Pseudogap Phase Boundary in Overdoped Bi_2Sr_2CaCu_2O_8 Studied by Measuring Out-of-plane Resistivity under the Magnetic Fields

The characteristic pseudogap temperature T* in Bi2Sr2CaCu2O8 system has been systematically evaluated as a function of doping, especially focusing on its overdoped region, by measuring the out-of-plane resistivity under the magnetic fields. Overdoped samples have been prepared by annealing TSFZ-grown Bi2Sr2CaCu2O8 single crystals under the high oxygen pressures (990 kgf/cm2). At a zero field, the out-of-plane resistivity showed a metallic behavior down to Tc (= 62 K), while under the magnetic fields of over 3 T,it showed typical upturn behavior from around 65 K upon decreasing temperature. This result suggests that the pseudogap and superconductivity are different phenomena.Comment: 2 pages, 2 figures. Final version accepted for the Proceedings of the M2S-IX Conference (Tokyo, September 2009

E3 Ubiquitin Ligase Synoviolin Is Involved in Liver Fibrogenesis

Chronic hepatic damage leads to liver fibrosis, which is characterized by the accumulation of collagen-rich extracellular matrix. However, the mechanism by which E3 ubiquitin ligase is involved in collagen synthesis in liver fibrosis is incompletely understood. This study aimed to explore the involvement of the E3 ubiquitin ligase synoviolin (Syno) in liver fibrosis.The expression and localization of synoviolin in the liver were analyzed in CCl(4)-induced hepatic injury models and human cirrhosis tissues. The degree of liver fibrosis and the number of activated hepatic stellate cells (HSCs) was compared between wild type (wt) and Syno(+/-) mice in the chronic hepatic injury model. We compared the ratio of apoptosis in activated HSCs between wt and Syno(+/-) mice. We also analyzed the effect of synoviolin on collagen synthesis in the cell line from HSCs (LX-2) using siRNA-synoviolin and a mutant synoviolin in which E3 ligase activity was abolished. Furthermore, we compared collagen synthesis between wt and Syno(-/-) mice embryonic fibroblasts (MEF) using quantitative RT-PCR, western blotting, and collagen assay; then, we immunohistochemically analyzed the localization of collagen in Syno(-/-) MEF cells.In the hepatic injury model as well as in cirrhosis, synoviolin was upregulated in the activated HSCs, while Syno(+/-) mice developed significantly less liver fibrosis than in wt mice. The number of activated HSCs was decreased in Syno(+/-) mice, and some of these cells showed apoptosis. Furthermore, collagen expression in LX-2 cells was upregulated by synoviolin overexpression, while synoviolin knockdown led to reduced collagen expression. Moreover, in Syno(-/-) MEF cells, the amounts of intracellular and secreted mature collagen were significantly decreased, and procollagen was abnormally accumulated in the endoplasmic reticulum.Our findings demonstrate the importance of the E3 ubiquitin ligase synoviolin in liver fibrosis

Composite structural motifs of binding sites for delineating biological functions of proteins

Most biological processes are described as a series of interactions between proteins and other molecules, and interactions are in turn described in terms of atomic structures. To annotate protein functions as sets of interaction states at atomic resolution, and thereby to better understand the relation between protein interactions and biological functions, we conducted exhaustive all-against-all atomic structure comparisons of all known binding sites for ligands including small molecules, proteins and nucleic acids, and identified recurring elementary motifs. By integrating the elementary motifs associated with each subunit, we defined composite motifs which represent context-dependent combinations of elementary motifs. It is demonstrated that function similarity can be better inferred from composite motif similarity compared to the similarity of protein sequences or of individual binding sites. By integrating the composite motifs associated with each protein function, we define meta-composite motifs each of which is regarded as a time-independent diagrammatic representation of a biological process. It is shown that meta-composite motifs provide richer annotations of biological processes than sequence clusters. The present results serve as a basis for bridging atomic structures to higher-order biological phenomena by classification and integration of binding site structures.Comment: 34 pages, 7 figure

Space Demonstration of Two-Layer Pop-Up Origami Deployable Membrane Reflectarray Antenna by 3U CubeSat OrigamiSat-2

3U CubeSat OrigamiSat-2 demonstrates a 50-cm × 50-cm two-layer pop-up Origami deployable membrane reflectarray antenna in space. The membrane has small stowage volume and high gain even though it has low flatness because of a large enough antenna area to cover its un-flatness. C-band transmitter is equipped in the CubeSat and offers 20-Mbps amateur satellite communication. In 3U size, a 1-m length deployable gravity gradient mast and magnetic torquer are equipped to stabilize and control its attitude. A camera is attached to the satellite to measure the shape of the membrane antenna. OrigamiSat-2 was selected as the Innovative Satellite Technology Demonstration-4 by Japan Aerospace Exploration Agency (JAXA) and is going to be launched in 2024 by Epsilon Launch Vehicle

The Ultrastructure of Tissue Damage by Amyloid Fibrils

Amyloidosis is a group of diseases that includes Alzheimer’s disease, prion diseases, transthyretin (ATTR) amyloidosis, and immunoglobulin light chain (AL) amyloidosis. The mechanism of organ dysfunction resulting from amyloidosis has been a topic of debate. This review focuses on the ultrastructure of tissue damage resulting from amyloid deposition and therapeutic insights based on the pathophysiology of amyloidosis. Studies of nerve biopsy or cardiac autopsy specimens from patients with ATTR and AL amyloidoses show atrophy of cells near amyloid fibril aggregates. In addition to the stress or toxicity attributable to amyloid fibrils themselves, the toxicity of non-fibrillar states of amyloidogenic proteins, particularly oligomers, may also participate in the mechanisms of tissue damage. The obscuration of the basement and cytoplasmic membranes of cells near amyloid fibrils attributable to an affinity of components constituting these membranes to those of amyloid fibrils may also play an important role in tissue damage. Possible major therapeutic strategies based on pathophysiology of amyloidosis consist of the following: (1) reducing or preventing the production of causative proteins; (2) preventing the causative proteins from participating in the process of amyloid fibril formation; and/or (3) eliminating already-deposited amyloid fibrils. As the development of novel disease-modifying therapies such as short interfering RNA, antisense oligonucleotide, and monoclonal antibodies is remarkable, early diagnosis and appropriate selection of treatment is becoming more and more important for patients with amyloidosis