Extinction map of the Small Magellanic Cloud based on SIRIUS and 6X 2MASS point source catalogs

In this paper, we present the first extinction map of the Small Magellanic Cloud (SMC) constructed using the color excess at near-infrared wavelengths. Using a new technique named "X percentile method", which we developed recently to measure the color excess of dark clouds embedded within a star distribution, we have derived an E(J – H) map based on the SIRIUS and 6X Two Micron All Sky Survey (2MASS) star catalogs. Several dark clouds are detected in the map derived from the SIRIUS star catalog, which is deeper than the 6X 2MASS catalog. We have compared the E(J – H) map with a model calculation in order to infer the locations of the clouds along the line of sight, and found that many of them are likely to be located in or elongated toward the far side of the SMC. Most of the dark clouds found in the E(J – H) map have counterparts in the CO clouds detected by Mizuno et al. with the NANTEN telescope. A comparison of the E(J – H) map with the virial mass derived from the CO data indicates that the dust-to-gas ratio in the SMC varies in the range A_V /N_H = 1-2 × 10^(–22) mag H^-1 cm^2 with a mean value of ~1.5 × 10^(–22) mag H^-1 cm^2. If the virial mass underestimates the true cloud mass by a factor of ~2, as recently suggested by Bot et al., the mean value would decrease to ~8×10^(–23) mag H^-1 cm^2, in good agreement with the value reported by Gordon et al., 7.59 × 10^(–23) mag H^-1 cm^2

Di-neutron correlation and soft dipole excitation in medium mass neutron-rich nuclei near drip-line

The neutron pairing correlation and the soft dipole excitation in medium-mass nuclei near drip-line are investigated from a viewpoint of the di-neutron correlation. Numerical analyses by means of the coordinate-space HFB and the continuum QRPA methods are performed for even-even $^{18-24}$O, $^{50-58}$Ca and $^{80-86}$Ni. A clear signature of the di-neutron correlation is found in the HFB ground state; two neutrons are correlated at short relative distances \lesim 2 fm with large probability $\sim 50$. The soft dipole excitation is influenced strongly by the neutron pairing correlation, and it accompanies a large transition density for pair motion of neutrons. This behavior originates from a coherent superposition of two-quasiparticle configurations $[l\times (l+1)]_{L=1}$ consisting of continuum states with high orbital angular momenta $l$ reaching an order of $l\sim 10$. It raises a picture that the soft dipole excitation under the influence of neutron pairing is characterized by motion of di-neutron in the nuclear exterior against the remaining $A-2$ subsystem. Sensitivity to the density dependence of effective pair force is discussed.Comment: 35 pages, 22 figure

Chronic inhibition of tumor cell-derived VEGF enhances the malignant phenotype of colorectal cancer cells

Abstract Background Vascular endothelial growth factor-a (VEGF)-targeted therapies have become an important treatment for a number of human malignancies. The VEGF inhibitors are actually effective in several types of cancers, however, the benefits are transiently, and the vast majority of patients who initially respond to the therapies will develop resistance. One of possible mechanisms for the acquired resistance may be the direct effect(s) of VEGF inhibitors on tumor cells expressing VEGF receptors (VEGFR). Thus, we investigated here the direct effect of chronic VEGF inhibition on phenotype changes in human colorectal cancer (CRC) cells. Methods To chronically inhibit cancer cell-derived VEGF, human CRC cell lines (HCT116 and RKO) were chronically exposed (2 months) to an anti-VEGF monoclonal antibody (mAb) or were disrupted the Vegf gene (VEGF-KO). Effects of VEGF family members were blocked by treatment with a VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI). Hypoxia-induced apoptosis under VEGF inhibited conditions was measured by TUNEL assay. Spheroid formation ability was assessed using a 3-D spheroid cell culture system. Results Chronic inhibition of secreted/extracellular VEGF by an anti-VEGF mAb redundantly increased VEGF family member (PlGF, VEGFR1 and VEGFR2), induced a resistance to hypoxia-induced apoptosis, and increased spheroid formation ability. This apoptotic resistance was partially abrogated by a VEGFR-TKI, which blocked the compensate pathway consisted of VEGF family members, or by knockdown of Vegf mRNA, which inhibited intracellular function(s) of all Vegf gene products. Interestingly, chronic and complete depletion of all Vegf gene products by Vegf gene knockout further augmented these phenotypes in the compensate pathway-independent manner. These accelerated phenotypes were significantly suppressed by knockdown of hypoxia-inducible factor-1α that was up-regulated in the VEGF-KO cell lines. Conclusions Our findings suggest that chronic inhibition of tumor cell-derived VEGF accelerates tumor cell malignant phenotypes.http://deepblue.lib.umich.edu/bitstream/2027.42/112625/1/12885_2012_Article_3866.pd

Statistical study of dust properties in LMC molecular clouds

The objective of this paper is to construct a catalog providing the dust properties and the star formation efficiency (SFE) of the molecular clouds in the Large Magellanic Cloud (LMC). We use the infrared (IR) data obtained with the Spitzer telescope as part of the ``Surveying the Agents of a Galaxy's Evolution'' (SAGE) Legacy survey as well as the IRAS data. We also work with extinction (Av) maps of the LMC. A total of 272 molecular clouds have been detected in the LMC in a previous molecular survey, accounting for 230 giant molecular clouds and 42 smaller clouds. We perform correlations between the IR emission/extinction, and atomic and molecular gas tracers. We compare the atomic gas that surrounds the molecular cloud with the molecular gas in the cloud. Using a dust emission model, we derive the physical properties of dust in and outside the clouds: equilibrium temperature, emissivity and extinction. We also determine the luminosity of the interstellar radiation field intercepted by the cloud, and the total IR luminosity. Statistically, we do not find any significant difference in the dust properties between the atomic and the molecular phases. In particular we do not find evidence for a systematic decrease of the dust temperature in the molecular phase, with respect to the surrounding, presumably atomic gas. This is probably because giant molecular clouds are the sites of star formation, which heat the dust, while the smallest clouds are unresolved. The ratio between the IR luminosity and the cloud mass (LDust/Mgas) does not seem to correlate with Mgas. The highest value of the ratio we derived is 18.1 Lsol/Msol in the 30 Doradus region, which is known to be the most prominent star formation region of the LMC, while the most likely value is 0.5 and is representative of quiescent clouds. We provide a prescription to associate the various stages of star formation with its LDust/Mgas.Comment: Accepted for publication in A

Downregulation of the CCL2/CCR2 and CXCL10/CXCR3 axes contributes to antitumor effects in a mouse model of malignant glioma

Glioblastoma multiforme involves glioma stem cells (GSCs) that are resistant to various therapeutic approaches. Here, we studied the importance of paracrine signaling in the glioma microenvironment by focusing on the celecoxib-mediated role of chemokines C–C motif ligand 2 (CCL2), C-X-C ligand 10 (CXCL10), and their receptors, CCR2 and CXCR3, in GSCs and a GSC-bearing malignant glioma model. C57BL/6 mice were injected with orthotopic GSCs intracranially and divided into groups administered either 10 or 30 mg/kg celecoxib, or saline to examine the antitumor effects associated with chemokine expression. In GSCs, we analyzed cell viability and expression of chemokines and their receptors in the presence/absence of celecoxib. In the malignant glioma model, celecoxib exhibited antitumor effects in a dose dependent manner and decreased protein and mRNA levels of Ccl2 and CxcL10 and Cxcr3 but not of Ccr2. CCL2 and CXCL10 co-localized with Nestin+ stem cells, CD16+ or CD163+ macrophages and Iba-1+ microglia. In GSCs, celecoxib inhibited Ccl2 and Cxcr3 expression in a nuclear factor-kappa B-dependent manner but not Ccr2 and CxcL10. Moreover, Ccl2 silencing resulted in decreased GSC viability. These results suggest that celecoxib-mediated regulation of the CCL2/CCR2 and CXCL10/ CXCR3 axes may partially contribute to glioma-specific antitumor effects

The Type Ic Hypernova SN 2002ap

Photometric and spectroscopic data of the energetic Type Ic supernova (SN) 2002ap are presented, and the properties of the SN are investigated through models of its spectral evolution and its light curve. The SN is spectroscopically similar to the "hypernova" SN 1997ef. However, its kinetic energy [$\sim (4-10) \times 10^{51}$ erg] and the mass ejected (2.5-5 $M_{\odot}$) are smaller, resulting in a faster-evolving light curve. The SN synthesized $\sim 0.07 M_{\odot}$ of $^{56}$Ni, and its peak luminosity was similar to that of normal SNe. Brightness alone should not be used to define a hypernova, whose defining character, namely very broad spectral features, is the result of a high kinetic energy. The likely main-sequence mass of the progenitor star was 20-25 $M_{\odot}$, which is also lower than that of both hypernovae SNe 1997ef and 1998bw. SN 2002ap appears to lie at the low-energy and low-mass end of the hypernova sequence as it is known so far. Observations of the nebular spectrum, which is expected to dominate by summer 2002, are necessary to confirm these values.Comment: 10 pages, 4 figures, accepted for publication in ApJL, 30 April 2002 (minor changes to match the accepted version, with figures being colored

Refinement of a 400-kb Critical Region Allows Genotypic Differentiation between Isolated Lissencephaly, Miller-Dieker Syndrome, and Other Phenotypes Secondary to Deletions of 17p13.3

Deletions of 17p13.3, including the LIS1 gene, result in the brain malformation lissencephaly, which is characterized by reduced gyration and cortical thickening; however, the phenotype can vary from isolated lissencephaly sequence (ILS) to Miller-Dieker syndrome (MDS). At the clinical level, these two phenotypes can be differentiated by the presence of significant dysmorphic facial features and a more severe grade of lissencephaly in MDS. Previous work has suggested that children with MDS have a larger deletion than those with ILS, but the precise boundaries of the MDS critical region and causative genes other than LIS1 have never been fully determined. We have completed a physical and transcriptional map of the 17p13.3 region from LIS1 to the telomere. Using fluorescence in situ hybridization, we have mapped the deletion size in 19 children with ILS, 11 children with MDS, and 4 children with 17p13.3 deletions not involving LIS1. We show that the critical region that differentiates ILS from MDS at the molecular level can be reduced to 400 kb. Using somatic cell hybrids from selected patients, we have identified eight genes that are consistently deleted in patients classified as having MDS. In addition, deletion of the genes CRK and 14-3-3ɛ delineates patients with the most severe lissencephaly grade. On the basis of recent functional data and the creation of a mouse model suggesting a role for 14-3-3ɛ in cortical development, we suggest that deletion of one or both of these genes in combination with deletion of LIS1 may contribute to the more severe form of lissencephaly seen only in patients with MDS

The Orbiting Carbon Observatory (OCO-2) Tracks 2-3 Peta-Gram Increase in Carbon Release to the Atmosphere During the 2014-2016 El Nino

The powerful El Nio event of 2015-2016 - the third most intense since the 1950s - has exerted a large impact on the Earth's natural climate system. The column-averaged CO2 dry-air mole fraction (XCO2) observations from satellites and ground based networks are analyzed together with in situ observations for the period of September 2014 to October 2016. From the differences between satellite (OCO-2) observations and simulations using an atmospheric chemistry-transport model, we estimate that, relative to the mean annual fluxes for 2014, the most recent El Nio has contributed to an excess CO2 emission from the Earth's surface (land+ocean) to the atmosphere in the range of 2.4+/-0.2 PgC (1 Pg = 10(exp 15) g) over the period of July 2015 to June 2016. The excess CO2 flux is resulted primarily from reduction in vegetation uptake due to drought, and to a lesser degree from increased biomass burning. It is about the half of the CO2 flux anomaly (range: 4.4-6.7 PgC) estimated for the 1997/1998 El Nio. The annual total sink is estimated to be 3.9+/-0.2 PgC for the assumed fossil fuel emission of 10.1 PgC. The major uncertainty in attribution arise from error in anthropogenic emission trends, satellite data and atmospheric transport

腫瘍細胞由来のVEGFを慢性的に阻害すると大腸がん細胞の悪性形質化を増強する

Background: Vascular endothelial growth factor-a (VEGF)-targeted therapies have become an important treatment for a number of human malignancies. The VEGF inhibitors are actually effective in several types of cancers, however, the benefits are transiently, and the vast majority of patients who initially respond to the therapies will develop resistance. One of possible mechanisms for the acquired resistance may be the direct effect(s) of VEGF inhibitors on tumor cells expressing VEGF receptors (VEGFR). Thus, we investigated here the direct effect of chronic VEGF inhibition on phenotype changes in human colorectal cancer (CRC) cells. Methods: To chronically inhibit cancer cell-derived VEGF, human CRC cell lines (HCT116 and RKO) were chronically exposed (2 months) to an anti-VEGF monoclonal antibody (mAb) or were disrupted the Vegf gene (VEGF-KO). Effects of VEGF family members were blocked by treatment with a VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI). Hypoxia-induced apoptosis under VEGF inhibited conditions was measured by TUNEL assay. Spheroid formation ability was assessed using a 3-D spheroid cell culture system. Results: Chronic inhibition of secreted/extracellular VEGF by an anti-VEGF mAb redundantly increased VEGF family member (PlGF, VEGFR1 and VEGFR2), induced a resistance to hypoxia-induced apoptosis, and increased spheroid formation ability. This apoptotic resistance was partially abrogated by a VEGFR-TKI, which blocked the compensate pathway consisted of VEGF family members, or by knockdown of Vegf mRNA, which inhibited intracellular function (s) of all Vegf gene products. Interestingly, chronic and complete depletion of all Vegf gene products by Vegf gene knockout further augmented these phenotypes in the compensate pathway-independent manner. These accelerated phenotypes were significantly suppressed by knockdown of hypoxia-inducible factor-1α that was up-regulated in the VEGF-KO cell lines. Conclusions: Our findings suggest that chronic inhibition of tumor cell-derived VEGF accelerates tumor cell malignant phenotypes