Electronic structure and magnetic properties of the spin-1/2 Heisenberg system CuSe2O5

A microscopic magnetic model for the spin-1/2 Heisenberg chain compound CuSe2O5 is developed based on the results of a joint experimental and theoretical study. Magnetic susceptibility and specific heat data give evidence for quasi-1D magnetism with leading antiferromagnetic (AFM) couplings and an AFM ordering temperature of 17 K. For microscopic insight, full-potential DFT calculations within the local density approximation (LDA) were performed. Using the resulting band structure, a consistent set of transfer integrals for an effective one-band tight-binding model was obtained. Electronic correlations were treated on a mean-field level starting from LDA (LSDA+U method) and on a model level (Hubbard model). In excellent agreement of experiment and theory, we find that only two couplings in CuSe2O5 are relevant: the nearest-neighbour intra-chain interaction of 165 K and a non-frustrated inter-chain coupling of 20 K. From a comparison with structurally related systems (Sr2Cu(PO4)2, Bi2CuO4), general implications for a magnetic ordering in presence of inter-chain frustration are made.Comment: 20 pages, 8 figures, 3 table

Spin-State Transition and Metal-Insulator Transition in La1−x_{1-x}Eux_xCoO3_3}

We present a study of the structure, the electric resistivity, the magnetic susceptibility, and the thermal expansion of La$_{1-x}$Eu$_x$CoO$_3$. LaCoO$_3$ shows a temperature-induced spin-state transition around 100 K and a metal-insulator transition around 500 K. Partial substitution of La$^{3+}$ by the smaller Eu$^{3+}$ causes chemical pressure and leads to a drastic increase of the spin gap from about 190 K in LaCoO$_3$ to about 2000 K in EuCoO$_3$, so that the spin-state transition is shifted to much higher temperatures. A combined analysis of thermal expansion and susceptibility gives evidence that the spin-state transition has to be attributed to a population of an intermediate-spin state with orbital order for $x<0.5$ and without orbital order for larger $x$. In contrast to the spin-state transition, the metal-insulator transition is shifted only moderately to higher temperatures with increasing Eu content, showing that the metal-insulator transition occurs independently from the spin-state distribution of the Co$^{3+}$ ions. Around the metal-insulator transition the magnetic susceptibility shows a similar increase for all $x$ and approaches a doping-independent value around 1000 K indicating that well above the metal-insulator transition the same spin state is approached for all $x$.Comment: 10 pages, 6 figure

Exercise training reverses myocardial dysfunction induced by CaMKIIδC overexpression by restoring Ca2+-homeostasis

Several conditions of heart disease, including heart failure and diabetic cardiomyopathy, are associated with upregulation of cytosolic Ca2+/calmodulin-dependent protein kinase II (CaMKIIδC) activity. In the heart, CaMKIIδC isoform targets several proteins involved in intracellular Ca2+ homeostasis. We hypothesized that high-intensity endurance training activates mechanisms that enable a rescue of dysfunctional cardiomyocyte Ca2+ handling and thereby ameliorate cardiac dysfunction despite continuous and chronic elevated levels of CaMKIIδC. CaMKIIδC transgenic (TG) and wild-type (WT) mice performed aerobic interval exercise training over 6 wk. Cardiac function was measured by echocardiography in vivo, and cardiomyocyte shortening and intracellular Ca2+ handling were measured in vitro. TG mice had reduced global cardiac function, cardiomyocyte shortening (47% reduced compared with WT, P &#60; 0.01), and impaired Ca2+ homeostasis. Despite no change in the chronic elevated levels of CaMKIIδC, exercise improved global cardiac function, restored cardiomyocyte shortening, and reestablished Ca2+ homeostasis to values not different from WT. The key features to explain restored Ca2+ homeostasis after exercise training were increased L-type Ca2+ current density and flux by 79 and 85%, respectively (P &#60; 0.01), increased sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) function by 50% (P &#60; 0.01), and reduced diastolic SR Ca2+ leak by 73% (P &#60; 0.01), compared with sedentary TG mice. In conclusion, exercise training improves global cardiac function as well as cardiomyocyte function in the presence of a maintained high CaMKII activity. The main mechanisms of exercise-induced improvements in TG CaMKIIδC mice are mediated via increased L-type Ca2+ channel currents and improved SR Ca2+ handling by restoration of SERCA2a function in addition to reduced diastolic SR Ca2+ leak

Evidence for a Low-Spin to Intermediate-Spin State Transition in LaCoO3

We present measurements of the magnetic susceptibility and of the thermal expansion of a LaCoO$_3$ single crystal. Both quantities show a strongly anomalous temperature dependence. Our data are consistently described in terms of a spin-state transition of the Co$^{3+}$ ions with increasing temperature from a low-spin ground state to an intermediate-spin state without (100K - 500K) and with (>500K) orbital degeneracy. We attribute the lack of orbital degeneracy up to 500K to (probably local) Jahn-Teller distortions of the CoO$_6$ octahedra. A strong reduction or disappearance of the Jahn-Teller distortions seems to arise from the insulator-to-metal transition around 500 K.Comment: an error in the scaling factor of Eq.(4) and consequently 2 values of table I have been corrected. The conclusions of the paper remain unchanged. See also: C. Zobel et al. Phys. Rev. B 71, 019902 (2005) and J. Baier et al. Phys. Rev. B 71, 014443 (2005

Variations of training load, monotony, and strain and dose-response relationships with maximal aerobic speed, maximal oxygen uptake, and isokinetic strength in professional soccer players

This study aimed to identify variations in weekly training load, training monotony, and training strain across a 10-week period (during both, pre- and in-season phases); and to analyze the dose-response relationships between training markers and maximal aerobic speed (MAS), maximal oxygen uptake, and isokinetic strength. Twenty-seven professional soccer players (24.9±3.5 years old) were monitored across the 10-week period using global positioning system units. Players were also tested for maximal aerobic speed, maximal oxygen uptake, and isokinetic strength before and after 10 weeks of training. Large positive correlations were found between sum of training load and extension peak torque in the right lower limb (r = 0.57, 90%CI[0.15;0.82]) and the ratio agonist/antagonist in the right lower limb (r = 0.51, [0.06;0.78]). It was observed that loading measures fluctuated across the period of the study and that the load was meaningfully associated with changes in the fitness status of players. However, those magnitudes of correlations were small-to-large, suggesting that variations in fitness level cannot be exclusively explained by the accumulated load and loading profile

Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training

Activation of the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays a critical role modulating cardiac function in both health and disease. Here, we determined the effect of chronic CaMKII inhibition during an exercise training program in healthy mice. CaMKII was inhibited by KN-93 injections. Mice were randomized to the following groups: sham sedentary, sham exercise, KN-93 sedentary, and KN-93 exercise. Cardiorespiratory function was evaluated by ergospirometry during treadmill running, echocardiography, and cardiomyocyte fractional shortening and calcium handling. The results revealed that KN-93 alone had no effect on exercise capacity or fractional shortening. In sham animals, exercise training increased maximal oxygen uptake by 8% (p < 0.05) compared to a 22% (p < 0.05) increase after exercise in KN-93 treated mice (group difference p < 0.01). In contrast, in vivo fractional shortening evaluated by echocardiography improved after exercise in sham animals only: from 25 to 32% (p < 0.02). In inactive mice, KN-93 reduced rates of diastolic cardiomyocyte re-lengthening (by 25%, p < 0.05) as well as Ca2+ transient decay (by 16%, p < 0.05), whereas no such effect was observed after exercise training. KN-93 blunted exercise training response on cardiomyocyte fractional shortening (63% sham vs. 18% KN-93; p < 0.01 and p < 0.05, respectively). These effects could not be solely explained by the Ca2+ transient amplitude, as KN-93 reduced it by 20% (p < 0.05) and response to exercise training was equal (64% sham and 47% KN-93; both p < 0.01). We concluded that chronic CaMKII inhibition increased time to 50% re-lengthening which were recovered by exercise training, but paradoxically led to a greater increase in maximal oxygen uptake compared to sham mice. Thus, the effect of chronic CaMKII inhibition is multifaceted and of a complex nature