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See detailHost DNA released by NETosis promotes rhinovirus-induced type-2 allergic asthma exacerbation.
Toussaint, Marie; Jackson, David J.; Swieboda, Dawid et al

in Nature Medicine (2017), 23

Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of the type-2 immune response is strongly implicated in asthma exacerbation, but how virus ... [more ▼]

Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of the type-2 immune response is strongly implicated in asthma exacerbation, but how virus infection boosts type-2 responses is poorly understood. We report a significant correlation between the release of host double-stranded DNA (dsDNA) following rhinovirus infection and the exacerbation of type-2 allergic inflammation in humans. In a mouse model of allergic airway hypersensitivity, we show that rhinovirus infection triggers dsDNA release associated with the formation of neutrophil extracellular traps (NETs), known as NETosis. We further demonstrate that inhibiting NETosis by blocking neutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopathology. Furthermore, the injection of mouse genomic DNA alone is sufficient to recapitulate many features of rhinovirus-induced type-2 immune responses and asthma pathology. Thus, NETosis and its associated extracellular dsDNA contribute to the pathogenesis and may represent potential therapeutic targets of rhinovirus-induced asthma exacerbations. [less ▲]

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See detailHost entry by gamma-herpesviruses-lessons from animal viruses?
Gillet, Laurent ULiege; Frederico, Bruno; Stevenson, Philip G.

in Current Opinion in Virology (2015), 15

The oncogenicity of gamma-herpesviruses (gammaHVs) motivates efforts to control them and their persistence makes early events key targets for intervention. Human gammaHVs are often assumed to enter naive ... [more ▼]

The oncogenicity of gamma-herpesviruses (gammaHVs) motivates efforts to control them and their persistence makes early events key targets for intervention. Human gammaHVs are often assumed to enter naive hosts orally and infect B cells directly. However, neither assumption is supported by direct evidence, and vaccination with the Epstein-Barr virus (EBV) gp350, to block virion binding to B cells, failed to reduce infection rates. Thus, there is a need to re-evaluate assumptions about gammaHV host entry. Given the difficulty of analysing early human infections, potentially much can be learned from animal models. Genomic comparisons argue that gammaHVs colonized mammals long before humans speciation, and so that human gammaHVs are unlikely to differ dramatically in behaviour from those of other mammals. Murid Herpesvirus-4 (MuHV-4), which like EBV and the Kaposi's Sarcoma-associated Herpesvirus (KSHV) persists in memory B cells, enters new hosts via olfactory neurons and exploits myeloid cells to spread. Integrating these data with existing knowledge of human and veterinary gammaHVs suggests a new model of host entry, with potentially important implications for infection control. [less ▲]

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See detailThe Host Galaxies of the Brightest Quasars: Gas-Rich Galaxies, Mergers, and Young Stars
Courbin, Frédéric; Letawe, Géraldine ULiege; Meylan, Georges et al

in The Messenger (2006), 124

Because they are faint and hidden in the glare of a much brighter unresolved source, quasar host galaxies still challenge the most powerful telescopes, instrumentation and processing techniques ... [more ▼]

Because they are faint and hidden in the glare of a much brighter unresolved source, quasar host galaxies still challenge the most powerful telescopes, instrumentation and processing techniques. Determining their basic morphological parameters and their integrated colours is feasible, but difficult, from imaging alone. However, detailed information on their stellar and gas contents and on their dynamics is achievable with deep spectroscopy. [less ▲]

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See detailThe host genomic environment of the provirus determines the abundance of HTLV-1-infected T-cell clones.
Gillet, Nicolas ULiege; Malani, Nirav; Melamed, Anat et al

in Blood (2011), 117(11), 3113-22

Human T-lymphotropic virus type 1 (HTLV-1) persists by driving clonal proliferation of infected T lymphocytes. A high proviral load predisposes to HTLV-1-associated diseases. Yet the reasons for the ... [more ▼]

Human T-lymphotropic virus type 1 (HTLV-1) persists by driving clonal proliferation of infected T lymphocytes. A high proviral load predisposes to HTLV-1-associated diseases. Yet the reasons for the variation within and between persons in the abundance of HTLV-1-infected clones remain unknown. We devised a high-throughput protocol to map the genomic location and quantify the abundance of > 91,000 unique insertion sites of the provirus from 61 HTLV-1(+) persons and > 2100 sites from in vitro infection. We show that a typical HTLV-1-infected host carries between 500 and 5000 unique insertion sites. We demonstrate that negative selection dominates during chronic infection, favoring establishment of proviruses integrated in transcriptionally silenced DNA: this selection is significantly stronger in asymptomatic carriers. We define a parameter, the oligoclonality index, to quantify clonality. The high proviral load characteristic of HTLV-1-associated inflammatory disease results from a larger number of unique insertion sites than in asymptomatic carriers and not, as previously thought, from a difference in clonality. The abundance of established HTLV-1 clones is determined by genomic features of the host DNA flanking the provirus. HTLV-1 clonal expansion in vivo is favored by orientation of the provirus in the same sense as the nearest host gene. [less ▲]

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See detailHost Interleukin 6 and Indoleamine 2,3 Dioxygenase Regulate Inflammation in the Brain during Graft Versus Host Disease
Belle, Ludovic ULiege; Koester, E; Hansen, E et al

in Blood (2016, December), 128

Graft versus host disease (GVHD) commonly induces pathological damage in peripheral target organs such as the skin, liver and gastrointestinal tract leading to well characterized organ-specific clinical ... [more ▼]

Graft versus host disease (GVHD) commonly induces pathological damage in peripheral target organs such as the skin, liver and gastrointestinal tract leading to well characterized organ-specific clinical manifestations. A number of studies, however, have shown that patients with GVHD can also have behavioral and mood alterations that can affect overall cognitive function and lead to significant impairments in quality of life. The extent to which GVHD contributes to cognitive dysfunction and induces inflammation within the central nervous system (CNS), however, has not been critically examined. To address this question, we conducted studies using two well-defined murine GVHD models [C57BL/6(H-2b)→Balb/c (H-2d) and B10.BR(H-2k)→B6 (H-2b)]. We observed that there was a significant increase in the number of donor-derived CD4+ and CD8+ T cells in the brains of GVHD recipients early (days 7 -14) and late (day 42) post transplantation compared to BM controls. Histological studies revealed activated microglial cells and CD3+ T cell infiltration in the periventricular regions of brains in GVHD recipients that were not present in BM animals. Real time q-PCR analysis also demonstrated significant increases in IFN-γ, TNF-α, and IL-6 mRNA expression indicative of a proinflammatory state. Notably, GVHD animals exhibited behavioral changes in the forced swim test and elevated plus maze which are validated assays of stress coping and anxiety, respectively. Since IL-6, in particular, plays a pivotal role in GVHD pathogenesis in murine models and humans, we examined whether blockade of IL-6 signaling altered neuroinflammation. Animals treated with an anti-IL-6R antibody had a significant reduction in the number of donor-derived CD4+ and CD8+T cells in the brain compared to isotype control-treated mice. Anti-IL-6R treatment of GVHD mice also resulted in significant reductions in IFN-γ, TNF-α, and IL-6 mRNA and normalized behavior in the forced swim test, indicative of a decreased inflammatory response. Since IL-6 is produced by a wide variety of cells, including microglial and T cells, both donor and recipient cells have the potential to modulate GVHD severity within the CNS. To define whether donor or host IL-6 production was most critical for inducing neuroinflammation, experiments were conducted employing IL-6-/- mice as either donors or recipients. Whereas the absence of IL-6 in donor-derived cells had no impact on the degree of inflammation within the CNS, recipient animals that lacked IL-6 had a significant decrease in the number of donor-derived T cells which accumulated in the brain as well as a marked reduction in inflammatory cytokines, indicating that host IL-6 production was critical. To define the downstream pathways of IL-6-mediated CNS inflammation, we examined the role of indoleamine 2,3-dioxygenase (IDO) since IL-6 has been shown to upregulate IDO-1 expression under inflammatory conditions. We observed that IDO-1 mRNA levels were significantly increased in the brains of GVHD animals, and that blockade of IL-6 signaling resulted in a marked decrease in IDO mRNA levels. Additionally, transplantation studies using IDO-/- mice revealed that host, but not donor, IDO production was required for maximal inflammatory effects. Serotoninergic projections to the prefrontal cortex (PFC), in particular, are sensitive to inflammation and contribute to stress coping behavior. Therefore, to further interrogate this pathway, we performed quantitative mass spectrometry of brain extracts from the PFC. We found that tryptophan and 5HT concentrations were not different between BM and GVHD groups. However, there was an increase in the IDO product, kynurenic acid, in GVHD recipients consistent with an increase in brain IDO expression. To provide additional support for the premise that IL-6 effects were mediated through the IDO pathway, recipient mice were treated with either 1-methyltryptophan (1-MT), a completive inhibitor of IDO, or a vehicle control. GVHD mice treated with 1-MT had decreased accumulation of T cells in the brain and normal behavior in the forced swim test, demonstrating that inhibition of IDO abrogated CNS inflammation and behavioral changes in the presence of intact IL-6 signaling. In summary, these studies demonstrate that host IL-6 and IDO regulate inflammation and adversely impact behavioral function within the brain during GVHD through the tryptophan metabolic pathway. [less ▲]

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See detailHost Interleukin 6 and Indoleamine 2,3 Dioxygenase Regulate Inflammation in the Brain during Graft Versus Host Disease
Belle, Ludovic ULiege; Koester, Erin; Hansen, Emily et al

Poster (2016)

Graft versus host disease (GVHD) commonly induces pathological damage in peripheral target organs such as the skin, liver and gastrointestinal tract leading to well characterized organ-specific clinical ... [more ▼]

Graft versus host disease (GVHD) commonly induces pathological damage in peripheral target organs such as the skin, liver and gastrointestinal tract leading to well characterized organ-specific clinical manifestations. A number of studies, however, have shown that patients with GVHD can also have behavioral and mood alterations that can affect overall cognitive function and lead to significant impairments in quality of life. The extent to which GVHD contributes to cognitive dysfunction and induces inflammation within the central nervous system (CNS), however, has not been critically examined. To address this question, we conducted studies using two well-defined murine GVHD models [C57BL/6(H-2b)→Balb/c (H-2d) and B10.BR(H-2k)→B6 (H-2b)]. We observed that there was a significant increase in the number of donor-derived CD4+ and CD8+ T cells in the brains of GVHD recipients early (days 7 -14) and late (day 42) post transplantation compared to BM controls. Histological studies revealed activated microglial cells and CD3+ T cell infiltration in the periventricular regions of brains in GVHD recipients that were not present in BM animals. Real time q-PCR analysis also demonstrated significant increases in IFN-γ, TNF-α, and IL-6 mRNA expression indicative of a proinflammatory state. Notably, GVHD animals exhibited behavioral changes in the forced swim test and elevated plus maze which are validated assays of stress coping and anxiety, respectively. Since IL-6, in particular, plays a pivotal role in GVHD pathogenesis in murine models and humans, we examined whether blockade of IL-6 signaling altered neuroinflammation. Animals treated with an anti-IL-6R antibody had a significant reduction in the number of donor-derived CD4+ and CD8+T cells in the brain compared to isotype control-treated mice. Anti-IL-6R treatment of GVHD mice also resulted in significant reductions in IFN-γ, TNF-α, and IL-6 mRNA and normalized behavior in the forced swim test, indicative of a decreased inflammatory response. Since IL-6 is produced by a wide variety of cells, including microglial and T cells, both donor and recipient cells have the potential to modulate GVHD severity within the CNS. To define whether donor or host IL-6 production was most critical for inducing neuroinflammation, experiments were conducted employing IL-6-/- mice as either donors or recipients. Whereas the absence of IL-6 in donor-derived cells had no impact on the degree of inflammation within the CNS, recipient animals that lacked IL-6 had a significant decrease in the number of donor-derived T cells which accumulated in the brain as well as a marked reduction in inflammatory cytokines, indicating that host IL-6 production was critical. To define the downstream pathways of IL-6-mediated CNS inflammation, we examined the role of indoleamine 2,3-dioxygenase (IDO) since IL-6 has been shown to upregulate IDO-1 expression under inflammatory conditions. We observed that IDO-1 mRNA levels were significantly increased in the brains of GVHD animals, and that blockade of IL-6 signaling resulted in a marked decrease in IDO mRNA levels. Additionally, transplantation studies using IDO-/- mice revealed that host, but not donor, IDO production was required for maximal inflammatory effects. Serotoninergic projections to the prefrontal cortex (PFC), in particular, are sensitive to inflammation and contribute to stress coping behavior. Therefore, to further interrogate this pathway, we performed quantitative mass spectrometry of brain extracts from the PFC. We found that tryptophan and 5HT concentrations were not different between BM and GVHD groups. However, there was an increase in the IDO product, kynurenic acid, in GVHD recipients consistent with an increase in brain IDO expression. To provide additional support for the premise that IL-6 effects were mediated through the IDO pathway, recipient mice were treated with either 1-methyltryptophan (1-MT), a completive inhibitor of IDO, or a vehicle control. GVHD mice treated with 1-MT had decreased accumulation of T cells in the brain and normal behavior in the forced swim test, demonstrating that inhibition of IDO abrogated CNS inflammation and behavioral changes in the presence of intact IL-6 signaling. In summary, these studies demonstrate that host IL-6 and IDO regulate inflammation and adversely impact behavioral function within the brain during GVHD through the tryptophan metabolic pathway. [less ▲]

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See detailHost location by the parasitoid, Nasonia vitripennis Walker (Hymenoptera : Pteromalidae)
Frederickx, Christine ULiege; Durieux, Delphine ULiege; Verheggen, François ULiege et al

Poster (2011, July 24)

Successful reproduction for parasitoids encompasses a series of behavioral steps commonly defined as host-habitat location, host location, host acceptance and host regulation. Successful host location ... [more ▼]

Successful reproduction for parasitoids encompasses a series of behavioral steps commonly defined as host-habitat location, host location, host acceptance and host regulation. Successful host location, where resources are patchily distributed within the environment, is dependent on the information value of stimuli used in the host location process. Chemical cues produced by either the host itself, products derived from the host play an important role in host location. This study investigated the role of odorant cues used during host location by the generalist parasitoid, Nasonia vitripennis Walker. N vitripennis is a common parasitoid of Dipteran pupae found in association with decaying carrion. The biological activity of eight of the volatile molecules constituting the odour of pupae were tested on the searching behavior of parasitoid females through chemoecological approache: olfactometry bioassays. [less ▲]

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See detailHost plasminogen activator inhibitor-1 promotes human skin carcinoma progression in a stage-dependent manner
Maillard, Catherine ULiege; Jost, M.; Romer, M. U. et al

in Neoplasia : An International Journal for Oncology Research (2005), 7(1), 57-66

Angiogenesis and tumor expansion are associated with extracellular matrix remodeling and involve various proteases such as the plasminogen (Plg)/plasminogen activator (PA) system. Recently, several ... [more ▼]

Angiogenesis and tumor expansion are associated with extracellular matrix remodeling and involve various proteases such as the plasminogen (Plg)/plasminogen activator (PA) system. Recently, several experimental data have implicated the plasminogen activator inhibitor-1 (PAI-1) in tumor angiogenesis in murine systems. However, little is known about PAI-1 functions in human skin carcinoma progression. By generating immunodeficient mice (in Rag-1(-/-) or nude background) deleted for PAI-1 gene (PAI-1(-/-)), we have evaluated the impact of host PAI-1 deficiency on the tumorigenicity of two malignant human skin keratinocyte cell lines HaCaT II-4 and HaCaT A5-RT3 forming low-grade and high-grade carcinomas, respectively. When using the surface transplantation model, angiogenesis and tumor invasion of these two cell lines are strongly reduced in PAI-1-deficient mice as compared to the wild-type control animals. After subcutaneous injection in PAI-1-/- mice, the tumor incidence is reduced for HaCaT II-4 cells, but not for those formed by HaCaT A5-RT3 cells. These data indicate that PAI-1 produced by host cells is an important contributor to earlier stages of human skin carcinoma progression. It exerts its tumor-promoting effect in a tumor stage-dependent manner, but PAI-1 deficiency is not sufficient to prevent neoplastic growth of aggressive tumors of the human skin. [less ▲]

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See detailHost-derived plasminogen activator inhibitor-1 (PAI-1) concentration is critical for in vivo tumoral angiogenesis and growth
Bajou, Khalid ULiege; Maillard, Catherine ULiege; Jost, M. et al

in Oncogene (2004), 23(41), 6986-6990

Plasminogen activator inhibitor type 1 (PAI-1) plays a key role in tumor progression and is believed to control proteolytic activity and cell migration during angiogenesis. We report here that host PAI-1 ... [more ▼]

Plasminogen activator inhibitor type 1 (PAI-1) plays a key role in tumor progression and is believed to control proteolytic activity and cell migration during angiogenesis. We report here that host PAI-1, at physiological concentration, promotes in vivo tumor invasion and angiogenesis. In sharp contrast, inhibition of tumor vascularization was observed when PAI-1 was produced at supraphysiologic levels, either by host cells (transgenic mice overexpressing PAI-1) or by tumor cells (after transfection with murine PAI-1 cDNA). This study provides for the first time in vivo evidence for a dose-dependent effect of PAI-1 on tumor angiogenesis. Of great interest is the finding that PAI-1 produced by tumor cells, even at high concentration, did not overcome the absence of PAI-1 in the host, emphasizing the importance of the cellular source of PAI-1. [less ▲]

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See detailHost-habitat location by the parasitoid, Nasonia vitripennis Walker (Hymenoptera: Pteromalidae).
Frederickx, Christine ULiege; Dekeirsschieter, Jessica ULiege; Verheggen, François ULiege et al

in Journal of Forensic Sciences (2014), 59

This study investigated the role of odorant cues used during host-habitat location by the generalist parasitoid, Nasonia vitripennis Walker. N vitripennis is a common parasitoid of Dipteran pupae found in ... [more ▼]

This study investigated the role of odorant cues used during host-habitat location by the generalist parasitoid, Nasonia vitripennis Walker. N vitripennis is a common parasitoid of Dipteran pupae found in association with decaying carrion. Behavioral assays were used to investigate the host-habitat searching behavior under different scenarios. First, we demonstrated N. vitripennis to be significantly attracted toward odorant cues associated with decaying meat. The biological activity of nine of the volatile molecules constituting the odor of decaying meat were tested on the searching behavior of parasitoid females through two complementary chemoecological approaches: electronantennography (EAG) and olfactometry bioassays. Butanoic acid and butan-1-ol elicited high olfactory responses, but no attraction was induced by these two chemicals. Behavioral assays showed that, among the VOCs tested, methyldisulfanylmethane (DMDS) was the only volatile chemical to induce attraction in N. vitripennis. [less ▲]

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See detailHost-induced bacterial cell wall decomposition mediates pattern-triggered immunity in Arabidopsis
Liu, X.; Grabherr, H.; Willmann, R. et al

in eLife (2014)

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See detailHost-microbe interactions have shaped the genetic architecture of inflammatory bowel disease.
Jostins, Luke; Ripke, Stephan; Weersma, Rinse K. et al

in Nature (2012), 491(7422), 119-24

Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome ... [more ▼]

Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome-wide association studies and subsequent meta-analyses of these two diseases as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD. [less ▲]

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See detailHost-parasite interactions in trypanosomiasis: On the way to an anti-disease strategy.
Antoine-Moussiaux, Nicolas ULiege; Buscher, Philippe; Desmecht, Daniel ULiege

in Infection and Immunity (2009), 77(4), 1276-1284

African trypanosomiasis (AT) is a family of parasitic conditions affecting both man and livestock, impairing development in sub-Saharan Africa, throughout the 10 million km(2) habitat zone of the common ... [more ▼]

African trypanosomiasis (AT) is a family of parasitic conditions affecting both man and livestock, impairing development in sub-Saharan Africa, throughout the 10 million km(2) habitat zone of the common vector, Glossina spp. ... [less ▲]

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See detailHost-pathogen interactome mapping for HTLV-1 and -2 retroviruses.
Simonis, Nicolas; Rual, Jean-Francois; Lemmens, Irma et al

in Retrovirology (2012), 9

BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1) and type 2 both target T lymphocytes, yet induce radically different phenotypic outcomes. HTLV-1 is a causative agent of Adult T-cell leukemia (ATL ... [more ▼]

BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1) and type 2 both target T lymphocytes, yet induce radically different phenotypic outcomes. HTLV-1 is a causative agent of Adult T-cell leukemia (ATL), whereas HTLV-2, highly similar to HTLV-1, causes no known overt disease. HTLV gene products are engaged in a dynamic struggle of activating and antagonistic interactions with host cells. Investigations focused on one or a few genes have identified several human factors interacting with HTLV viral proteins. Most of the available interaction data concern the highly investigated HTLV-1 Tax protein. Identifying shared and distinct host-pathogen protein interaction profiles for these two viruses would enlighten how they exploit distinctive or common strategies to subvert cellular pathways toward disease progression. RESULTS: We employ a scalable methodology for the systematic mapping and comparison of pathogen-host protein interactions that includes stringent yeast two-hybrid screening and systematic retest, as well as two independent validations through an additional protein interaction detection method and a functional transactivation assay. The final data set contained 166 interactions between 10 viral proteins and 122 human proteins. Among the 166 interactions identified, 87 and 79 involved HTLV-1 and HTLV-2 -encoded proteins, respectively. Targets for HTLV-1 and HTLV-2 proteins implicate a diverse set of cellular processes including the ubiquitin-proteasome system, the apoptosis, different cancer pathways and the Notch signaling pathway. CONCLUSIONS: This study constitutes a first pass, with homogeneous data, at comparative analysis of host targets for HTLV-1 and -2 retroviruses, complements currently existing data for formulation of systems biology models of retroviral induced diseases and presents new insights on biological pathways involved in retroviral infection. [less ▲]

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See detailHost-plant specialization in bees
Michez, Denis; Vanderplanck, Maryse ULiege

Conference (2010)

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See detailHot and cold contrasts in high resolution Tc-99m planar scintigraphy: a survey of fifty-two camera heads using the PICKER thyroid phantom
Seret, Alain ULiege

in Physica Medica : An International Journal Devoted to the Applications of Physics to Medicine and Biology : Official Journal of the Italian Association of Biomedical Physics (AIFB) [=PM] (2010), 26(3), 166-172

This study aimed at comparing the sensitivity and hot and cold contrasts obtained when imaging the Picker thyroid phantom using gamma cameras fitted with either their ultra-high or high-resolution low ... [more ▼]

This study aimed at comparing the sensitivity and hot and cold contrasts obtained when imaging the Picker thyroid phantom using gamma cameras fitted with either their ultra-high or high-resolution low energy parallel hole collimator. Seventeen camera models from Elscint, General Electric, Siemens and Sopha Medical Vision were involved in the study for a total of 30 cameras and 52 camera heads. A single operator conducted the study in order to minimize the impact of human factors. The phantom contained about 74 MBq 99mTc and was imaged at 10-cm from the collimator face with the energy window recommended by the camera manufacturer. A total of 1 million counts were accumulated. Hot and cold contrasts were in mean about 0.05 higher when using an ultra-high-resolution than when using a high-resolution low energy collimator. This higher contrast was obtained at the expense of a mean reduction in sensitivity of 30%. In particular, Elscint cameras demonstrated a 30% lower sensitivity whatever the collimator type. The Sopha Medical Vision DST and DSX cameras and the General Electric Magicam camera offered the lowest contrasts among the cameras with a high-resolution collimator. Although this was accompanied by a higher than the mean sensitivity for the DST and DSX, the Magicam demonstrated sensitivity roughly identical to the mean of all the cameras with a high-resolution collimator. [less ▲]

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See detailHot and cool: two emission-line stars with constrasting behaviours in the same XMM-Newton field
Nazé, Yaël ULiege; Rauw, Grégor ULiege; Ud-Doula, A.

in Astronomy and Astrophysics (2010), 510

High-energy emissions are good indicators of peculiar behaviours in stars. We have therefore obtained an XMM-Newton observation of HD 155806 and 1RXS J171502.4-333344, and derived their spectral ... [more ▼]

High-energy emissions are good indicators of peculiar behaviours in stars. We have therefore obtained an XMM-Newton observation of HD 155806 and 1RXS J171502.4-333344, and derived their spectral properties for the first time. The X-ray spectrum of HD 155806 appears soft, even slightly softer than usual for O-type stars (as shown by a comparison with the O9 star HD 155889 in the same XMM-Newton field). It is well-fitted with a two-component thermal model with low temperatures (0.2 and 0.6 keV), and it shows no overluminosity (log[L_X/L_BOL] = -6.75). The high-resolution spectrum, though noisy, reveals a few broad, symmetric X-ray lines (FWHMË 2500 km s[SUP]-1[/SUP]). The X-ray emission is compatible with the wind-shock model and therefore appears unaffected by the putative dense equatorial regions at the origin of the Oe classification. 1RXS J171502.4-333344 is a nearby flaring source of moderate X-ray luminosity (log[L_X/L_BOL] = -3), with a soft thermal spectrum composed of narrow lines and presenting a larger abundance of elements (e.g. Ne) with a high first ionization potential (FIP) compared to lower-FIP elements. All the evidence indicates a coronal origin for the X-ray emission, in agreement with the dMe classification of this source. Based on observations collected with XMM-Newton, an ESA Science Mission with instruments and contributions directly funded by ESA Member States and the USA (NASA).Research Associate FNRS. [less ▲]

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