151 research outputs found
Cu Nuclear Quadrupole Resonance Study of Site-Disorder and Chemical Pressure Effects on Y(Ba1-xSrx)2Cu4O8
We report a zero-field Cu nuclear quadrupole resonance (NQR) study on the
effects of nonmagnetic Sr substitution for high-Tc superconductors,
Y(Ba1-xSrx)2Cu4O8 (Tc=82-80 K for x=0-0.4), using a spin-echo technique. The
site-disordering and chemical pressure effects associated with doping Sr were
observed in the broadened, shifted Cu NQR spectra. Nevertheless, the site
disorder did not significantly affect the homogeneity of Cu electron spin
dynamics, in contrast to the in-plane impurity. The peak shift of Cu NQR
spectrum due to Sr was different between the chain- and the plane-Cu sites,
more remarkably than those under a hydrostatic physical pressure, suggesting
anisotropic or nonuniform local structural strains. The small decrease of Tc
due to Sr can be traced back to either a cancellation effect on Tc between the
disorder and the pressure, or an anisotropic or nonuniform chemical pressure
effect on Tc.Comment: 4 pages, 5 figure
Physical origin of the buckling in CuO: Electron-phonon coupling and Raman spectra
It is shown theoretically that the buckling of the CuO planes in
certain cuprate systems can be explained in terms of an electric field across
the planes which originates from different valences of atoms above and below
the plane. This field results also in a strong coupling of the Raman-active
out-of-phase vibration of the oxygen atoms ( mode) to the electronic
charge transfer between the two oxygens in the CuO plane. Consequently,
the electric field can be deduced from the Fano-type line shape of the
phonon. Using the electric field estimated from the electron-phonon coupling
the amplitude of the buckling is calculated and found to be in good agreement
with the structural data. Direct experimental support for the idea proposed is
obtained in studies of YBaCuO and
BiSr(CaY)CuO with different oxygen and
yttrium doping, respectively, including antiferromagnetic samples. In the
latter compound, symmetry breaking by replacing Ca partially by Y leads to an
enhancement of the electron-phonon coupling by an order of magnitude.Comment: 12 pages, 4 figures, and 1 tabl
Excitonic Instability in the Transition from the Black Phase to the Golden Phase of SmS under Pressure Investigated by Infrared Spectroscopy
We report the pressure-dependent optical reflectivity spectra of a strongly
correlated insulator, samarium monosulfide (SmS), in the far- and
middle-infrared regions to investigate the origin of the pressure-induced phase
transition from the black phase to the golden phase. The energy gap becomes
narrow with increasing pressure in the black phase. A valence transition from
Sm2+ in the black phase to mainly Sm3+ in the golden phase accompanied by
spectral change from insulator to metal were observed at the transition
pressure of 0.65 GPa. The black-to-golden phase transition occurs when the
energy gap size of black SmS becomes the same as the binding energy of the
exciton at the indirect energy gap before the gap closes. This result indicates
that the valence transition originates from an excitonic instability.Comment: 5 pages, 4 figures. To be published in J. Phys. Soc. Jpn. Vol. 77,
No. 1
The CDK-Activating Kinase (CAK) Csk1 Is Required for Normal Levels of Homologous Recombination and Resistance to DNA Damage in Fission Yeast
BACKGROUND: Cyclin-dependent kinases (CDKs) perform essential roles in cell division and gene expression in all eukaryotes. The requirement for an upstream CDK-activating kinase (CAK) is also universally conserved, but the fission yeast Schizosaccharomyces pombe appears to be unique in having two CAKs with both overlapping and specialized functions that can be dissected genetically. The Mcs6 complex--orthologous to metazoan Cdk7/cyclin H/Mat1--activates the cell-cycle CDK, Cdk1, but its non-redundant essential function appears to be in regulation of gene expression, as part of transcription factor TFIIH. The other CAK is Csk1, an ortholog of budding yeast Cak1, which activates all three essential CDKs in S. pombe--Cdk1, Mcs6 and Cdk9, the catalytic subunit of positive transcription elongation factor b (P-TEFb)--but is not itself essential. METHODOLOGY/PRINCIPAL FINDINGS: Cells lacking csk1(+) are viable but hypersensitive to agents that damage DNA or block replication. Csk1 is required for normal levels of homologous recombination (HR), and interacts genetically with components of the HR pathway. Tests of damage sensitivity in csk1, mcs6 and cdk9 mutants indicate that Csk1 acts pleiotropically, through Cdk9 and at least one other target (but not through Mcs6) to preserve genomic integrity. CONCLUSIONS/SIGNIFICANCE: The two CAKs in fission yeast, which differ with respect to their substrate range and preferences for monomeric CDKs versus CDK/cyclin complexes as substrates, also support different functions of the CDK network in vivo. Csk1 plays a non-redundant role in safeguarding genomic integrity. We propose that specialized activation pathways dependent on different CAKs might insulate CDK functions important in DNA damage responses from those capable of triggering mitosis
Flux Phase as a Dynamic Jahn-Teller Phase: Berryonic Matter in the Cuprates?
There is considerable evidence for some form of charge ordering on the
hole-doped stripes in the cuprates, mainly associated with the low-temperature
tetragonal phase, but with some evidence for either charge density waves or a
flux phase, which is a form of dynamic charge-density wave. These three states
form a pseudospin triplet, demonstrating a close connection with the E X e
dynamic Jahn-Teller effect, suggesting that the cuprates constitute a form of
Berryonic matter. This in turn suggests a new model for the dynamic Jahn-Teller
effect as a form of flux phase. A simple model of the Cu-O bond stretching
phonons allows an estimate of electron-phonon coupling for these modes,
explaining why the half breathing mode softens so much more than the full
oxygen breathing mode. The anomalous properties of provide a coupling
(correlated hopping) which acts to stabilize density wave phases.Comment: Major Revisions: includes comparisons with specific cuprate phonon
modes, 16 eps figures, revte
Number and type of vertebral deformities: Epidemiological characteristics and relation to back pain and height loss
Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine
[This corrects the article DOI: 10.1186/s13054-016-1208-6.]
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Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro
BACKGROUND: Mammalian cardiac myocytes withdraw from the cell cycle during post-natal development, resulting in a non-proliferating, fully differentiated adult phenotype that is unable to repair damage to the myocardium, such as occurs following a myocardial infarction. We and others previously have shown that forced expression of certain cell cycle molecules in adult cardiac myocytes can promote cell cycle progression and division in these cells. The mitotic serine/threonine kinase, Polo-like kinase-1 (Plk1), is known to phosphorylate and activate a number of mitotic targets, including Cdc2/Cyclin B1, and to promote cell division. PRINCIPAL FINDINGS: The mammalian Plk family are all differentially regulated during the development of rat cardiac myocytes, with Plk1 showing the most dramatic decrease in both mRNA, protein and activity in the adult. We determined the potential of Plk1 to induce cell cycle progression and division in cultured rat cardiac myocytes. A persistent and progressive loss of Plk1 expression was observed during myocyte development that correlated with the withdrawal of adult rat cardiac myocytes from the cell cycle. Interestingly, when Plk1 was over-expressed in cardiac myocytes by adenovirus infection, it was not able to promote cell cycle progression, as determined by cell number and percent binucleation. CONCLUSIONS: We conclude that, in contrast to Cdc2/Cyclin B1 over-expression, the forced expression of Plk1 in adult cardiac myocytes is not sufficient to induce cell division and myocardial repair
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