Magnetic exchange interactions in Mn doped ZnSnAs₂ chalcopyrite

Accurate ab initio full-potential augmented plane wave (FP-LAPW) electronic calculations within generalized gradient approximation have been performed for Mn doped ZnSnAs₂ chalcopyrites, focusing on their electronic and magnetic properties as a function of the geometry related to low Mn-impurity concentration and the spin magnetic alignment (i.e., ferromagnetic vs antiferromagnetic). As expected, Mn is found to be a source of holes and localized magnetic moments of about 4 µB per Mn atom are calculated which are sufficiently large. The defect calculations are firstly performed by replacing a single cation (namely Zn and Sn) with a single Mn atom in the pure chalcopyrite ZnSnAs₂ supercell, and their corresponding formation energies show that the substitution of a Sn atom (rather than Zn) by Mn is strongly favored. Thereafter, a comparison of total energy differences between ferromagnetic (FM) and antiferromagnetic (AFM) are given. Surprisingly, the exchange interaction between a Mn pairs is found to oscillate with the distance between them. Consequently, the AFM alignment is energetically favored in Mn-doped ZnSnAs₂ compounds, except for low impurity concentration associated with lower distances between neighboring Mn impurities, in this case the stabilization of FM increases. Moreover, the ferromagnetic alignment in the Mn-doped ZnSnAs₂ systems behaves half-metallic; the valence band for majority spin orientation is partially filled while there is a gap in the density of states for the minority spin orientation. This semiconducting gap of ~1 eV opened up in the minority channel and is due to the large bonding–antibonding splitting from the p–d hybridization. Our findings suggest that the Mn-doped ZnSnAs₂ chalcopyrites could be a different class of ferromagnetic semiconductors

Chronic Nicotine Modifies Skeletal Muscle Na,K-ATPase Activity through Its Interaction with the Nicotinic Acetylcholine Receptor and Phospholemman

Our previous finding that the muscle nicotinic acetylcholine receptor (nAChR) and the Na,K-ATPase interact as a regulatory complex to modulate Na,K-ATPase activity suggested that chronic, circulating nicotine may alter this interaction, with long-term changes in the membrane potential. To test this hypothesis, we chronically exposed rats to nicotine delivered orally for 21–31 days. Chronic nicotine produced a steady membrane depolarization of ∼3 mV in the diaphragm muscle, which resulted from a net change in electrogenic transport by the Na,K-ATPase α2 and α1 isoforms. Electrogenic transport by the α2 isoform increased (+1.8 mV) while the activity of the α1 isoform decreased (−4.4 mV). Protein expression of Na,K-ATPase α1 or α2 isoforms and the nAChR did not change; however, the content of α2 subunit in the plasma membrane decreased by 25%, indicating that its stimulated electrogenic transport is due to an increase in specific activity. The physical association between the nAChR, the Na,K-ATPase α1 or α2 subunits, and the regulatory subunit of the Na,K-ATPase, phospholemman (PLM), measured by co-immuno precipitation, was stable and unchanged. Chronic nicotine treatment activated PKCα/β2 and PKCδ and was accompanied by parallel increases in PLM phosphorylation at Ser63 and Ser68. Collectively, these results demonstrate that nicotine at chronic doses, acting through the nAChR-Na,K-ATPase complex, is able to modulate Na,K-ATPase activity in an isoform-specific manner and that the regulatory range includes both stimulation and inhibition of enzyme activity. Cholinergic modulation of Na,K-ATPase activity is achieved, in part, through activation of PKC and phosphorylation of PLM

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

Hypoxia, AMPK activation and uterine artery vasoreactivity

This is the author accepted manuscript. The final version is available from Wiley via http://dx.doi.org/10.1113/JP270995Genes near adenosine monophosphate-activated protein kinase-α1 (PRKAA1) have been implicated in the greater uterine artery (UtA) blood flow and relative protection from fetal growth restriction seen in altitude-adapted Andean populations. Adenosine monophosphate-activated protein kinase (AMPK) activation vasodilates multiple vessels but whether AMPK is present in UtA or placental tissue and influences UtA vasoreactivity during normal or hypoxic pregnancy remains unknown. We studied isolated UtA and placenta from near-term C57BL/6J mice housed in normoxia (n = 8) or hypoxia (10% oxygen, n = 7-9) from day 14 to day 19, and placentas from non-labouring sea level (n = 3) or 3100 m (n = 3) women. Hypoxia increased AMPK immunostaining in near-term murine UtA and placental tissue. RT-PCR products for AMPK-α1 and -α2 isoforms and liver kinase B1 (LKB1; the upstream kinase activating AMPK) were present in murine and human placenta, and hypoxia increased LKB1 and AMPK-α1 and -α2 expression in the high- compared with low-altitude human placentas. Pharmacological AMPK activation by A769662 caused phenylephrine pre-constricted UtA from normoxic or hypoxic pregnant mice to dilate and this dilatation was partially reversed by the NOS inhibitor l-NAME. Hypoxic pregnancy sufficient to restrict fetal growth markedly augmented the UtA vasodilator effect of AMPK activation in opposition to PE constriction as the result of both NO-dependent and NO-independent mechanisms. We conclude that AMPK is activated during hypoxic pregnancy and that AMPK activation vasodilates the UtA, especially in hypoxic pregnancy. AMPK activation may be playing an adaptive role by limiting cellular energy depletion and helping to maintain utero-placental blood flow in hypoxic pregnancy.Funding for these studies was provided by the Wellcome Trust (084804/2/08/Z) to G.J.B., the British Heart Foundation and the Wellcome Trust to D.A.G., the Biotechnology and Biological Sciences Research Council (BBSRC) to A.L.F., a UK Wellcome Trust Programme Grant (WT081195MA) to A.M.E. and A.D.M., a BBSRC studentship and in vivo skills award to J.S.H., a National Health Medical Research Council and Centre for Trophoblast Research fellowship to A.N.S.-P., and a NIH RO1 grant (HLBI-079647) to L.G.M. along with sabbatical support from Wake Forest University

A group contribution model for determining the vaporization enthalpy of organic compounds at the standard reference temperature of 298K

Article on a group contribution model for determining the vaporization enthalpy of organic compounds at the standard reference temperature of 298 K

Ab initio study of structural, electronic and thermodynamic properties of tungstate double perovskites Ba₂MWO₆ (M = Mg, Ni, Zn)

The structural and electronic properties of the double perovskite Ba₂MWO₆ with M = Mg, Ni, Zn have been studied using the full-potential linearized augmented plane wave (FP-LAPW) method by employing both the local density approximation (LDA) and the generalized gradient approximation (GGA), which are based on exchange–correlation energy optimization to calculate the total energy. Also we have used the Engel–Vosko GGA formalism, which optimizes the corresponding potential for band structure calculations. However, we have evaluated the ground state quantities such as lattice parameter, bulk modulus and its pressure derivative. Also, we have presented the results of the band structures and densities of states. These results were in favorable agreement with previous theoretical works and the existing experimental data. To complete the fundamental characteristics of these compounds we have analyzed the thermodynamic properties such as thermal expansion coefficient, heat capacities and other structural parameters in the whole pressure range from 0 to 20 GPa and temperature range from 0 to 1000 K

The role of HIV1 Nef in T-cell activation: Nef impairs induction of Th1 cytokines and interacts with the Src family tyrosine kinase Lck

International audienc

Similarity between Nef of primate lentiviruses and p15E of murine and feline leukaemia viruses

International audienc