Strange filamentary structures ("fireballs") around a merger galaxy in the Coma cluster of galaxies

We found an unusual complex of narrow blue filaments, bright blue knots, and H-alpha emitting filaments and clouds, which morphologically resembled a complex of ``fireballs,'' extending up to 80 kpc south from an E+A galaxy RB199 in the Coma cluster. The galaxy has a highly disturbed morphology indicative of a galaxy--galaxy merger remnant. The narrow blue filaments extend in straight shapes toward the south from the galaxy, and several bright blue knots are located at the southern ends of the filaments. The Rc band absolute magnitudes, half light radii and estimated masses of the bright knots are -12 - -13 mag, 200 - 300 pc and 10^6-7 Msolar, respectively. Long, narrow H-alpha emitting filaments are connected at the south edge of the knots. The average color of the fireballs is B - Rc = 0.5, which is bluer than RB199 (B - R = 0.99), suggesting that most of the stars in the fireballs were formed within several times 10^8 yr. The narrow blue filaments exhibit almost no H-alpha emission. Strong H-alpha and UV emission appear in the bright knots. These characteristics indicate that star formation recently ceased in the blue filaments and now continues in the bright knots. The gas stripped by some mechanism from the disk of RB199 may be traveling in the intergalactic space, forming stars left along its trajectory. The most plausible fireball formation mechanism is ram pressure stripping by high-speed collision between the galaxy and the hot intra-cluster medium. The fireballs may be a snapshot of diffuse intra-cluster population formation, or halo star population formation in a cluster galaxy.Comment: 13 pages, 14 figures, submitted to Ap

Update on the Keio collection of Escherichia coli single-gene deletion mutants

The Keio collection (Baba et al, 2006) has been established as a set of single‐gene deletion mutants of Escherichia coli K‐12. These mutants have a precisely designed deletion from the second codon from the seventh to the last codon of each predicted ORF. Further information is available at http://sal.cs.purdue.edu:8097/GB7/index.jsp or http://ecoli.naist.jp/. The distribution is now being handled by the National Institute of Genetics of Japan (http://www.shigen.nig.ac.jp/ecoli/pec/index.jsp). To date more than 4 million samples have been distributed worldwide. As we described earlier (Baba et al, 2006), gene amplification during construction is likely to have led to a small number of mutants with genetic duplications

MicroRNA induction by copy number gain is associated with poor outcome in squamous cell carcinoma of the lung

Abstract Copy number gains in cancer genomes have been shown to induce oncogene expression and promote carcinogenesis; however, their role in regulating oncogenic microRNAs (onco-miRNAs) remains largely unknown. Our aim was to identify onco-miRNAs induced by copy number gains in human squamous cell carcinoma (Sq) of the lung. We performed a genome-wide screen of onco-miRNAs from 245 Sqs using data sets from RNA-sequencing, comparative genomic hybridization, and the corresponding clinical information from The Cancer Genome Atlas. Among 1001 miRNAs expressed in the samples, 231 were correlated with copy number alternations, with only 11 of these being highly expressed in Sq compared to adenocarcinoma and normal tissues. Notably, miR-296-5p, miR-324-3p, and miR-3928-3p expression was significantly associated with poor prognosis. Multivariate analysis using the Cox proportional hazards model showed that miRNA expression and smoking were independent prognostic factors and were associated with poor prognosis. Furthermore, the three onco-miRNAs inhibited FAM46C to induce MYC expression, promoting proliferation of Sq cells. We found that copy number gains in Sq of the lung induce onco-miRNA expression that is associated with poor prognosis

Analgesic Mechanisms of Steroid Ointment against Oral Ulcerative Mucositis in a Rat Model

Despite the long history of use of steroid ointments for oral mucositis, the analgesic mechanism has not been fully elucidated. In this study, we examined the effects of triamcinolone acetonide (Tmc) on oral ulcerative mucositis-induced pain in conscious rats by our proprietary assay system. Based on evaluations of the physical properties and retention periods in the oral mucosa of human volunteers and rats, we selected TRAFUL® ointment as a long-lasting base. In oral ulcerative mucositis model rats, TRAFUL® with Tmc suppressed cyclooxygenase-dependent inflammatory responses with upregulations of glucocorticoid receptor-induced anti-inflammatory genes and inhibited spontaneous nociceptive behavior. When an ointment with a shorter residual period was used, the effects of Tmc were not elicited or were induced to a lesser extent. Importantly, TRAFUL® with Tmc also improved oral ulcerative mucositis-induced mechanical allodynia, which has been reported to be independent of cyclooxygenase. Ca2+ imaging in dissociated trigeminal ganglion neurons showed that long-term preincubation with Tmc inhibited the hypertonic stimulation-induced Ca2+ response. These results suggest that the representative steroid Tmc suppresses oral ulcerative mucositis-induced pain by general anti-inflammatory actions and inhibits mechanical sensitivity in peripheral nerves. For drug delivery, long-lasting ointments such as TRAFUL® are needed to sufficiently induce the therapeutic effects