NMR evidence for very slow carrier density fluctuations in the organic metal (TMTSF)2_2ClO4_4

We have investigated the origin of the large increase in spin-echo decay rates for the $^{77}$Se nuclear spins at temperatures near to $T=30K$ in the organic superconductor (TMTSF)$_2$ClO$_4$. The measured angular dependence of $T_2^{-1}$ demonstrates that the source of the spin-echo decays lies with carrier density fluctuations rather than fluctuations in TMTSF molecular orientation. The very long time scales are directly associated with the dynamics of the anion ordering occurring at $T=25K$, and the inhomogeneously broadened spectra at lower temperatures result from finite domain sizes. Our results are similar to observations of line-broadening effects associated with charge-ordering transitions in quasi-two dimensional organic conductors.Comment: 5 pages, 4 figure

Ikaros has a crucial role in regulation of B cell receptor signaling

transcription factor Ikaros, a key regulator of hematopoiesis, has an essential role in lymphocyte development. In mice, fetal lymphoid differentiation is blocked in the absence of Ikaros, and whereas T cells develop postnatally, B cells are totally absent. The significance of Ikaros in the B cell development is evident, but how Ikaros regulates B cell function has neither been established nor previously been studied with B cells that lack Ikaros expression. Here we show that disruption of Ikaros in the chicken B cell line DT40 induces a B cell receptor (BCR) signaling defect with reduced phospholipase C gamma 2 phosphorylation and impaired intracellular calcium mobilization, which is restored by Ikaros reintroduction. Furthermore, we show that lack of Ikaros induces hyperphosphorylation of Casitas B lymphoma protein subsequent to BCR activation. These results indicate that the absolute need of Ikaros for development, cell fate decisions and maintenance of B cells is due to the enhancement of BCR signaling

Phospholipase C-γ2 and Vav cooperate within signaling microclusters to propagate B cell spreading in response to membrane-bound antigen

B cell receptor (BCR) recognition of membrane-bound antigen initiates a spreading and contraction response, the extent of which is controlled through the formation of signaling-active BCR-antigen microclusters and ultimately affects the outcome of B cell activation. We followed a genetic approach to define the molecular requirements of BCR-induced spreading and microcluster formation. We identify a key role for phospholipase C-γ2 (PLCγ2), Vav, B cell linker, and Bruton's tyrosine kinase in the formation of highly coordinated “microsignalosomes,” the efficient assembly of which is absolutely dependent on Lyn and Syk. Using total internal reflection fluorescence microscopy, we examine at high resolution the recruitment of PLCγ2 and Vav to microsignalosomes, establishing a novel synergistic relationship between the two. Thus, we demonstrate the importance of cooperation between components of the microsignalosome in the amplification of signaling and propagation of B cell spreading, which is critical for appropriate B cell activation

Exact diagonalization study of Mott transition in the Hubbard model on an anisotropic triangular lattice

We study Mott transition in the two-dimensional Hubbard model on an anisotropic triangular lattice. We use the Lanczos exact diagonalization of finite-size clusters up to eighteen sites, and calculate Drude weight, charge gap, double occupancy and spin structure factor. We average these physical quantities over twisted boundary conditions in order to reduce finite-size effects. We find a signature of the Mott transition in the dependence of the Drude weight and/or charge gap on the system size. We also examine the possibility of antiferromagnetic order from the spin structure factor. Combining these information, we propose a ground-state phase diagram which has a nonmagnetic insulating phase between a metallic phase and an insulating phase with antiferromagnetic order. Finally, we compare our results with those reported in the previous theoretical studies, and discuss the possibility of an unconventional insulating state.Comment: 10 pages, 11 figure

Association study with Wegener granulomatosis of the human phospholipase Cγ2 gene

BACKGROUND: Wegener Granulomatosis (WG) is a multifactorial disease of yet unknown aetiology characterized by granulomata of the respiratory tract and systemic necrotizing vasculitis. Analyses of candidate genes revealed several associations, e.g. with α(1)-antitrypsin, proteinase 3 and with the HLA-DPB1 locus. A mutation in the abnormal limb mutant 5 (ALI5) mouse in the region coding for the hydrophobic ridge loop 3 (HRL3) of the phospholipaseCγ2 (PLCγ-2) gene, corresponding to human PLCγ-2 exon 27, leads to acute and chronic inflammation and granulomatosis. For that reason, we screened exons 11, 12 and 13 coding for the hydrophobic ridge loop 1 and 2 (HRL1 and 2, respectively) and exon 27 of the PLCγ-2 protein by single strand conformation polymorphism (SSCP), sequencing and PCR/ restriction fragment length polymorphism (RFLP) analyses. In addition, we screened indirectly for disease association via 4 microsatellites with pooled DNA in the PLCγ-2 gene. RESULTS: Although a few polymorphisms in these distinct exons were observed, significant differences in allele frequencies were not identified between WG patients and respective controls. In addition, the microsatellite analyses did not reveal a significant difference between our patient and control cohort. CONCLUSION: This report does not reveal any hints for an involvement of the PLCγ-2 gene in the pathogenesis of WG in our case-control study

Generation of a new mouse model of glaucoma characterized by reduced expression of the AP-2β and AP-2δ proteins

We generated 6 transgenic lines with insertion of an expression plasmid for the R883/M xanthine dehydrogenase (XDH) mutant protein. Approximately 20% of the animals deriving from one of the transgenic lines show ocular abnormalities and an increase in intra-ocular pressure which are consistent with glaucoma. The observed pathologic phenotype is not due to expression of the transgene, but rather the consequence of the transgene insertion site, which has been defined by genome sequencing. The insertion site maps to chromosome 1qA3 in close proximity to the loci encoding AP-2\u3b2 and AP-2\u3b4, two proteins expressed in the eye. The insertion leads to a reduction in AP-2\u3b2 and AP-2\u3b4 levels. Down-regulation of AP-2\u3b2 expression is likely to be responsible for the pathologic phenotype, as conditional deletion of the Tfap2b gene in the neural crest has recently been shown to cause defective development of the eye anterior segment and early-onset glaucoma. In these conditional knock-out and our transgenic mice, the morphological/histological features of the glaucomatous pathology are surprisingly similar. Our transgenic mouse represents a model of angle-closure glaucoma and a useful tool for the study of the pathogenesis and the development of innovative therapeutic strategies

The unprecedented optical outburst of the quasar 3C 454.3. The WEBT campaign of 2004-2005

The radio quasar 3C 454.3 underwent an exceptional optical outburst lasting more than 1 year and culminating in spring 2005. The maximum brightness detected was R = 12.0, which represents the most luminous quasar state thus far observed (M_B ~ -31.4). In order to follow the emission behaviour of the source in detail, a large multiwavelength campaign was organized by the Whole Earth Blazar Telescope (WEBT). Continuous optical, near-IR and radio monitoring was performed in several bands. ToO pointings by the Chandra and INTEGRAL satellites provided additional information at high energies in May 2005. The historical radio and optical light curves show different behaviours. Until about 2001.0 only moderate variability was present in the optical regime, while prominent and long-lasting radio outbursts were visible at the various radio frequencies, with higher-frequency variations preceding the lower-frequency ones. After that date, the optical activity increased and the radio flux is less variable. This suggests that the optical and radio emissions come from two separate and misaligned jet regions, with the inner optical one acquiring a smaller viewing angle during the 2004-2005 outburst. Moreover, the colour-index behaviour (generally redder-when-brighter) during the outburst suggests the presence of a luminous accretion disc. A huge mm outburst followed the optical one, peaking in June-July 2005. The high-frequency (37-43 GHz) radio flux started to increase in early 2005 and reached a maximum at the end of our observing period (end of September 2005). VLBA observations at 43 GHz during the summer confirm theComment: 7 pages, 4 figures, to be published in A&

The WEBT Campaign on the Blazar 3C279 in 2006

The quasar 3C279 was the target of an extensive multiwavelength monitoring campaign from January through April 2006, including an optical-IR-radio monitoring campaign by the Whole Earth Blazar Telescope (WEBT) collaboration. In this paper we focus on the results of the WEBT campaign. The source exhibited substantial variability of optical flux and spectral shape, with a characteristic time scale of a few days. The variability patterns throughout the optical BVRI bands were very closely correlated with each other. In intriguing contrast to other (in particular, BL Lac type) blazars, we find a lag of shorter- behind longer-wavelength variability throughout the RVB ranges, with a time delay increasing with increasing frequency. Spectral hardening during flares appears delayed with respect to a rising optical flux. This, in combination with the very steep IR-optical continuum spectral index of ~ 1.5 - 2.0, may indicate a highly oblique magnetic field configuration near the base of the jet. An alternative explanation through a slow (time scale of several days) acceleration mechanism would require an unusually low magnetic field of < 0.2 G, about an order of magnitude lower than inferred from previous analyses of simultaneous SEDs of 3C279 and other FSRQs with similar properties.Comment: Accepted for publication in Ap