Mid-Infrared Identification of Faint Submillimeter Sources

Faint submillimeter sources detected with the Submillimeter Common-User Bolometer Array on the James Clerk Maxwell Telescope have faced an identification problem due to the telescope's broad beam profile. Here we propose a new method to identify such submillimeter sources with a mid-infrared image having a finer point spread function. The Infrared Space Observatory has provided a very deep 6.7 um image of the Hawaii Deep Field SSA13. All three faint 850 um sources in this field have their 6.7 um counterparts. They have been identified with interacting galaxy pairs in optical images. These pairs are also detected in the radio. Two of them are optically faint and very red (I>24, I-K>4), one of which has a hard X-ray detection with the Chandra satellite. As these observing properties are similar to those of local ultraluminous infrared galaxies, their photometric redshifts are derived based on submillimeter to mid-infrared flux ratios assuming a spectral energy distribution (SED) of Arp220. Other photometric redshifts are obtained via chi^2 minimization between the available photometry data and template SEDs. Both estimates are in the range z=1-2, in good agreement with a spectroscopic redshift and a millimetric one. The reconstructed Arp220 SEDs with these redshift estimates are consistent with all the photometry data except Chandra's hard X-ray detection. The sources would be a few times more luminous than Arp220. With an assumption that AGN contributions are negligible, it appears that extremely high star formation rates are occurring in galaxies at high redshifts with massive stellar contents already in place.Comment: 6 pages, 2 figures, ApJL (accepted), a version with color figures at http://www.ioa.s.u-tokyo.ac.jp/~ysato/pub/2/sato-c.ps.g

KAIKObase: An integrated silkworm genome database and data mining tool

<p>Abstract</p> <p>Background</p> <p>The silkworm, <it>Bombyx mori</it>, is one of the most economically important insects in many developing countries owing to its large-scale cultivation for silk production. With the development of genomic and biotechnological tools, <it>B. mori </it>has also become an important bioreactor for production of various recombinant proteins of biomedical interest. In 2004, two genome sequencing projects for <it>B. mori </it>were reported independently by Chinese and Japanese teams; however, the datasets were insufficient for building long genomic scaffolds which are essential for unambiguous annotation of the genome. Now, both the datasets have been merged and assembled through a joint collaboration between the two groups.</p> <p>Description</p> <p>Integration of the two data sets of silkworm whole-genome-shotgun sequencing by the Japanese and Chinese groups together with newly obtained fosmid- and BAC-end sequences produced the best continuity (~3.7 Mb in N50 scaffold size) among the sequenced insect genomes and provided a high degree of nucleotide coverage (88%) of all 28 chromosomes. In addition, a physical map of BAC contigs constructed by fingerprinting BAC clones and a SNP linkage map constructed using BAC-end sequences were available. In parallel, proteomic data from two-dimensional polyacrylamide gel electrophoresis in various tissues and developmental stages were compiled into a silkworm proteome database. Finally, a <it>Bombyx </it>trap database was constructed for documenting insertion positions and expression data of transposon insertion lines.</p> <p>Conclusion</p> <p>For efficient usage of genome information for functional studies, genomic sequences, physical and genetic map information and EST data were compiled into KAIKObase, an integrated silkworm genome database which consists of 4 map viewers, a gene viewer, and sequence, keyword and position search systems to display results and data at the level of nucleotide sequence, gene, scaffold and chromosome. Integration of the silkworm proteome database and the <it>Bombyx </it>trap database with KAIKObase led to a high-grade, user-friendly, and comprehensive silkworm genome database which is now available from URL: <url>http://sgp.dna.affrc.go.jp/KAIKObase/</url>.</p

Faint 6.7um Galaxies and their Contributions to the Stellar Mass Density in the Universe

We discuss the nature of faint 6.7um galaxies detected with the mid-infrared camera ISOCAM on board the Infrared Space Observatory (ISO). The 23 hour integration on the Hawaii Deep Field SSA13 has provided a sample of 65 sources down to 6uJy at 6.7um. For 57 sources, optical or near-infrared counterparts were found with a statistical method. All four Chandra sources, three SCUBA sources, and one VLA/FIRST source in this field were detected at 6.7um with high significance. Using their optical to mid-infrared colors, we divided the 6.7um sample into three categories: low redshift galaxies with past histories of rapid star formation, high redshift ancestors of these, and other star forming galaxies. Rapidly star forming systems at high redshifts dominate the faintest end. Spectroscopically calibrated photometric redshifts were derived from fits to a limited set of template SEDs. They show a high redshift tail in their distribution with faint (1. The 6.7um galaxies tend to have brighter K magnitudes and redder I-K colors than the blue dwarf population at intermediate redshifts. Stellar masses of the 6.7um galaxies were estimated from their rest-frame near-infrared luminosities. Massive galaxies (M_star~10e11M_sun) were found in the redshift range of z=0.2-3. Epoch dependent stellar mass functions indicate a decline of massive galaxies' comoving space densities with redshift. Even with such a decrease, the contributions of the 6.7um galaxies to the stellar mass density in the universe are found to be comparable to those expected from UV bright galaxies detected in deep optical surveys.Comment: 31 pages, 15 figures, AJ (accepted), a version with color figures at http://www.ioa.s.u-tokyo.ac.jp/~ysato/pub/3/p3c-ysato.ps.g

Structural Features and Biological Properties of Ellagitannins in Some Plant Families of the Order Myrtales

Plant tannins, including hydrolysable and condensed varieties, are well known antioxidants in medicinal plants, foods, and edible fruits. Their diverse biological properties and potential for disease prevention have been demonstrated by various in vitro and in vivo assays. A number of ellagitannins, the largest group of hydrolysable tannins, have been isolated from dicotyledoneous angiosperms and characterized. This diverse class of tannins is sub-grouped into simple ellagitannins, C-glycosidic ellagitannins, complex tannins (condensates of C-glycosidic tannins with flavan-3-ol), and oligomers up to pentamers. This review outlines and describes the chemotaxonomic significance of structural features in various types of ellagitannins found in plants belonging to the Myrtaceae, Onagraceae, and Melastomataceae families, which are all included in the order Myrtales. Any biological activities that have been reported, including antitumor and antibacterial effects as well as enzyme inhibition, are also reviewed

Disposition of protein-bound 3-nitrotyrosine in rat plasma analysed by a novel protocol for HPLC-ECD

金沢大学医薬保健研究域医学系3-Nitrotyrosine (NTyr) is considered as a biomarker of the generation of reactive nitrogen species (RNS). However, it is still difficult to determine its concentration in biological samples. To develop a reliable and high-throughput method, we optimized the conditions for high performance liquid chromatography and electrochemical detection (HPLC-ECD). The best separation of NTyr was achieved using a highly acidic mobile phase (pH 2.5). The concentration of protein-bound NTyr in plasma protein was 593.6 ± 53.8 fmol/mg in rats treated with lipopolysaccharide (LPS) and 114.4 ± 27.6 fmol/mg in control. After intravenous administration of in vitro-nitrated plasma protein, NTyr concentration decreased; the half-life was 63.4 ± 16.8 h. Consistently, protein-bound NTyr concentration in plasma after LPS treatment declined gradually, but was detectable for 1 week. Our protocol is reproducible and suitable for analysing multiple clinical samples to study RNS production in vivo. © 2007 The Japanese Biochemical Society

Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism.

Low body temperature predicts a poor outcome in patients with heart failure, but the underlying pathological mechanisms and implications are largely unknown. Brown adipose tissue (BAT) was initially characterised as a thermogenic organ, and recent studies have suggested it plays a crucial role in maintaining systemic metabolic health. While these reports suggest a potential link between BAT and heart failure, the potential role of BAT dysfunction in heart failure has not been investigated. Here, we demonstrate that alteration of BAT function contributes to development of heart failure through disorientation in choline metabolism. Thoracic aortic constriction (TAC) or myocardial infarction (MI) reduced the thermogenic capacity of BAT in mice, leading to significant reduction of body temperature with cold exposure. BAT became hypoxic with TAC or MI, and hypoxic stress induced apoptosis of brown adipocytes. Enhancement of BAT function improved thermogenesis and cardiac function in TAC mice. Conversely, systolic function was impaired in a mouse model of genetic BAT dysfunction, in association with a low survival rate after TAC. Metabolomic analysis showed that reduced BAT thermogenesis was associated with elevation of plasma trimethylamine N-oxide (TMAO) levels. Administration of TMAO to mice led to significant reduction of phosphocreatine and ATP levels in cardiac tissue via suppression of mitochondrial complex IV activity. Genetic or pharmacological inhibition of flavin-containing monooxygenase reduced the plasma TMAO level in mice, and improved cardiac dysfunction in animals with left ventricular pressure overload. In patients with dilated cardiomyopathy, body temperature was low along with elevation of plasma choline and TMAO levels. These results suggest that maintenance of BAT homeostasis and reducing TMAO production could be potential next-generation therapies for heart failure.We thank Kaori Yoshida, Keiko Uchiyama, Satomi Kawai, Naomi Hatanaka, Yoko Sawaguchi, Runa Washio, Takako Ichihashi, Nanako Koike, Keiko Uchiyama, Masaaki Nameta (Niigata University), Kaori Igarashi, Kaori Saitoh, Keiko Endo, Hiroko Maki, Ayano Ueno, Maki Ohishi, Sanae Yamanaka, Noriko Kagata (Keio University) for their excellent technical assistance, C. Ronald Kahn (Joslin Diabetes Center and Harvard Medical School) for providing the BAT cell line, Evan Rosen (Harvard Medical School) for providing us Ucp-Cre mice, Kosuke Morikawa (Kyoto University), Tomitake Tsukihara (University of Hyogo) and Shinya Yoshikawa (University of Hyogo) for their professional opinions and suggestions. Tis work was supported by a Grant-in-Aid for Scientifc Research (A) (20H00533) from MEXT, AMED under Grant Numbers JP20ek0210114, and AMED-CREST under Grant Number JP20gm1110012, and Moonshot Research and Development Program (21zf0127003s0201), MEXT Supported Program for the Strategic Research Foundation at Private Universities Japan, Private University Research Branding Project, and Leading Initiative for Excellent Young Researchers, and grants from the Takeda Medical Research Foundation, the Vehicle Racing Commemorative Foundation, Ono Medical Research Foundation, and the Suzuken Memorial Foundation (to T.M.). Support was also provided by a Grants-in-Aid for Young Scientists (Start-up) (26893080), and grants from the Uehara Memorial Foundation, Kowa Life Science Foundation, Manpei Suzuki Diabetes Foundation, SENSHIN Medical Research Foundation, ONO Medical Research Foundation, Tsukada Grant for Niigata University Medical Research, Te Nakajima Foundation, SUZUKEN memorial foundation, HOKUTO Corporation, Mochida Memorial Foundation for Medical & Pharmaceutical Research, Grants-in-Aid for Encouragement of Young Scientists (A) (16H06244), Daiichi Sankyo Foundation of Life Science, AMED Project for Elucidating and Controlling Mechanisms of Aging and Longevity under Grant Number JP17gm5010002, JP18gm5010002, JP19gm5010002, JP20gm5010002, JP21gm5010002, Astellas Foundation for Research on Metabolic Disorders, Research grant from Naito Foundation, Te Japan Geriatrics Society (to I.S.); by a Grant-in-Aid for Scientifc Research (C) (19K08974), Yujin Memorial Grant, Sakakibara Memorial Research Grant from Te Japan Research Promotion Society for Cardiovascular Diseases, TERUMO Life Science Foundation, Kanae Foundation (to Y.Y.), JST ERATO (JPMJER1902), AMED-CREST (JP20gm1010009), the Takeda Science Foundation, the Food Science Institute Foundation (to S.F.), and by a grant from Bourbon (to T.M., I.S. and Y.Y.).S

Structural insight into the TFIIE–TFIIH interaction: TFIIE and p53 share the binding region on TFIIH

RNA polymerase II and general transcription factors (GTFs) assemble on a promoter to form a transcription preinitiation complex (PIC). Among the GTFs, TFIIE recruits TFIIH to complete the PIC formation and regulates enzymatic activities of TFIIH. However, the mode of binding between TFIIE and TFIIH is poorly understood. Here, we demonstrate the specific binding of the C-terminal acidic domain (AC-D) of the human TFIIEα subunit to the pleckstrin homology domain (PH-D) of the human TFIIH p62 subunit and describe the solution structures of the free and PH-D-bound forms of AC-D. Although the flexible N-terminal acidic tail from AC-D wraps around PH-D, the core domain of AC-D also interacts with PH-D. AC-D employs an entirely novel binding mode, which differs from the amphipathic helix method used by many transcriptional activators. So the binding surface between PH-D and AC-D is much broader than the specific binding surface between PH-D and the p53 acidic fragments. From our in vitro studies, we demonstrate that this interaction could be a switch to replace p53 with TFIIE on TFIIH in transcription

Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families

Painful peripheral neuropathy has been correlated with various voltage-gated sodium channel mutations in sensory neurons. Recently Nav1.9, a voltage-gated sodium channel subtype, has been established as a genetic influence for certain peripheral pain syndromes. In this study, we performed a genetic study in six unrelated multigenerational Japanese families with episodic pain syndrome. Affected participants (n = 23) were characterized by infantile recurrent pain episodes with spontaneous mitigation around adolescence. This unique phenotype was inherited in an autosomal-dominant mode. Linkage analysis was performed for two families with 12 affected and nine unaffected members, and a single locus was identified on 3p22 (LOD score 4.32). Exome analysis (n = 14) was performed for affected and unaffected members in these two families and an additional family. Two missense variants were identified: R222H and R222S in SCN11A. Next, we generated a knock-in mouse model harboring one of the mutations (R222S). Behavioral tests (Hargreaves test and cold plate test) using R222S and wild-type C57BL/6 (WT) mice, young (8-9 weeks old; n = 10-12 for each group) and mature (36-38 weeks old; n = 5-6 for each group), showed that R222S mice were significantly (p < 0.05) more hypersensitive to hot and cold stimuli than WT mice. Electrophysiological studies using dorsal root ganglion neurons from 8-9-week-old mice showed no significant difference in resting membrane potential, but input impedance and firing frequency of evoked action potentials were significantly increased in R222S mice compared with WT mice. However, there was no significant difference among Nav1.9 (WT, R222S, and R222H)-overexpressing ND7/23 cell lines. These results suggest that our novel mutation is a gain-of-function mutation that causes infantile familial episodic pain. The mouse model developed here will be useful for drug screening for familial episodic pain syndrome associated with SCN11A mutations