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 relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. Diabetogenic activity could be demonstrated between the doses of 25 and 100 mg/kg, all indices used showing some degree of correlation with the dose administered. Ketonuria was only seen with the largest dose, 100 mg/kg. The most striking and precise correlation was that between the dose and the pancreatic IRI content 24 hr after administration of the drug, and it is suggested that this represents a convenient test system either for both related and unrelated beta cytotoxic compounds or for screening for modifying agents or antidiabetic substances of a novel type. Ability to produce graded depletion of pancreatic IRI storage capacity led to an analysis of the relationship between pancreatic IRI content and deranged carbohydrate metabolism. Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached two-thirds and three-quarters, respectively. The mild yet persistent anomaly produced by the lowest effective streptozotocin dose, 25 mg/kg, exhibits characteristics resembling the state of chemical diabetes in humans and might thus warrant further study as a possible model. Finally, the loss of the diabetogenic action of streptozotocin by pretreatment with nicotinamide was confirmed and was shown to be a function of the relative doses of nicotinamide and streptozotocin and of the interval between injections.

/pdf/diabetogenic-action-of-streptozotocin-relationship-of-dose-2a2gw8ducg.pdf

Diabetogenic action of streptozotocin: relationship of dose to metabolic response.

SummaryStreptozotocin is a highly effective cytotoxic agent for pancreatic B-cells. After intravenous administration of 65 mg streptozotocin per kg, damage to B-cells is apparent as early as one hour after intravenous administration of the drug. Frank necrosis associated with phagocytosis is best seen after 7 hours, when pancreatic insulin release and hypoglycemia are also noted. By 24 hours, pancreatic insulin content is reduced to 5% of normal or less. While the B-cytotoxic effects of streptozotocin resemble those of alloxan, their specificity is very much greater, as demonstrated by the wide margin between diabetogenic dose and general toxicity.

Studies of the diabetogenic action of streptozotocin.

${\mathrm{SrRuO}}_{3}$ is a metallic ferromagnet. Its electrical resistivity is reported for temperatures up to 1000 K, its Hall coefficient for temperatures up to 300 K, and its specific heat for temperatures up to 230 K. The energy bands have been calculated by self-consistent spin-density functional theory, which finds a ferromagnetic ordered moment of 1.45${\mathrm{\ensuremath{\mu}}}_{\mathit{B}}$ per Ru atom. The measured linear specific heat coefficient \ensuremath{\gamma} is 30 mJ/mol, which exceeds the theoretical value by a factor of 3.7. A transport mean free path at room temperature of \ensuremath{\approxeq}10 \AA{} is found. The resistivity increases nearly linearly with temperature to 1000 K in spite of such a short mean free path that resistivity saturation would be expected. The Hall coefficient is small and positive above the Curie temperature, and exhibits both a low-field and a high-field anomalous behavior below the Curie temperature. \textcopyright{} 1996 The American Physical Society.

https://arxiv.org/pdf/cond-mat/9601106.pdf

Transport properties, thermodynamic properties, and electronic structure of SrRuO3.

The specific heat C of a sintered polycrystalline sample of MgB 2 with a bulk superconducting transition temperature T c =36.7 K is measured as a function of the temperature (2–300 K) and magnetic field (0–16 T), together with magnetic properties (normal-state susceptibility, superconducting-state magnetization, etc.). The Sommerfeld constant γ =0.89±0.05 mJ/K 2 /gat (2.7 mJ/K 2 /mol) is determined in the normal state above H c2 . The normal- and superconducting-state entropies are equal at T c . Several moments of the PDOS are obtained from the lattice specific heat. We report bulk values for: the thermodynamic critical field, B c (0)=0.26 T; the slope of the upper critical field, (d B c2 /d T ) T c =0.56 T/K; the Ginzburg–Landau parameter, κ =38; the coherence length, ξ ≅5 nm; the lower critical field, B c1 ≅0.018 T; the London penetration depth, λ (0)≅180 nm. These results characterize MgB 2 as a type-II superconductor. The nearly quadratic dependence of C ( T ) versus T at T ≪ T c , its non-linear field dependence, and the discrepancy between the electron–phonon coupling constant λ ep as determined by the renormalization of the electron density of states ( λ ep ≅0.6) and by McMillan's equation for isotropic superconductors ( λ ep ≅1.1), are inconsistent with a single isotropic gap. In addition to high phonon frequencies, anisotropy or two-band gap structure may explain why the critical temperature of this superconductor is high in spite of its low condensation energy, which does not exceed 1/16 of that of YBa 2 Cu 3 O 7 and 1/4 of that of Nb 3 Sn.

Specific heat in the superconducting and normal state (2–300 K, 0–16 T), and magnetic susceptibility of the 38 K superconductor MgB2: evidence for a multicomponent gap

The authors show that the specific heat of the superconductor MgB{sub 2} in zero field, for which significant non-BCS features have been reported, can be fitted, essentially within experimental error, over the entire range of temperature to T{sub c} by a phenomenological two-gap model. The resulting gap parameters agree with previous determinations from band-structure calculations, and from various spectroscopic experiments. The determination from specific heat, a bulk property, shows that the presence of two superconducting gaps in MgB{sub 2} is a volume effect.

/pdf/phenomenological-two-gap-model-for-the-specific-heat-of-mgb2-17kgq7off5.pdf

Alain Junod

Papers

Diabetogenic action of streptozotocin: relationship of dose to metabolic response.

Studies of the diabetogenic action of streptozotocin.

Transport properties, thermodynamic properties, and electronic structure of SrRuO3.

Specific heat in the superconducting and normal state (2–300 K, 0–16 T), and magnetic susceptibility of the 38 K superconductor MgB2: evidence for a multicomponent gap

Phenomenological two-gap model for the specific heat of MgB2