Microscopic annealing process and its impact on superconductivity in T'-structure electron-doped copper oxides

High-transition-temperature superconductivity arises in copper oxides when holes or electrons are doped into the CuO2 planes of their insulating parent compounds. While hole-doping quickly induces metallic behavior and superconductivity in many cuprates, electron-doping alone is insufficient in materials such as R2CuO4 (R is Nd, Pr, La, Ce, etc.), where it is necessary to anneal an as-grown sample in a low-oxygen environment to remove a tiny amount of oxygen in order to induce superconductivity. Here we show that the microscopic process of oxygen reduction repairs Cu deficiencies in the as-grown materials and creates oxygen vacancies in the stoichiometric CuO2 planes, effectively reducing disorder and providing itinerant carriers for superconductivity. The resolution of this long-standing materials issue suggests that the fundamental mechanism for superconductivity is the same for electron- and hole-doped copper oxides.Comment: 23 pages, 3 figures, accepted for publication in Nature Material

Bladder hyperactivity and increased excitability of bladder afferent neurons associated with reduced expression of Kv1.4 α-subunit in rats with cystitis

Hyperexcitability of C-fiber bladder afferent pathways has been proposed to contribute to urinary frequency and bladder pain in chronic bladder inflammation including interstitial cystitis. However, the detailed mechanisms inducing afferent hyperexcitability after bladder inflammation are not fully understood. Thus, we investigated changes in the properties of bladder afferent neurons in rats with bladder inflammation induced by intravesical application of hydrochloric acid. Eight days after the treatment, bladder function and bladder sensation were analyzed using cystometry and an electrodiagnostic device of sensory function (Neurometer), respectively. Whole cell patch-clamp recordings and immunohistochemical staining were also performed in dissociated bladder afferent neurons identified by a retrograde tracing dye, Fast Blue, injected into the bladder wall. Cystitis rats showed urinary frequency that was inhibited by pretreatment with capsaicin and bladder hyperalgesia mediated by C-fibers. Capsaicin-sensitive bladder afferent neurons from sham rats exhibited high thresholds for spike activation and a phasic firing pattern, whereas those from cystitis rats showed lower thresholds for spike activation and a tonic firing pattern. Transient A-type K+ current density in capsaicin-sensitive bladder afferent neurons was significantly smaller in cystitis rats than in sham rats, although sustained delayed-rectifier K+ current density was not altered after cystitis. The expression of voltage-gated K+ Kv1.4 α-subunits, which can form A-type K+ channels, was reduced in bladder afferent neurons from cystitis rats. These data suggest that bladder inflammation increases bladder afferent neuron excitability by decreasing expression of Kv1.4 α-subunits. Similar changes in capsaicin-sensitive C-fiber afferent terminals may contribute to bladder hyperactivity and hyperalgesia due to acid-induced bladder inflammation