Optical conductivity in the CuO double chains of PrBa_2Cu_4O_8: Consequences of charge fluctuation

We calculate the optical conductivity of the CuO double chains of PrBa$_2$Cu$_4$O$_8$ by the mean-field approximation for the coupled two-chain Hubbard model around quarter filling. We show that the $\sim$40 meV peak structure, spectral shape, and small Drude weight observed in experiment are reproduced well by the present calculation provided that the stripe-type charge ordering presents. We argue that the observed anomalous optical response may be due to the presence of stripe-type fluctuations of charge carriers in the CuO double chains; the fast time scale of the optical measurement should enable one to detect slowly fluctuating order parameters as virtually a long-range order.Comment: 7 pages, 5 eps figure

Anomalous behaviors of the charge and spin degrees of freedom in the CuO double chains of PrBa2_2Cu4_4O8_8

The density-matrix renormalization-group method is used to study the electronic states of a two-chain Hubbard model for CuO double chains of PrBa$_2$Cu$_4$O$_8$. We show that the model at quarter filling has the charge ordered phases with stripe-type and in-line--type patterns in the parameter space, and in-between, there appears a wide region of vanishing charge gap; the latter phase is characteristic of either Tomonaga-Luttinger liquid or a metallic state with a spin gap. We argue that the low-energy electronic state of the CuO double chains of PrBa$_2$Cu$_4$O$_8$ should be in the metallic state with a possibly small spin gap.Comment: REVTEX 4, 10 pages, 9 figures; submitted to PR

Up regulated expression of tumour necrosis factor α converting enzyme in peripheral monocytes of patients with early systemic sclerosis

Background: Systemic sclerosis (SSc) is accompanied by abnormalities in humoral and cellular immune systems. Objective: To determine the genes specifically expressed in the immune system in SSc by analysis of the gene expression profile of peripheral blood mononuclear cells (PBMC) from patients with SSc, including those treated with haematopoietic stem cell transplantation (HSCT). Additionally, to investigate the clinical significance of the up regulation of tumour necrosis factor α (TNFα) converting enzyme (TACE). Methods: PBMC from patients with SSc (n = 23) and other autoimmune diseases (systemic lupus erythematosus (SLE, n = 16), rheumatoid arthritis (RA, n = 29)), and from disease-free controls (n = 36) were examined. Complementary DNA arrays were used to evaluate gene expression of PBMC, in combination with real time quantitative polymerase chain reactions. TACE protein expression in PBMC was examined by fluorescence activated cell sorter (FACS). Results: In patients with SSc 118 genes were down regulated after HSCT. Subsequent comparative analysis of SSc without HSCT and healthy controls indicated SSc-specific up regulation for three genes: monocyte chemoattractant protein-3 (p = 0.0015), macrophage inflammatory protein 3α (p = 0.0339), and TACE (p = 0.0251). In the FACS analysis, TACE protein was mainly expressed on CD14(+) monocytes both in patients with SSc and controls. TACE expression on CD14(+) cells was significantly increased in patients with early SSc (p = 0.0096), but not in those with chronic SSc, SLE, or RA. TACE protein levels in SSc monocytes correlated with the intracellular CD68 levels (p = 0.0016). Conclusions: Up regulation of TACE expression was a unique profile in early SSc, and may affect the function of TNFα and other immunoregulatory molecules

Serum levels of soluble Fas/APO-1 (CD95) and its molecular structure in patients with systemic lupus erythematosus (SLE) and other autoimmune diseases

There are two major forms of the Fas molecule, membranous Fas and soluble Fas (sFas). To clarify the clinical significance of sFas in autoimmune diseases, we designed a sandwich ELISA to determine serum concentrations of sFas and its molecular structure, and we then analysed the correlation between levels of sFas and laboratory findings in patients with SLE and other autoimmune diseases. The levels of serum sFas were significantly higher in SLE patients than in subjects with other autoimmune diseases and in healthy donors, and the frequency of a positive serum sFas was much greater in SLE patients with high SLE disease activity index scores than in those with low scores. In addition, sFas-positive SLE patients showed a significant difference in various laboratory parameters from sFas-negative SLE patients. Serial measurements of serum sFas levels in SLE patients with active disease revealed that the elevated level of sFas dramatically decreased with improvement in clinical and laboratory findings, following corticosteroid therapy. We propose that the serum level of sFas can serve as an appropriate marker for evaluating SLE disease activity. Serum sFas is heterogeneous with respect to molecular structure, thus several mechanisms are involved in the generation of sFas