Lattice effects on the physical properties of half doped perovskite ruthenates

We investigate the unusual phase transitions in SrRuO$_{3}$ and Sr$_{0.5}$Ca$_{0.5}$Ru$_{1-x}$Cr$_{x}$O$_{3}$ (x=0,0.05 and 0.1) employing x-ray diffraction, resistivity, magnetic studies and x-ray photoemission spectroscopy. Our results show the compounds undergo crossover from $itinerant$ ferromagnetism to $localised$ ferromagnetism. The combined studies suggests Ru and Cr to be in 4+ valence state. A Griffith phase and an enhancement in Curie temperature (Tc) from 38 K to 107 K is observed with Cr doping. A shift in the chemical potential towards the valence band is observed with Cr doping. In the metallic samples, interestingly, a direct link between the resistivity and orthorhombic strain is observed. Detailed studies in this direction will be helpful to understand the nature of interactions and hence manoeuvre its properties. In the non metallic samples, the resistivity is mainly governed by disorder and electron-electron correlation effects. The value of the resistivity for the 5% Cr doped sample suggests semi metallic behaviour. Understanding its nature in detail using electron spectroscopic techniques could unravel the possibility of its utility in high mobility transistors at room temperature and its combined property with ferromagnetism will be helpful in making spintronic devices

Strong in-plane anisotropy in the electronic structure of fixed-valence β\beta-LuAlB4_4

The origin of intrinsic quantum criticality in the heavy-fermion superconductor $\beta$-YbAlB$_4$ has been attributed to strong Yb valence fluctuations and its peculiar crystal structure. Here, we assess these contributions individually by studying the isostructural but fixed-valence compound $\beta$-LuAlB$_4$. Quantum oscillation measurements and DFT calculations reveal a Fermi surface markedly different from that of $\beta$-YbAlB$_4$, consistent with a `large' Fermi surface there. We also find an unexpected in-plane anisotropy of the electronic structure, in contrast to the isotropic Kondo hybridization in $\beta$-YbAlB$_4$.Comment: 6 pages, 4 figure

Exercise training enhances in vivo clearance of endotoxin and attenuates inflammatory responses by potentiating Kupffer cell phagocytosis

The failure of Kupffer cells (KCs) to remove endotoxin is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, the effects of exercise training on KC function were studied in terms of in vivo endotoxin clearance and inflammatory responses. Mice were allocated into rest and exercise groups. KC bead phagocytic capacity and plasma steroid hormone levels were determined following exercise training. Endotoxin and inflammatory cytokine levels in plasma were determined over time following endotoxin injection. KC bead phagocytic capacity was potentiated and clearance of exogenously-injected endotoxin was increased in the exercise group. Inflammatory cytokine (TNF-α and IL-6) levels were lower in the exercise group. We found that only DHEA was increased in the plasma of the exercise group. In an in vitro experiment, the addition of DHEA to RAW264.7 cells increased bead phagocytic capacity and attenuated endotoxin-induced inflammatory responses. These results suggest that exercise training modulates in vivo endotoxin clearance and inflammatory responses in association with increased DHEA production. These exercise-induced changes in KC capacity may contribute to a slowing of disease progression in NAFLD patients

Nuclear factor (erythroid derived 2)-like 2 activation increases exercise endurance capacity via redox modulation in skeletal muscles

Sulforaphane (SFN) plays an important role in preventing oxidative stress by activating the nuclear factor (erythroid derived 2)-like 2 (Nrf2) signalling pathway. SFN may improve exercise endurance capacity by counteracting oxidative stress-induced damage during exercise. We assessed running ability based on an exhaustive treadmill test (progressive-continuous all-out) and examined the expression of markers for oxidative stress and muscle damage. Twelve- to 13-week-old Male wild-type mice (Nrf2+/+) and Nrf2-null mice (Nrf2−/−) on C57BL/6J background were intraperitoneally injected with SFN or vehicle prior to the test. The running distance of SFN-injected Nrf2+/+ mice was significantly greater compared with that of uninjected mice. Enhanced running capacity was accompanied by upregulation of Nrf2 signalling and downstream genes. Marker of oxidative stress in SFN-injected Nrf2+/+ mice were lower than those in uninjected mice following the test. SFN produced greater protection against muscle damage during exhaustive exercise conditions in Nrf2+/+ mice than in Nrf2−/− mice. SFN-induced Nrf2 upregulation, and its antioxidative effects, might play critical roles in attenuating muscle fatigue via reduction of oxidative stress caused by exhaustive exercise. This in turn leads to enhanced exercise endurance capacity. These results provide new insights into SFN-induced upregulation of Nrf2 and its role in improving exercise performance