Electronic Correlations within Fermionic Lattice Models

We investigate two-site electronic correlations within generalized Hubbard model, which incorporates the conventional Hubbard model (parameters: $t$ (hopping between nearest neighbours), $U$ (Coulomb repulsion (attraction)) supplemented by the intersite Coulomb interactions (parameters: $J^{(1)}$(parallel spins), $J^{(2)}$ (antiparellel spins)) and the hopping of the intrasite Cooper pairs (parameter: $V$). As a first step we find the eigenvalues $E_{\alpha}$ and eigenvectors $|E_{\alpha}>$ of the dimer and we represent each partial Hamiltonian $E_{\alpha} |E_{\alpha} > < E_{\alpha} |$ ($\alpha =1,2,..,16$) in the second quantization with the use of the Hubbard and spin operators. Each dimer energy level possesses its own Hamiltonian describing different two-site interactions which can be active only in the case when the level will be occupied by the electrons. A typical feature is the appearence of two generalized $t-J$ interactions ascribed to two different energy levels which do not vanish even for $$ and their coupling constants are equal to $\pm t$ in this case. The competition between ferromagnetism, antiferromagnetism and superconductivity (intrasite and intersite pairings) is also a typical feature of the model because it persists in the case $U=J^{(1)}=J^{(2)}=V=0$ and $t\neq 0$. The same types of the electronic, competitive interactions are scattered between different energy levels and therefore their thermodynamical activities are dependent on the occupation of these levels. It qualitatively explains the origin of the phase diagram of the model. We consider also a real lattice as a set of interacting dimers to show that the competition between magnetism and superconductivity seems to be universal for fermonic lattice models.Comment: 12 page

Hubbard Hamiltonian in the dimer representation. Large U limit

We formulate the Hubbard model for the simple cubic lattice in the representation of interacting dimers applying the exact solution of the dimer problem. By eliminating from the considerations unoccupied dimer energy levels in the large U limit (it is the only assumption) we analytically derive the Hubbard Hamiltonian for the dimer (analogous to the well-known t-J model), as well as, the Hubbard Hamiltonian for the crystal as a whole by means of the projection technique. Using this approach we can better visualize the complexity of the model, so deeply hidden in its original form. The resulting Hamiltonian is a mixture of many multiple ferromagnetic, antiferromagnetic and more exotic interactions competing one with another. The interplay between different competitive interactions has a decisive influence on the resulting thermodynamic properties of the model, depending on temperature, model parameters and assumed average number of electrons per lattice site. A simplified form of the derived Hamiltonian can be obtained using additionally Taylor expansion with respect to $x=\frac{t}{U}$ (t-hopping integral between nearest neighbours, U-Coulomb repulsion). As an example, we present the expansion including all terms proportional to t and to $\frac{t^2}U$ and we reproduce the exact form of the Hubbard Hamiltonian in the limit $U\to \infty$. The nonperturbative approach, presented in this paper, can, in principle, be applied to clusters of any size, as well as, to another types of model Hamiltonians.Comment: 26 pages, 1 figure, LaTeX; added reference

Histone deacetylases in RA: epigenetics and epiphenomena

Reduced synovial expression of histone deacetylases (HDACs) is proposed to contribute to pathology in rheumatoid arthritis (RA) by enhancing histone-dependent access of transcription factors to promoters of inflammatory genes. In the previous issue of Arthritis Research & Therapy, Kawabata and colleagues provided independent evidence that HDAC activity is increased in the synovium and fibroblast-like synoviocytes (FLSs) of patients with RA and is paralleled by increased HDAC1 expression and synovial tumor necrosis factor-alpha (TNFα) production. Remarkably, stimulation of RA FLSs with TNFα specifically increases HDAC activity and HDAC1 expression, suggesting that changes in synovial HDAC activity and expression may be secondary to local inflammatory status

A Pixel Vertex Tracker for the TESLA Detector

In order to fully exploit the physics potential of a e+e- linear collider, such as TESLA, a Vertex Tracker providing high resolution track reconstruction is required. Hybrid Silicon pixel sensors are an attractive sensor technology option due to their read-out speed and radiation hardness, favoured in the high rate TESLA environment, but have been so far limited by the achievable single point space resolution. A novel layout of pixel detectors with interleaved cells to improve their spatial resolution is introduced and the results of the characterisation of a first set of test structures are discussed. In this note, a conceptual design of the TESLA Vertex Tracker, based on hybrid pixel sensors is presentedComment: 20 pages, 11 figure

Targeting histone deacetylase activity in rheumatoid arthritis and asthma as prototypes of inflammatory disease: should we keep our HATs on?

Cellular activation, proliferation and survival in chronic inflammatory diseases is regulated not only by engagement of signal trans-duction pathways that modulate transcription factors required for these processes, but also by epigenetic regulation of transcription factor access to gene promoter regions. Histone acetyl trans-ferases coordinate the recruitment and activation of transcription factors with conformational changes in histones that allow gene promoter exposure. Histone deacetylases (HDACs) counteract histone acetyl transferase activity through the targeting of both histones as well as nonhistone signal transduction proteins important in inflammation. Numerous studies have indicated that depressed HDAC activity in patients with inflammatory airway diseases may contribute to local proinflammatory cytokine production and diminish patient responses to corticosteroid treatment. Recent observations that HDAC activity is depressed in rheumatoid arthritis patient synovial tissue have predicted that strategies restoring HDAC function may be therapeutic in this disease as well. Pharmacological inhibitors of HDAC activity, however, have demonstrated potent therapeutic effects in animal models of arthritis and other chronic inflammatory diseases. In the present review we assess and reconcile these outwardly paradoxical study results to provide a working model for how alterations in HDAC activity may contribute to pathology in rheumatoid arthritis, and highlight key questions to be answered in the preclinical evaluation of compounds modulating these enzymes

Influence of viscosity modifying agent on some rheological properties, segregation resistance and compressive strength of self-compacting concrete

Rheological properties of self-compacting concrete mixes containing a viscosity modifying agent (VMA) in their composition were studied. After preliminary studies self-compacting concrete mixes and, particularly, a fluid concrete mix prone to segregation of its ingredients were chosen. VMA was added in various amounts to that concrete mix to check how it performed in fresh and hardened concrete. Main studies focused on the influence of VMA on the following properties of concrete mixes: the slump flow, the flow time into the diameter of 500 mm and the resistance to segregation in the vertical direction. Moreover, the air content of concrete mixes and the 28-day compressive strength of concrete were measured. Test results showed that VMA significantly influenced the rheological properties of concrete mix, stabilised it and reduced the segregation. It was proved, that the concrete mix modified by VMA used in the optimal amount, featured the smallest scatter of concrete strength results. Besides, the Tukey's test showed that a reduction of the concrete compressive strength is possible to be statistically insignificant when compared to the reference level. First published online: 19 Oct 201

High resolution pixel detectors for e+e- linear colliders

The physics goals at the future e+e- linear collider require high performance vertexing and impact parameter resolution. Two possible technologies for the vertex detector of an experimental apparatus are outlined in the paper: an evolution of the Hybrid Pixel Sensors already used in high energy physics experiments and a new detector concept based on the monolithic CMOS sensors.Comment: 8 pages, to appear on the Proceedings of the International Workshop on Linear Colliders LCWS99, Sitges (Spain), April 28 - May 5, 199

Histone deacetylase inhibitors suppress rheumatoid arthritis fibroblast-like synoviocyte and macrophage IL-6 production by accelerating mRNA decay

Background Histone deacetylase inhibitors (HDACi) display potent therapeutic efficacy in animal models of arthritis and suppress inflammatory cytokine production in rheumatoid arthritis (RA) synovial macrophages and tissue. Objectives To determine the molecular mechanisms contributing to the suppressive effects of HDACi on RA synovial cell activation, using interleukin 6 (IL-6) regulation as a model. Methods RA fibroblast-like synoviocytes (FLS) and healthy donor macrophages were treated with IL-1 beta, tumour necrosis factor (TNF)alpha, lipopolysaccharide or polyinosinic: polycytidylic acid (poly(I:C)) in the absence or presence of the HDACi trichostatin A (TSA) or ITF2357 (givinostat). IL-6 production and mRNA expression was measured by ELISA and quantitative PCR (qPCR), respectively. Protein acetylation and the activation of intracellular signalling pathways were assessed by immunoblotting. The DNA-binding activity of nuclear factor kappa B (NF kappa B) and activator protein 1 (AP-1) components was measured by ELISA-based assays. Results HDACi (0.25-1.0 mu M) suppressed RA FLS IL-6 production induced by IL-1 beta, TNF alpha and Toll-like receptor ligands. Phosphorylation of mitogen-activated protein kinases and inhibitor of kappa B alpha (I kappa B alpha) following IL-1 beta stimulation were unaffected by HDACi, as were AP-1 composition and binding activity, and c-Jun induction. TSA induced a significant reduction in nuclear retention of NF kappa B in FLS 24 h after IL-1 beta stimulation, but this did not reduce NF kappa B transcriptional activity or correlate temporally with reductions in IL-6 mRNA accumulation. HDACi significantly reduced the stability of IL-6 mRNA in FLS and macrophages. Conclusions Our study identifies a novel, shared molecular mechanism by which HDACi can disrupt inflammatory cytokine production in RA synovial cells, namely the promotion of mRNA decay, and suggests that targeting HDAC activity may be clinically useful in suppressing inflammation in R