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We investigate the specific influence of structural disorder on the suppression of antiferromagnetic order and on the emergence of cuprate superconductivity. We single out pure disorder, by focusing on a series of Y<sub>z</sub>Eu<sub>1-z</sub>Ba<sub>2</sub>Cu<sub>3</sub>O<sub>6.35</sub> samples at fixed oxygen content y=0.35, in the range 0 ≦ z ≦1. The gradual Y/Eu isovalent substitution smoothly drives the system through the Mott-insulator to superconductor transition from a full antiferromagnet with Néel transition T<sub>N</sub>=320 K at z=0 to a bulk superconductor with superconducting critical temperature T<sub>c</sub>=18 K at z=1, YBa<sub>2</sub>Cu<sub>3</sub>O<sub>6.35</sub>. The electronic properties are finely tuned by gradual lattice deformations induced by the different cationic radii of the two lanthanides, inducing a continuous change of the basal Cu(1)-O chain length, as well as a controlled amount of disorder in the active Cu(2)O<sub>2</sub> bilayers. We check that internal charge transfer from the basal to the active plane is entirely responsible for the doping of the latter and we show that superconductivity emerges with orthorhombicity. By comparing transition temperatures with those of the isoelectronic clean system we determine the influence of pure structural disorder connected with the Y/Eu alloy.
This article was published in the following journal.
Name: Journal of physics. Condensed matter : an Institute of Physics journal
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Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
The interval between two successive CELL DIVISIONS during which the CHROMOSOMES are not individually distinguishable. It is composed of the G phases (G1 PHASE; G0 PHASE; G2 PHASE) and S PHASE (when DNA replication occurs).
Functionalization of exogenous substances to prepare them for conjugation in PHASE II DETOXIFICATION. Phase I enzymes include CYTOCHROME P450 enzymes and some OXIDOREDUCTASES. Excess induction of phase I over phase II detoxification leads to higher levels of FREE RADICALS that can induce CANCER and other cell damage. Induction or antagonism of phase I detoxication is the basis of a number of DRUG INTERACTIONS.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
Studies that are usually controlled to assess the effectiveness and dosage (if appropriate) of diagnostic, therapeutic, or prophylactic drugs, devices, or techniques. These studies are performed on several hundred volunteers, including a limited number of patients with the target disease or disorder, and last about two years. This concept includes phase II studies conducted in both the U.S. and in other countries.