16 research outputs found

    MHV Rules for Higgs Plus Multi-Gluon Amplitudes

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    We use tree-level perturbation theory to show how non-supersymmetric one-loop scattering amplitudes for a Higgs boson plus an arbitrary number of partons can be constructed, in the limit of a heavy top quark, from a generalization of the scalar graph approach of Cachazo, Svrcek and Witten. The Higgs boson couples to gluons through a top quark loop which generates, for large top mass, a dimension-5 operator H tr G^2. This effective interaction leads to amplitudes which cannot be described by the standard MHV rules; for example, amplitudes where all of the gluons have positive helicity. We split the effective interaction into the sum of two terms, one holomorphic (selfdual) and one anti-holomorphic (anti-selfdual). The holomorphic interactions give a new set of MHV vertices -- identical in form to those of pure gauge theory, except for momentum conservation -- that can be combined with pure gauge theory MHV vertices to produce a tower of amplitudes with more than two negative helicities. Similarly, the anti-holomorphic interactions give anti-MHV vertices that can be combined with pure gauge theory anti-MHV vertices to produce a tower of amplitudes with more than two positive helicities. A Higgs boson amplitude is the sum of one MHV-tower amplitude and one anti-MHV-tower amplitude. We present all MHV-tower amplitudes with up to four negative-helicity gluons and any number of positive-helicity gluons (NNMHV). These rules reproduce all of the available analytic formulae for Higgs + n-gluon scattering (n<=5) at tree level, in some cases yielding considerably shorter expressions.Comment: 34 pages, 8 figures; v2, references correcte

    Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

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    <p>Abstract</p> <p>Background</p> <p>Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub>2</sub>) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts E<sub>2 </sub>to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less E<sub>2 </sub>in their brains than females.</p> <p>Results</p> <p>Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain.</p> <p>Conclusions</p> <p>Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub>2 </sub>metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p

    Consensus guidelines for the use and interpretation of angiogenesis assays

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    The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference
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