157 research outputs found

    High-redshift Ly alpha emitters with a large equivalent width: Properties of i-dropout galaxies with an NB921-band depression in the Subaru Deep Field

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    We report new follow-up spectroscopy of i-dropout galaxies with an NB921-band depression found in the Subaru Deep Field. The NB921-depressed i-dropout selection method is expected to select galaxies with large equivalent width Ly alpha emission over a wide redshift range, 6.0<z<6.5. Two of four observed targets show a strong emission line with a clear asymmetric profile, identified as Ly alpha emitters at z=6.11 and 6.00. Their rest-frame equivalent widths are 153A and 114A, which are lower limits on the intrinsic equivalent widths. Through our spectroscopic observations (including previous ones) of NB921-depressed i-dropout galaxies, we identified 5 galaxies in total with a rest-frame equivalent width larger than 100A at 6.0<z<6.5 out of 8 photometric candidates, which suggests that the NB921-depressed i-dropout selection method is possibly an efficient way to search for Ly alpha emitters with a large Ly alpha equivalent width, in a wider redshift range than usual narrow-band excess techniques. By combining these findings with our previous observational results, we infer that the fraction of broad-band selected galaxies having a rest-frame equivalent width larger than 100A is significantly higher at z~6 (the cosmic age of ~1 Gyr) than that at z~3 (~2 Gyr), being consistent with the idea that the typical stellar population of galaxies is significantly younger at z~6 than that at z~3. The NB921-depressed i-dropout galaxies may be interesting candidates for hosts of massive, zero-metallicity Population III stars.Comment: 9 pages, 5 figures, accepted for publication in A&

    Large-scale Filamentary Structure around the Protocluster at Redshift z=3.1

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    We report the discovery of a large-scale coherent filamentary structure of Lyman alpha emitters in a redshift space at z=3.1. We carried out spectroscopic observations to map the three dimensional structure of the belt-like feature of the Lyman alpha emitters discovered by our previous narrow-band imaging observations centered on the protocluster at z=3.1. The feature was found to consist of at least three physical filaments connecting with each other. The result is in qualitative agreement with the prediction of the 'biased' galaxy-formation theories that galaxies preferentially formed in large-scale filamentary or sheet-like mass overdensities in the early Universe. We also found that the two known giant Lyman alpha emission-line nebulae showing high star-formation activities are located near the intersection of these filaments, which presumably evolves into a massive cluster of galaxies in the local Universe. This may suggest that massive galaxy formation occurs at the characteristic place in the surrounding large-scale structure at high redshift.Comment: 11 pages, 3 figures, accepted for publication in ApJ Letter

    Genetic mapping of putative Chrna7 and Luzp2 neuronal transcriptional enhancers due to impact of a transgene-insertion and 6.8 Mb deletion in a mouse model of Prader-Willi and Angelman syndromes

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    BACKGROUND: Prader-Willi and Angelman syndrome (PWS and AS) patients typically have an ~5 Mb deletion of human chromosome 15q11-q13, of opposite parental origin. A mouse model of PWS and AS has a transgenic insertion-deletion (TgPWS/TgAS) of chromosome 7B/C subsequent to paternal or maternal inheritance, respectively. In this study, we define the deletion endpoints and examine the impact on expression of flanking genes. RESULTS: Using molecular and cytological methods we demonstrate that 13 imprinted and 11 non-imprinted genes are included in the TgPWS/TgAS deletion. Normal expression levels were found in TgPWS brain for genes extending 9.1- or 5.6-Mb centromeric or telomeric of the deletion, respectively. Our molecular cytological studies map the proximal deletion breakpoint between the Luzp2 and Siglec-H loci, and we show that overall mRNA levels of Luzp2 in TgPWS and TgAS brain are significantly reduced by 17%. Intriguingly, 5' Chrna7 shows 1.7-fold decreased levels in TgPWS and TgAS brain whereas there is a ≥15-fold increase in expression in neonatal liver and spleen of these mouse models. By isolating a Chrna7-Tg fusion transcript from TgAS mice, we mapped the telomeric deletion breakpoint in Chrna7 intron 4. CONCLUSION: Based on the extent of the deletion, TgPWS/TgAS mice are models for PWS/AS class I deletions. Other than for the first gene promoters immediately outside the deletion, since genes extending 5.6–9.1 Mb away from each end of the deletion show normal expression levels in TgPWS brain, this indicates that the transgene array does not induce silencing and there are no additional linked rearrangements. Using gene expression, non-coding conserved sequence (NCCS) and synteny data, we have genetically mapped a putative Luzp2 neuronal enhancer responsible for ~33% of allelic transcriptional activity. The Chrna7 results are explained by hypothesizing loss of an essential neuronal transcriptional enhancer required for ~80% of allelic Chrna7 promoter activity, while the Chrna7 promoter is upregulated in B lymphocytes by the transgene immunoglobulin enhancer. The mapping of a putative Chrna7 neuronal enhancer inside the deletion has significant implications for understanding the transcriptional regulation of this schizophrenia-susceptibility candidate gene

    In vivo imaging of autophagy in a mouse stroke model

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    Recent studies have suggested that autophagy is involved in a neural death pathway following cerebral ischemia. In vivo detection of autophagy could be important for evaluating ischemic neural cell damage for human stroke patients. Using novel green fluorescent protein (GFP)-fused microtubule-associated protein 1 light chain 3 (LC3) transgenic (Tg) mice, in vivo imaging of autophagy was performed at 1, 3 and 6 d after 60 min transient middle cerebral artery occlusion (tMCAO). Ex vivo imaging of autophagy, testing of the autophagy inhibitor 3-methyladenine (3-MA), estern blot analysis, immunohistochemistry, terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) and fluorescent analyses were performed on brain sections following tMCAO. In vivo fluorescent signals were detected above the ischemic hemisphere through the skull bone at 1, 3 and 6 d after tMCAO, with a peak at 1 d. Similar results were obtained with ex vivo fluorescence imaging. western blot analysis revealed maximum LC3-I and LC3-II expression at 1 d after tMCAO and fluorescence immunohistochemistry demonstrated that GFP-LC3-positive cells were primarily neuronal, not astroglial or microglial, cells. The number of GFP-LC3/TUNEL double-positive cells was greater in the peri-ischemic area than in the core. These results provided evidence of in vivo autophagy detection, with a peak at 1 d, in a live animal model following cerebral ischemia. This novel technique could be valuable for monitoring autophagic processes in vivo in live stroke patients, as well as for clarifying the detailed role of autophagy in the ischemic brain, as well as in other neurological diseases

    A 1.5-Mb PAC/BAC Contig Spanning the Prader-Willi Syndrome Critical Region (PWCR)

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    Prader-Willi syndrome (PWS) is a multiple anomalies/mental retardation syndrome. The putative PWS gene(s) remains unknown, and its occurrence is based on genomic imprinting at chromosome 15q11-q13. We have constructed a 1.5- Mb, fine, physical map of PWS critical region (PWCR) between two markers, D15S9 and D15S174 at 15q11-q13. The map is composed of 32 PAC and 3 BAC clones without any gaps. By the PAC/BAC-end sequencing procedure, a total of 26 sequence tag site (STS) markers were newly generated, and 5 expressed sequence tags (ESTs) were mapped in the region. The contig map was verified by both STS and fluorescence in situ hybridization analyses. Our map has higher resolution, compared with a previous YAC-based map of PWCR. It is useful for further genome analysis, especially on genomic imprinting of this region

    Phosphodiesterase Inhibitors Suppress Lactobacillus casei Cell-Wall-Induced NF-κB and MAPK Activations and Cell Proliferation through Protein Kinase A—or Exchange Protein Activated by cAMP-Dependent Signal Pathway

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    Specific strains of Lactobacillus have been found to be beneficial in treating some types of diarrhea and vaginosis. However, a high mortality rate results from underlying immunosuppressive conditions in patients with Lactobacillus casei bacteremia. Cyclic AMP (cAMP) is a small second messenger molecule that mediates signal transduction. The onset and progression of inflammatory responses are sensitive to changes in steady-state cAMP levels. L. casei cell wall extract (LCWE) develops arteritis in mice through Toll-like receptor-2 signaling. The purpose of this study was to investigate whether intracellular cAMP affects LCWE-induced pathological signaling. LCWE was shown to induce phosphorylation of the nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways and cell proliferation in mice fibroblast cells. Theophylline and phosphodiesterase inhibitor increased intracellular cAMP and inhibited LCWE-induced cell proliferation as well as phosphorylation of NF-κB and MAPK. Protein kinase A inhibitor H89 prevented cAMP-induced MAPK inhibition, but not cAMP-induced NF-κB inhibition. An exchange protein activated by cAMP (Epac) agonist inhibited NF-κB activation but not MAPK activation. These results indicate that an increase in intracellular cAMP prevents LCWE induction of pathological signaling pathways dependent on PKA and Epac signaling

    Evidence for Association of the rs17822931-A Allele in ABCC11 with a Decreased Risk of Estrogen Receptor-negative Breast Cancer

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    The rs17822931 SNP of the human ABCC11 gene determines earwax types, and is also associated with some functions of apocrine glands, including the mammary gland. Nevertheless, whether the ABCC11 polymorphism is correlated with estrogen receptor (ER) status of breast cancer (BC) remains unclear. To investigate the correlation between rs17822931 and BC, we screened the genotypes in a total of 276 and 295 histological BC samples collected from Japanese and Ukrainian BC patients, and 269 and 264 ethnically-matched healthy individuals, respectively, using TaqManTM PCR. Genotype frequencies at rs178229131 in Japanese and Ukrainian BC patients were not significantly different from those in their respective control populations. Consistently, no correlation between rs178229131 and the susceptibility to BC was found. The AA genotype, which corresponds to dry earwax, occurred less frequently in ER -negative BC in Japanese [odds ratio, 0.48; 95% confidential interval, 0.29-0.80] but not in Ukrainian patients although a similar correlation was weakly observed. Our results indicate that the rs178229131-A allele may be important in reducing the risk of ER -negative BC development
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