171 research outputs found
Charge dynamics of Ca_{2-x}Na_{x}CuO_{2}Cl_{2} as a correlated electron system with the ideal tetragonal lattice
We report the reflectivity and the resistivity measurement of
Ca_{2-x}Na_{x}CuO_{2}Cl_{2} (CNCOC), which has a single-CuO2-plane lattice with
no orthorhombic distortion. The doping dependence of the in-plane optical
conductivity spectra for CNCOC is qualitatively the same to those of other
cuprates, but a slight difference between CNCOC and LSCO, i.e., the absence of
the 1.5 eV peak in CNCOC, can be attributed to the smaller charge-stripe
instability in CNCOC. The temperature dependence of the optical onductivity
spectra of CNCOC has been analyzed both by the two-component model
(Drude+Lorentzian) and by the one-component model (extended-Drude analysis).
The latter analysis gives a universal trend of the scattering rate Gamma(omega)
with doping. It was also found that Gamma(omega) shows a saturation behavior at
high frequencies, whose origin is the same as that of resistivity saturation at
high temperatures.Comment: 8 pages, 11 figures, to be published in Phys. Rev.
Visualizing the emergence of the pseudogap state and the evolution to superconductivity in a lightly hole-doped Mott insulator
Superconductivity emerges from the cuprate antiferromagnetic Mott state with
hole doping. The resulting electronic structure is not understood, although
changes in the state of oxygen atoms appear paramount. Hole doping first
destroys the Mott state yielding a weak insulator where electrons localize only
at low temperatures without a full energy gap. At higher doping, the
'pseudogap', a weakly conducting state with an anisotropic energy gap and
intra-unit-cell breaking of 90\degree-rotational (C4v) symmetry appears.
However, a direct visualization of the emergence of these phenomena with
increasing hole density has never been achieved. Here we report atomic-scale
imaging of electronic structure evolution from the weak-insulator through the
emergence of the pseudogap to the superconducting state in Ca2-xNaxCuO2Cl2. The
spectral signature of the pseudogap emerges at lowest doping from a weakly
insulating but C4v-symmetric matrix exhibiting a distinct spectral shape. At
slightly higher hole-density, nanoscale regions exhibiting pseudogap spectra
and 180\degree-rotational (C2v) symmetry form unidirectional clusters within
the C4v-symmetric matrix. Thus, hole-doping proceeds by the appearance of
nanoscale clusters of localized holes within which the broken-symmetry
pseudogap state is stabilized. A fundamentally two-component electronic
structure11 then exists in Ca2-xNaxCuO2Cl2 until the C2v-symmetric clusters
touch at higher doping, and the long-range superconductivity appears.Comment: See the Nature Physics website for the published version available at
http://dx.doi.org/10.1038/Nphys232
Visualizing the atomic scale electronic structure of the Ca2CuO2Cl2 Mott insulator
Although the mechanism of superconductivity in the cuprates remains elusive,
it is generally agreed that at the heart of the problem is the physics of doped
Mott insulators. The cuprate parent compound has one unpaired electron per Cu
site, and is predicted by band theory to be a half-filled metal. The strong
onsite Coulomb repulsion, however, prohibits electron hopping between
neighboring sites and leads to a Mott insulator ground state with
antiferromagnetic (AF) ordering. Charge carriers doped into the CuO2 plane
destroy the insulating phase and superconductivity emerges as the carrier
density is sufficiently high. The natural starting point for tackling high Tc
superconductivity is to elucidate the electronic structure of the parent Mott
insulator and the behavior of a single doped charge. Here we use a scanning
tunneling microscope to investigate the atomic scale electronic structure of
the Ca2CuO2Cl2 parent Mott insulator of the cuprates. The full electronic
spectrum across the Mott-Hubbard gap is uncovered for the first time, which
reveals the particle-hole symmetric and spatially uniform Hubbard bands. A
single electron donated by surface defect is found to create a broad in-gap
electronic state that is strongly localized in space with spatial
characteristics intimately related to the AF spin background. The unprecedented
real space electronic structure of the parent cuprate sheds important new light
on the origion of high Tc superconductivity from the doped Mott insulator
perspective.Comment: 26 pages, 4 figures, supplementary information include
Mixture models for analysis of melting temperature data
<p>Abstract</p> <p>Background</p> <p>In addition to their use in detecting undesired real-time PCR products, melting temperatures are useful for detecting variations in the desired target sequences. Methodological improvements in recent years allow the generation of high-resolution melting-temperature (T<sub>m</sub>) data. However, there is currently no convention on how to statistically analyze such high-resolution T<sub>m </sub>data.</p> <p>Results</p> <p>Mixture model analysis was applied to T<sub>m </sub>data. Models were selected based on Akaike's information criterion. Mixture model analysis correctly identified categories in T<sub>m </sub>data obtained for known plasmid targets. Using simulated data, we investigated the number of observations required for model construction. The precision of the reported mixing proportions from data fitted to a preconstructed model was also evaluated.</p> <p>Conclusion</p> <p>Mixture model analysis of T<sub>m </sub>data allows the minimum number of different sequences in a set of amplicons and their relative frequencies to be determined. This approach allows T<sub>m </sub>data to be analyzed, classified, and compared in an unbiased manner.</p
Global analysis of DNA methylation in early-stage liver fibrosis
<p>Abstract</p> <p>Background</p> <p>Liver fibrosis is caused by chemicals or viral infection. The progression of liver fibrosis results in hepatocellular carcinogenesis in later stages. Recent studies have revealed the importance of DNA hypermethylation in the progression of liver fibrosis to hepatocellular carcinoma (HCC). However, the importance of DNA methylation in the early-stage liver fibrosis remains unclear.</p> <p>Methods</p> <p>To address this issue, we used a pathological mouse model of early-stage liver fibrosis that was induced by treatment with carbon tetrachloride (CCl<sub>4</sub>) for 2 weeks and performed a genome-wide analysis of DNA methylation status. This global analysis of DNA methylation was performed using a combination of methyl-binding protein (MBP)-based high throughput sequencing (MBP-seq) and bioinformatic tools, IPA and Oncomine. To confirm functional aspect of MBP-seq data, we complementary used biochemical methods, such as bisulfite modification and <it>in-vitro</it>-methylation assays.</p> <p>Results</p> <p>The genome-wide analysis revealed that DNA methylation status was reduced throughout the genome because of CCl<sub>4 </sub>treatment in the early-stage liver fibrosis. Bioinformatic and biochemical analyses revealed that a gene associated with fibrosis, <it>secreted phosphoprotein 1 </it>(<it>Spp1</it>), which induces inflammation, was hypomethylated and its expression was up-regulated. These results suggest that DNA hypomethylation of the genes responsible for fibrosis may precede the onset of liver fibrosis. Moreover, <it>Spp1 </it>is also known to enhance tumor development. Using the web-based database, we revealed that <it>Spp1 </it>expression is increased in HCC.</p> <p>Conclusions</p> <p>Our study suggests that hypomethylation is crucial for the onset of and in the progression of liver fibrosis to HCC. The elucidation of this change in methylation status from the onset of fibrosis and subsequent progression to HCC may lead to a new clinical diagnosis.</p
The Subcellular Distribution of Acyltransferases which Catalyze the Synthesis of Phosphoglycerides
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65213/1/j.1432-1033.1969.tb00602.x.pd
Medium Chain Fatty Acids Are Selective Peroxisome Proliferator Activated Receptor (PPAR) γ Activators and Pan-PPAR Partial Agonists
Thiazolidinediones (TZDs) act through peroxisome proliferator activated receptor (PPAR) γ to increase insulin sensitivity in type 2 diabetes (T2DM), but deleterious effects of these ligands mean that selective modulators with improved clinical profiles are needed. We obtained a crystal structure of PPARγ ligand binding domain (LBD) and found that the ligand binding pocket (LBP) is occupied by bacterial medium chain fatty acids (MCFAs). We verified that MCFAs (C8–C10) bind the PPARγ LBD in vitro and showed that they are low-potency partial agonists that display assay-specific actions relative to TZDs; they act as very weak partial agonists in transfections with PPARγ LBD, stronger partial agonists with full length PPARγ and exhibit full blockade of PPARγ phosphorylation by cyclin-dependent kinase 5 (cdk5), linked to reversal of adipose tissue insulin resistance. MCFAs that bind PPARγ also antagonize TZD-dependent adipogenesis in vitro. X-ray structure B-factor analysis and molecular dynamics (MD) simulations suggest that MCFAs weakly stabilize C-terminal activation helix (H) 12 relative to TZDs and this effect is highly dependent on chain length. By contrast, MCFAs preferentially stabilize the H2-H3/β-sheet region and the helix (H) 11-H12 loop relative to TZDs and we propose that MCFA assay-specific actions are linked to their unique binding mode and suggest that it may be possible to identify selective PPARγ modulators with useful clinical profiles among natural products
Intracellular Phospholipase A1 and Acyltransferase, Which Are Involved in Caenorhabditis elegans Stem Cell Divisions, Determine the sn-1 Fatty Acyl Chain of Phosphatidylinositol
Phosphatidylinositol (PI) is unique in the abundance of stearic acid at the sn-1 position. This fatty acid is thought to be incorporated through fatty acid remodeling. Here, we identified a phospholipase and acyltransferases involved in the fatty acid remodeling at the sn-1 position of PI and provide a link between the sn-1 fatty acid of PI and asymmetric cell division
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