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Y Kohsaka

Publications and source records attributed to Y Kohsaka.

9 recordsLinked to original sources

Nodal quasiparticles and antinodal charge ordering in Ca2-xNaxCuO2Cl2.

Understanding the role of competing states in the cuprates is essential for developing a theory for high-temperature superconductivity. We report angle-resolved photoemission spectroscopy experiments which probe the 4a0 x 4a0 charge-ordered state discovered by scanning tunneling microscopy in the lightly doped cuprate superconductor Ca2-xNaxCuO2Cl2. Our measurements reveal a marked dichotomy between the real- and momentum-space probes, for which charge ordering is emphasized in the tunneling measurements and photoemission is most sensitive to excitations near the node of the d-wave superconducting gap. These results emphasize the importance of momentum anisotropy in determining the complex electronic properties of the cuprates and places strong constraints on theoretical models of the charge-ordered state.

Journal Article↗

Missing quasiparticles and the chemical potential puzzle in the doping evolution of the cuprate superconductors.

The evolution of Ca2-xNaxCuO2Cl2 from Mott insulator to superconductor was studied using angle-resolved photoemission spectroscopy. By measuring both the excitations near the Fermi energy as well as nonbonding states, we tracked the doping dependence of the electronic structure and the chemical potential with unprecedented precision. Our work reveals failures in the standard weakly interacting quasiparticle scenario, including the broad line shapes of the insulator and the apparently paradoxical shift of the chemical potential within the Mott gap. To resolve this, we develop a model where the quasiparticle is vanishingly small at half filling and grows upon doping, allowing us to unify properties such as the dispersion and Fermi wave vector with the chemical potential.

Journal Article↗

Imaging nanoscale electronic inhomogeneity in the lightly doped Mott insulator Ca(2-x)NaxCuO2Cl2.

The spatial variation of electronic states was imaged in the lightly doped Mott insulator Ca(2-x)NaxCuO2Cl2 using scanning tunneling microscopy or spectroscopy. We observed nanoscale domains with a high local density of states within an insulating background. The observed domains have a characteristic length scale of 2 nm (approximately 4-5a, a: lattice constant) with preferred orientations along the tetragonal [100] direction. We argue that such spatially inhomogeneous electronic states are inherent to slightly doped Mott insulators and play an important role for the insulator to metal transition.

Journal Article↗

A 'checkerboard' electronic crystal state in lightly hole-doped Ca2-xNaxCuO2Cl2.

The phase diagram of hole-doped copper oxides shows four different electronic phases existing at zero temperature. Familiar among these are the Mott insulator, high-transition-temperature superconductor and metallic phases. A fourth phase, of unknown identity, occurs at light doping along the zero-temperature bound of the 'pseudogap' regime. This regime is rich in peculiar electronic phenomena, prompting numerous proposals that it contains some form of hidden electronic order. Here we present low-temperature electronic structure imaging studies of a lightly hole-doped copper oxide: Ca2-xNaxCuO2Cl2. Tunnelling spectroscopy (at energies |E| > 100 meV) reveals electron extraction probabilities greatly exceeding those for injection, as anticipated for a doped Mott insulator. However, for |E| < 100 meV, the spectrum exhibits a V-shaped energy gap centred on E = 0. States within this gap undergo intense spatial modulations, with the spatial correlations of a four CuO2-unit-cell square 'checkerboard', independent of energy. Intricate atomic-scale electronic structure variations also exist within the checkerboard. These data are consistent with an unanticipated crystalline electronic state, possibly the hidden electronic order, existing in the zero-temperature pseudogap regime of Ca2-xNaxCuO2Cl2.

Journal Article↗

The effect of chronic treatment with trandolapril on cyclic AMP-and cyclic GMP-dependent relaxations in aortic segments of rats with chronic heart failure.

1 Characteristics of cyclic GMP- and cyclic AMP-mediated relaxation in aortic segments of rats with chronic heart failure (CHF) and the effects of chronic treatment with an angiotensin I converting enzyme (ACE) inhibitor, trandolapril, were examined 8 weeks after coronary artery ligation. 2 Cardiac output indices of coronary artery-ligated and sham-operated rats were 125+/-8 and 189+/-10 ml min(-1) kg(-1), respectively (P<0.05), indicating the development of CHF at this period. 3 The maximal relaxant response of aortic segments to 10 microM acetylcholine in rats with CHF and sham-operated rats was 64.0+/-5.7 and 86.9+/-1.9%, respectively (P<0.05), whereas the relaxant response to sodium nitroprusside (SNP) remained unchanged. Tissue cyclic GMP content in rats with CHF was lower than that of sham-operated rats. 4 In endothelium-intact segments of rats with CHF, the maximal relaxant response to 10 microM isoprenaline (44.5+/-6.7%) was lower that sham-operated rats (81.3+/-2.5%, P<0.05) and the concentration-response curve for NKH477, a water-soluble forskolin, was shifted to the right without a reduction in the maximal response. Isoprenaline-induced relaxation of aortic segments was attenuated by NG-nitro-L-arginine methyl ester (L-NAME) in sham-operated rats, but not in rats with CHF. Relaxation to 30 microM dibutyryl cyclic AMP in rats with CHF (26.8+/-2.7%) was lower than that in sham-operated rats (63.4+/-11.8%, P<0.05). 5 Trandolapril (3 mg kg(-1) day(-1)) was orally administered from the 2nd to 8th week after the operation. Aortic blood flow of rats with CHF (38.5+/-3.6 ml min(-1)) was lower than that of sham-operated rats (55.0+/-3.0 ml min(-1)), and this reduction was reversed (54.1+/-3.4 ml min(-1)) by treatment with trandolapril. The diminished responsiveness described above was normalized in the trandolapril-treated rat with CHF (i.e., the maximal relaxation to acetylcholine, 94.7+/-1.0%; that to isoprenaline, 80.5+/-2.8%; that to dibutyryl cyclic AMP, 54.7+/-6.2%). However, aortic segments of trandolapril-treated rats with CHF, L-NAME did not attenuate isoprenaline-induced relaxation and the tissue cyclic GMP level was not fully restored, suggesting that the ability of the endothelium to produce NO was still partially damaged. 6 The results suggest that vasorelaxation in CHF, diminished mainly due to dysfunction in endothelial nitric oxide (NO) production and cyclic AMP-mediated signal transduction, was partially restored by long-term treatment with trandolapril. The mechanism underlying the restoration may be attributed in part to prevention of CHF-induced endothelial dysfunction.

Acetylcholine↗

Modulation of cAMP-mediated vasorelaxation by endothelial nitric oxide and basal cGMP in vascular smooth muscle.

Recent in vitro evidence shows a role of endothelial nitric oxide (NO) in the modulation of isoproterenol-induced vasorelaxation. To elucidate roles of endothelial cells and NO in cyclic adenosine monophosphate (cAMP)-mediated vasodilators we examined the effects of removal of endothelium and a NO synthase (NOS) inhibitor on relaxant responses in vitro of rat aortic strips to beta-adrenoceptor stimulants and colforsin dapropate, a water-soluble forskolin, and changes in cAMP and cyclic guanosine monophosphate (cGMP) contents. Relaxant responses of rat aorta to isoproterenol, denopamine, salbutamol, colforsin, and dibutyryl cAMP (dbcAMP) were blunted by removal of endothelial cells or treatment with NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). Relaxant response of endothelium-intact segments to isoproterenol was associated with increases in tissue cAMP and cGMP contents. Removal of endothelium or treatment with L-NAME markedly reduced basal cGMP and abolished the isoproterenol-induced increase in cGMP but not cAMP content. In endothelium-removed segments, pretreatment with sodium nitroprusside (SNP) restored the diminished relaxant response to isoproterenol and increased basal cGMP (from 0.08 +/- 0.01 to 0.16 +/- 0.02 pmol/mg protein), whereas it did not affect the isoproterenol-induced increase in cAMP. The diminished relaxant response of endothelium-removed segments to dbcAMP was not restored by SNP pretreatment. The results suggest that relaxant response of rat aorta to cAMP-mediated vasodilators is mediated, in part, by NO production in endothelium and subsequent increase in cGMP in vascular smooth-muscle cells.

Adrenergic beta-Agonists↗

Serial changes in endogenous erythropoietin levels in patients with myelodysplastic syndromes and aplastic anemia undergoing erythropoietin treatment.

Recombinant human erythropoietin (rhEpo) was administered to 14 patients with myelodysplastic syndrome (MDS) and seven patients with aplastic anemia (AA). In 19 patients, doses of 6000 units were given intravenously three times a week (t.i.w.) with the dose being doubled up to 24,000 units every 8 weeks until a response was obtained. RhEpo was given subcutaneously in two patients. Seven patients, four with MDS and three with AA, showed a significant response with an increase of hemoglobin concentration during therapy. The response occurred at doses of 12,000 units in five and 24,000 units in two patients. Responding patients with both MDS and AA had a relatively low serum Epo (s-Epo) level prior to Epo therapy. MDS responders had either refractory anemia (RA) or RA with ring sideroblasts (RARS), while two of the Epo responders in AA had a severe form of the disease. However, since some of the Epo responders had a high initial s-Epo concentration, a high s-Epo level does not preclude the use of rhEpo. Serial determination of s-Epo levels showed a progressive decline in six of the seven responders even when they were on rhEpo therapy, while the s-Epo levels remained elevated or further increased with time in most nonresponders. RhEpo was well tolerated by all patients. The results suggest that rhEpo is a safe and effective treatment for a certain proportion of patients with MDS and AA. Moreover, serial determination of s-Epo during therapy may be useful in monitoring and predicting the therapeutic effect of rhEpo.

Adolescent↗