We present a review of experimental and theoretical studies of the anomalous Hall effect (AHE), focusing on recent developments that have provided a more complete framework for understanding this subtle phenomenon and have, in many instances, replaced controversy by clarity. Synergy between experimental and theoretical work, both playing a crucial role, has been at the heart of these advances. On the theoretical front, the adoption of Berry-phase concepts has established a link between the AHE and the topological nature of the Hall currents which originate from spin-orbit coupling. On the experimental front, new experimental studies of the AHE in transition metals, transition-metal oxides, spinels, pyrochlores, and metallic dilute magnetic semiconductors, have more clearly established systematic trends. These two developments in concert with first-principles electronic structure calculations, strongly favor the dominance of an intrinsic Berry-phase-related AHE mechanism in metallic ferromagnets with moderate conductivity. The intrinsic AHE can be expressed in terms of Berry-phase curvatures and it is therefore an intrinsic quantum mechanical property of a perfect cyrstal. An extrinsic mechanism, skew scattering from disorder, tends to dominate the AHE in highly conductive ferromagnets. We review the full modern semiclassical treatment of the AHE together with the more rigorous quantum-mechanical treatments based on the Kubo and Keldysh formalisms, taking into account multiband effects, and demonstrate the equivalence of all three linear response theories in the metallic regime. Finally we discuss outstanding issues and avenues for future investigation.

/pdf/anomalous-hall-effect-tyeyld308t.pdf

Anomalous hall effect

The first suggestion that physical exercise results in free radical-mediated damage to tissues appeared in 1978, and the past three decades have resulted in a large growth of knowledge regarding exercise and oxidative stress. Although the sources of oxidant production during exercise continue to be debated, it is now well established that both resting and contracting skeletal muscles produce reactive oxygen species and reactive nitrogen species. Importantly, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Furthermore, oxidants can modulate a number of cell signaling pathways and regulate the expression of multiple genes in eukaryotic cells. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, DNA repair proteins, and mitochondrial electron transport proteins. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species promote contractile dysfunction resulting in muscle weakness and fatigue. Ongoing research continues to probe the mechanisms by which oxidants influence skeletal muscle contractile properties and to explore interventions capable of protecting muscle from oxidant-mediated dysfunction.

/pdf/exercise-induced-oxidative-stress-cellular-mechanisms-and-4a18810890.pdf

Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production

http://www.biblioteca.uma.es/bbldoc/articulos/16689835.pdf?origin=publication_detail

Antioxidant enzymes and human diseases

The Na+/Ca2+ exchanger, an ion transport protein, is expressed in the plasma membrane (PM) of virtually all animal cells. It extrudes Ca2+ in parallel with the PM ATP-driven Ca2+ pump. As a reversible transporter, it also mediates Ca2+ entry in parallel with various ion channels. The energy for net Ca2+ transport by the Na+/Ca2+ exchanger and its direction depend on the Na+, Ca2+, and K+ gradients across the PM, the membrane potential, and the transport stoichiometry. In most cells, three Na+ are exchanged for one Ca2+. In vertebrate photoreceptors, some neurons, and certain other cells, K+ is transported in the same direction as Ca2+, with a coupling ratio of four Na+ to one Ca2+ plus one K+. The exchanger kinetics are affected by nontransported Ca2+, Na+, protons, ATP, and diverse other modulators. Five genes that code for the exchangers have been identified in mammals: three in the Na+/Ca2+ exchanger family (NCX1, NCX2, and NCX3) and two in the Na+/Ca2+ plus K+ family (NCKX1 and NCKX2). Genes homologous to NCX1 have been identified in frog, squid, lobster, and Drosophila. In mammals, alternatively spliced variants of NCX1 have been identified; dominant expression of these variants is cell type specific, which suggests that the variations are involved in targeting and/or functional differences. In cardiac myocytes, and probably other cell types, the exchanger serves a housekeeping role by maintaining a low intracellular Ca2+ concentration; its possible role in cardiac excitation-contraction coupling is controversial. Cellular increases in Na+ concentration lead to increases in Ca2+ concentration mediated by the Na+/Ca2+ exchanger; this is important in the therapeutic action of cardiotonic steroids like digitalis. Similarly, alterations of Na+ and Ca2+ apparently modulate basolateral K+ conductance in some epithelia, signaling in some special sense organs (e.g., photoreceptors and olfactory receptors) and Ca2+-dependent secretion in neurons and in many secretory cells. The juxtaposition of PM and sarco(endo)plasmic reticulum membranes may permit the PM Na+/Ca2+ exchanger to regulate sarco(endo)plasmic reticulum Ca2+ stores and influence cellular Ca2+ signaling.

https://www.physiology.org/doi/pdf/10.1152/physrev.1999.79.3.763

Sodium/Calcium Exchange: Its Physiological Implications

Increases in the intracellular levels of reactive oxygen species (ROS), frequently referred to as oxidative stress, represents a potentially toxic insult which if not counteracted will lead to membrane dysfunction, DNA damage and inactivation of proteins. Chronic oxidative stress has numerous pathological consequences including cancer, arthritis and neurodegenerative disease. Glutathione-associated metabolism is a major mechanism for cellular protection against agents which generate oxidative stress. It is becoming increasingly apparent that the glutathione tripeptide is central to a complex multifaceted detoxification system, where there is substantial inter-dependence between separate component members. Glutathione participates in detoxification at several different levels, and may scavenge free radicals, reduce peroxides or be conjugated with electrophilic compounds. Thus, glutathione provides the cell with multiple defences not only against ROS but also against their toxic products. This article discusses how glutathione biosynthesis, glutathione peroxidases, glutathione S-transferases and glutathione S-conjugate efflux pumps function in an integrated fashion to allow cellular adaption to oxidative stress. Co-ordination of this response is achieved, at least in part, through the antioxidant responsive element (ARE) which is found in the promoters of many of the genes that are inducible by oxidative and chemical stress. Transcriptional activation through this enhancer appears to be mediated by basic leucine zipper transcription factors such as Nrf and small Maf proteins. The nature of the intracellular sensor(s) for ROS and thiol-active chemicals which induce genes through the ARE is described. Gene activation through the ARE appears to account for the enhanced antioxidant and detoxification capacity of normal cells effected by many cancer chemopreventive agents. In certain instances it may also account for acquired resistance of tumours to cancer chemotherapeutic drugs. It is therefore clear that determining the mechanisms involved in regulation of ARE-driven gene expression has enormous medical implications.

Glutathione and glutathione-dependent enzymes represent a co-ordinately regulated defence against oxidative stress

The range of thermal fluctuations in ‘classical’ bulk superconductors is extremely small and especially in low-fields hardly experimentally accessible. With a new type of calorimeter we were able to detect a tiny lambda anomaly in the specific-heat of the superconductor Nb3Sn within a narrow temperature range around the Hc2 line. We show that the evolution of the anomaly as a function of magnetic field follows scaling laws expected in the presence of critical thermal fluctuations.

Thermal fluctuations in the classical superconductor Nb3Sn from high-resolution specific-heat measurements

A New Elaboration Process of the Superconducting Tl2Ba2Cu1O6 Phase with Tc = 90 K.

We have attempted to substitute calcium on the yttrium and barium sites in the “247” superconducting phase, i.e. (Y1 - x Cax)2Ba4 Cu7O15 + δ and Y2(Ba1 - xCax)4Cu7O15 + δ. X-Ray diffraction and microprobe analyses indicate that calcium enters the structure but preferentially occupies the barium site. The solubility of calcium in the “247” phase is clearly lower than 10% (x < 0.1). The samples are not single phase even for small substitutions (x = 0.05). Higher values of x result in a higher amount of impurity phases. The (Y1 - xCax)2Ba4Cu7O15 + δ samples contain BaCuO2 as the major impurity, whereas in Y2 (Ba1 - xCax)4Cu7O15 + δ a new phase is found. This new phase was identified by microprobe analysis to have the composition YCaCu2O4.5 ± δ. No increase is observed in the critical temperature Tc as a function of calcium substitution. This is in contrast with the calcium-substituted “124” superconductor (Y1 - xCax)Ba2Cu4O8 where Tc increases from 80 K (x = 0) to about 90 K (x = 0.1).

Calcium Substitution in the Y2Ba4Cu7O15+δ Superconducting Phase.

Ca doping effects in YBa2Cu4O8 (124) phase are investigated by the citrate pyrolysis method under both atmospheric and high oxygen pressure. The decomposition temperature of (124) to the Y2Ba4Cu7O15−δ (247) and the YBa2Cu3O7−δ (123) phases decreases with Ca doping. The onset Tc measured by DC susceptibility increases linearly from 81K to 89K with increasing Ca content, x, from x=0 to x=0. 15 in nominal compositions Y1−xCaxBa2Cu4O8. The

Ca Doping Effects in YBa2Cu4O8 Prepared by the Citrate Pyrolysis Method

We investigate the specific heat in high fields (0-14T, 40-150K) of (Ca0.4La0.6)(Ba1.35La0.65)Cu3Oδ ceramics with different oxygen concentrations δ. The specific heat jump ΔC/Tc≅13 mJ/K2mole is about three times smaller for the compound with δ=7.19 compared to YBa2Cu3O6.94. The field dependence of the specific heat of oxidized samples is comparable to that of YBa2Cu3O7, whereas that of reduced samples is similar to that of Bi2Sr2CaCu2Oδ.

Alain Junod

Papers

Thermal fluctuations in the classical superconductor Nb3Sn from high-resolution specific-heat measurements

A New Elaboration Process of the Superconducting Tl2Ba2Cu1O6 Phase with Tc = 90 K.

Calcium Substitution in the Y2Ba4Cu7O15+δ Superconducting Phase.

Ca Doping Effects in YBa2Cu4O8 Prepared by the Citrate Pyrolysis Method

Specific heat of (Ca{sub 0.4}La{sub 0.6})(Ba{sub 1.35}La{sub 0.65})Cu{sub 3}O{sub {delta}} for different oxygen concentrations