Magnetic Order in the 2D Heavy-Fermion System CePt2In7 studied by muSR

The low-temperature microscopic magnetic properties of the quasi-2D heavyfermion compound, CePt2In7 are investigated by using a positive muon-spin rotation and relaxation (?muSR) technique. Clear evidence for the formation of a commensurate antiferromagnetic order below TN=5.40 K is presented. The magnetic order parameter is shown to fit well to a modified BSC gap-energy function in a strong-coupling scenario.Comment: Accepted in Journal of Physics: Conference Series (2014

Modest phenotypic improvements in ASA-deficient mice with only one UDP-galactose:ceramide-galactosyltransferase gene

BACKGROUND: Arylsulfatase A (ASA)-deficient mice are a model for the lysosomal storage disorder metachromatic leukodystrophy. This lipidosis is characterised by the lysosomal accumulation of the sphingolipid sulfatide. Storage of this lipid is associated with progressive demyelination. We have mated ASA-deficient mice with mice heterozygous for a non-functional allele of UDP-galactose:ceramide-galactosyltransferase (CGT). This deficiency is known to lead to a decreased synthesis of galactosylceramide and sulfatide, which should reduce sulfatide storage and improve pathology in ASA-deficient mice. RESULTS: ASA-/- CGT+/- mice, however, showed no detectable decrease in sulfatide storage. Neuronal degeneration of cells in the spiral ganglion of the inner ear, however, was decreased. Behavioural tests showed small but clear improvements of the phenotype in ASA-/- CGT+/- mice. CONCLUSION: Thus the reduction of galactosylceramide and sulfatide biosynthesis by genetic means overall causes modest improvements of pathology

The dual string sigma-model of the SU_q(3) sector

In four-dimensional N=4 super Yang-Mills (SYM) the SU(3) sub-sector spanned by purely holomorphic fields is isomorphic to the corresponding mixed one spanned by both holomorphic and antiholomorphic fields. This is no longer the case when one considers the marginally deformed N=4 SYM. The mixed SU(3) sector marginally deformed by a complex parameter beta, i.e. SU_q(3) with q=e^{2 i\pi\beta}, has been shown to be integrable at one-loop hep-th/0703150, while it is not the case for the corresponding purely holomorphic one. Moreover, the marginally deformed N=4 SYM also has a gravity dual constructed by Lunin and Maldacena in hep-th/0502086. However, the mixed SU_q(3) sector has not been studied from the supergravity point of view. Hence in this note, for the case of purely imaginary marginal $\beta$-deformations, we compute the superstring SU_q(3) \sigma-model in the fast spinning string limit and show that, for rational spinning strings, it reproduces the energy computed via Bethe equations.Comment: 20 page

Multiple phenotypic changes in mice after knockout of the B3gnt5 gene, encoding Lc3 synthase--a key enzyme in lacto-neolacto ganglioside synthesis

<p>Abstract</p> <p>Background</p> <p>Ganglioside biosynthesis occurs through a multi-enzymatic pathway which at the lactosylceramide step is branched into several biosynthetic series. Lc3 synthase utilizes a variety of galactose-terminated glycolipids as acceptors by establishing a glycosidic bond in the beta-1,3-linkage to GlcNaAc to extend the lacto- and neolacto-series gangliosides. In order to examine the lacto-series ganglioside functions in mice, we used gene knockout technology to generate Lc3 synthase gene <it>B3gnt5-</it>deficient mice by two different strategies and compared the phenotypes of the two null mouse groups with each other and with their wild-type counterparts.</p> <p>Results</p> <p><it>B3gnt5 </it>gene knockout mutant mice appeared normal in the embryonic stage and, if they survived delivery, remained normal during early life. However, about 9% developed early-stage growth retardation, 11% died postnatally in less than 2 months, and adults tended to die in 5-15 months, demonstrating splenomegaly and notably enlarged lymph nodes. Without lacto-neolacto series gangliosides, both homozygous and heterozygous mice gradually displayed fur loss or obesity, and breeding mice demonstrated reproductive defects. Furthermore, <it>B3gnt5 </it>gene knockout disrupted the functional integrity of B cells, as manifested by a decrease in B-cell numbers in the spleen, germinal center disappearance, and less efficiency to proliferate in hybridoma fusion.</p> <p>Conclusions</p> <p>These novel results demonstrate unequivocally that lacto-neolacto series gangliosides are essential to multiple physiological functions, especially the control of reproductive output, and spleen B-cell abnormality. We also report the generation of anti-IgG response against the lacto-series gangliosides 3'-isoLM1 and 3',6'-isoLD1.</p

Yangians in Deformed Super Yang-Mills Theories

We discuss the integrability structure of deformed, four-dimensional N=4 super Yang-Mills theories using Yangians. We employ a recent procedure by Beisert and Roiban that generalizes the beta deformation of Lunin and Maldacena to produce N=1 superconformal gauge theories, which have the superalgebra SU(2,2|1)xU(1)xU(1). The deformed theories, including those with the more general twist, were shown to have retained their integrable structure. Here we examine the Yangian algebra of these deformed theories. In a five field subsector, we compute the two cases of SU(2)xU(1)xU(1)xU(1) and SU(2|1)xU(1)xU(1) as residual symmetries of SU(2,2|1)xU(1)xU(1). We compute a twisted coproduct for these theories, and show that only for the residual symmetry do we retain the standard coproduct. The twisted coproduct thus provides a method for symmetry breaking. However, the full Yangian structure of SU(2|3) is manifest in our subsector, albeit with twisted coproducts, and provides for the integrability of the theory.Comment: 17 page

Solving matrix models using holomorphy

We investigate the relationship between supersymmetric gauge theories with moduli spaces and matrix models. Particular attention is given to situations where the moduli space gets quantum corrected. These corrections are controlled by holomorphy. It is argued that these quantum deformations give rise to non-trivial relations for generalized resolvents that must hold in the associated matrix model. These relations allow to solve a sector of the associated matrix model in a similar way to a one-matrix model, by studying a curve that encodes the generalized resolvents. At the level of loop equations for the matrix model, the situations with a moduli space can sometimes be considered as a degeneration of an infinite set of linear equations, and the quantum moduli space encodes the consistency conditions for these equations to have a solution.Comment: 38 pages, JHEP style, 1 figur

Four-loop anomalous dimensions in Leigh-Strassler deformations

We determine the scalar part of the four-loop chiral dilatation operator for Leigh-Strassler deformations of N=4 super Yang-Mills. This is sufficient to find the four-loop anomalous dimensions for operators in closed scalar subsectors. This includes the SU(2) subsector of the (complex) beta-deformation, where we explicitly compute the anomalous dimension for operators with a single impurity. It also includes the "3-string null" operators of the cubic Leigh-Strassler deformation. Our four-loop results show that the rational part of the anomalous dimension is consistent with a conjecture made in arXiv:1108.1583 based on the three-loop result of arXiv:1008.3351 and the N=4 magnon dispersion relation. Here we find additional zeta(3) terms.Comment: Latex, feynmp, 21 page

Intranasal Administration of poly(I:C) and LPS in BALB/c Mice Induces Airway Hyperresponsiveness and Inflammation via Different Pathways

BACKGROUND: Bacterial and viral infections are known to promote airway hyperresponsiveness (AHR) in asthmatic patients. The mechanism behind this reaction is poorly understood, but pattern recognizing Toll-like receptors (TLRs) have recently been suggested to play a role. MATERIALS AND METHODS: To explore the relation between infection-induced airway inflammation and the development of AHR, poly(I:C) activating TLR3 and LPS triggering TLR4, were chosen to represent viral and bacterial induced interactions, respectively. Female BALB/c or MyD88-deficient C57BL/6 mice were treated intranasally with either poly(I:C), LPS or PBS (vehicle for the control group), once a day, during 4 consecutive days. RESULTS: When methacholine challenge was performed on day 5, BALB/c mice responded with an increase in airway resistance. The maximal resistance was higher in the poly(I:C) and LPS treated groups than among the controls, indicating development of AHR in response to repeated TLR activation. The proportion of lymphocytes in broncheoalveolar lavage fluid (BALF) increased after poly(I:C) treatment whereas LPS enhanced the amount of neutrophils. A similar cellular pattern was seen in lung tissue. Analysis of 21 inflammatory mediators in BALF revealed that the TLR response was receptor-specific. MyD88-deficient C57BL/6 mice responded to poly (I:C) with an influx of lymphocytes, whereas LPS caused no inflammation. CONCLUSION: In vivo activation of TLR3 and TLR4 in BALB/c mice both caused AHR in conjunction with a local inflammatory reaction. The AHR appeared to be identical regardless of which TLR that was activated, whereas the inflammation exhibited a receptor specific profile in terms of both recruited cells and inflammatory mediators. The inflammatory response caused by LPS appeared to be dependent on MyD88 pathway. Altogether the presented data indicate that the development of AHR and the induction of local inflammation might be the result of two parallel events, rather than one leading to another