Electron paramagnetic resonance of Cu<SUP>2+</SUP> ion in CsCl single crystals

Electron paramagnetic resonance spectrum of the Cu2+ ion in CsCl is studied at different temperatures. The local symmetry at the Cu2+ site is found to be tetragonal. A model of substitutional Cu2+ ion associated with a first neighbour cation vacancy is proposed to explain the observed spectrum

Electrochemical and lithium-ion transport properties of layered Li-rich Li1.10(Ni0.32X0.01Co0.33Mn0.33)O2 (X = Dy/Gd/Ho) positive electrodes

864-876Layer structured Li1.10(Ni0.32X0.01Co0.33Mn0.33)O2 (X = Dy/Gd/Ho) compounds were synthesized via the microwave assisted solvothermal route. The impacts of doping on the electrical and electrochemical properties of Li1.10 (Ni0.32X0.01Co0.33Mn0.33)O2 compounds were investigated. Rietveld refined XRD pattern showed Li1.10 (Ni0.32X0.01Co0.33Mn0.33)O2 compounds with layered hexagonal structure. SEM images revealed the compounds with micrometer sized grains. The Li1.10 (Ni0.33Co0.33Mn0.33)O2 compound delivered an initial discharge capacity of 197 mAh/g at 0.2C and retained a capacity of 163mAh/g after 50th cycle in the voltage window of 2.5-4.6V. The cycling stability of Li1.10(Ni0.33Co0.33Mn0.33)O2 compound was improved with rare earth doping. Li1.10(Ni0.32Dy0.01Co0.33Mn0.33)O2 compound delivered the discharge capacity of 166 mAh/g after50th cycle in the potential window 2.5-4.6V at 0.2C with 100% capacity retention. AC impedance studies displayed the electrical conductivity in the order of 10-6 S/cm. Wagner polarization analysis revealed the improvement in electronic transference number via rare earth doping

GWA study data mining and independent replication identify cardiomyopathy-associated 5 (CMYA5) as a risk gene for schizophrenia

We conducted data-mining analyses using the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) and molecular genetics of schizophrenia genome-wide association study supported by the genetic association information network (MGS-GAIN) schizophrenia data sets and performed bioinformatic prioritization for all the markers with P-values ≤0.05 in both data sets. In this process, we found that in the CMYA5 gene, there were two non-synonymous markers, rs3828611 and rs10043986, showing nominal significance in both the CATIE and MGS-GAIN samples. In a combined analysis of both the CATIE and MGS-GAIN samples, rs4704591 was identified as the most significant marker in the gene. Linkage disequilibrium analyses indicated that these markers were in low LD (3 828 611–rs10043986, r2 = 0.008; rs10043986–rs4704591, r2 = 0.204). In addition, CMYA5 was reported to be physically interacting with the DTNBP1 gene, a promising candidate for schizophrenia, suggesting that CMYA5 may be involved in the same biological pathway and process. On the basis of this information, we performed replication studies for these three single-nucleotide polymorphisms. The rs3828611 was found to have conflicting results in our Irish samples and was dropped out without further investigation. The other two markers were verified in 23 other independent data sets. In a meta-analysis of all 23 replication samples (family samples, 912 families with 4160 subjects; case–control samples, 11 380 cases and 15 021 controls), we found that both markers are significantly associated with schizophrenia (rs10043986, odds ratio (OR) = 1.11, 95% confidence interval (CI) = 1.04–1.18, P = 8.2 × 10−4 and rs4704591, OR = 1.07, 95% CI = 1.03–1.11, P = 3.0 × 10−4). The results were also significant for the 22 Caucasian replication samples (rs10043986, OR = 1.11, 95% CI = 1.03–1.17, P = 0.0026 and rs4704591, OR = 1.07, 95% CI = 1.02–1.11, P = 0.0015). Furthermore, haplotype conditioned analyses indicated that the association signals observed at these two markers are independent. On the basis of these results, we concluded that CMYA5 is associated with schizophrenia and further investigation of the gene is warranted

The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

BACKGROUND: A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. PRESENTATION OF THE HYPOTHESIS: Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia. TESTING THE HYPOTHESIS: Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. IMPLICATIONS OF THE HYPOTHESIS: The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments

Electron paramagnetic resonance of Mn<SUP>2+</SUP> in (NH<SUB>4</SUB>)<SUB>2</SUB>SO<SUB>4</SUB> single crystal

Electron paramagnetic resonance investigation of Mn<SUP>2+</SUP> in (NH<SUB>4</SUB>)<SUB>2</SUB>SO<SUB>4</SUB> single crystal is discussed both in paraelectric and ferroelectric phases of the crystal. Mn<SUP>2+</SUP> is found to substitute one of the two possible types (&#945; and&#946; ) of NH<SUB>4</SUB><SUP>+</SUP> ions and get associated with the second type of NH<SUB>4</SUB><SUP>+</SUP> vacancy, the vacancy being the second distant neighbour in thebc-plane. As The line joining Mn<SUP>2+</SUP> substituted NH<SUB>4</SUB><SUP>+</SUP> site and NH<SUB>4</SUB><SUP>+</SUP> vacancy lies at an angle of 18&#176; from the crystallographicb-axis in the bc-plane. As the temperature is lowered to &#8722;56&#176; C the crystal becomes ferroelectric and the spectrum in the paraelectric phase splits into two from which it appears that two sets of Mn<SUP>2+</SUP> sites which are magnetically equivalent in the paraelectric phase become inequivalent in the ferroelectric phase. The spin Hamiltonian analysis is presented for the spectrum in the paraelectric phase

Electron paramagnetic resonance of Mn<SUP>2&#177;</SUP> in K<SUB>2</SUB>SO<SUB>4</SUB> single crystal

The paramagnetic resonance spectrum of divalent manganese ion in single crystals of potassium sulfate is described in detail over a large temperature range. Mn<SUP>2&#177;</SUP> is found to substitute for K<SUP>&#177;</SUP> and becomes associated with first-, second-, and third-neighbor potassium ion vacancies. The different spectra obtained at room temperature have been analyzed. Variation in the fine-structure spread with temperature has been studied for one of these spectra and the variation indicates a probable phase change at about &#8722;130<SUP>&#176;</SUP> C. This was supported by the observation that some of the resonance lines appear to begin to split into two as the temperature is lowered below &#8722;130<SUP>&#176;</SUP>C