The process gg -> WW as a background to the Higgs signal at the LHC

The production of W pairs from the one-loop gluon fusion process is studied. Formulas are presented for the helicity amplitudes keeping the top mass finite, but all other quark masses zero. The correlations among the leptons coming from the W bosons are kept. The contribution of this background to the Higgs boson search in the WW decay mode at the LHC is estimated by applying the cuts foreseen in experimental searches using the PYTHIA Monte Carlo program. Kinematic distributions for the final state leptons are compared to those of the Higgs boson signal and of the q qbar -> WW background. After applying final cuts, the gg background is found to be large, at the level of 35% of the q qbar background.The characteristics of the gg background are very similar to those of the signal. Therefore, an experimental normalization of this background component appears to be very difficult and the uncertainty must largely be determined by theory. As a result, the significance of a Higgs signal in the gg -> H -> WW mode at the LHC is reduced.Comment: 24 pages, 4 figure

Neurotransmitter alterations in embryonic succinate semialdehyde dehydrogenase (SSADH) deficiency suggest a heightened excitatory state during development

<p>Abstract</p> <p>Background</p> <p>SSADH (aldehyde dehydrogenase 5a1 (Aldh5a1); γ-hydroxybutyric (GHB) aciduria) deficiency is a defect of GABA degradation in which the neuromodulators GABA and GHB accumulate. The human phenotype is that of nonprogressive encephalopathy with prominent bilateral discoloration of the globi pallidi and variable seizures, the latter displayed prominently in Aldh5a1^-/-mice with lethal convulsions. Metabolic studies in murine neural tissue have revealed elevated GABA [and its derivatives succinate semialdehyde (SSA), homocarnosine (HC), 4,5-dihydroxyhexanoic acid (DHHA) and guanidinobutyrate (GB)] and GHB [and its analogue D-2-hydroxyglutarate (D-2-HG)] at birth. Because of early onset seizures and the neurostructural anomalies observed in patients, we examined metabolite features during Aldh5a1^-/-embryo development.</p> <p>Methods</p> <p>Embryos were obtained from pregnant dams sacrificed at E (embryo day of life) 10–13, 14–15, 16–17, 18–19 and newborn mice. Intact embryos were extracted and metabolites quantified by isotope dilution mass spectrometry (n = 5–15 subjects, Aldh5a1^+/+and Aldh5a1^-/-) for each gestational age group. Data was evaluated using the <it>t </it>test and one-way ANOVA with Tukey post hoc analysis. Significance was set at the 95^thcentile.</p> <p>Results</p> <p>GABA and DHHA were significantly elevated at all gestational ages in Aldh5a1^-/-mice, while GB was increased only late in gestation; SSA was not elevated at any time point. GHB and D-2-HG increased in an approximately linear fashion with gestational age. Correlative studies in human amniotic fluid from SSADH-deficient pregnancies (n = 5) also revealed significantly increased GABA.</p> <p>Conclusion</p> <p>Our findings indicate early GABAergic alterations in Aldh5a1^-/-mice, possibly exacerbated by other metabolites, which likely induce a heightened excitatory state that may predispose neural networks to epilepsy in these animals.</p

Education and the boarding school novel : examining the work of José Régio

This thesis is centred on the work of Portuguese writer José Régio (1901-1969). He was a teacher-writer and, arguably, the most philosophical of Portuguese school novel authors. In his novel ‘A Drop of Blood’ (1945), Régio shows interest in the formation of the artist as the special object of education – the ‘marked man’ –, whose sensitivity distances him irremediably from the crowd. He adopted the radical individualism of Nietzsche not in order to be ‘for’ or ‘against’ this or that schooling model but to exemplify the perpetual clash, inherent in mankind, between the individual and the group, the artist and the non-artistic person, the young and the adult, the son and the father and the self and the world. Published Proquest ebook version: http://ebookcentral.proquest.com/lib/canterbury/detail.action?docID=4799556 (UC Staff and Student use only

Preparation of Powder Precursors and Evaporation of Photoconductive Indium Sulfide Films

We have demonstrated significant photoconductance in indium sulfide thin films prepared by thermal vacuum evaporation ofIn2$3 powders synthesized in-house by chemical precipitation ofInCl3 or In(CH3COO)3, and (NH4)2S or Na2S. The Delta G lambda/Gdark values have been as high as 0.1 in the initial unoptimized films. Excess sulfur (via a mixture of polysulfide and sulfide ions in the synthesis bath) appears to be important in achieving reproducible and large photoconductivities. In2S3 is particularly attractive as a lower toxicity alternative to CdS in optoelectronic applications such as photovoltaic and photoconductive cells

Self-amplified photo-induced gap quenching in a correlated electron material.

Capturing the dynamic electronic band structure of a correlated material presents a powerful capability for uncovering the complex couplings between the electronic and structural degrees of freedom. When combined with ultrafast laser excitation, new phases of matter can result, since far-from-equilibrium excited states are instantaneously populated. Here, we elucidate a general relation between ultrafast non-equilibrium electron dynamics and the size of the characteristic energy gap in a correlated electron material. We show that carrier multiplication via impact ionization can be one of the most important processes in a gapped material, and that the speed of carrier multiplication critically depends on the size of the energy gap. In the case of the charge-density wave material 1T-TiSe2, our data indicate that carrier multiplication and gap dynamics mutually amplify each other, which explains-on a microscopic level-the extremely fast response of this material to ultrafast optical excitation

Gluon-induced W-boson pair production at the LHC

Pair production of W bosons constitutes an important background to Higgs boson and new physics searches at the Large Hadron Collider LHC. We have calculated the loop-induced gluon-fusion process gg -> W*W* -> leptons, including intermediate light and heavy quarks and allowing for arbitrary invariant masses of the W bosons. While formally of next-to-next-to-leading order, the gg -> W*W* -> leptons process is enhanced by the large gluon flux at the LHC and by experimental Higgs search cuts, and increases the next-to-leading order WW background estimate for Higgs searches by about 30%. We have extended our previous calculation to include the contribution from the intermediate top-bottom massive quark loop and the Higgs signal process. We provide updated results for cross sections and differential distributions and study the interference between the different gluon scattering contributions. We describe important analytical and numerical aspects of our calculation and present the public GG2WW event generator.Comment: 20 pages, 4 figure

A new case of GABA transaminase deficiency facilitated by proton MR spectroscopy

BACKGROUND: Deficiency of 4-aminobutyrate aminotransferase (GABA-T) is a rare disorder of GABA catabolism, with only a single sibship reported. We report on a third case, a Japanese female infant with severe psychomotor retardation and recurrent episodic lethargy with intractable seizures, with the diagnosis facilitated by proton magnetic resonance (MR) spectroscopy ((1)H-MRS). METHODS: Neuroimaging was performed at the first episode of lethargy. For (1)H-MRS, locations were placed in the semioval center and the basal ganglia. Quantification of metabolite concentrations were derived using the LCModel. We confirmed the diagnosis subsequently by enzyme and molecular studies, which involved direct DNA sequence analysis and the development of a novel multiplex ligation-dependent probe amplification test. RESULTS: (1)H-MRS analysis revealed an elevated GABA concentration in the basal ganglia (2.9 mmol/l). Based on the results of quantitative (1)H-MRS and clinical findings, GABA-T deficiency was suspected and confirmed in cultured lymphoblasts. Molecular studies of the GABA-T gene revealed compound heterozygosity for a deletion of one exon and a missense mutation, 275G>A, which was not detected in 210 control chromosomes. CONCLUSIONS: Our results suggest that excessive prenatal GABA exposure in the central nervous system (CNS) was responsible for the clinical manifestations of GABA transaminase deficiency. Our findings suggest the dual nature of GABA as an excitatory molecule early in life, followed by a functional switch to an inhibitory species later in development. Furthermore, quantitative (1)H-MRS appears to be a useful, noninvasive tool for detecting inborn errors of GABA metabolism in the CNS

Dynamic rerouting of the carbohydrate flux is key to counteracting oxidative stress

<p>Abstract</p> <p>Background</p> <p>Eukaryotic cells have evolved various response mechanisms to counteract the deleterious consequences of oxidative stress. Among these processes, metabolic alterations seem to play an important role.</p> <p>Results</p> <p>We recently discovered that yeast cells with reduced activity of the key glycolytic enzyme triosephosphate isomerase exhibit an increased resistance to the thiol-oxidizing reagent diamide. Here we show that this phenotype is conserved in <it>Caenorhabditis elegans </it>and that the underlying mechanism is based on a redirection of the metabolic flux from glycolysis to the pentose phosphate pathway, altering the redox equilibrium of the cytoplasmic NADP(H) pool. Remarkably, another key glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), is known to be inactivated in response to various oxidant treatments, and we show that this provokes a similar redirection of the metabolic flux.</p> <p>Conclusion</p> <p>The naturally occurring inactivation of GAPDH functions as a metabolic switch for rerouting the carbohydrate flux to counteract oxidative stress. As a consequence, altering the homoeostasis of cytoplasmic metabolites is a fundamental mechanism for balancing the redox state of eukaryotic cells under stress conditions.</p