Browsing by Author "Huang, Tzu-Wen"

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Magnetic fluctuations in FeSe(1-delta) and Cu-doped FeSe(1-delta): (77)Se NMR experiments
(2010-04-01)
Young, Ben-Li
;
Wu, Jack
;
Huang, Tzu-Wen
;
Yeh, Kuo-Wei
;
Wu, Maw-Kuen
The roles of Se deficiency and Fe atoms, for the superconductivity of FeSe, have been, respectively, investigated in FeSe(1-delta) and (Fe(1-x)Cu(x))Se(1-delta), by our NMR experiments. The data, for nuclear spin-lattice relaxation rate (1/T(1)), show that the spin fluctuations are weakened at a larger delta, and are correlated with the superconductivity in FeSe. The superconducting volume fraction, estimated by our ac susceptibility experiments, is found to vary inversely with delta. Our findings suggest that the Se-deficient FeSe has an inhomogeneous phase, where the superconductivity is associated with the regions having few or no Se vacancies. As for (Fe(1-x)Cu(x))Se(1-delta), T(c) is rapidly suppressed by Cu doping and vanishes around x=0.03. The (77)Se and the (63)Cu NMR linewidths suggest that a local moment is induced at the Fe sites and not at the Cu sites. However, 1/T(1) shows no obvious change with the Cu doping. We suspect that other effects, such as disorder or change in the density of states, have more influence on T(c) suppression since a metal-insulator transition, induced by Cu substitution, occurs in the resistivity measurements.
Magnetic fluctuations in FeSe1-delta and Cu-doped FeSe1-delta: Se-77 NMR experiments
(2010-04-01)
Young, Ben-Li
;
Wu, Jack
;
Huang, Tzu-Wen
;
Yeh, Kuo-Wei
;
Wu, Maw-Kuen
The roles of Se deficiency and Fe atoms, for the superconductivity of FeSe, have been, respectively, investigated in FeSe1-delta and (Fe1-xCux)Se1-delta, by our NMR experiments. The data, for nuclear spin-lattice relaxation rate (1/T-1), show that the spin fluctuations are weakened at a larger delta, and are correlated with the superconductivity in FeSe. The superconducting volume fraction, estimated by our ac susceptibility experiments, is found to vary inversely with delta. Our findings suggest that the Se-deficient FeSe has an inhomogeneous phase, where the superconductivity is associated with the regions having few or no Se vacancies. As for (Fe1-xCux)Se1-delta, T-c is rapidly suppressed by Cu doping and vanishes around x=0.03. The Se-77 and the Cu-63 NMR linewidths suggest that a local moment is induced at the Fe sites and not at the Cu sites. However, 1/T-1 shows no obvious change with the Cu doping. We suspect that other effects, such as disorder or change in the density of states, have more influence on T-c suppression since a metal-insulator transition, induced by Cu substitution, occurs in the resistivity measurements.
Tigecycline-non-susceptible hypervirulent Klebsiella pneumoniae strains in Taiwan
(2020-02-01)
Cheng, Yi-Hsiang
;
Huang, Tzu-Wen
;
Juan, Chih-Han
;
Chou, Sheng-Hua
;
Tseng, Yao-Yi
Objectives Emergent antimicrobial-resistant hypervirulent Klebsiella pneumoniae (hvKp) is an important public health issue. We aimed to investigate resistance mechanisms and hypervirulent traits among tigecycline-non-susceptible (TNS) K. pneumoniae clinical strains, focusing on one hvKp strain with in vivo evolution of tigecycline resistance. Methods TNS K. pneumoniae strains causing invasive diseases in a medical centre in Taiwan between July 2015 and April 2018 were collected. Resistance mechanisms were determined and hvKp strains were defined as rmpA/rmpA2-carrying strains. Isogenic strains with and without tigecycline resistance were subjected to WGS and in vivo virulence testing. Further, site-directed mutagenesis was used to confirm the resistance mechanism. Results In total, 31 TNS K. pneumoniae strains were isolated, including six hypervirulent strains. Tigecycline resistance mechanisms were mostly caused by overexpression of AcrAB and OqxAB together with up-regulation of RamA or RarA, respectively. One TNS hypervirulent strain (KP1692; MIC=6mg/L) derived from its tigecycline-susceptible counterpart (KP1677; MIC=0.75mg/L) showed acrAB overexpression. WGS revealed four genetic variations between KP1677 and KP1692. In addition, using site-directed mutagenesis, we confirmed that a 1bp insertion in the ramA upstream region (RamR-binding site), leading to ramA and acrAB overexpression in KP1692, was responsible for tigecycline resistance. The in vivo virulence experiment showed that the TNS hvKp strain KP1692 still retained its high virulence compared with KP1677. Conclusions hvKp strains accounted for 19.4% among TNS strains. We identified alterations in the ramA upstream region as a mechanism of in vivo tigecycline resistance development in an hvKp strain.