3,828 research outputs found

    In-plane thermal conductivity of large single crystals of Sm-substituted (Y1x_{1-x}Smx_{x})Ba2_{2}Cu3_{3}O7δ_{7-\delta}

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    We have investigated the in-plane thermal conductivity κab(T,H)\kappa_{ab}(T,H) of large single crystals of optimally oxygen-doped (Y1x_{1-x},Smx_{x})Ba2_{2}Cu3_{3}O7δ_{7-\delta} (xx=0, 0.1, 0.2 and 1.0) and YBa2_{2}(Cu1y_{1-y}Zny_{y})3_{3}O7δ_{7-\delta}(yy=0.0071) as functions of temperature and magnetic field (along the c axis). For comparison, the temperature dependence of κab\kappa_{ab} for as-grown crystals with the corresponding compositions are presented. The nonlinear field dependence of κab\kappa_{ab} for all crystals was observed at relatively low fields near a half of TcT_{c}. We make fits of the κ(H)\kappa(H) data to an electron contribution model, providing both the mean free path of quasiparticles 0\ell_{0} and the electronic thermal conductivity κe\kappa_{e}, in the absence of field. The local lattice distortion due to the Sm substitution for Y suppresses both the phonon and electron contributions. On the other hand, the light Zn doping into the CuO 2_{2} planes affects solely the electron component below TcT_{c}, resulting in a substantial decrease in 0\ell_{0} .Comment: 7 pages,4 figures,1 tabl

    Reactive Hall constant of Strongly Correlated Electrons

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    The zero-temperature Hall response within tight-binding models of correlated electrons is studied. Using the linear response theory and a linearization in the magnetic field B, a general relation for the reactive (zero frequency) Hall constant in the fast (transport) limit is derived, involving only matrix elements between the lowest excited states at B=0; for noninteracting fermions, the Boltzmann expression is reproduced. For a Fermi liquid with a well defined Fermi surface and linear gapless excitations an analogous expression is found more generally. In the specific case of quasi-one-dimensional correlated systems a relation of RH0R^0_H to the charge stiffness D is recovered. Similar analysis is performed and discussed for D and the compressibility.Comment: 8 pages, submitted to Phys.Rev.

    Microcystic cyanobacteria causes mitochondrial membrane potential alteration and reactive oxygen species formation in primary cultured rat hepatocytes.

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    Cyanobacteria contamination of water has become a growing public health problem worldwide. Microcystis aeruginosa is one of the most common toxic cyanobacteria. It is capable of producing microcystins, a group of cyclic heptapeptide compounds with potent hepatotoxicity and tumor promotion activity. The present study investigated the effect of microcystic cyanobacteria on primary cultured rat hepatocytes by examining mitochondrial membrane potential (MMP) changes and intracellular reactive oxygen species (ROS) formation in cells treated with lyophilized freshwater microcystic cyanobacteria extract (MCE). Rhodamine 123 (Rh-123) was used as a fluorescent probe for changes in mitochondrial fluorescence intensity. The mitochondrial Rh-123 fluorescence intensity in MCE-treated hepatocytes, examined using a laser confocal microscope, responded in a dose- and time-dependent manner. The results thus indicate that the alteration of MMP might be an important event in the hepatotoxicity caused by cyanobacteria. Moreover, the parallel increase of ROS formation detected using another fluorescent probe, 2',7'-dichlorofluorescin diacetate also suggests the involvement of oxidative stress in the hepatotoxicity caused by cyanobacteria. The fact that MMP changes precede other cytotoxic parameters such as nuclear staining by propidium iodide and cell morphological changes suggests that mitochondrial damage is closely associated with MCE-induced cell injury in cultured rat hepatocytes

    Transport Properties of Doped t-J Ladders

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    Conductivity and Hall coefficient for various types of t-J ladders are calculated as a function of temperature and frequency by numerical diagonalization. A crossover from an incoherent to a coherent charge dynamics is found at a temperature T_{coh}. There exists another crossover at T_{PG} below which a pseudogap opens in the optical spectra, induced by the opening of a spin gap. In the absence of the spin gap, T_{coh} and the coherent weight are suppressed especially with increasing dimensionality. On the contrary, T_{coh} is strongly enhanced by the pseudogap formation below T_{PG}, where the coherent Drude weight decreases with increasing dimensionality. The Hall coefficient shows a strong crossover at T_{PG} below which it has large amplitude for small doping concentration.Comment: 4 pages, RevTeX, 5 PostScript figure

    Microcystic cyanobacteria extract induces cytoskeletal disruption and intracellular glutathione alteration in hepatocytes.

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    Microcystins are a group of highly liver-specific toxins, although their exact mechanisms of action remain unclear. We examined the effects of microcystic cyanobacteria extract (MCE) collected from a contaminated water source on the organization of cellular microtubules (MTs) and microfilaments (MFs) in hepatocytes. We also investigated the effects on lactate dehydrogenase (LDH) leakage and intracellular glutathione (GSH). Primary cultured rat hepatocytes exposed to MCE (equivalent to 125 microg/mL lyophilized algae cells) showed a characteristic disruption of MTs and MFs in a time-dependent manner. Under these conditions, MCE caused aggregation of MTs and MFs and a severe loss of MTs in some cells. Moreover, MCE-induced cytoskeletal alterations preceded the LDH leakage. On the other hand, the treatment of cells with MCE led to a dose-dependent increase of intracellular GSH. However, time-course study showed a biphasic change of intracellular GSH levels with a significant increase in the initial stage followed by a decrease after prolonged treatment. Furthermore, pretreatment with N-acetylcystein (NAC), a GSH precursor, significantly enhanced the intracellular GSH level and decreased the MCE-induced cytotoxicity as well as cytoskeleton changes. In contrast, buthionine-(S, R)-sulfoximine, a specific GSH synthesis inhibitor, increased the cell susceptibility to MCE-induced cytotoxicity by depleting the intracellular GSH level. These findings suggest that intracellular GSH plays an important role in MCE-induced cytotoxicity and cytoskeleton changes in primary cultured rat hepatocytes. Increasing intracellular GSH levels protect cells from MCE-induced cytotoxicity and cytoskeleton changes
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