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1

Roumeguere, T., A. Noël, F. Aoun, S. Albisinni, M. Paesman, R. Van Velthoven, and A. Peltier. "Apport des biopsies ciblées par fusion d’image (us/irmmp) en complément à des biopsies systématisées chez des patients maintenant une suspicion de cancer prostatique après une ou plusieurs séries de biopsies systématisées négatives." Progrès en Urologie 26, no. 13 (November 2016): 811–12. http://dx.doi.org/10.1016/j.purol.2016.07.281.

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2

Richter, S., A. Alonso, W. De Bolle, H. Kühn, A. Verbruggen, R. Wellum, and P. D. P. Taylor. "Re-certification of a series of uranium isotope reference materials: IRMM-183, IRMM-184, IRMM-185, IRMM-186 and IRMM-187." International Journal of Mass Spectrometry 247, no. 1-3 (December 2005): 37–39. http://dx.doi.org/10.1016/j.ijms.2005.07.008.

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3

Mossialos, Dimitris, Jean-Marie Meyer, Herbert Budzikiewicz, Ulrich Wolff, Nico Koedam, Christine Baysse, Vanamala Anjaiah, and Pierre Cornelis. "Quinolobactin, a New Siderophore ofPseudomonas fluorescens ATCC 17400, the Production of Which Is Repressed by the Cognate Pyoverdine." Applied and Environmental Microbiology 66, no. 2 (February 1, 2000): 487–92. http://dx.doi.org/10.1128/aem.66.2.487-492.2000.

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ABSTRACT Transposon mutant strain 3G6 of Pseudomonas fluorescensATCC 17400 which was deficient in pyoverdine production, was found to produce another iron-chelating molecule; this molecule was identified as 8-hydroxy-4-methoxy-quinaldic acid (designated quinolobactin). The pyoverdine-deficient mutant produced a supplementary 75-kDa iron-repressed outer membrane protein (IROMP) in addition to the 85-kDa IROMP present in the wild type. The mutant was also characterized by substantially increased uptake of 59Fe-quinolobactin. The 75-kDa IROMP was produced by the wild type after induction by quinolobactin-containing culture supernatants obtained from the pyoverdine-negative mutant or by purified quinolobactin. Conversely, adding purified wild-type pyoverdine to the growth medium resulted in suppression of the 75-kDa IROMP in the pyoverdine-deficient mutant; however, suppression was not observed when Pseudomonas aeruginosa PAO1 pyoverdine, a siderophore utilized by strain 3G6, was added to the culture. Therefore, we assume that the quinolobactin receptor is the 75-kDa IROMP and that the quinolobactin-mediated iron uptake system is repressed by the cognate pyoverdine.
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4

Lapitajs, G., F. Hendrickx, A. Verbruggen, and A. Lamberty. "An IRMM 87Rb isotopic reference material IRMM-618." International Journal of Mass Spectrometry and Ion Processes 152, no. 1 (January 1996): 69–77. http://dx.doi.org/10.1016/0168-1176(95)04328-4.

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5

Chibber, Sanjay, and Sonia B. Bhardwaj. "Protection in a mouse peritonitis model mediated by iron-regulated outer-membrane protein of Salmonella typhi coupled to its Vi antigen." Journal of Medical Microbiology 53, no. 7 (July 1, 2004): 705–9. http://dx.doi.org/10.1099/jmm.0.05378-0.

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Vi polysaccharide and iron-regulated outer-membrane proteins (IROMPs) were extracted and purified from the standard strain of Salmonella typhi, Ty2. These were then conjugated by chemical coupling using the carbodimide method. Vi–IROMP conjugate was tested for its ability to protect against colonization by S. typhi in different organs. Mice immunized with 2.5 μg Vi–IROMP conjugate showed the most protection, as the least bacterial colonization of spleen, liver and Peyer's patches was observed. Peritoneal macrophages obtained from conjugate-treated mice phagocytosed bacteria efficiently. Circulating antibodies and the delayed type hypersensitivity response elucidated by mouse foot-pad swelling was significantly higher in conjugate-treated animals. These results clearly demonstrate that an IROMP and polysaccharide conjugate of S. typhi prepared from the same strain has the potential to protect animals against challenge.
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6

Duta, Steluta, Michael Berglund, and Philip Taylor. "Updated certified values of the lithium isotopic reference materials IRMM-016, IRMM-015 and IRMM-615." Rapid Communications in Mass Spectrometry 23, no. 6 (March 30, 2009): 937–38. http://dx.doi.org/10.1002/rcm.3930.

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7

Cocchieri, Riccardo, Bertus van de Wetering, Sjoerd van Tuijl, Iman Mousavi, Robert Riezebos, and Bastian de Mol. "At the Crossroads of Minimally Invasive Mitral Valve Surgery—Benching Single Hospital Experience to a National Registry: A Plea for Risk Management Technology." Journal of Cardiovascular Development and Disease 9, no. 8 (August 11, 2022): 261. http://dx.doi.org/10.3390/jcdd9080261.

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Almost 30 years after the first endoscopic mitral valve repair, Minimally Invasive Mitral Valve Surgery (MIMVS) has become the standard at many institutions due to optimal clinical results and fast recovery. The question that arises is can already good results be further improved by an Institutional Risk Management Performance (IRMP) system in decreasing risks in minimally invasive mitral valve surgery (MIMVS)? As of yet, there are no reports on IRMP and learning systems in the literature. (2) Methods: We described and appraised our five-year single institutional experience with MIMVS in isolated valve surgery included in the Netherlands Heart Registry (NHR) and investigated root causes of high-impact complications. (3) Results: The 120-day and 12-month mortality were 1.1% and 1.9%, respectively, compared to the average of 4.3% and 5.3% reported in the NHR. The regurgitation rate was 1.4% compared to 5.2% nationwide. The few high-impact complications appeared not to be preventable. (4) Discussion: In MIMVS, freedom from major and minor complications is a strong indicator of an effective IRMP but remains concealed from physicians and patients, despite its relevance to shared decision making. Innovation adds to the complexity of MIMVS and challenges surgical competence. An IRMP system may detect and control new risks earlier. (5) Conclusion: An IRMP system contributes to an effective reduction of risks, pain and discomfort; provides relevant input for shared decision making; and warrants the safe introduction of new technology. Crossroads conclusions: investment in machine learning and AI for an effective IRMP system is recommended and the roles for commanding and operating surgeons should be considered.
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8

Reggiani, Henrique, Kevin C. Schlaufman, and Andrew R. Casey. "Iron-rich Metal-poor Stars and the Astrophysics of Thermonuclear Events Observationally Classified as Type Ia Supernovae. I. Establishing the Connection." Astronomical Journal 166, no. 3 (August 25, 2023): 128. http://dx.doi.org/10.3847/1538-3881/ace68c.

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Abstract The progenitor systems and explosion mechanisms responsible for the thermonuclear events observationally classified as Type Ia supernovae are uncertain and difficult to uniquely constrain using traditional observations of Type Ia supernova host galaxies, progenitors, light curves, and remnants. For the subset of thermonuclear events that are prolific producers of iron, we use published theoretical nucleosynthetic yields to identify a set of elemental abundance ratios infrequently observed in metal-poor stars but shared across a range of progenitor systems and explosion mechanisms: [Na, Mg, Co/Fe] < 0. We label stars with this abundance signature “iron-rich metal-poor,” or IRMP stars. We suggest that IRMP stars formed in environments dominated by thermonuclear nucleosynthesis and consequently that their elemental abundances can be used to constrain both the progenitor systems and explosion mechanisms responsible for thermonuclear explosions. We identify three IRMP stars in the literature and homogeneously infer their elemental abundances. We find that the elemental abundances of BD +80 245, HE 0533–5340, and SMSS J034249.53–284216.0 are best explained by the (double) detonations of sub-Chandrasekhar-mass CO white dwarfs. If our interpretation of IRMP stars is accurate, then they should be very rare in globular clusters and more common in the Magellanic Clouds and dwarf spheroidal galaxies than in the Milky Way’s halo. We propose that future studies of IRMP stars will quantify the relative occurrences of different thermonuclear event progenitor systems and explosion mechanisms.
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9

Reeves, Zachary, Kevin C. Schlaufman, and Henrique Reggiani. "The Dependence of Iron-rich Metal-poor Star Occurrence on Galactic Environment Supports an Origin in Thermonuclear Supernova Nucleosynthesis." Astronomical Journal 166, no. 3 (August 25, 2023): 127. http://dx.doi.org/10.3847/1538-3881/ace68d.

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Abstract It has been suggested that a class of chemically peculiar metal-poor stars called iron-rich metal-poor (IRMP) stars formed from molecular cores with metal contents dominated by thermonuclear supernova nucleosynthesis. If this interpretation is accurate, then IRMP stars should be more common in environments where thermonuclear supernovae were important contributors to chemical evolution. Conversely, IRMP stars should be less common in environments where thermonuclear supernovae were not important contributors to chemical evolution. At constant [Fe/H] ≲ −1, the Milky Way’s satellite classical dwarf spheroidal (dSph) galaxies and the Magellanic Clouds have lower [α/Fe] than the Milky Way field and globular cluster populations. This difference is thought to demonstrate the importance of thermonuclear supernova nucleosynthesis for the chemical evolution of the Milky Way’s satellite classical dSph galaxies and the Magellanic Clouds. We use data from the Sloan Digital Sky Survey Apache Point Observatory Galactic Evolution Experiment and Gaia to infer the occurrence of IRMP stars in the Milky Way’s satellite classical dSph galaxies η dSph and the Magellanic Clouds η Mag, as well as in the Milky Way field η MWF and globular cluster populations η MWGC. In order of decreasing occurrence, we find η dSph = 0.07 − 0.02 + 0.02 , η Mag = 0.037 − 0.006 + 0.007 , η MWF = 0.0013 − 0.0005 + 0.0006 , and a 1σ upper limit η MWGC < 0.00057. These occurrences support the inference that IRMP stars formed in environments dominated by thermonuclear supernova nucleosynthesis and that the time lag between the formation of the first and second stellar generations in globular clusters was longer than the thermonuclear supernova delay time.
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10

Hambsch, F. J., S. Oberstedt, S. Zeynalov, N. Kornilov, I. Fabry, R. Borcea, and A. Al-Adili. "Fission Research at IRMM." EPJ Web of Conferences 2 (2010): 07002. http://dx.doi.org/10.1051/epjconf/20100207002.

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11

Stollings, Lindsay, Binfeng Lu, and Yan Xu. "Immunomodulation of volatile anesthetics (IRM9P.726)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 128.9. http://dx.doi.org/10.4049/jimmunol.192.supp.128.9.

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Abstract Introduction: The impact of anesthetic exposure on the immune system is relatively unknown at both mechanistic and clinical levels. In this in vitro study, we employ immunological assays and understanding of immune cell function to evaluate the effect of volatile anesthetic (VA) exposure on bone marrow dendritic cells (BMDCs). BMDCc play a critical role in antigen presentation and link the innate and adaptive arms of the immune response. Hypothesis: We believe that VA exposure may modulate immune responses, specifically BMDC function. Methods: Bone marrow cells were harvested from C57BL/6 mice and cultured for six days to generate BMDCs. They were stimulated with low and high dose lipopolysaccharide (LPS). Simultaneously, the cells were exposed to 1.5% isoflurane and incubated for 5 hours. Upon completion of VA exposure, the BMDCs were lysed with Trizol, RNA extracted, and reverse transcript PCR used to generate cDNA. RT-qPCR was performed to evaluate gene expression of common BMDC cytokines. Results: BMDC exposure to isoflurane resulted in decreased gene expression of IL-10, IL-6, and IL-1β. RT-qPCR data indicated 2-4 fold decreases in gene expression of these cytokines. Conclusions: BMDCs exposed to VA in vitro displayed decreased gene expression of inflammatory cytokines. Significance: Better understanding of immunomodulation by anesthetics is critical for optimizing patient outcomes and improved perioperative management.
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12

Hult, Mikael, Timotheos Altzitzoglou, Bruno Denecke, Leif Persson, Goedele Sibbens, and Dietmar F. G. Reher. "Standardisation of 204Tl at IRMM." Applied Radiation and Isotopes 52, no. 3 (March 2000): 493–98. http://dx.doi.org/10.1016/s0969-8043(99)00200-6.

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13

Ostermann, Markus, Michael Berglund, P. Taylor, and M. Máriássy. "Certification of the chlorine content of the isotopic reference materials IRMM-641 and IRMM-642." Fresenius’ Journal of Analytical Chemistry 371, no. 6 (October 13, 2001): 721–25. http://dx.doi.org/10.1007/s002160101015.

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14

Lamberty, A., and H. Emons. "Reference materials: from CBNM to IRMM." Accreditation and Quality Assurance 16, no. 8-9 (April 30, 2011): 393–98. http://dx.doi.org/10.1007/s00769-011-0781-2.

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15

Richter, S., S. Konegger-Kappel, S. F. Boulyga, G. Stadelmann, A. Koepf, and H. Siegmund. "Linearity testing and dead-time determination for MC-ICP-MS ion counters using the IRMM-072 series of uranium isotope reference materials." Journal of Analytical Atomic Spectrometry 31, no. 8 (2016): 1647–57. http://dx.doi.org/10.1039/c6ja00203j.

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16

Hawse, WIlliam, Natasa Miskov-Zivanov, James Faeder, and Penelope Morel. "PTEN regulates CD4+ T cell differentiation (IRM6P.716)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 63.8. http://dx.doi.org/10.4049/jimmunol.192.supp.63.8.

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Abstract Naïve CD4+ T cells differentiate into either helper (Th) or regulatory (Treg) cells following encounter with antigen. T cell fate is in part determined by signaling strength where lower TCR and AKT/mTOR signaling favors Treg differentiation and higher TCR and AKT/mTOR signaling drives Th differentiation. AKT/mTOR signaling is regulated by PTEN, a phosphatase that is highly expressed in Tregs. We recently published a computational model that suggested a critical role for PTEN in T cell differentiation. Our current work focuses on validating the model predictions and explaining how PTEN is regulated during T cell differentiation. We demonstrate that PTEN inhibition increases Akt/mTOR signaling leading to increased Th induction. When the TCR signal strength is high, PTEN is ubiquitinated and phosphorylated and PTEN protein levels are dramatically reduced. Conversely, PTEN levels only decrease transiently when TCR signal strength is low and the resulting Treg express higher PTEN levels. We are exploring the transcriptional regulation of PTEN. One potential regulator is FOXO1, which has been shown by ChIP-Seq to bind the PTEN promoter. High Akt/mTOR signaling results in phosphorylation of FOXO1 and exclusion of FOXO1 from the nucleus. Low Akt/mTOR signaling results in minimal phosphorylation and sustained FOXO1 nuclear localization. Thus, PTEN protein levels are tightly controlled by TCR signal strength and regulation of PTEN plays an important role in determining T cell fate.
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17

König, Jan C. L. "https://econjournals.com/index.php/irmm/article/view/10187." International Review of Management and Marketing 10, no. 5 (September 1, 2020): 127–37. http://dx.doi.org/10.32479/irmm.10187.

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18

Hambsch, F. J., S. Oberstedt, A. Al-Adil, R. Borcea, A. Oberstedt, A. Tudora, and Sh Zeynalov. "Investigation of the Fission Process at IRMM." Journal of the Korean Physical Society 59, no. 2(3) (August 12, 2011): 1654–59. http://dx.doi.org/10.3938/jkps.59.1654.

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19

Lamberty, A., G. Lapitajs, L. Van Nevel, A. Götz, J. R. Moody, D. E. Erdmann, and P. De Bievre. "The IRMM—International Measurement Evaluation Program (IMEP)." Biological Trace Element Research 43-45, no. 1 (December 1994): 571–83. http://dx.doi.org/10.1007/bf02917360.

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20

Lamberty, A., L. Van Nevel, J. R. Moody, and P. De Bièvre. "The IRMM - International Measurement Evaluation Programme, IMEP." Accreditation and Quality Assurance 1, no. 2 (March 18, 1996): 71–82. http://dx.doi.org/10.1007/s007690050038.

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21

Pauwels, Jean. "Latest news on BCR/IRMM reference materials." Accreditation and Quality Assurance 6, no. 7 (July 1, 2001): 328–29. http://dx.doi.org/10.1007/s007690100355.

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22

Dragomir, Florin, Paul Ciprian Patic, and Otilia Elena Dragomir. "Intelligent Robot with Microcontroller for Obstacles Avoiding." Solid State Phenomena 166-167 (September 2010): 179–84. http://dx.doi.org/10.4028/www.scientific.net/ssp.166-167.179.

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The paper describes a intelligent robot with two stepper motor and microcontroller PIC16F84A for obstacles avoiding (IRSMP). An experimental prototype, based on a stepper motor, microcontroller PIC16F84A and infrared sensors, has been realized using conventional digital circuits. The proposed control scheme can be usefully applied to any intelligent robot. The infrared sensors has using for obstacles avoiding. The program for microcontroller is making in assembler language.
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23

Hutchinson, John, and Vicky Dunn. "Development of the community based individual risk mitigation profile (IRMP) for people who have intellectual disability and are at risk of offending." Journal of Intellectual Disabilities and Offending Behaviour 7, no. 2 (June 13, 2016): 66–74. http://dx.doi.org/10.1108/jidob-09-2015-0033.

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Purpose – The purpose of this paper is to discuss the development of the community-based individual risk mitigation profile (IRMP) and to examine its effectiveness for people who have an intellectual disability, and are at risk of offending, through the use of a case study. Design/methodology/approach – Case study and literature review. Findings – The tool has been found to be useful and accessible by clinicians. It has a particular focus on joint sharing of opinion on risk and decision making in a structured and contained multi-disciplinary forum, that is evidence-based and defensible. This multi-disciplinary approach meets recommendations in best practice in relation to risk. Research limitations/implications – A current limitation is that the IRMP has not been evaluated for reliability and validity, though a research study is being planned. Originality/value – The paper highlights the usefulness of a community-based risk profile assessment and linked risk mitigation process.
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24

Hurtado-Bermúdez, Santiago, and José Luis Mas. "Determination of 210Po in low-level wild bilberries reference material for quality control assurance in environmental analysis using extraction chromatography and α-particle spectroscopy." Radiochimica Acta 108, no. 2 (January 28, 2020): 99–103. http://dx.doi.org/10.1515/ract-2019-3141.

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AbstractCertified reference materials (CRM) are being widely used for quality control assurance in environmental analysis. For certain CRM, the analytes and/or the range of concentrations are not be available or certified at all. The Joint Research Centre – Institute for Reference Materials and Measurements (JRC-IRMM) of the European Commission has issued a CRM of Wild Berries (IRMM-426) in order to validate radionuclide measurement methods for activity concentrations of the natural radionuclide 40K and the anthropogenic nuclides 90Sr and 137Cs, but not for 210Po. The aim of the work was to determine low-level activity concentration of 210Po in these wild berries. The activity concentration of 210Po was assessed by α-particle spectroscopy after dissolution of the sample by wet digestion and chemical isolation of Po by extraction chromatography. According to the time elapsed since sample collection, the results here shown can be useful not only for ultra low-level analysis of 210Po but also for 210Pb in the reference material.
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Gupta, Neetu, Debasis Pore, Neetha Parameswaran, Ken Matsui, Matthew Stone, Ichiko Saotome, Andrea McClatchey, and Sarah Veatch. "Ezrin tunes the magnitude of humoral immunity. (IRM8P.709)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 127.10. http://dx.doi.org/10.4049/jimmunol.192.supp.127.10.

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Abstract Ezrin is a member of the Ezrin-Radixin-Moesin (ERM) family of membrane-actin cytoskeleton crosslinkers that participate in a variety of cellular processes. In B cells, phosphorylation of ezrin at different sites regulates multiple processes such as lipid raft coalescence, BCR diffusion, microclustering, and endosomal JNK activation. In this study, we generated mice with conditional deletion of ezrin in the B cell lineage to investigate the physiological significance of ezrin’s function in antigen receptor-mediated B cell activation and humoral immunity. B cell development, as well as the proportion and numbers of major B cell subsets in peripheral lymphoid organs were unaffected by the loss of ezrin. Using super resolution imaging methods we show that in the absence of ezrin, BCRs respond to antigen binding by accumulating into larger and more stable signaling microclusters. Loss of ezrin led to delayed BCR capping and accelerated lipid raft coalescence. Although proximal signaling proteins showed stronger activation in the absence of ezrin, components of the distal BCR signaling components displayed distinct effects. Ezrin deficiency resulted in increased B cell proliferation and differentiation into antibody-secreting cells ex vivo, and stronger T cell-independent and -dependent responses to antigen in vivo. Overall, our data demonstrate that ezrin regulates amplification of BCR signals and tunes the strength of B cell activation and humoral immunity.
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Poltorak, Alexander, Bridget Larkin, Guy Surpris, and Vladimir Ilyuha. "The role of STING in T lymphocytes (IRM5P.643)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 59.8. http://dx.doi.org/10.4049/jimmunol.194.supp.59.8.

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Abstract The cytoplasmic protein Stimulator of Interferon Genes (STING) plays an essential role in sensing intracellular pathogens and initiating type I IFN responses in myeloid cells. STING detects the presence of cytoplasmic DNA presented by various DNA-binding proteins (e.g. IFI16, DDX41, DAI, RNA Pol III); it also directly binds cyclic dinucleotides produced by intracellular bacteria or by the DNA-binding cyclic GAMP synthase (c-GAS). Once activated, STING phosphorylates TBK1 and IRF3 to trigger type I IFN production. To date STING has only been studied in macrophages and dendritic cells, but early reports showed expression of STING in a variety of tissues including the thymus and spleen, prompting us to ask whether STING might have a functional role in T cells, which account for the majority of cells in the thymus and a larger proportion of cells in the spleen than macrophages and dendritic cells. Here, we show that STING can be activated in T cells by the small molecule DMXAA, resulting in IFNβ production and increased expression of numerous interferon stimulated genes (ISG)—the first evidence to our knowledge of type I IFN production by T cells. Furthermore, RNA-sequencing data revealed unanticipated differences between unstimulated wild type and STING-/- T cells, with STING -/- T cells exhibiting increased expression of genes associated with cytotoxic T lymphocytes, indicating that STING-mediated signaling in T cells may regulate the development of particular T cell subsets.
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Shu, Qiang, Chi Chen, Dongyan Zhao, Xiwang Liu, QiXing Chen, and XiangMing Fang. "TRIM22 enhances staurosporine-induced apoptosis in monocytes (IRM7P.492)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 126.17. http://dx.doi.org/10.4049/jimmunol.192.supp.126.17.

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Abstract Background TRIM22 was first identified as an interferon-induced gene, and constitutively expressed in peripheral blood leukocytes and lymphoid tissues, especially expressed at high levels in monocytes. Researches suggest that TRIM22 may have an impact on monocyte fate in immune response. However, the direct evidence of TRIM22 on monocyte apoptosis remains absent. Methods TRIM22 was constructed and transfected into a monocytic cell line THP-1 cell. Apoptosis of transfected cells was induced by STS and tested by flow cytometry. The caspase pathways involved in TRIM22-related apoptosis were illustrated by inhibitory experiments. Proapoptotic/antiapoptotic protein were measured by immunoblot. Results Overexpression of TRIM22 in THP-1 cells caused extensive apoptosis induced by STS; The activation of caspase-9 and caspase-3, and the release of cytochrome c were increased in TRIM22-overexpressing cells; Inhibition of caspase activation protected the cells from apoptosis augmented by TRIM22; Bak was upregulated in TRIM22 overexpressing monocytes. Conclusions Overexpression of TRIM22 in human acute monocytic leukemia cell THP-1 caused extensive apoptosis induced by STS both in absence and presence of lipopolysaccharide, which was associated with elevated cleavage of caspase-9 and caspase-3, and release of cytochrome c. Z-VAD-fmk, a pan caspase inhibitor, prevented TRIM22-induced apoptosis. Western blot found that Bak was upregulated in TRIM22 overexpressing monocytes.
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Wang, Jinghua, Brian Manick, Guoping Wu, and Ruyi Hao. "Biofunctions of three new B7 family members (IRM7P.486)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 126.11. http://dx.doi.org/10.4049/jimmunol.192.supp.126.11.

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Abstract Recently, three new B7 family members, B7-H5 (VISTA, Gi24, or Dies1), B7-H6, and B7-H7 (HHLA2) were identified. However, the functions of the three new B7 family members remain uncertain. We expressed the human B7-H5, B7-H6, and B7-H7 extracellular domain human IgG1 Fc Chimera in mammalian cell line and investigated the functions of the purified recombinant B7-H5/Fc, B7-H6/Fc, and B7-H7/Fc in vitro. To determine the functions of B7-H5 and B7-H7, human T cells were treated with plate-bound anti-CD3 and either B7-H5/Fc, B7-H7/Fc or control IgG1 Fc. The cytokine levels of supernatant were measured using the Proteome Profiler Human Cytokine Array and Quantikine ELISA kit. B7-H5 significantly reduced production of seven cytokines from T cells including IFN-γ, IL-2, IL-4, IL-8, IL-13, IL-16, and TNF-α. B7-H7 markedly decreased four cytokines including IFN-γ, IL-2, IL-8, and TNF-α. To investigate the bioactivity of B7-H6, NK92 cells were treated with plate-bound B7-H6/Fc or control IgG1 Fc. B7-H6/Fc induced IFN-γ production in NK cells in a dose dependent manner. Furthermore, B7-H6/Fc showed binding to recombinant human NKp30/Fc. Taken together, our data suggest that B7-H5 and B7-H7 are co-inhibitory molecules for T cell activation. Our data also indicate that B7-H6, a major NKp30 ligand, triggers NKp30-dependent NK cell activation.
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Kuhns, Michael, Mark Lee, Caleb Glassman, Neha Deshpande, and Heather Parrish. "Evidence for a pivot upon TCR engagement (IRM7P.700)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 61.1. http://dx.doi.org/10.4049/jimmunol.194.supp.61.1.

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Abstract The T cell receptor (TCR)-CD3 complex is the chief determinant for T cell development, activation, differentiation and the execution of effector functions. The TCR module (TCRα+TCRβ) relays highly specific information about antigenic peptides embedded within major histocompatibility complex molecules (pMHC) to the intracellular signaling domains of the associated CD3γε, CD3δε, and CD3ζζ signaling modules to initiate intracellular signaling. It is unclear how mechanical information is transferred from the TCR-pMHC interface, across the plasma membrane, and on to the intracellular signaling domains of the CD3 subunits. The complexity of this molecular machinery, and the lack of obvious parallels with other receptor systems, has hindered progress in resolving these issues. We tested the hypothesis that the juxtamembrane regions of the CD3 signaling subunits are held in a spatial relationship that keeps the complex ‘off’ until TCR engagement triggers a change in this spatial relationship that converts the complex to an ‘on’ conformation. This would be akin to cytokine receptors, receptor tyrosine kinases, and even integrins. Our data indicate that unengaged TCRs enforce a divaricated conformation of the cytosolic juxtamembrane regions of key TCR-CD3 complex subunits at steady state. We interpret this to represent an off conformation. TCR engagement then triggers the intra-complex apposition of these regions into what we interpret to represent an on conformation.
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Stolarz, Anna, Roger Eykens, Andre Moens, and Yetunde Aregbe. "Actinide target preparation at IRMM—then and now." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 613, no. 3 (February 2010): 351–56. http://dx.doi.org/10.1016/j.nima.2009.09.074.

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31

Kramer, G. N., J. Pauwels, L. Le Guern, H. Schimmel, and S. Trapmann. "Recent production of candidate reference materials at IRMM." Fresenius' Journal of Analytical Chemistry 370, no. 2-3 (June 1, 2001): 142–46. http://dx.doi.org/10.1007/s002160100730.

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32

Varga, Zsolt, Célia Venchiarutti, Adrian Nicholl, Judit Krajkó, Rožle Jakopič, Klaus Mayer, Stephan Richter, and Yetunde Aregbe. "IRMM-1000a and IRMM-1000b uranium reference materials certified for the production date. Part I: methodology, preparation and target characteristics." Journal of Radioanalytical and Nuclear Chemistry 307, no. 2 (June 20, 2015): 1077–85. http://dx.doi.org/10.1007/s10967-015-4227-x.

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33

Richter, S., C. Venchiarutti, C. Hennessy, U. Jacobsson, R. Bujak, J. Truyens, and Y. Aregbe. "Preparation and certification of the uranium nitrate solution reference materials series IRMM-2019 to IRMM-2029 for the isotopic composition." Journal of Radioanalytical and Nuclear Chemistry 318, no. 2 (September 1, 2018): 1359–68. http://dx.doi.org/10.1007/s10967-018-6166-9.

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34

Zhang, Jinyu, Zihai Li, and Beichu Guo. "ER stress-induced inflammasome activation promotes liver steatosis (IRM9P.723)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 128.6. http://dx.doi.org/10.4049/jimmunol.192.supp.128.6.

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Abstract Recent evidences suggest that obese animal exhibits increased endoplasmic reticulum (ER) stress and inflammation in the liver tissue. However, it is largely unknown how ER stress contributes to hepatic steatosis. In this study, we demonstrated that ER stress induced inflammasome activation and IL-1 beta production, leading to hepatic inflammation and steatosis. Our results show that tunicamycin (TM), an ER stress inducer, caused NLRP3 inflammasome activation, leading to increased IL-1 beta processing and production in macrophages and hepatocytes. We found that caspase-1 knockout (KO) mice treated with TM exhibited a less characterization of hepatic steatosis and inflammation compared with WT mice. Our data also demonstrated that ER stress-induced inflammasome activation and hepatic steatosis were partially attenuated by treatment with ER stress inhibitor tauroursodeoxycholic acid (TUDCA) and IRE1α inhibitor (4µ8C). Notably, hepatocytes from WT mice showed marked hepatocyte pyroptotic cell death with more than a fivefold increase compared with caspase-1 KO mice. Furthermore, our results show that ER stress promoted inflammasome activation and IL-1 beta production through IRE1α pathways. Taken together, our findings demonstrate that ER stress-mediated inflammasome activation plays an important role in liver inflammation and steatosis. Thus, ER stress could be potential targets for a novel therapeutic approach to prevent impaired inflammatory related liver diseases.
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35

Kumar, Satyendra, and Amy Kenter. "Immunoglobulin isotype switching during early B cell development (IRM8P.702)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 127.3. http://dx.doi.org/10.4049/jimmunol.192.supp.127.3.

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Abstract During B cell lymphopoiesis in the bone marrow (BM), V(D)J joining assembles immunoglobulin (Ig) VH and VL genes mediated by RAG recombinase. Mature splenic B cells undergo class switch recombination (CSR) and somatic hypermutation initiated by activation induced deaminase (AID). However, the strict ontological separation of these processes may breakdown under some circumstances. Several immunodeficiencies including Omenn syndrome display increased serum IgE despite undetectable numbers of B cells. We hypothesized that CSR occurs in BM pro- or pre-B cells. Earlier, we showed that Rag1 and Mb1 deficient pro-B cells can be induced to undergo robust CSR, albeit to a restricted subset of IgH isotypes, including IgG2b and IgE. Immunization of Rag1-/- mice with LPS, promoted IgG2b switching in BM pro-B cells. We demonstrated that V(D)J joining can be induced to follow CSR. We found a unique stage specific chromatin conformation of Igh locus in pro-B cells that may repress IgG3 and IgG1 switching (Genes Dev. 27:2439). Here we show that CSR is inducible in WT pro-B cells. Using an elegant mouse model to irreversibly mark AID expressing cells, a knockin carrying AIDcre/+RosaYFP (Nat Imm. 10:1292), we assess the frequency of AID expression in BM pro-B cells activated in vitro and in vivo with LPS. These findings have implications for the hyper-IgE phenotype in Omenn syndrome, autoimmune repertoire development and leukemagenesis via the co-expression of the RAG and AID recombinases.
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36

Peron, Jean Pierre, Wesley Nogueira Brandão, Cristiano Rossato, and Niels Olsen Camara. "Glutamate ionotropic receptor (NMDAR) modulates T cell survival (IRM7P.712)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 61.13. http://dx.doi.org/10.4049/jimmunol.194.supp.61.13.

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Abstract Introduction: T cells play a crucial role in adaptive immune responses and neuroinflammatory diseases such as multiple sclerosis. Glutamate is one of the most abundant neurotransmitter in the central nervous system; it can acts through two different receptor families: metabotropic and ionotropic. It has been demonstrated that T cells can be the target of glutamate during antigen presentation and immunological synapses, however, little is known about its role on T cell survival. Methods and Results: To evaluate whether NMDAr ligands exert a role in T cell survival, we harvested spleen cells from C57BL/6 female mice and cultivated in the presence of anti-CD3 (1µg/mL) in vitro for 5 days. On day 5, cells were stained for CD4+/CD8+ and 7-AAD and data were acquired by flow cytometric analysis. NMDAr blockage by MK801 induced cell death while NMDA agonist did not affect T proliferation and T cell numbers. Conclusion: Our data demonstrate that NMDAr exert a crucial role in T cell survival. These findings not only contribute to the advantage of the neuroimmunology field but also suggest that T cells which infiltrate the central nervous system could be target of the neurotransmitter glutamate via NMDAr in neuroinflammatory diseases.
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37

LEE, TAEYUN, Sungwook Lee, and Boyoun Park. "The nucleolus contains immune-related RNAs during infection. (IRM5P.644)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 59.9. http://dx.doi.org/10.4049/jimmunol.194.supp.59.9.

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Abstract The nucleolus is a subnuclear structure that is involved in ribosomal RNA (rRNA) synthesis and ribosome assembly, and it is also the location of viral replication or cellular stress sensing. However, the function of the nucleolus in the immune response is still unclear. Here, we report that the nucleoli are fused in both macrophages and dendritic cells during lipopolysaccharide (LPS) or CpG-DNA stimulation, which activates the Toll-like receptor 4 (TLR4) or Toll-like receptor 9 (TLR9) signaling pathway. Our results from RNA-sequencing analysis reveal that the nucleolus contains diverse RNA transcripts in response to LPS. Furthermore, gene ontology term analysis shows that these RNA species are highly correlated with immune-related functions. More interestingly, intron-containing RNA transcripts are existed in the nucleolus. Our results provide new insight into another mechanism of nucleolus in the immune system.
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38

Tat, Connie, Ken Hayama, Hong Zan, and Paolo Casali. "Rad52 deficiency Increases immunoglobulin class switch DNA recombination (IRM8P.714)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 127.15. http://dx.doi.org/10.4049/jimmunol.192.supp.127.15.

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Abstract Class switch DNA recombination (CSR) plays a central role in the maturation of the antibody response. CSR entails the generation of double-strand DNA breaks (DSBs) mediated by activation-induced cytidine deaminase (AID). Resolution of these DSBs can occur through Ku70/Ku86 dependent classical non-homologous end-joining (C-NHEJ), or through an undefined alternative-end joining (A-EJ) that introduces microhomologies in the S-S junctions. Here we investigate the role of Rad52, an important DSB repair factor in CSR. We found that Rad52 deficiency elicits an increase in NP-specific IgG1 and IgG3 responses to T-dependent and T-independent antigens. The increased antibody response is not due to alterations in lymphoid differentiation, B cell proliferation or cell division but rather a direct effect on the CSR machinery. This phenomenon is B cell intrinsic, as CSR to IgG1, IgG2a, IgG3 and IgA virtually double in Rad52-/- B cells stimulated with LPS and respective cytokines. In CSR, both Rad52 and Ku70/Ku86 are specifically recruited to S region DNA in an AID-dependent manner. In the absence of Rad52, the recruitment of Ku70/Ku86 to the S regions was significantly increased. Finally, the frequency and length of microhomologies in the S-S junctions was significantly reduced in Rad52-/- B cells. Altogether, our findings suggest that Rad52 competes with Ku70/Ku86 in binding S region to repair DSBs in CSR possibly utilizing an alternative end-joining pathway.
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39

Ponzevera, Emmanuel, Christophe R. Quétel, Michael Berglund, Philip D. P. Taylor, Peter Evans, Robert D. Loss, and Giuseppino Fortunato. "Mass discrimination during MC-ICPMS isotopic ratio measurements: Investigation by means of synthetic isotopic mixtures (IRMM-007 series) and application to the calibration of natural-like zinc materials (including IRMM-3702 and IRMM-651)." Journal of the American Society for Mass Spectrometry 17, no. 10 (October 2006): 1413–27. http://dx.doi.org/10.1016/j.jasms.2006.06.001.

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40

Oliveira, Adriano Teixeira de, Paloma de Almeida Rodrigues, Alexandre Mendes Ramos Filho, Maria Fernanda da Silva Gomes, Ariany Rabello da Silva Liebl, Júlia Vianna de Pinho, Paulo Henrique Rocha Aride, and Carlos Adam Conte-Junior. "Levels of Total Mercury and Health Risk Assessment of Consuming Freshwater Stingrays (Chondrichthyes: Potamotrygoninae) of the Brazilian Amazon." International Journal of Environmental Research and Public Health 20, no. 21 (October 28, 2023): 6990. http://dx.doi.org/10.3390/ijerph20216990.

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Mercury is an element with potential risk to fish and those who consume it. Thus, this study aimed to determine the levels of total mercury (THg), carry out a health risk assessment related to the consumption of the freshwater stingrays Potamotrygon motoro, and determine the physical and chemical properties of the water where stingrays occur. Stingrays of the species P. motoro were obtained from the Amazon River, and samples of the animals’ musculature were collected to determine THg levels. Risk assessment was conducted using pre-established formulas of estimated monthly intake (EMI), maximum monthly intake rate (IRmm), and hazard quotient (HQ). Three population scenarios were evaluated, considering both sexes and differences between rural and urban areas. There was no relationship between weight and THg concentration nor between total length and THg concentration. Higher EMI values were observed in rural children; for the IRmm, male children had the lowest consumption levels. For the hazard quotient, there was a similarity between the three age groups when comparing the male and female sexes. In addition, the representatives of the rural area always had lower values than the urban area. Freshwater stingrays, like other elasmobranchs, can be crucial animal species because they act as sentinels in studies that assess harmful chemicals like mercury.
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41

Pauwels, J., and M. Grasserbauer. "The view of IRMM on accreditation of CRM producers." Accreditation and Quality Assurance 7, no. 12 (December 1, 2002): 516–19. http://dx.doi.org/10.1007/s00769-002-0515-6.

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42

Valkiers, S., T. Ding, K. Ruße, P. De Bièvre, and P. D. P. Taylor. "Absolute sulfur isotope amount ratios in two batches of high purity SO2 gas: sulfur isotope reference materials IRMM-2012 and IRMM-2013." International Journal of Mass Spectrometry 242, no. 2-3 (April 2005): 303–8. http://dx.doi.org/10.1016/j.ijms.2004.11.021.

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43

Venchiarutti, C., Z. Varga, S. Richter, A. Nicholl, J. Krajko, R. Jakopič, K. Mayer, and Y. Aregbe. "IRMM-1000a and IRMM-1000b: uranium reference materials certified for the production date based on the 230Th/234U radiochronometer. Part II: certification." Journal of Radioanalytical and Nuclear Chemistry 308, no. 1 (September 4, 2015): 105–11. http://dx.doi.org/10.1007/s10967-015-4368-y.

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44

Leong, Jeff, Stephanie Schneider, Ryan Sullivan, and Todd Fehniger. "PTEN regulates natural killer cell trafficking and effector functions (IRM7P.484)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 126.9. http://dx.doi.org/10.4049/jimmunol.192.supp.126.9.

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Abstract Phosphatase and tensin homolog (PTEN) is a critical negative regulator of the PI3 kinase pathway, members of which are essential for regulating natural killer (NK) cell signaling and activation. To evaluate whether PTEN was required for normal NK cell functions, we utilized a mouse model of NK specific PTEN deficiency (Ncr1iCre knockin x PTENflox). PTEN deletion resulted in significant loss of NK cells in the bone marrow and other lymphoid tissues, but markedly increased numbers within the peripheral blood and lung. Surprisingly, we observed near equivalent NK cell maturation within peripheral organs regardless of PTEN expression, suggesting that PTEN operates to re-distribute NK cells during development. Similarly, despite impaired migration to chemoattractants in vitro, PTEN-deficient NK cells egress more efficiently from the bone marrow and preferentially reside in sinusoidal compartments, but are specifically retained in the lung and peripheral vasculature. Given the inappropriate localization in the absence of PTEN, we further evaluated whether cytotoxic functions were altered. While PTEN deficient NK cells have enhanced cytotoxicity against co-localized RMAS tumors, they are unable to migrate to distal tumor sites. These data suggest that PTEN is required for the trafficking of NK cells during both homeostasis and in the presence of malignancy, during which it represses cytotoxic functions.
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45

Mohamed, Eslam, Henrique Lemos, Lei Huang, Rong Ou, Gabriella Pacholczyk, Yoshihrio Hayakawa, David Munn, and Andrew Mellor. "DNA sensing via STING regulates autoimmunity and tumor immunity. (IRM5P.648)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 59.13. http://dx.doi.org/10.4049/jimmunol.194.supp.59.13.

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Abstract The Stimulator of Interferon Genes (STING) is activated by cytosolic DNA sensors such as cyclic GMP-AMP Synthase (cGAS) to induce interferon type I (IFN-I). Dendritic cells (DCs) that engulf dying tumor cells incite anti-tumor T cell immunity by sensing tumor cell DNA to activate STING/IFN-I signaling. Paradoxically, we find that DNA sensing to activate STING/IFN-I signaling induces DCs to express indoleamine 2, 3 dioxygenase (IDO), which activates regulatory T cells (Tregs). Thus treatment with DNA nanoparticles (DNPs) or cyclic dinucleotides (CDNs) to activate STING attenuated Experimental Autoimmune Encephalomyelitis (EAE), arthritis, and therapeutic responses were dependent on STING/IFN-I signaling to induce IDO. DNP and CDN treatments were also effective in slowing Type I Diabetes (T1D) progression in susceptible female Non-Obese Diabetic (NOD) mice. STING ablation also abolished IDO-dependent regulatory responses to apoptotic cells, suggesting that DNA from dying cells is sensed to activate the STING/IFN-I pathway and induce IDO to suppress autoimmunity. Moreover, cGAS and STING ablation abolished the ability of Lewis Lung carcinoma (LLC) tumor cells to induce local IDO, which suppresses anti-tumor immunity. These findings support the hypothesis that DNA from dying cells is sensed to activate STING/IFN-I in regulatory DCs that suppress T cell immunity and autoimmunity at sites of chronic inflammation associated with autoimmunity and tumor growth.
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46

Schwerk, Johannes, Kerri Thomas, Lauren Aarreberg, Abigail Jarret, MeeAe Hong, and Ram Savan. "Post-transcriptional regulation of interferon lambda during viral infection (IRM5P.640)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 59.5. http://dx.doi.org/10.4049/jimmunol.194.supp.59.5.

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Abstract Interferon lambda (IFN-λ) has gained increasing attention recently as an important mediator of antiviral protection in hepatitis C virus (HCV) infection. Similar to many cytokines, we have shown that expression of IFNL is regulated on a post-transcriptional level. Interestingly, single nucleotide polymorphisms (SNPs) within the IFNL genes dictate the outcome of acute HCV infection and serve as a prognostic marker for therapy of chronic HCV infection. Previously, we demonstrated that a functional SNP (rs4803217) within the 3'-untranslated region (UTR) of IFNL3 affects transcript stability and correlates with HCV clearance (G/G) or persistence (T/T) in infected patients and this is mediated by miRNAs and AU-rich elements. In our current study we have identified RNA-binding protein(s) (RBPs) that differentially regulate IFNL3 variants. We identified RBP candidates by carrying out mass spectrometry analysis on both variants of IFNL3 mRNA. We found that these candidates exclusively interact with the IFNL3 (T/T) mRNA. Intriguingly, gene expression of one candidate RBP is strongly induced upon stimulation of cells with HCV RNA or viral PAMP. Collectively, our data suggest that IFNL3 mRNA is post-transcriptionally regulated by miRNA and RBP-mediated mechanisms and that HCV potentially hijacks these regulatory mechanisms to suppress host antiviral responses.
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47

Tang, Daolin, Rui Kang, Michael Lotze, and Herbert Zeh. "Endogenous HMGB1 prevents nuclear catastrophe and proinflammatory nucleosomal release (IRM9P.719)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 128.2. http://dx.doi.org/10.4049/jimmunol.192.supp.128.2.

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Abstract The mechanisms by which tissue injury alerts the immune system and drives a systemic inflammatory response syndrome remain unknown. Here we identify a high mobility group box 1 (HMGB1)-mediated nuclear regulatory mechanism for the control of the inflammatory response during tissue injury. We show that conditional knockout of HMGB1 within the pancreas, while benign without provocation, rendered mice dramatically more susceptible to experimental acute severe pancreatitis, as manifested by accelerated tissue injury and animal lethality. Deficiency of endogenous pancreatic HMGB1 led to exaggeration of L-arginine-induced nuclear catastrophe and nucleosome release, which then recruited and activated inflammatory cells with subsequent HMGB1 release locally and into the circulation. Serum levels of tissue enzymes (e.g., amylase, lactate dehydrogenase, and pancreatic myeloperoxidase) and pro-inflammatory cytokines were significantly higher in conditional pancreas-specific HMGB1 knockout mice compared to their wild-type control littermates. Moreover, neutralizing extracellular histone and HMGB1 conferred protection against acute pancreatitis in conditional pancreas-specific HMGB1 knockout mice. Thus, intracellular HMGB1 may serve as a previously underappreciated negative regulator of inflammation, shedding light on the role of the innate immune response in infection and tissue damage.
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48

Trapmann, Stefanie, Heinz Schimmel, Gerard Nico Kramer, Guy van den Eede, and Jean Pauwels. "Production of Certified Reference Materials for the Detection of Genetically Modified Organisms." Journal of AOAC INTERNATIONAL 85, no. 3 (May 1, 2002): 775–79. http://dx.doi.org/10.1093/jaoac/85.3.775.

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Abstract Certified reference materials (CRMs) are an essential tool in the quality assurance of analytical measurements. They are produced, certified, and used in accordance with relevant ISO (International Organization for Standardization) and BCR (Community Bureau of Reference) guidelines. The Institute for Reference Materials and Measurements (IRMM; Geel, Belgium) has produced the first powdery genetically modified organism (GMO) CRMs in cooperation with the Institute for Health and Consumer Protection (Ispra, Italy). Until now, different weight percentages in the range of 0–5%for 4 GMOs in Europe were produced and certified: Bt (Bacillus thuringiensis)-11 and Bt-176 maize, Roundup Ready® soybean, and MON810 maize. Bt-11 and Bt-176 maize and Roundup Ready soybean were produced by IRMM on behalf of Fluka Chemie AG (Buchs, Switzerland). Characterization of used base material is the first step in production and is especially important for GMO CRMs. The production of powdery GMO CRMs and methods used for production control are described. Thorough control of homogeneity and stability are essential for certification of reference materials and ensure validity of the certificate for each bottle of a batch throughout a defined shelf-life. Because production of reference materials and their maintenance are very labor- and cost-intensive tasks, the usefulness of new types of GMO CRMs must be estimated carefully.
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49

Roebben, G., A. Lamberty, and J. Pauwels. "Certification of Charpy V-Notch Reference Test Pieces at IRMM." Journal of ASTM International 2, no. 7 (2005): 12870. http://dx.doi.org/10.1520/jai12870.

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50

Gawlik, B. M., S. Trapmann, T. P. J. Linsinger, A. Lamberty, and H. Emons. "Preservation of sensitive CRMs and monitoring their stability at IRMM." Analytical and Bioanalytical Chemistry 378, no. 5 (March 1, 2004): 1168–74. http://dx.doi.org/10.1007/s00216-003-2214-5.

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