XMM-Newton and Chandra Cross Calibration Using HIFLUGCS Galaxy Clusters: Systematic Temperature Differences and Cosmological Impact

Cosmological constraints from clusters rely on accurate gravitational mass estimates, which strongly depend on cluster gas temperature measurements. Therefore, systematic calibration differences may result in biased, instrument-dependent cosmological constraints. This is of special interest in the light of the tension between the Planck results of the primary temperature anisotropies of the CMB and Sunyaev-Zel'dovich plus X-ray cluster counts analyses. We quantify in detail the systematics and uncertainties of the cross-calibration of the effective area between five X-ray instruments, EPIC-MOS1/MOS2/PN onboard XMM-Newton and ACIS-I/S onboard Chandra, and the influence on temperature measurements. Furthermore, we assess the impact of the cross calibration uncertainties on cosmology. Using the HIFLUGCS sample, consisting of the 64 X-ray brightest galaxy clusters, we constrain the ICM temperatures through spectral fitting in the same, mostly isothermal, regions and compare them. Our work is an extension to a previous one using X-ray clusters by the IACHEC. Performing spectral fitting in the full energy band we find that best-fit temperatures determined with XMM-Newton/EPIC are significantly lower than Chandra/ACIS temperatures. We demonstrate that effects like multitemperature structure and different relative sensitivities of the instruments at certain energy bands cannot explain the observed differences. We conclude that using XMM-Newton/EPIC, instead of Chandra/ACIS to derive full energy band temperature profiles for cluster mass determination results in an 8% shift towards lower OmegaM values and <1% shift towards higher sigma8 values in a cosmological analysis of a complete sample of galaxy clusters. Such a shift is insufficient to significantly alleviate the tension between Planck CMB anisotropies and SZ plus XMM-Newton cosmological constraints.Comment: Accepted by A&A; Python-Script for modification of XMM-Newton/EPIC and Chandra/ACIS effective areas according to the stacked residual ratios: https://wikis.mit.edu/confluence/display/iachec/Data

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Suzaku observations of X-ray excess emission in the cluster of galaxies A3112

We analysed the Suzaku XIS1 data of the A3112 cluster of galaxies in order to examine the X-ray excess emission in this cluster reported earlier with the XMM-Newton and Chandra satellites. The best-fit temperature of the intracluster gas depends strongly on the choice of the energy band used for the spectral analysis. This proves the existence of excess emission component in addition to the single-temperature MEKAL in A3112. We showed that this effect is not an artifact due to uncertainties of the background modeling, instrument calibration or the amount of Galactic absorption. Neither does the PSF scatter of the emission from the cool core nor the projection of the cool gas in the cluster outskirts produce the effect. Finally we modeled the excess emission either by using an additional MEKAL or powerlaw component. Due to the small differencies between thermal and non-thermal model we can not rule out the non-thermal origin of the excess emission based on the goodness of the fit. Assuming that it has a thermal origin, we further examined the Differential Emission Measure (DEM) models. We utilised two different DEM models, a Gaussian differential emission measure distribution (GDEM) and WDEM model, where the emission measure of a number of thermal components is distributed as a truncated power law. The best-fit XIS1 MEKAL temperature for the 0.4-7.0 keV band is 4.7+-0.1 keV, consistent with that obtained using GDEM and WDEM models.Comment: 8 pages, 10 figures, accepted to A&

A possible Chandra and Hubble Space Telescope detection of extragalactic WHIM towards PG 1116+215

(Abridged) We have analyzed Chandra LETG and XMM-Newton RGS spectra towards the z=0.177 quasar PG 1116+215, a sightline that is rendered particularly interesting by the HST detection of several OVI and HI broad Lyman-alpha absorption lines that may be associated with the warm-hot intergalactic medium. We performed a search for resonance K-alpha absorption lines from OVII and OVIII at the redshifts of the detected far-ultraviolet lines. We detected an absorption line in the Chandra spectra at 5.2 sigma confidence level at wavelengths corresponding to OVIII K-alpha at z=0.0911+-0.0004+-0.0005 (statistical followed by systematic error). This redshift is within 3 sigma of that of a HI broad Lyman-alpha of b=130 km/s at z=0.09279+-0.00005. We have also analyzed the available XMM-Newton RGS data towards PG 1116+215. Unfortunately, the XMM-Newton data are not suitable to investigate this line because of instrumental features at the wavelengths of interest. At the same redshift, the Chandra and XMM-Newton spectra have OVII K-alpha absorption line features of significance 1.5 sigma and 1.8 sigma, respectively. We also analyzed the available SDSS spectroscopic galaxy survey data towards PG 1116+215 in the redshift range of interest. We found evidence for a galaxy filament that intersects the PG 1116+215 sightline and additional galaxy structures that may host WHIM. The combination of HST, Chandra, XMM-Newton and SDSS data indicates that we have likely detected a multi-temperature WHIM at z=0.091-0.093 towards PG 1116+215.Comment: Accepted for publication in MNRA

Exosome-mediated Transfer of αvβ3 Integrin from Tumorigenic to Nontumorigenic Cells Promotes a Migratory Phenotype.

The αvβ3 integrin is known to be highly upregulated during cancer progression and promotes a migratory and metastatic phenotype in many types of tumors. We hypothesized that the αvβ3 integrin is transferred through exosomes and, upon transfer, has the ability to support functional aberrations in recipient cells. Here, for the first time, it is demonstrated that αvβ3 is present in exosomes released from metastatic PC3 and CWR22Pc prostate cancer cells. Exosomal β3 is transferred as a protein from donor to nontumorigenic and tumorigenic cells as β3 protein or mRNA levels remain unaffected upon transcription or translation inhibition in recipient cells. Furthermore, it is shown that upon exosome uptake, de novo expression of an αvβ3 increases adhesion and migration of recipient cells on an αvβ3 ligand, vitronectin. To evaluate the relevance of these findings, exosomes were purified from the blood of TRAMP mice carrying tumors where the expression of αvβ3 is found higher than in exosomes from wild-type mice. In addition, it is demonstrated that αvβ3 is coexpressed with synaptophysin, a biomarker for aggressive neuroendocrine prostate cancer. IMPLICATIONS: Overall this study reveals that the αvβ3 integrin is transferred from tumorigenic to nontumorigenic cells via exosomes, and its de novo expression in recipient cells promotes cell migration on its ligand. The increased expression of αvβ3 in exosomes from mice bearing tumors points to its clinical relevance and potential use as a biomarker. Mol Cancer Res; 14(11); 1136-46. ©2016 AACR

Androgen receptor-dependent and -independent mechanisms driving prostate cancer progression: Opportunities for therapeutic targeting from multiple angles.

Despite aggressive treatment for localized cancer, prostate cancer (PC) remains a leading cause of cancer-related death for American men due to a subset of patients progressing to lethal and incurable metastatic castrate-resistant prostate cancer (CRPC). Organ-confined PC is treated by surgery or radiation with or without androgen deprivation therapy (ADT), while options for locally advanced and disseminated PC include radiation combined with ADT, or systemic treatments including chemotherapy. Progression to CRPC results from failure of ADT, which targets the androgen receptor (AR) signaling axis and inhibits AR-driven proliferation and survival pathways. The exact mechanisms underlying the transition from androgen-dependent PC to CRPC remain incompletely understood. Reactivation of AR has been shown to occur in CRPC despite depletion of circulating androgens by ADT. At the same time, the presence of AR-negative cell populations in CRPC has also been identified. While AR signaling has been proposed as the primary driver of CRPC, AR-independent signaling pathways may represent additional mechanisms underlying CRPC progression. Identification of new therapeutic strategies to target both AR-positive and AR-negative PC cell populations and, thereby, AR-driven as well as non-AR-driven PC cell growth and survival mechanisms would provide a two-pronged approach to eliminate CRPC cells with potential for synthetic lethality. In this review, we provide an overview of AR-dependent and AR-independent molecular mechanisms which drive CRPC, with special emphasis on the role of the Jak2-Stat5a/b signaling pathway in promoting castrate-resistant growth of PC through both AR-dependent and AR-independent mechanisms

Adverse reactions from consumption of oral rabies vaccine baits in dogs in Finland

Background Oral rabies vaccination of wildlife has effectively reduced the incidence of rabies in wildlife and has led to the elimination of rabies in large areas of Europe. The safety of oral rabies vaccines has been assessed in both target (red fox and raccoon dog) and several non-target species. Case presentation Since 2011, the competent authority in Finland has received a few reports of dogs experiencing adverse reactions that have been assumed to be caused by the consumption of baits containing oral rabies vaccine. The dogs usually exhibited gastrointestinal symptoms (vomiting, inappetence, constipation or diarrhoea) or behavioral symptoms (restlessness, listlessness and unwillingness to continue hunting). Conclusions Nevertheless, these adverse reactions are transient and non-life threatening. Even though the adverse reactions are unpleasant to individual dogs and their owners, the benefits of oral rabies vaccination clearly outweigh the risks

Transcription factor signal transducer and activator of transcription 5 promotes growth of human prostate cancer cells in vivo

Purpose: Stat5a/b is the key mediator of prolactin (Prl) effects in prostate cancer cells via activation of Jak2. Prl is locally produced growth factor in human prostate cancer. Prl protein expression and constitutive activation of Stat5a/b are associated with high histological grade of clinical prostate cancer. Moreover, activation of Stat5a/b in primary prostate cancer predicts early disease recurrence. Here, we inhibited Stat5a/b by several different methodological approaches. Our goal was to establish a proof-of-principle that Stat5a/b is critical for prostate cancer cell viability in vitro and for prostate tumor growth in vivo. Experimental Design: We inhibited Stat5a/b protein expression by antisense oligonucleotides or RNA interference and transcriptional activity of Stat5a/b by adenoviral expression of a dominant-negative mutant of Stat5a/b in prostate cancer cells in culture. Moreover, Stat5a/b activity was suppressed in human prostate cancer xenograft tumors in nude mice. Stat5a/b regulation of BclXL and Cyclin-D1 protein levels was demonstrated by antisense suppression of Stat5a/b protein expression followed by Western blotting. Results and Conclusions: We show here that inhibition of Stat5a/b by antisense oligonuleotides, RNA interference, or adenoviral expression of DNStat5a/b all effectively kill prostate cancer cells. Moreover, we demonstrate that Stat5a/b is critical for human prostate cancer xenograft growth in nude mice. Stat5a/b effects on the viability of on prostate cancer cells involve Stat5a/b-regulation of BclXL and Cyclin-D1 protein levels, but not the expression or activation of Stat3. This work establishes Stat5a/b as a therapeutic target protein for prostate cancer. Pharmacological inhibition of Stat5a/b in prostate cancer can be achieved by small-molecule inhibitors of transactivation, dimerization or DNA-binding of Stat5a/b