced performance in Gallium Nitride (GaN) based high electron mobility transistors (HEMTs) as a result of self-heating has been well-documented. A new approach, termed “diamond-before-gate" is shown to improve the thermal budget of the deposition process and enables large area diamond without degrading the gate metal NCD capped devices had a 20% lower channel temperature at equivalent power dissipation

    From Effective Lagrangians, to Chiral Bags, to Skyrmions with the Large-N_c Renormalization Group

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    We explicitly relate effective meson-baryon Lagrangian models, chiral bags, and Skyrmions in the following way. First, effective Lagrangians are constructed in a manner consistent with an underlying large-N_c QCD. An infinite set of graphs dress the bare Yukawa couplings at *leading* order in 1/N_c, and are summed using semiclassical techniques. What emerges is a picture of the large-N_c baryon reminiscent of the chiral bag: hedgehog pions for r > 1/\Lambda patched onto bare nucleon degrees of freedom for r < 1/\Lambda, where the ``bag radius'' 1/\Lambda is the UV cutoff on the graphs. Next, a novel renormalization group (RG) is derived, in which the bare Yukawa couplings, baryon masses and hyperfine baryon mass splittings run with \Lambda. Finally, this RG flow is shown to act as a *filter* on the renormalized Lagrangian parameters: when they are fine-tuned to obey Skyrme-model relations the continuum limit \Lambda --> \infty exists and is, in fact, a Skyrme model; otherwise there is no continuum limit.Comment: Figures included (separate file). This ``replaced'' version corrects the discussion of backwards-in-time baryon

    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

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    Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

    Populist Mobilization: A New Theoretical Approach to Populism*

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112280/1/j.1467-9558.2011.01388.x.pd
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