Starburst models of merging galaxies

In the past decade, infrared observations have shown that interacting and merging galaxies have higher luminosities than isolated systems, with the luminosities in mergers as high as 10(exp 12) solar luminosity. However, the origin of the luminosity found in mergers is controversial, with two main competing theories. The first is the starburst scenario. As two gas rich galaxies start to merge, cloud-cloud collisions induce fast shocks in the molecular gas. This gas cools, collapses, and fragments, producing a blast of star formation. The main rival to this theory is that the infrared luminosity is produced by a dust embedded active nucleus, the merger of two gas rich galaxies providing the 'fuel to feed the monster'. There has even been speculation that there is an evolutionary link between starbursts and active nuclei, and that possibly active galactic nuclei (AGN's) and QSO's were formed from a starburst. Assuming that the infrared luminosity in merging galaxies is due to star formation, there should be ionizing photons produced from the high mass stars, giving rise to recombination line emission. The objective is to use a simple starburst model to test the hypothesis that the extreme infrared luminosity of merging galaxies is due to a starburst

Radio Emission from an Ultraluminous X-Ray Source

The physical nature of ultraluminous x-ray sources is uncertain. Stellar mass black holes with beamed radiation and intermediate mass black holes with isotropic radiation are two plausible explanations. We discovered radio emission from an ultraluminous x-ray source in the dwarf irregular galaxy NGC 5408. The x-ray, radio and optical fluxes as well as the x-ray spectral shape are consistent with beamed relativistic jet emission from an accreting stellar black hole. If confirmed, this would suggest that the ultraluminous x-ray sources may be stellar-mass rather than intermediate mass black holes. However, interpretation of the source as a jet-producing intermediate-mass black hole cannot be ruled out at this time.Comment: 8 pages, one color figure. appeared in Science 299: 365-367 (January 17, 2003

The Connection Between X-ray Binaries and Star Clusters in NGC 4449

We present 23 candidate X-ray binaries with luminosities down to 1.8x10^36 erg/s, in the nearby starburst galaxy NGC 4449, from observations totaling 105 ksec taken with the ACIS-S instrument on the Chandra Space Telescope. We determine count rates, luminosities, and colors for each source, and perform spectral fits for sources with sufficient counts. We also compile a new catalog of 129 compact star clusters in NGC 4449 from high resolution, multi-band optical images taken with the Hubble Space Telescope, doubling the number of clusters known in this galaxy. The UBVI,Ha luminosities of each cluster are compared with predictions from stellar evolution models to estimate their ages and masses. We find strong evidence for a population of very young massive, black-hole binaries, which comprise nearly 50% of the detected X-ray binaries in NGC 4449. Approximately a third of these remain within their parent star clusters, which formed t < 6-8 Myr ago, while others have likely been ejected from their parent clusters. We also find evidence for a population of somewhat older X-ray binaries, including both supergiant and Be-binaries, which appear to be associated with somewhat older t ~ 100-400 Myr star clusters, and one X-ray binary in an ancient (t ~ 10 Gyr) globular cluster. Our results suggest that detailed information on star clusters can significantly improve constraints on X-ray binary populations in star-forming galaxies

Viral-mediated oncolysis is the most critical factor in the late-phase of the tumor regression process upon vaccinia virus infection

<p>Abstract</p> <p>Background</p> <p>In principle, the elimination of malignancies by oncolytic virotherapy could proceed by different mechanisms - e.g. tumor cell specific oncolysis, destruction of the tumor vasculature or an anti-tumoral immunological response. In this study, we analyzed the contribution of these factors to elucidate the responsible mechanism for regression of human breast tumor xenografts upon colonization with an attenuated vaccinia virus (VACV).</p> <p>Methods</p> <p>Breast tumor xenografts were analyzed 6 weeks post VACV infection (p.i.; regression phase) by immunohistochemistry and mouse-specific expression arrays. Viral-mediated oncolysis was determined by tumor growth analysis combined with microscopic studies of intratumoral virus distribution. The tumor vasculature was morphologically characterized by diameter and density measurements and vessel functionality was analyzed by lectin perfusion and extravasation studies. Immunological aspects of viral-mediated tumor regression were studied in either immune-deficient mouse strains (T-, B-, NK-cell-deficient) or upon cyclophosphamide-induced immunosuppression (MHCII⁺-cell depletion) in nude mice.</p> <p>Results</p> <p>Late stage VACV-infected breast tumors showed extensive necrosis, which was highly specific to cancer cells. The tumor vasculature in infected tumor areas remained functional and the endothelial cells were not infected. However, viral colonization triggers hyperpermeability and dilatation of the tumor vessels, which resembled the activated endothelium in wounded tissue. Moreover, we demonstrated an increased expression of genes involved in leukocyte-endothelial cell interaction in VACV-infected tumors, which orchestrate perivascular inflammatory cell infiltration. The immunohistochemical analysis of infected tumors displayed intense infiltration of MHCII-positive cells and colocalization of tumor vessels with MHCII⁺/CD31⁺vascular leukocytes. However, GI-101A tumor growth analysis upon VACV-infection in either immunosuppressed nude mice (MHCII⁺-cell depleted) or in immune-deficient mouse strains (T-, B-, NK-cell-deficient) revealed that neither MHCII-positive immune cells nor T-, B-, or NK cells contributed significantly to VACV-mediated tumor regression. In contrast, tumors of immunosuppressed mice showed enhanced viral spreading and tumor necrosis.</p> <p>Conclusions</p> <p>Taken together, these results indicate that VACV-mediated oncolysis is the primary mechanism of tumor shrinkage in the late regression phase. Neither the destruction of the tumor vasculature nor the massive VACV-mediated intratumoral inflammation was a prerequisite for tumor regression. We propose that approaches to enhance viral replication and spread within the tumor microenvironment should improve therapeutical outcome.</p

Calibration of the ROSAT HRI Spectral Response

The ROSAT High Resolution Imager has a limited (2-band) spectral response. This spectral capability can give X-ray hardness ratios on spatial scales of 5 arcseconds. The spectral response of the center of the detector was calibrated before the launch of ROSAT, but the gain decreases with time and also is a function of position on the detector. To complicate matters further, the satellite is 'wobbled', possibly moving a source across several spatial gain states. These difficulties have prevented the spectral response of the ROSAT High Resolution Imager (HRI) from being used for scientific measurements. We have used Bright Earth data and in-flight calibration sources to map the spatial and temporal gain changes, and written software which will allow ROSAT users to generate a calibrated XSPEC (an x ray spectral fitting package) response matrix and hence determine a calibrated hardness ratio. In this report, we describe the calibration procedure and show how to obtain a response matrix. In Section 2 we give an overview of the calibration procedure, in Section 3 we give a summary of HRI spatial and temporal gain variations. Section 4 describes the routines used to determine the gain distribution of a source. In Sections 5 and 6, we describe in detail how, the Bright Earth database and calibration sources are used to derive a corrected response matrix for a given observation. Finally, Section 7 describes how to use the software