Widely Extended [OIII] 88 um Line Emission around the 30 Doradus Region Revealed with AKARI FIS-FTS

We present the distribution map of the far-infrared [OIII] 88um line emission around the 30 Doradus (30 Dor) region in the Large Magellanic Cloud obtained with the Fourier Transform Spectrometer of the Far-Infrared Surveyor onboard AKARI. The map reveals that the [OIII] emission is widely distributed by more than 10' around the super star cluster R136, implying that the 30 Dor region is affluent with interstellar radiation field hard enough to ionize O^{2+}. The observed [OIII] line intensities are as high as (1-2) x 10^{-6} W m^{-2} sr^{-1} on the peripheral regions 4'-5' away from the center of 30 Dor, which requires gas densities of 60-100 cm^{-3}. However the observed size of the distribution of the [OIII] emission is too large to be explained by massive stars in the 30 Dor region enshrouded by clouds with the constant gas density of 10^2 cm^{-3}. Therefore the surrounding structure is likely to be highly clumpy. We also find a global correlation between the [OIII] and the far-infrared continuum emission, suggesting that the gas and dust are well mixed in the highly-ionized region where the dust survives in clumpy dense clouds shielded from the energetic photons.Comment: 17 pages, 9 figures, accepted for publication in Publications of the Astronomical Society of Japan (PASJ

Identification of novel candidate genes for treatment response to risperidone and susceptibility for schizophrenia: integrated analysis among pharmacogenomics, mouse expression, and genetic case-control association approaches

Background: Pharmacogenomic approaches based on genomewide sets of single nucleotide polymorphisms (SNPs) are now feasible and offer the potential to uncover variants that influence drug response. Methods: To detect potential predictor gene variants for risperidone response in schizophrenic subjects, we performed a convergent analysis based on 1) a genomewide (100K SNP) SNP pharmacogenetic study of risperidone response and 2) a global transcriptome study of genes with mRNA levels influenced by risperidone exposure in mouse prefrontal cortex. Results: Fourteen genes were highlighted as of potential relevance to risperidone activity in both studies: ATP2B2, HS3ST2, UNC5C, BAG3, PDE7B, PAICS, PTGFRN, NR3C2, ZBTB20, ST6GAL2, PIP5K1B, EPHA6, KCNH5, and AJAP1. The SNPs related to these genes that were associated in the pharmacogenetic study were further assessed for evidence for association with schizophrenia in up to three case-control series comprising 1564 cases and 3862 controls in total (Japanese [JPN] 1st and 2nd samples and UK sample). Of 14 SNPs tested, one (rs9389370) in PDE7B showed significant evidence for association with schizophrenia in a discovery sample (pallele � .026 in JPN_1st, two-tailed). This finding replicated in a joint analysis of two independent case-control samples (pJPN_2nd�UK � .008, one-tailed, uncorrected) and in all combined data sets (pall � .0014, two-tailed, uncorrected and pall � .018, two-tailed, Bonferroni correction). Conclusions: We identified novel candidate genes for treatment response to risperidone and provide evidence that one of these additionally may confer susceptibility to schizophrenia. Specifically, PDE7B is an attractive candidate gene, although evidence from integrated methodology, including pharmacogenomics, pharmacotranscriptomic, and case-control association approaches