Structural Evolutions and Crystal Field Characterizations of Tm-Doped YAlO₃: New Theoretical Insights

The recent renaissance of the use of rare-earth-doped yttrium orthoaluminate as an ideal laser material has generated significant interest; however, the unique structural features underlying many of its outstanding optical properties still require elucidation. To solve this intriguing problem, we performed a systematic first-principles study; the results of the study reveal a new stable phase for Tm³⁺-doped YAlO₃ (YAP), of monoclinic <i>Pm</i> symmetry, with an 80-atom per unit cell. An unbiased CALYPSO structure search indicates that the Tm³⁺ impurity ion tends to substitute the position of Y³⁺ in the YAP crystal lattice. Electronic band structure calculations reveal that the insulated behaviors of YAP are significantly eliminated after doping the impure Tm³⁺ ions, as evidenced by the minor energy gap of about 0.4 eV, which is close to the band gap energy of a 2 μm emitter source. On the basis of our developed crystal-field theory method, the 4f¹² electronic structures and energies of Tm³⁺ ions in the YAP crystal are calculated. The theoretical results indicate that the electric-dipole-induced transition ³H₄ → ³H₅ is mainly responsible for producing the light wave at approximately 2.3 μm. The present results provide an essential understanding of the rare-earth-ion-doped lasing materials and serve as a practical tool for further exploration of such materials

Differential Phosphorylation of GluN1-MAPKs in Rat Brain Reward Circuits following Long-Term Alcohol Exposure

<div><p>The effects of long-term alcohol consumption on the mitogen-activated protein kinases (MAPKs) pathway and N-methyl-D-aspartate-type glutamate receptor 1 (GluN1) subunits in the mesocorticolimbic system remain unclear. In the present study, rats were allowed to consume 6% (v/v) alcohol solution for 28 consecutive days. Locomotor activity and behavioral signs of withdrawal were observed. Phosphorylation and expression of extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), p38 protein kinase and GluN1 in the nucleus accumbens, caudate putamen, amygdala, hippocampus and prefrontal cortex of these rats were also measured. Phosphorylation of ERK, but not JNK or p38, was decreased in all five brain regions studied in alcohol-drinking rats. The ratio of phospho/total-GluN1 subunit was reduced in all five brain regions studied. Those results suggest that the long-term alcohol consumption can inhibits GluN1 and ERK phosphorylation, but not JNK or p38 in the mesocorticolimbic system, and these changes may be relevant to alcohol dependence. To differentiate alcohol-induced changes in ERK and GluN1 between acute and chronic alcohol exposure, we have determined levels of phospho-ERK, phospho-GluN1 and total levels of GluN1 after acute alcohol exposure. Our data show that 30 min following a 2.5 g/kg dose of alcohol (administered intragastrically), levels of phospho-ERK are decreased while those of phospho-GluN1 are elevated with no change in total GluN1 levels. At 24 h following the single alcohol dose, levels of phospho-ERK are elevated in several brain regions while there are no differences between controls and alcohol treated animals in phospho-GluN1 or total GluN1. Those results suggest that alcohol may differentially regulate GluN1 function and ERK activation depending on alcohol dose and exposure time in the central nervous system.</p> </div

Global withdrawal severity (sum of somatic withdrawal scores across the 5 behavioral signs) measured between 2 and 72 hours after the removal of the 6% v/v alcohol solution.

<p>(Inset) Somatic withdrawal signs measured at 6^th h of the alcohol withdrawal (n = 10 per group). Rats of water-drinking group were evaluated as a control. The values represent the mean ± SD. *<i>p</i><0.05; **<i>p</i><0.01; ***<i>p</i><0.0001 different from water-control group;</p

Gene structure of human <i>GRIN2A</i> and the relative positions of the 40 variations used in our study.

<p>Gene structure of human <i>GRIN2A</i> and the relative positions of the 40 variations used in our study.</p

Analysis of Variations in the Glutamate Receptor, N-Methyl D-Aspartate 2A (<i>GRIN2A</i>) Gene Reveals Their Relative Importance as Genetic Susceptibility Factors for Heroin Addiction

<div><p>The glutamate receptor, N-methyl D-aspartate 2A (<i>GRIN2A</i>) gene that encodes the 2A subunit of the N-methyl D-aspartate (NMDA) receptor was recently shown to be involved in the development of opiate addiction. Genetic polymorphisms in <i>GRIN2A</i> have a plausible role in modulating the risk of heroin addiction. An association of <i>GRIN2A</i> single-nucleotide polymorphisms (SNPs) with heroin addiction was found earlier in African Americans. To identify markers that contribute to the genetic susceptibility to heroin addiction, we examined the potential association between heroin addiction and forty polymorphisms of the <i>GRIN2A</i> gene using the MassARRAY system and GeneScan in this study. The frequency of the (GT)26 repeats (rs3219790) in the heroin addiction group was significantly higher than that in the control group (<i>χ²</i> = 5.360, <i>P</i> = 0.021). The allele frequencies of three polymorphisms (rs1102972, rs1650420, and rs3104703 in intron 3) were strongly associated with heroin addiction (<i>P</i><0.001, 0.0002, and <0.001, after Bonferroni correction). Three additional SNPs from the same intron (rs1071502, rs6497730, and rs1070487) had nominally significant <i>P</i> values for association (<i>P</i><0.05), but did not pass the threshold value. Haplotype analysis revealed that the G-C-T-C-C-T-A (block 6) and T-T (block 10) haplotypes of the <i>GRIN2A</i> gene displayed a protective effect (<i>P</i> = <0.001 and 0.003). These findings point to a role for <i>GRIN2A</i> polymorphisms in heroin addiction among the Han Chinese from Shaanxi province, and may be informative for future genetic or neurobiological studies on heroin addiction.</p></div

HPLC chromatogram of the black rice extract detected at 520 nm.

<p>Peak 1, cyanidin-3,5-diglucoside; Peak 2, not identified; Peak 3, cyanidin-3-glucoside; Peak 4, cyanidin-3-rutinoside; Peak 5, peonidin-3-glucoside; and Peak 6, peonidin-3-rutinoside.</p

Relative content of C3G metabolites produced by Bifidobacteria and Lactobacilli at different incubation times in anaerobic conditions at 37 °C.

<p>Relative content of C3G metabolites produced by Bifidobacteria and Lactobacilli at different incubation times in anaerobic conditions at 37 °C.</p

MS, MS/MS spectra of the six peaks in the HPLC analysis and the chemical structure of the anthocyanin monomers detected in the black rice extract.

<p>a (Peak 1), cyanidin-3,5-diglucoside; b (peak 2), not identified; c (peak 3), cyanidin-3-glucoside; d (peak 4), cyanidin-3-rutinoside; e (peak 5), peonidin-3-glucoside; and f (peak 6), peonidin-3-rutinoside.</p

Decreased extracellular signal-regulated kinase (ERK) (Thr202/Tyr204) phosphorylation was found in the nucleus accumbens (NAc), caudate putamen (CPu), amygdala (Amy), hippocampus (Hip) and the prefrontal cortex (PFC) in rats following 28 d of 6% (v/v) alcohol exposure.

<p>Ratios of phospho/total-ERK protein levels in the five brain regions were analyzed. Data were expressed as mean ± SD relative to water-drinking controls that were set as 100%. β-actin was used as loading control. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 <i>vs.</i> water-controls.</p

Genotype and allele frequencies of the <i>GRIN2A</i> gene SNPs in cases and controls and the results of their associations with risk of heroin addiction.

a<p>values for Hardy-Weinberg equilibrium in controls.</p>b<p>values for genotype frequency dirrerence.</p>c<p>values for allele frequency dirrerence.</p>d<p>values for allele frequency dirrerence.</p><p>Alpha value is adjusted by Bonferroni correction and significant results (<i>P</i><0.0013).</p