Optical and hidden transport properties of BaFe1.91Ni0.09As2film.

Optical spectroscopy was used to study the electrodynamics and hidden transport properties of a BaFe1.91Ni0.09As2thin superconducting (SC) film. We analyzed the normal state data using a Drude-Lorentz model with two Drude components: one narrow (D1) and another broad one (D2). In the SC state, two gaps with2Δ0(2)/kBTc=1.9-2.0 and2Δ0(1)/kBTc=4.0-4.3 are formed from the narrow component D1while the broad component D2remains ungapped. The calculated total DC resistivity of the film and the low-temperature scattering rate for the narrow Drude component show a hidden Fermi-liquid behavior. The change of total electron-boson coupling (λtot) and representative energy (Ω0) in the normal state with respect to the SC state is typical of other iron-based materials as well as high-temperature superconducting (HTSC) cuprates.

Direct study of structural phase transformation in single crystalline bulk and thin film BaFe2As2.

The ternary iron arsenide compound BaFe2As2 exhibits a structural phase transition from tetragonal to orthorhombic at a temperature of about 140 K. The twin lamellae arising below this transition temperature were studied in undoped single crystalline bulk and epitaxial thin film samples using electron backscatter diffraction in a scanning electron microscope equipped with a helium cryostat. Applying this technique on bulk single crystals a characteristic twin lamella size in the range of 0.1 µm up to a few µm was observed. In contrast, in epitaxially strained thin films the phase transition is not observed at temperatures above 19 K.

Pushing the limits of applicability of REBCO coated conductor films through fine chemical tuning and nanoengineering of inclusions.

An outstanding current carrying performance (namely critical current density, Jc) over a broad temperature range of 10-77 K for magnetic fields up to 12 T is reported for films of YBa2Cu3O7-x with Ba2Y(Nb,Ta)O6 inclusion pinning centres (YBCO-BYNTO) and thicknesses in the range of 220-500 nm. Jc values of 10 MA cm-2 were measured at 30 K - 5 T and 10 K - 9 T with a corresponding maximum of the pinning force density at 10 K close to 1 TN m-3. The system is very flexible regarding properties and microstructure tuning, and the growth window for achieving a particular microstructure is wide, which is very important for industrial processing. Hence, the dependence of Jc on the magnetic field angle was readily controlled by fine tuning the pinning microstructure. Transmission electron microscopy (TEM) analysis highlighted that higher growth rates induce more splayed and denser BYNTO nanocolumns with a matching field as high as 5.2 T. Correspondingly, a strong peak at the B||c-axis is noticed when the density of vortices is lower than the nanocolumn density. YBCO-BYNTO is a very robust and reproducible composite system for high-current coated conductors over an extended range of magnetic fields and temperatures.

Selective mass enhancement close to the quantum critical point in BaFe2(As1-x P x )2.

A quantum critical point (QCP) is currently being conjectured for the BaFe2(As1-x P x )2 system at the critical value x c ≈ 0.3. In the proximity of a QCP, all thermodynamic and transport properties are expected to scale with a single characteristic energy, given by the quantum fluctuations. Such a universal behavior has not, however, been found in the superconducting upper critical field H c2. Here we report H c2 data for epitaxial thin films extracted from the electrical resistance measured in very high magnetic fields up to 67 Tesla. Using a multi-band analysis we find that H c2 is sensitive to the QCP, implying a significant charge carrier effective mass enhancement at the doping-induced QCP that is essentially band-dependent. Our results point to two qualitatively different groups of electrons in BaFe2(As1-x P x )2. The first one (possibly associated to hot spots or whole Fermi sheets) has a strong mass enhancement at the QCP, and the second one is insensitive to the QCP. The observed duality could also be present in many other quantum critical systems.

Controlling the near-surface superfluid density in underdoped YBa2Cu3O(6+x) by photo-illumination.

The interaction with light weakens the superconducting ground state in classical superconductors. The situation in cuprate superconductors is more complicated: illumination increases the charge carrier density, a photo-induced effect that persists below room temperature. Furthermore, systematic investigations in underdoped YBa2Cu3O(6+x) (YBCO) have shown an enhanced critical temperature Tc. Until now, studies of photo-persistent conductivity (PPC) have been limited to investigations of structural and transport properties, as well as the onset of superconductivity. Here we show how changes in the magnetic screening profile of YBCO in the Meissner state due to PPC can be determined on a nanometer scale utilizing low-energy muons. The data obtained reveal a strongly increased superfluid density within the first few tens of nanometers from the sample surface. Our findings suggest a non-trivial modification of the near-surface band structure and give direct evidence that the superfluid density of YBCO can be controlled by light illumination.

Strain induced superconductivity in the parent compound BaFe2As2.

The discovery of superconductivity with a transition temperature, Tc, up to 65 K in single-layer FeSe (bulk Tc=8 K) films grown on SrTiO3 substrates has attracted special attention to Fe-based thin films. The high Tc is a consequence of the combined effect of electron transfer from the oxygen-vacant substrate to the FeSe thin film and lattice tensile strain. Here we demonstrate the realization of superconductivity in the parent compound BaFe2As2 (no bulk Tc) just by tensile lattice strain without charge doping. We investigate the interplay between strain and superconductivity in epitaxial BaFe2As2 thin films on Fe-buffered MgAl2O4 single crystalline substrates. The strong interfacial bonding between Fe and the FeAs sublattice increases the Fe-Fe distance due to the lattice misfit, which leads to a suppression of the antiferromagnetic spin density wave and induces superconductivity with bulk Tc≈10 K. These results highlight the role of structural changes in controlling the phase diagram of Fe-based superconductors.

Nanostructural control in solution-derived epitaxial Ce(1-x)Gd(x)O(2-y) films.

A novel mechanism based on aliovalent doping, allowing fine tuning of the nanostructure and surface topography of solution-derived ceria films, is reported. While under reducing atmospheric conditions, non-doped ceria films are inherently polycrystalline due to an interstitial amorphous Ce(2)C(3) phase that inhibits grain growth, a high quality epitaxial film can be achieved simply by doping with Gd(3+) cations. Gd(3+) [Formula: see text] Ce(4+) substitutions within the lattice are accompanied by charge-compensating oxygen vacancies throughout the volume of the crystallites acting as an efficient vehicle to reduce the barrier for grain boundary motion caused by interstitial Ce(2)C(3). In this way, the original nanostructure is self-purified by pushing the amorphous Ce(2)C(3) phase towards the free surface of the film. Once a full epitaxial cube-on-cube oriented ceria film is obtained, its surface morphology is dictated by the interplay between faceting on low energy {110} and/or {111} pyramidal planes and truncation of those pyramids by (001) ones. The development of the latter requires the suppression of their polar character which is thought to be achieved by charge compensation between the dopand and oxygen along [Formula: see text] directions.

Potentiation of 3-hydroxyglutarate neurotoxicity following induction of astrocytic iNOS in neonatal rat hippocampal cultures.

Neuronal damage in glutaryl-CoA dehydrogenase deficiency (GDD) has previously been addressed to N-methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity of the accumulating neurotoxic metabolite 3-hydroxyglutarate. However, acute encephalopathic crises in GDD patients are typically precipitated by febrile illness or even routine vaccinations, suggesting a potentiating role of inflammatory cytokines. In the present study we investigated the effect of interleukin-1beta and interferon-gamma on 3-hydroxyglutarate toxicity in rat cortical astrocyte cultures and neonatal rat hippocampal cultures. A cotreatment of both culture systems with interleukin-1beta and interferon-gamma induced the protein expression of astrocytic inducible nitric oxide synthase (iNOS), resulting in increased nitric oxide (NO) production. Cytokine pretreatment alone had no effect on cell viability but potentiated 3-hydroxyglutarate neurotoxicity. NOS inhibition by aminoguanidine and L-NAME prevented an iNOS-mediated potentiation of 3-hydroxyglutarate neurotoxicity but failed to protect neurons against 3-hydroxyglutarate alone. In contrast, superoxide dismutase/catalase as well as MK-801 prevented toxicity of 3-hydroxyglutarate alone as well as its potentiation by iNOS, supporting a central role of NMDA receptor stimulation with subsequently increased superoxide anion production. It is concluded that the potentiation of 3-hydroxyglutarate neurotoxicity is most probably due to an induction of astrocytic iNOS and concomitantly increased NO production, enabling enhanced peroxynitrite formation. Thus, we provide evidence for a neuroimmunological approach to the precipitation of acute encephalopathic crises in GDD by inflammatory cytokines.

Neuroprotective effects of NV-31, a bilobalide-derived compound: evidence for an antioxidative mechanism.

In previous studies we have already shown that the extract of Ginkgo biloba, and some of its constituents, such as ginkgolide B and bilobalide, protected cultured neurons against apoptotic and excitotoxic damage and reduced the infarct volume after focal cerebral ischemia in mice and rats. In this work, we determined the neuroprotective and antioxidative effects of 4-hydroxy-4-tert-butyl-2,3,5,6-tetrahydrothiopyran-1-oxide (NV-31), a stable compound which was synthesized to mimic the pharmacological activity profile of bilobalide. In pure neuronal cultures from chick embryo telencephalon, damage was induced by serum deprivation (24 h) and exposure to staurosporine (200 nM, 24 h) which caused an increase in the percentage of apoptotic neurons from 14 (controls) to 30 and 55%, respectively. NV-31 (1-100 nM) protected dose-dependently chick neurons against both serum deprivation- and staurosporine-induced apoptosis. Similarly, NV-31 (100 nM) reduced staurosporine (300 nM, 24 h)-induced neuronal damage in mixed cultures of neurons and astrocytes from neonatal rat hippocampus. The cellular ROS content increased 6-fold 4 h after serum deprivation as well as 4 h after the exposure to staurosporine and this increase was reduced by 50% in the presence of 10 and 100 nM NV-31, respectively. In mice, a treatment with 10 and 20 mg/kg NV-31 60 min before and immediately after focal cerebral ischemia, respectively, significantly reduced the infarct area compared with vehicle-treated animals. In the present study, we show that NV-31 promotes neuronal survival and we suggest that its antioxidative property contributes to the mechanism of neuroprotection.

Retinoic acid potentiated the protective effect of NGF against staurosporine-induced apoptosis in cultured chick neurons by increasing the trkA protein expression.

Nerve growth factor (NGF) has already been shown to protect neurons and PC12 cells from cell death induced by different stimuli. When chick embryonic neurons were exposed to staurosporine (200 nM, 24 hr), the percentage of apoptotic neurons increased from 15% in controls to 80%, but the treatment with NGF alone did not show any neuroprotection. In the presence of retinoic acid (RA, 5 microM), however, NGF (20 pg/ml) reduced staurosporine-induced damage to 42% apoptotic neurons compared to 58% in the presence of RA (5 icroM) alone. TrkA protein expression in chick neurons was markedly reduced by staurosporine, but was found to be increased in the presence of RA and NGF compared with the treatment with staurosporine alone. The antiapoptotic effect caused by RA and NGF was abolished by the tyrosine kinase inhibitor K-252a, as well as by anti-trkA antibodies and anti-NGF antibodies suggesting that the increase in trkA protein expression contributed to its mechanism of action. In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Increasing the endogenous synthesis of growth factors as well as the expression of their receptors by small, blood-brain barrier-permeable drugs was suggested as a promising concept for neuroprotection.

The resolvase encoded by Xanthomonas campestris transposable element ISXc5 constitutes a new subfamily closely related to DNA invertases.

BACKGROUND: Conservative site-specific recombination is responsible for the resolution of cointegrates which result during the transposition of class II transposable elements. Resolution is catalysed by a transposon-encoded recombinase, resolvase, that belongs to a large family of recombinases, including DNA invertases. Resolvases and the related invertases are likely to employ similar reaction mechanisms during recombination. There are important differences, however. Resolvases require two accessory DNA binding sites within each of the two directly repeated recombination sites. Invertases instead need a host factor, Fis, and an enhancer type DNA sequence, in addition to two inversely orientated recombination sites. RESULTS: The resolvase encoded by transposable element ISXc5 from the gram-negative phytopathogen Xanthomonas campestris shows two features which distinguish it from other known resolvases. First, it is more closely phylogenetically related to invertases than other resolvases. In particular, two functionally important regions seem highly conserved between this resolvase and members of the invertase subfamily. Second, the enzyme exhibits a large extension of its carboxy-terminal domain with unknown function. We purified ISXc5 resolvase and analysed its resolution reaction in vitro. Our biochemical and DNA topological analysis reveals that critical features of resolution are similar, if not identical, to that carried out by gammadelta resolvase. However, despite its apparent similarity to invertases, we were unable to detect recombination on standard substrates for DNA inversion, in either the presence or absence of Fis. CONCLUSIONS: ISXc5 resolvase employs a reaction mechanism which is common to members of the resolvase family. Its position near the evolutionary borderline to invertases and its high degree of identity within two functionally important regions with members of the DNA invertase subfamily suggest that only a few replacements of critical residues may suffice to convert this resolvase into a functional, possibly Fis-dependent invertase.

How AraC interacts specifically with its target DNAs.

Previous work indicates that one subunit of the AraC protein dimer binds to a DNA target araI1, of 17 base-pairs. We systematically substituted every base-pair in a synthetic araI1 target with the three possible alternatives and then tested binding of araI1 and of these 51 DNA targets to AraC by quantitative gel shift analysis in the presence of L-arabinose. We found that every substitution of the underlined bases reduces AraC binding tenfold or more: 5' TAGCATTTTTATCCATA 3'. Substitutions at other bases have little or no effect. In the absence of L-arabinose we observed a sixfold reduction of binding of AraC to araI1. We have designated the 5' AGC sequence the A-box and the 5'TCCATA sequence the B-box. We synthesised DNA targets containing either two A or two B-boxes with the natural araI1-I2 spacing. Wild-type AraC binds both targets in the presence of L-arabinose in a gel shift-experiment. In the absence of L-arabinose, AraC binds only to the double B-box. We then tested various AraC mutant proteins in the same way. S208A and H212A bind to the double B-box but not to the double A-box in the presence or absence of L-arabinose. D256A binds to the double A-box, but not to the double B-box, in the presence of L-arabinose but not in its absence. The implications of these results for the mechanism of AraC induction by L-arabinose are discussed.