8 research outputs found
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