Enhanced Star Formation of Less Massive Galaxies in a Proto-Cluster at z=2.5

We investigate a correlation between star-formation rate (SFR) and stellar mass for Halpha emission line galaxies (HAEs) in one of the richest proto-clusters ever known at z~2.5, USS 1558-003 proto-cluster. This study is based on a 9.7-hour narrow-band imaging data with MOIRCS on the Subaru telescope. We are able to construct a sample, in combination with additional H-band data taken with WFC3 on Hubble Space Telescope (HST), of 100 HAEs reaching the dust-corrected SFRs down to 3 Msun/yr and the stellar masses down to $10^{8.0}$ Msun. We find that while the star-forming galaxies with >$10^{9.3}$ Msun are located on the universal SFR-mass main sequence irrespective of the environment, less massive star-forming galaxies with <$10^{9.3}$ Msun show a significant upward scatter from the main sequence in this proto-cluster. This suggests that some less massive galaxies are in a starburst phase, although we do not know yet if this is due to environmental effects.Comment: 5 pages, 3 figures, 1 table, accepted for publication in the ApJ Letter

Development of spontaneous neuropathy in NF-κBp50-deficient mice by calcineurin-signal involving impaired NF-κB activation

信州大学博士（医学）・学位論文・平成24年3月28日授与（乙第21144号）・中村朋子Purpose: The transcriptional regulator, nuclear factor-kappa B (NF-kappa B)/Rel family are involved in neuronal cell death and survival. Previously, we reported that NF-kappa Bp50-deficient (p50-deficient) mice exhibit many features resembling human normal tension glaucoma (NTG). The developmental mechanism of human NTG is not clearly understood, and a radical curative treatment has yet to be established. Our aim is to elucidate the signal cascade which mediates the spontaneous optic neuropathy in p50-deficient mice as a model of NTG. Methods: To demonstrate the expression and activation of pro-apoptotic factors, which mediate the death of retinal ganglion cells (RGCs) in p50-deficient mice, western blot (WB) and luciferase reporter assays with retinas from p50-deficient and wild type mice, and cultured RGC-5 cells were performed. Furthermore, we tested the neuroprotective effects of chemical reagents (memantine, lomerizine, and tacrolimus) against N-methyl-D-aspartate (NMDA)-susceptible RGC damage according to in vitro experiments with RGC-5 cells. To elucidate the NF-kappa B-mediated death signaling, the effects of chemical reagents on spontaneous optic neuropathy were examined by histopathological studies. Results: WB experiments and luciferase reporter assays showed that NF-kappa B-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells. Further, the constitutively active cleaved forms of calcineurin (CaN), which have been reported to lead to apoptosis, were detected in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells. Pre-treatment with tacrolimus markedly protected RGC-5 cells from NMDA-induced neurotoxicity, and then both spontaneous RGC death and degenerative changes to the optic nerve in p50-deficient mice were significantly reduced by the chronic administration of tacrolimus. The experiments with cultured RGC-5 cells supported the results of histological examinations with p50-deficient mice, suggesting that CaN activation leads to NF-kappa B-induced Bax activation and caspase 3 activation, and mediates spontaneous optic neuropathy in p50-deficient mice. Conclusions: Research findings show that the chronic administration of tacrolimus significantly reduces spontaneous optic neuropathy in p50-deficient mice. We demonstrated a potential CaN signal cascade, which spontaneously induces age-dependent RGC death and degenerative optic nerve changes in p50-deficient mice.ArticleMOLECULAR VISION. 17:2157-2170 (2011)journal articl

Development of spontaneous neuropathy in NF-kappa Bp50-deficient mice by calcineurin-signal involving impaired NF-kappa B activation

信州大学博士（医学）・学位論文・平成24年3月28日授与（乙第21144号）・中村朋子Purpose: The transcriptional regulator, nuclear factor-kappa B (NF-kappa B)/Rel family are involved in neuronal cell death and survival. Previously, we reported that NF-kappa Bp50-deficient (p50-deficient) mice exhibit many features resembling human normal tension glaucoma (NTG). The developmental mechanism of human NTG is not clearly understood, and a radical curative treatment has yet to be established. Our aim is to elucidate the signal cascade which mediates the spontaneous optic neuropathy in p50-deficient mice as a model of NTG. Methods: To demonstrate the expression and activation of pro-apoptotic factors, which mediate the death of retinal ganglion cells (RGCs) in p50-deficient mice, western blot (WB) and luciferase reporter assays with retinas from p50-deficient and wild type mice, and cultured RGC-5 cells were performed. Furthermore, we tested the neuroprotective effects of chemical reagents (memantine, lomerizine, and tacrolimus) against N-methyl-D-aspartate (NMDA)-susceptible RGC damage according to in vitro experiments with RGC-5 cells. To elucidate the NF-kappa B-mediated death signaling, the effects of chemical reagents on spontaneous optic neuropathy were examined by histopathological studies. Results: WB experiments and luciferase reporter assays showed that NF-kappa B-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells. Further, the constitutively active cleaved forms of calcineurin (CaN), which have been reported to lead to apoptosis, were detected in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells. Pre-treatment with tacrolimus markedly protected RGC-5 cells from NMDA-induced neurotoxicity, and then both spontaneous RGC death and degenerative changes to the optic nerve in p50-deficient mice were significantly reduced by the chronic administration of tacrolimus. The experiments with cultured RGC-5 cells supported the results of histological examinations with p50-deficient mice, suggesting that CaN activation leads to NF-kappa B-induced Bax activation and caspase 3 activation, and mediates spontaneous optic neuropathy in p50-deficient mice. Conclusions: Research findings show that the chronic administration of tacrolimus significantly reduces spontaneous optic neuropathy in p50-deficient mice. We demonstrated a potential CaN signal cascade, which spontaneously induces age-dependent RGC death and degenerative optic nerve changes in p50-deficient mice.ArticleMOLECULAR VISION. 17:2157-2170 (2011)journal articl

Evolutionary phases of gas-rich galaxies in a galaxy cluster at z=1.46

We report a survey of molecular gas in galaxies in the XMMXCS J2215.9-1738 cluster at $z=1.46$. We have detected emission lines from 17 galaxies within a radius of $R_{200}$ from the cluster center, in Band 3 data of the Atacama Large Millimeter/submillimeter Array (ALMA) with a coverage of 93 -- 95 GHz in frequency and 2.33 arcmin$^2$ in spatial direction. The lines are all identified as CO $J$=2--1 emission lines from cluster members at $z\sim1.46$ by their redshifts and the colors of their optical and near-infrared (NIR) counterparts. The line luminosities reach down to $L'_{\rm CO(2-1)}=4.5\times10^{9}$ K km s$^{-1}$ pc$^2$. The spatial distribution of galaxies with a detection of CO(2--1) suggests that they disappear from the very center of the cluster. The phase-space diagram showing relative velocity versus cluster-centric distance indicates that the gas-rich galaxies have entered the cluster more recently than the gas-poor star-forming galaxies and passive galaxies located in the virialized region of this cluster. The results imply that the galaxies have experienced ram-pressure stripping and/or strangulation during the course of infall towards the cluster center and then the molecular gas in the galaxies at the cluster center is depleted by star formation.Comment: 7 pages, 4 figures, 1 table, accepted for publication in the ApJ Letter