Metal-Insulator Transitions in Degenerate Hubbard Models and Ax_xC60_{60}

Mott-Hubbard metal-insulator transitions in $N$-fold degenerate Hubbard models are studied within the Gutzwiller approximation. For any rational filling with $x$ (integer) electrons per site it is found that metal-insulator transition occurs at a critical correlation energy $U_c(N,x)=U_c(N,2N-x)=\gamma(N,x)|\bar{\epsilon}(N,x)|$, where $\bar{\epsilon}$ is the band energy per particle for the uncorrelated Fermi-liquid state and $\gamma(N,x)$ is a geometric factor which increases linearly with $x$. We propose that the alkali metal doped fullerides $A_xC_{60}$ can be described by a 3-fold degenerate Hubbard model. Using the current estimate of band width and correlation energy this implies that most of ${\rm A_xC_{60}}$, at integer $x$, are Mott-Hubbard insulators and ${\rm A_3C_{60}}$ is a strongly correlated metal.Comment: 10 pages, Revte

Kulturkammervorrichtung zur Erzeugung von flusslosen und zeitstabilen Gradienten

Kulturkammervorrichtung zur Erzeugung von flusslosen und zeitstabilen Gradienten (1), umfassend eine Beobachtungskammer (2), in der ein Konzentrationsgefüge dreidimensional einstellbar ist, mehrere Versorgungskanäle (4) zur Durchströmung mit einem Versorgungsfluid (10), jeweils eine Trennwand (13) zwischen den Versorgungskanälen (4) und der Beobachtungskammer (2), wobei die Trennwand (13) Poren (5) zur Diffusion von Versorgungsfluid zwischen dem jeweiligen Versorgungskanal (4) und der Beobachtungskammer (2) aufweist, wobei eine erste Anordnung von Versorgungskanälen (4O) oberhalb der Beobachtungskammer (2) und eine zweite Anordnung von Versorgungskanälen (4U) unterhalb der Beobachtungskammer (2) angeordnet sind

Gaps and excitations in fullerides with partially filled bands : NMR study of Na2C60 and K4C60

We present an NMR study of Na2C60 and K4C60, two compounds that are related by electron-hole symmetry in the C60 triply degenerate conduction band. In both systems, it is known that NMR spin-lattice relaxation rate (1/T1) measurements detect a gap in the electronic structure, most likely related to singlet-triplet excitations of the Jahn-Teller distorted (JTD) C60^{2-} or C60^{4-}. However, the extended temperature range of the measurements presented here (10 K to 700 K) allows to reveal deviations with respect to this general trend, both at high and low temperatures. Above room temperature, 1/T1 deviates from the activated law that one would expect from the presence of the gap and saturates. In the same temperature range, a lowering of symmetry is detected in Na2C60 by the appearance of quadrupole effects on the 23Na spectra. In K4C60, modifications of the 13C spectra lineshapes also indicate a structural modification. We discuss this high temperature deviation in terms of a coupling between JTD and local symmetry. At low temperatures, 1/T$_1$T tends to a constant value for Na2C60, both for 13C and 23Na NMR. This indicates a residual metallic character, which emphasizes the proximity of metallic and insulting behaviors in alkali fullerides.Comment: 12 pages, 13 figure

Expanding the set of rhodococcal Baeyer–Villiger monooxygenases by high-throughput cloning, expression and substrate screening

To expand the available set of Baeyer–Villiger monooxygenases (BVMOs), we have created expression constructs for producing 22 Type I BVMOs that are present in the genome of Rhodococcus jostii RHA1. Each BVMO has been probed with a large panel of potential substrates. Except for testing their substrate acceptance, also the enantioselectivity of some selected BVMOs was studied. The results provide insight into the biocatalytic potential of this collection of BVMOs and expand the biocatalytic repertoire known for BVMOs. This study also sheds light on the catalytic capacity of this large set of BVMOs that is present in this specific actinomycete. Furthermore, a comparative sequence analysis revealed a new BVMO-typifying sequence motif. This motif represents a useful tool for effective future genome mining efforts.

A single gene defect causing claustrophobia

Claustrophobia, the well-known fear of being trapped in narrow/closed spaces, is often considered a conditioned response to traumatic experience. Surprisingly, we found that mutations affecting a single gene, encoding a stress-regulated neuronal protein, can cause claustrophobia. Gpm6a-deficient mice develop normally and lack obvious behavioral abnormalities. However, when mildly stressed by single-housing, these mice develop a striking claustrophobia-like phenotype, which is not inducible in wild-type controls, even by severe stress. The human GPM6A gene is located on chromosome 4q32-q34, a region linked to panic disorder. Sequence analysis of 115 claustrophobic and non-claustrophobic subjects identified nine variants in the noncoding region of the gene that are more frequent in affected individuals (P=0.028). One variant in the 3′untranslated region was linked to claustrophobia in two small pedigrees. This mutant mRNA is functional but cannot be silenced by neuronal miR124 derived itself from a stress-regulated transcript. We suggest that loosing dynamic regulation of neuronal GPM6A expression poses a genetic risk for claustrophobia

100G Flexible IM-DD 850 nm VCSEL Transceiver with Fractional Bit Rate Using Eight-Dimensional PAM

We demonstrate a novel optical transceiver scheme with a net flexible bit rate up to 100Gbit/s with 5 Gbit/s granularity, using an eight-dimensional modulation format family, and investigate its performance on capacity, reach, and power tolerance

Toward the Assessment of Food Toxicity for Celiac Patients: Characterization of Monoclonal Antibodies to a Main Immunogenic Gluten Peptide

13 pages, 8 figures.-- PMID: 18509534 [PubMed].-- PMCID: PMC2386552.[Background and Aims] Celiac disease is a permanent intolerance to gluten prolamins from wheat, barley, rye and, in some patients, oats. Partially digested gluten peptides produced in the digestive tract cause inflammation of the small intestine. High throughput, immune-based assays using monoclonal antibodies specific for these immunotoxic peptides would facilitate their detection in food and enable monitoring of their enzymatic detoxification. Two monoclonal antibodies, G12 and A1, were developed against a highly immunotoxic 33-mer peptide. The potential of each antibody for quantifying food toxicity for celiac patients was studied.[Methods] Epitope preferences of G12 and A1 antibodies were determined by ELISA with gluten-derived peptide variants of recombinant, synthetic or enzymatic origin.[Results] The recognition sequences of G12 and A1 antibodies were hexameric and heptameric epitopes, respectively. Although G12 affinity for the 33-mer was superior to A1, the sensitivity for gluten detection was higher for A1. This observation correlated to the higher number of A1 epitopes found in prolamins than G12 epitopes. Activation of T cell from gluten digested by glutenases decreased equivalently to the detection of intact peptides by A1 antibody. Peptide recognition of A1 included gliadin peptides involved in the both the adaptive and innate immunological response in celiac disease.[Conclusions] The sensitivity and epitope preferences of the A1 antibody resulted to be useful to detect gluten relevant peptides to infer the potential toxicity of food for celiac patients as well as to monitor peptide modifications by transglutaminase 2 or glutenases.This work was supported by the Asociación de Celiacos de Madrid (to Carolina Sousa), by the CTA (Corporación Tecnológica de Andalucía) and IDEA (Agencia de Innovación y Desarrollo de Andalucía) (to Angel Cebolla) and by grants BFU2007-64999 from Plan Nacional de Investigación científica, Desarrollo e Innovación tecnológica (Miniterio de Educación y Ciencia) and RICET-RD06/0021-0014, Spain (to Manuel C. López). Belén Morón was supported by a fellowship from Consejo Andaluz de Colegios Oficiales de Farmacéuticos.Peer reviewe

Pleiotropy of Glycogen Synthase Kinase-3 Inhibition by CHIR99021 Promotes Self-Renewal of Embryonic Stem Cells from Refractory Mouse Strains

Background: Inhibition of glycogen synthase kinase-3 (GSK-3) improves the efficiency of embryonic stem (ES) cell derivation from various strains of mice and rats, as well as dramatically promotes ES cell self-renewal potential. b-catenin has been reported to be involved in the maintenance of self-renewal of ES cells through TCF dependent and independent pathway. But the intrinsic difference between ES cell lines from different species and strains has not been characterized. Here, we dissect the mechanism of GSK-3 inhibition by CHIR99021 in mouse ES cells from refractory mouse strains. Methodology/Principal Findings: We found that CHIR99021, a GSK-3 specific inhibitor, promotes self-renewal of ES cells from recalcitrant C57BL/6 (B6) and BALB/c mouse strains through stabilization of b-catenin and c-Myc protein levels. Stabilized b-catenin promoted ES self-renewal through two mechanisms. First, b-catenin translocated into the nucleus to maintain stem cell pluripotency in a lymphoid-enhancing factor/T-cell factor–independent manner. Second, b-catenin binds plasma membrane-localized E-cadherin, which ensures a compact, spherical morphology, a hallmark of ES cells. Further, elevated c-Myc protein levels did not contribute significantly to CH-mediated ES cell self-renewal. Instead, the role of c-Myc is dependent on its transformation activity and can be replaced by N-Myc but not L-Myc. b-catenin and c-Myc have similar effects on ES cells derived from both B6 and BALB/c mice. Conclusions/Significance: Our data demonstrated that GSK-3 inhibition by CH promotes self-renewal of mouse ES cell

Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ molecules

Celiac disease is caused by an abnormal intestinal T-cell response to gluten proteins of wheat, barley and rye. Over the last few years, a number of gluten T-cell epitopes restricted by celiac disease associated HLA-DQ molecules have been characterized. In this work, we give an overview of these epitopes and suggest a comprehensive, new nomenclature