50 research outputs found

    Electronic Collective Modes and Superconductivity in Layered Conductors

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    A distinctive feature of layered conductors is the presence of low-energy electronic collective modes of the conduction electrons. This affects the dynamic screening properties of the Coulomb interaction in a layered material. We study the consequences of the existence of these collective modes for superconductivity. General equations for the superconducting order parameter are derived within the strong-coupling phonon-plasmon scheme that account for the screened Coulomb interaction. Specifically, we calculate the superconducting critical temperature Tc taking into account the full temperature, frequency and wave-vector dependence of the dielectric function. We show that low-energy plasmons may contribute constructively to superconductivity. Three classes of layered superconductors are discussed within our model: metal-intercalated halide nitrides, layered organic materials and high-Tc oxides. In particular, we demonstrate that the plasmon contribution (electronic mechanism) is dominant in the first class of layered materials. The theory shows that the description of so-called ``quasi-two-dimensional superconductors'' cannot be reduced to a purely 2D model, as commonly assumed. While the transport properties are strongly anisotropic, it remains essential to take into account the screened interlayer Coulomb interaction to describe the superconducting state of layered materials.Comment: Final version (minor changes) 14 pages, 6 figure

    Electronic correlation in the infrared optical properties of the quasi two dimensional κ\kappa-type BEDT-TTF dimer system

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    The polarized optical reflectance spectra of the quasi two dimensional organic correlated electron system κ\kappa-(BEDT-TTF)2_{2}Cu[N(CN)2_{2}]YY, Y=Y = Br and Cl are measured in the infrared region. The former shows the superconductivity at TcT_{\rm c} \simeq 11.6 K and the latter does the antiferromagnetic insulator transition at TNT_{\rm N} \simeq 28 K. Both the specific molecular vibration mode ν3(ag)\nu_{3}(a_{g}) of the BEDT-TTF molecule and the optical conductivity hump in the mid-infrared region change correlatively at TT^{*} \simeq 38 K of κ\kappa-(BEDT-TTF)2_{2}Cu[N(CN)2_{2}]Br, although no indication of TT^{*} but the insulating behaviour below TinsT_{\rm ins} \simeq 50-60 K are found in κ\kappa-(BEDT-TTF)2_{2}Cu[N(CN)2_{2}]Cl. The results suggest that the electron-molecular vibration coupling on the ν3(ag)\nu_{3}(a_{g}) mode becomes weak due to the enhancement of the itinerant nature of the carriers on the dimer of the BEDT-TTF molecules below TT^{*}, while it does strong below TinsT_{\rm ins} because of the localized carriers on the dimer. These changes are in agreement with the reduction and the enhancement of the mid-infrared conductivity hump below TT^{*} and TinsT_{\rm ins}, respectively, which originates from the transitions between the upper and lower Mott-Hubbard bands. The present observations demonstrate that two different metallic states of κ\kappa-(BEDT-TTF)2_{2}Cu[N(CN)2_{2}]Br are regarded as {\it a correlated good metal} below TT^{*} including the superconducting state and {\it a half filling bad metal} above TT^{*}. In contrast the insulating state of κ\kappa-(BEDT-TTF)2_{2}Cu[N(CN)2_{2}]Cl below TinsT_{\rm ins} is the Mott insulator.Comment: 8 pages, 7 figure

    Riboflavin alleviates cardiac failure in Type I diabetic cardiomyopathy

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    Heart failure (HF) is a common and serious comorbidity of diabetes. Oxidative stress has been associated with the pathogenesis of chronic diabetic complications including cardiomyopathy. The ability of antioxidants to inhibit injury has raised the possibility of new therapeutic treatment for diabetic heart diseases. Riboflavin constitutes an essential nutrient for humans and animals and it is an important food additive. Riboflavin, a precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), enhances the oxidative folding and subsequent secretion of proteins. The objective of this study was to investigate the cardioprotective effect of riboflavin in diabetic rats. Diabetes was induced in 30 rats by a single injection of streptozotocin (STZ) (70 mg /kg). Riboflavin (20 mg/kg) was orally administered to animals immediately after induction of diabetes and was continued for eight weeks. Rats were examined for diabetic cardiomyopathy by left ventricular (LV) remadynamic function. Myocardial oxidative stress was assessed by measuring the activity of superoxide dismutase (SOD), the level of malondialdehyde (MDA) as well as heme oxygenase-1 (HO-1) protein level. Myocardial connective tissue growth factor (CTGF) level was measured by Western blot in all rats at the end of the study. In the untreated diabetic rats, left ventricular systolic pressure (LVSP) rate of pressure rose (+dp/dt), and rate of pressure decay (−dp/dt) were depressed while left ventricular end-diastolic pressure (LVEDP) was increased, which indicated the reduced left ventricular contractility and slowing of left ventricular relaxation. The level of SOD decreased, CTGF and HO-1 protein expression and MDA content rose. Riboflavin treatment significantly improved left ventricular systolic and diastolic function in diabetic rats, there were persistent increases in significant activation of SOD and the level of HO-1 protein, and a decrease in the level of CTGF. These results suggest that riboflavin treatment ameliorates myocardial function and improves heart oxidant status, whereas raising myocardial HO-1 and decreasing myocardial CTGF levels have beneficial effects on diabetic cardiomyopathy

    Incoherent Interplane Conductivity of kappa-(BEDT-TTF)2Cu[N(CN)2]Br

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    The interplane optical spectrum of the organic superconductor kappa-(BEDT-TTF)2Cu[N(CN)2]Br was investigated in the frequency range from 40 to 40,000 cm-1. The optical conductivity was obtained by Kramers-Kronig analysis of the reflectance. The absence of a Drude peak at low frequency is consistent with incoherent conductivity but in apparent contradiction to the metallic temperature dependence of the DC resistivity. We set an upper limit to the interplane transfer integral of tb = 0.1 meV. A model of defect-assisted interplane transport can account for this discrepancy. We also assign the phonon lines in the conductivity to the asymmetric modes of the ET molecule.Comment: 7 pages with embedded figures, submitted to PR

    Influence of internal disorder on the superconducting state in the organic layered superconductor kappa-(BEDT-TTF)2Cu[N(CN)2]Br

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    We report high-sensitivity AC susceptibility measurements of the penetration depth in the Meissner state of the layered organic superconductor kappa-(BEDT-TTF)2Cu[N(CN)2]Br. We have studied nominally pure single crystals from the two different syntheses and employed controlled cooling procedures in order to minimize intrinsic remnant disorder at low temperatures associated with the glass transition, caused by ordering of the ethylene moieties in BEDT-TTF molecule at T_G = 75 K. We find that the optimal cooling procedures (slow cooling of -0.2 K/h or annealing for 3 days in the region of T_G) needed to establish the ground state, depend critically on the sample origin indicating different relaxation times of terminal ethylene groups. We show that, in the ground state, the behavior observed for nominally pure single crystals from both syntheses is consistent with unconventional d-wave order parameter. The in-plane penetration depth lambda_in(T) is strongly linear, whereas the out-of-plane component lambda_out(T) varies as T^2. In contrast, the behavior of single crystals with long relaxation times observed after slow (-0.2 K/h) cooling is as expected for a d-wave superconductor with impurities (i.e. lambda_in(T) propto lambda_out(T) propto T^2) or might be also reasonably well described by the s-wave model. Our results might reconcile the contradictory findings previously reported by different authors.Comment: 13 pages, 10 figures, submitted to Phys. Rev.

    The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism

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    Although multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions

    Heterozygous ANKRD17 loss-of-function variants cause a syndrome with intellectual disability, speech delay, and dysmorphism

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    ANKRD17 is an ankyrin repeat-containing protein thought to play a role in cell cycle progression, whose ortholog in Drosophila functions in the Hippo pathway as a co-factor of Yorkie. Here, we delineate a neurodevelopmental disorder caused by de novo heterozygous ANKRD17 variants. The mutational spectrum of this cohort of 34 individuals from 32 families is highly suggestive of haploinsufficiency as the underlying mechanism of disease, with 21 truncating or essential splice site variants, 9 missense variants, 1 in-frame insertion-deletion, and 1 microdeletion (1.16 Mb). Consequently, our data indicate that loss of ANKRD17 is likely the main cause of phenotypes previously associated with large multi-gene chromosomal aberrations of the 4q13.3 region. Protein modeling suggests that most of the missense variants disrupt the stability of the ankyrin repeats through alteration of core structural residues. The major phenotypic characteristic of our cohort is a variable degree of developmental delay/intellectual disability, particularly affecting speech, while additional features include growth failure, feeding difficulties, non-specific MRI abnormalities, epilepsy and/or abnormal EEG, predisposition to recurrent infections (mostly bacterial), ophthalmological abnormalities, gait/balance disturbance, and joint hypermobility. Moreover, many individuals shared similar dysmorphic facial features. Analysis of single-cell RNA-seq data from the developing human telencephalon indicated ANKRD17 expression at multiple stages of neurogenesis, adding further evidence to the assertion that damaging ANKRD17 variants cause a neurodevelopmental disorder.Neurolog
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