Relevant bibliographies by topics / Gitern

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Gitern'

Author: Grafiati
Published: 24 April 2022

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Journal articles on the topic "Gitern"

1

Gan, Xiaoxia, Xiaoke Feng, Lei Gu, Wenfeng Tan, Xiaoxuan Sun, Chengyin Lv, and Miaojia Zhang. "Correlation of Increased Blood Levels of GITR and GITRL with Disease Severity in Patients with Primary Sjögren’s Syndrome." Clinical and Developmental Immunology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/340751.

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Glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) is a type I transmembrane protein belonging to the TNFR superfamily. After activated by its ligand GITRL, GITR could influence the activity of effector and regulatory T cells, participating in the development of several autoimmune and inflammatory diseases included rheumatoid arthritis and autoimmune thyroid disease. We previously reported that serum GITRL levels are increased in systemic lupus erythematosus (SLE) patients compared with healthy controls (HC). Here, we tested serum soluble GITR (sGITR) and GITRL levels in 41 primary Sjögren’s syndrome (pSS) patients and 29 HC by ELISA and correlated sGITR and GITRL levels with clinical and laboratory variables. GITR and GITRL expression in labial salivary glands was detected by immunohistochemistry. pSS patients had significantly increased serum levels of sGITR and GITRL compared with controls (GITR: 5.66 ± 3.56 ng/mL versus 0.50 ± 0.31 ng/mL;P<0.0001; GITRL: 6.17 ± 7.10 ng/mL versus 0.36 ± 0.28 ng/mL;P<0.0001). Serum sGITR and GITRL levels were positively correlated with IgG (GITRL:r=0.6084,P<0.0001; sGITR:r=0.6820,P<0.0001) and ESR (GITRL:r=0.8315,P<0.0001; sGITR:r=0.7448,P<0.0001). Moreover, GITR and GITRL are readily detected in the lymphocytic foci and periductal areas of the LSGs. In contrast, the LSGs of HC subjects did not express GITR or GITRL. Our findings indicate the possible involvement of GITR-GITRL pathway in the pathogenesis of pSS. Further studies may facilitate the development of targeting this molecule pathway for the treatment of pSS.
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2

Krausz, Ludovic Tibor, Rodolfo Bianchini, Simona Ronchetti, Katia Fettucciari, Giuseppe Nocentini, and Carlo Riccardi. "GITR-GITRL System, A Novel Player in Shock and Inflammation." Scientific World JOURNAL 7 (2007): 533–66. http://dx.doi.org/10.1100/tsw.2007.106.

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Glucocorticoid-induced TNFR-Related (GITR) protein is a member of the tumor necrosis factor receptor superfamily that modulates acquired and natural immune response. It is expressed in several cells and tissues, including T cells, natural killer cells, and, at lower levels, in cells of innate immunity. GITR is activated by its ligand, GITRL, mainly expressed on antigen presenting and endothelial cells. Recent evidence suggests that the GITR/GITRL system participates in the development of inflammatory responses, including shock, either due to early response of neutrophils and macrophages, or together with autoimmune/allergic pathogenesis. The pro-inflammatory role of the GITR/GITRL system is due to: 1) modulation of the extravasation process, 2) activation of innate immunity cells, 3) activation of effector T cells also favored by partial inhibition of suppressor T cells and modulation of dendritic function. This review summarizes thein vivorole of the GITR/GITRL system in inflammation and shock, explaining the mechanisms responsible for their effects, considering the interplay among the different cells of the immune system and transduction pathways activated by GITR and GITRL triggering. The hidden aspects about GITR/GITRL function, crucial for treatment planning of inflammatory diseases and shock by modulation of this system is stressed.
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3

Krusch, Matthias, Katrin M. Baltz, Tina Baessler, Mercedes Kloss, Ingrid Kumbier, Andrea Peterfi, Lothar Kanz, and Helmut R. Salih. "Expression of Glucocorticoid-Induced TNF Receptor Ligand on Acute Myeloid Leukemia Cells Mediates the Release of Immunosuppressive Cytokines and Impairs NK Cell-Mediated Immune Surveillance." Blood 108, no. 11 (November 16, 2006): 1941. http://dx.doi.org/10.1182/blood.v108.11.1941.1941.

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Abstract NK cells play an important role in the reciprocal interaction of tumor cells with the immune system and participate in the surveillance of hematological malignancies including acute myeloid leukemia (AML). Among the molecules influencing host-tumor interaction are many members of the TNF superfamily, which mediate multiple cellular functions including cellular proliferation, differentiation and cell death. The TNF family member Glucocorticoid-induced TNF Receptor (GITR) costimulates effector T cells, modulates apoptosis and nuclear factor kappa B and abrogates suppression of murine but not human regulatory T cells. Its cognate ligand GITRL has been found in various healthy tissues. Recently we reported that NK cells express GITR, while solid tumors express GITR ligand (GITRL), and GITR/GITRL interaction downregulates NK cell cytotoxicity and IFN-γ production. Here we analyzed the role of GITR and its ligand in AML. We report for the first time that GITRL is expressed on primary AML cells in 18 of 30 patients as determined by FACS and RT-PCR analysis. Reverse signaling through GITRL using a recombinant GITR-Ig fusion protein induces the release of the immunoregulatory cytokines IL-10 and TNF as determined by ELISA. GITRL-mediated cytokine production of AML cells is abrogated by inhibition of mitogen activated protein kinase (MAPK) pathways as demonstrated by addition of the specific p38 MAPK inhibitor SB202190, the specific JNK inhibitor SP600125 and the specific ERK Inhibitor II. Furthermore, binding of AML-expressed GITRL to GITR on NK cells downregulates cellular cytotoxicity and IFN-γ production in AML-NK cell cocultures, which can be overcome by addition of GITR-blocking antibodies as determined by cytotoxicity assays and ELISA. Thus, our data indicate that GITRL expression in AML substantially influences tumor immunoediting and enables the escape of leukemia cells from NK cell-mediated immunosurveillance.
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4

Baltz, Katrin M., Matthias Krusch, Radsak P. Markus, Frank Mayer, Lothar Kanz, and Helmut R. Salih. "Human GITR Ligand Is Expressed on Tumor Cells and Reduces Cytokine Production and Cellular Cytotoxicity of NK Cells Identified to Express GITR." Blood 106, no. 11 (November 16, 2005): 3310. http://dx.doi.org/10.1182/blood.v106.11.3310.3310.

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Abstract Members of the tumor necrosis factor (TNF) superfamily mediate multiple cellular functions including cellular proliferation, differentiation, and cell death. Human Glucocorticoid-induced TNF Receptor (GITR) has been shown to be expressed on T cells, is upregulated following activation and mediates costimulatory signals. The human GITR ligand (GITRL) has been reported to be expressed on antigen presenting cells and various healthy nonlymphoid tissues including small intestine, ovary, testis, kidney and endothelial cells. We analyzed multiple tumor cell lines of hematopoietic and epithelial origin as well as of germ cell lineage and various gliomas by RT-PCR and FACS analysis. Both GITRL m-RNA and protein are expressed in various carcinomas, gliomas and tumor cells of germ cell lineage, but not in hematopoietic tumor cells. Furthermore, we demonstrate that human NK cells constitutively express low levels of GITR, and this expression is upregulated following activation by, e.g., IL-2 or IL-15 as detected by quantitative PCR and FACS analysis. To address the functional interaction of GITRL with its receptor on NK cells, we generated a GITRL-IgG fusion protein (GITRL-Ig). Stimulation of activated NK cells with GITRL-Ig lead to significantly reduced IFN-g production of NK cells as measured by ELISA. Similarly, a significant reduction of IFN-g release was observed following coculture of GITR expressing NK cells with C1R cells transfected with GITRL but not with the respective mock transfectants. Furthermore, ligation of GITR on NK cells lead to significantly decreased killing of target cells as demonstrated by cellular cytotoxicity assays. Taken together, our data demonstrate that GITR not only plays an important role in adaptive immunity but is also involved in the regulation of NK cell effector functions. Since tumor cells express significant levels of GITRL, and ligation of GITR on NK cells markedly reduces cytokine production and cellular cytotoxicity, our data indicate that GITR-GITRL interactions play an important role in the escape of tumor cells from innate immune surveillance.
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Kondo, Yukio, Takamasa Katagiri, Kinya Ohata, and Shinji Nakao. "GITR Ligand on Leukemic Myeloid Dendritic Cells Suppresses Induction of Leukemia-Associated Antigen-Specific CTLs from Naïve CD8+ T Cells." Blood 112, no. 11 (November 16, 2008): 2347. http://dx.doi.org/10.1182/blood.v112.11.2347.2347.

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Abstract Glucocorticoid-induced TNFR-related protein (GITR), a member of the TNF receptor superfamily, is expressed at low levels on resting T cells and is up-regulated following activation. Triggering of GITR with its ligand (GITRL) has been described to abrogate the function of CD4+CD25+ regulatory T cells and stimulate effector T cells in mice, but little is known about roles of GITR-GITRL interaction in humans. Recent evidence suggests that the interaction between GITR on NK cell and GITRL, which is constitutively expressed on tumor cells, negatively regulates NK cell-mediated anti-tumor activity in cancer patients. Leukemic myeloid dendritic cells (mDCs) can induce cyclin-dependent kinase (CDK2)- specific cytotoxic T lymphocytes (CTLs) from naïve T cells and CDK2-specific CTLs are detectable in MRD+ patients with leukemia after allo-SCT (Blood. 110 (11): a3228. 2007). The GITR-GITRL interaction may affect this process and a modification of the interaction may improve the efficiency of inducing CDK2-specific CTLs. Therefore, the expression of GITRL on leukemic cells and leukemic mDCs was examined to determine whether an engagement of GITR controls the priming of leukemia-associated-antigen (LAA)-specific CD8+ T cells. When cryopreserved BMMCs obtained at diagnosis from 5 patients with AML were assessed using flow cytometry, GITRL expression was detectable on leukemic cells in 3 patients. Leukemic mDCs were enriched from PBMCs of HLA-A24+ patients with anti-CD1c mAb-conjugated magnetic beads and were assessed for their ability to stimulate HLA-A24+ naïve CD8+ T cells to acquire cytotoxicity specific to CDK2-peptides (CDK2 158–166, CDK2 178–186). A three days culture of immature leukemic mDCs in the presence of TNFα up-regulated the expression of GITRL along with CD83 and CD40 expression. Naïve CD8+ T cells isolated from healthy individuals and cord blood were cultured with the GITRL-expressing leukemic mDCs in the presence or absence of anti- GITR monoclonal antibodies (mAbs) for 14 days and stained for CDK2 158–166/A24, CDK2 178–186/A24 pentamers. Blocking of GITR with the mAbs augmented induction of CDK2 158–166- and CDK2 178–186- specific CD8+ T cells from 0.37% to 1.17% and from 0.45% to 1.64%, respectively (Fig). Anti-GITR mAbs did not enhance induction of CDK2-specific T cells by peptide-pulsed monocyte-derived DCs which do not express GITRL. These data suggest that the expression of GITRL on circulating leukemic mDCs may suppress induction of CTLs specific to LAAs and induce cancer immunoediting in patients with leukemia. Administration of anti-GITR mAb after allo-SCT may enhance graft versus leukemia effect by CDK2-specific CTLs without vaccination of CDK2-peptides. Fig Blocking of GITR on T cells augments induction of CDK2-specific CTLs Fig. Blocking of GITR on T cells augments induction of CDK2-specific CTLs
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Buechele, Corina, Tina Baessler, Benjamin J. Schmiedel, Lothar Kanz, and Helmut R. Salih. "Glucocorticoid-Induced TNFR-Related Protein (GITR) Ligand Mediates Tumor Immunoediting in Chronic Lymphocytic Leukemia and Impairs Direct and Rituximab-Induced NK Cell Anti-Leukemia Reactivity." Blood 114, no. 22 (November 20, 2009): 4403. http://dx.doi.org/10.1182/blood.v114.22.4403.4403.

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Abstract Abstract 4403 Members of the TNF/TNF receptor (TNFR) family of proteins govern differentiation, proliferation, activation, and death of both tumor and immune effector cells and thus play an important role in tumor immunoediting, the reciprocal interaction of tumor cells and anti-tumor immunity. Activation of the TNFR family member GITR has recently been shown to stimulate T cell-mediated anti-tumor immunity in mice. However, available data suggest that GITR mediates different effects in mice and men, and may impair anti-tumor immunity of human NK cells. Here we studied the expression and function of GITR ligand (GITRL) in patients with chronic lymphocytic leukemia (CLL) and the consequences of GITR-GITRL interaction for NK cell reactivity against CLL cells. Substantial GITRL expression was detected on primary B-CLL cells in 38 of 48 (79%) investigated patients. Upon interaction with its cognate receptor, GITRL induced the release of immunoregulatory cytokines like TNF by the leukemia cells, which demonstrated that CLL-expressed GITRL is functional and capable to transduce bidirectional signals. Moreover, disruption of GITR-GITRL interaction in cultures of allogenic NK cells with patient CLL cells by addition of blocking antibody caused a significant increase in NK cell granule mobilization, cytotoxicity and IFN-γ production. The inhibitory effect of tumor-expressed GITRL on the reactivity of human NK cells was also confirmed in cocultures of C1R lymphoma cells transfected to express GITRL with mock transfectants serving as control. In addition, blocking GITR-GITRL interaction also considerably augmented both antibody-dependent cellular cytotoxicity (ADCC) and antibody-induced IFN-γ production of NK cells in cultures with allogenic CLL cells upon Rituximab exposure. Of note, GITR blockade also significantly enhanced anti-leukemia reactivity of autologous NK cells among PBMC of B-CLL patients, and this reinforcement of NK cell effector functions was observed both regarding the direct and, more pronounced, Rituximab-induced anti-leukemia reactivity (both n=10, p<0.01, Student's T test). Thus, expression of functional GITRL by CLL cells potently influences tumor immunoediting and impairs anti-tumor immunity by diminishing both direct and Rituximab-dependent anti-leukemia reactivity of NK cells. Modulation of the GITR-GITRL system might therefore serve to enhance the efficacy of therapeutic approaches in CLL which, like Rituximab-induced ADCC or stem cell transplantation, rely on a sufficient NK cell anti-tumor response. Disclosures: No relevant conflicts of interest to declare.
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Steinbacher, Julia, Benjamin J. Schmiedel, Antje Werner, Tina Nuebling, Corina Buechele, Ludger Grosse-Hovest, Lothar Kanz, and Helmut R. Salih. "Bimodal Induction of NK Cell Reactivity Against Acute Myeloid (AML) and Chronic Lymphoid Leukemia (CLL) by Fc-Engineered GITR-Fc Fusion Proteins." Blood 120, no. 21 (November 16, 2012): 2143. http://dx.doi.org/10.1182/blood.v120.21.2143.2143.

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Abstract Abstract 2143 NK cells play an important role in anti-tumor immunity and largely contribute to the efficacy of therapeutic strategies like allogenic stem cell transplantation in AML and application of Rituximab that induces antibody-dependent cellular cytotoxicity (ADCC) in CLL. Recently, we demonstrated that the TNF family member GITR ligand (GITRL) is expressed on leukemia cells in a high proportion of AML and CLL patients and impairs direct and Rituximab-induced reactivity of NK cells which constitutively express its counterpart GITR (e.g., Buechele et al., Leukemia 2012). Here we developed a strategy to reinforce NK anti-leukemia reactivity by combining disruption of NK-inhibitory GITR-GITRL interaction with induction of ADCC against the GITRL-expressing leukemia cells using GITR-Ig fusion proteins with modified Fc moieties. Fc parts were engineered by amino acid exchange as previously described (Lazar et al., PNAS 2006; Armour et al., Eur. J. Immunol. 1999). Compared to wild type GITR-Ig (GITR-Fc-WT), our mutants (S239D/I332E and E233P/L234V/L235A/deltaG236/A327G/A330S) displayed highly enhanced (GITR-Fc-ADCC) and abrogated (GITR-Fc-KO) affinity to the Fc(gamma)RIIIa receptor (CD16) expressed on NK cells, respectively. In functional analyses of NK cells and primary leukemia cells, GITR-Fc-KO, which does not induce ADCC, already increased NK reactivity due to disruption of GITR-GITRL interaction. Treatment with GITR-Fc-WT further enhanced NK reactivity due to modest induction of ADCC, while GITR-Fc-ADCC induced highly increased NK-mediated target cell lysis, degranulation and cytokine production in a target-antigen dependent manner. With CLL cells, combined treatment with GITR-Fc-ADCC fusion protein and Rituximab caused additive effects, resulting in significantly enhanced NK cell ADCC. Notably, the effects of our fusion proteins were observed both in an allogenic setting and when employing NK cells of patients with autologous leukemia cells as targets. Our results demonstrate that Fc-engineered GITR-Fc-ADCC fusion protein may combine both neutralization of the NK-inhibitoryeffects of GITR-GITRL interaction and targeting GITRL-expressing malignant cells for NK anti-tumor reactivity and thus constitute an attractive immunotherapeutic means for the treatment of AML and CLL. Disclosures: No relevant conflicts of interest to declare.
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Schilling, Susanne R., Jörn R. Sparfeldt, Detlef H. Rost, and Grete Nickels. "Schulische Selbstkonzepte - Zur Validität einer erweiterten Version des Differentiellen Selbstkonzept Gitters (DISK-Gitter)." Diagnostica 51, no. 1 (January 2005): 21–28. http://dx.doi.org/10.1026/0012-1924.51.1.21.

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Zusammenfassung. Die Validität des erweiterten Differentiellen Selbstkonzept Gitters (DISK-Gitter; Rost & Sparfeldt, 2002 ) - ein Verfahren zur Erfassung schulfachspezifischer Selbstkonzepte - wird an N = 999 Schülern der 7. bis 10. Klassenstufe überprüft. Das DISK-Gitter mit den hier betrachteten sechs Facetten “Mathematik“, “Deutsch“, “Physik“, “Geschichte“, “Englisch“ und “Biologie“ erweist sich konfirmatorisch als faktoriell valide. Konvergente und divergente Validitätsaspekte können anhand der Beziehungen zu ausgewählten Skalen des Self-Description Questionnaire II (SDQ II; Marsh, 1990a ), zur Skala zur Erfassung schulischer Leistungen und Fähigkeiten (SKSLF; Rost & Lamsfuß, 1992 ), zu Schulzensuren sowie in Bezug auf Geschlechtsunterschiede belegt werden. Es ergeben sich hypothesenkonforme Korrelationsmuster und Mittelwertsunterschiede. Insgesamt erweist sich das erweiterte DISK-Gitter als ökonomisches, reliables und valides Instrument zur Messung schulfachspezifischer Selbstkonzepte.
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Baltz, Katrin M., Matthias Krusch, Tina Baessler, Mercedes Kloss, Ingrid Kumbier, Andrea Peterfi, Lothar Kanz, and Helmut R. Salih. "Down-Regulation of Glucocorticoid-Induced TNF Receptor (GITR) Ligand on Human Tumors by Proteolytic Shedding Increases Anti-Tumor Reactivity of NK Cells." Blood 108, no. 11 (November 16, 2006): 926. http://dx.doi.org/10.1182/blood.v108.11.926.926.

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Abstract Members of the TNF superfamily mediate multiple cellular functions, including cellular proliferation, differentiation and cell death. Many members of this protein family are shed from the cell surface as soluble forms, which affects cell-cell interactions by reduction of ligand densities and distally modulates effector cells bearing the respective receptor. The TNF family member Glucocorticoid-induced TNF Receptor (GITR) costimulates effector T cells, modulates apoptosis and NFkappaB and abrogates suppression of murine but not human regulatory T cells. Its cognate ligand GITRL has been found in various healthy tissues. Recently we reported that NK cells express GITR, while tumor cells express GITR ligand (GITRL), and GITR/GITRL interaction downregulates NK cell-mediated anti-tumor effector mechanisms like cytotoxicity and IFN-gamma production. Here we report that human tumor cells spontaneously release a soluble form of GITRL (sGITRL) detectable in culture supernatants by ELISA. Furthermore, we found elevated levels of sGITRL in sera of patients with various malignancies compared to healthy controls. We demonstrate that the release of GITRL from tumor cells can be blocked by inhibition of metalloproteinases, concomitantly causing accumulation of GITRL on the tumor cell surface as determined by FACS analysis. Upregulated GITRL surface expression further increased inhibition of NK cell anti-tumor effector mechanisms, while, in contrast, presence of sGITRL in cocultures of GITRL-expressing tumor cells and GITR-positive NK cells enhanced NK cell cytotoxicity and IFN-gamma production. Thus, in line with the results obtained with other TNF family members, conversion of membrane bound GITRL to its soluble form is associated with downregulation of its function, potentially due to blocking its cognate receptor. Thus, release of sGITRL substantially influences the interaction of tumor cells with NK cells. In addition, determination of sGITRL levels may be implemented as a diagnostic marker in patients with malignancies. Further prospective studies are currently being conducted addressing the value of GITRL as a tumor marker in different tumor entities.
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Placke, Theresa, Hans-Georg Kopp, and Helmut Rainer Salih. "Glucocorticoid-Induced TNFR-Related (GITR) Protein and Its Ligand in Antitumor Immunity: Functional Role and Therapeutic Modulation." Clinical and Developmental Immunology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/239083.

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The ability of the tumor necrosis factor receptor (TNFR) family member GITR to modulate immune responses has been the subject of multiple studies. Initially thought to be critically involved in governing functions of regulatory T cells, GITR and its ligand GITRL have meanwhile been found to modulate the reactivity of various different cell types and to influence a broad variety of immunological conditions including the immune response against tumors. Not only GITR, but also GITRL is capable of transducing signals, and the consequences of GITR-GITRL interaction may vary among different effector cell types, differ upon signal transduction via the receptor, the ligand, or both, depend on the level of an ongoing immune response, and even differ among mice and men. In this paper, we address available data on GITR and its ligand in immune responses and discuss the role and potential therapeutic modulation of this molecule system in antitumor immunity.
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Dissertations / Theses on the topic "Gitern"

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Wanka, Rolf. "Paralleles Sortieren auf mehrdimensionalen Gittern /." Aachen : Shaker, 1995. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=017006701&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Hemkemeier, Boris [Verfasser]. "Algorithmische Konstruktionen von Gittern / Boris Hemkemeier." Dortmund : Universitätsbibliothek Technische Universität Dortmund, 2004. http://d-nb.info/1011531712/34.

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Reinelt, Rolf. "Simulation inkompressibler Strömungen mit unstrukturierten Gittern." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964902508.

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Kreiter, Maximilian. "Oberflächenplasmonen-artige Resonanzen auf metallischen Gittern." [S.l. : s.n.], 2000. http://ArchiMeD.uni-mainz.de/pub/2000/0074/diss.pdf.

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Voigt, Sebastian. "Drucksensorkatheter auf Basis von Faser-Bragg-Gittern." Doctoral thesis, Universitätsbibliothek Chemnitz, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:ch1-qucosa-83302.

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Die vorliegende Arbeit beschreibt die Entwicklung eines Drucksensorkatheters auf Basis von Faser-Bragg-Gittern. Dazu werden der medizinische Hintergrund aus technischer Sicht strukturiert dargelegt und bereits verfügbare Messmethoden für Manometrieuntersuchungen erörtert. Der Stand der Technik bei Faser-Bragg-Gitter basierten Sensoren und deren Auswertegeräten wird im Zusammenhang mit den aus dem medizinischen Hintergrund und dem Vergleich mit den anderen Messmethoden erwachsenden Anforderungen dargestellt. Die Entwicklung eines zweistufigen für die Herstellung mittels Koextrusion geeigneten Mantels für die optischen Fasern wird beschrieben. Mehrere Funktionsmuster für einen Drucksensorkatheter werden experimentell charakterisiert und die Ergebnisse hinsichtlich der Medizineignung bewertet.
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Rom, Tim. "Bosonische und fermionische Quantengase in dreidimensionalen optischen Gittern." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-116800.

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Yan, Jianping. "Effiziente Simulation komplexer Strömungen auf semi-strukturierten Gittern." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968439802.

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Friedrich, Oliver. "Gewichtete wesentlich nicht-oszillierende Verfahren auf unstrukturierten Gittern." [S.l. : s.n.], 1999. http://www.sub.uni-hamburg.de/disse/62/Disse.pdf.

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Graf, Frank. "Numerische Simulation dreidimensionaler kompressibler Strömungen auf unstrukturierten Gittern." München Verl. Dr. Hut, 2007. http://d-nb.info/988229218/04.

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Rieth, Thomas Herbert. "Untersuchung der Lokalisierung elektronischer Zustaende in quasiperiodischen Gittern." Doctoral thesis, [S.l. : s.n.], 1996. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10324485.

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Books on the topic "Gitern"

1

Grünberg, Karol. Gitler: Biografii︠a︡ Fi︠u︡rera, ss--chernai︠a︡ gvardii︠a︡ Gitlera. Moscow: Respublika, 1995.

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Klinge, Aleksandr. Zapreshchennyĭ Gitler: Vraga nado znatʹ : 10 mifov o Gitlere. Moskva: ︠I︡Auza-Press, 2011.

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Nihongo giten. Tōkyō: Yayoi Shobō, 1985.

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Nihongo giten. Tōkyō: Yayoi Shobō, 1985.

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Gitara dlia vsekh: Samouchitel igry na shestistrunnoi gitare : akkompanement pesen : tablitsy akkordov. Moskva: Izd. V. Katanskogo, 2002.

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Ochmann, Nadine. Gesundheit hinter Gittern. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9.

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"Gde Gitler?": Povtornoe rassledovanie NKVD-MVD SSSR obstoi︠a︡telʹstv ischeznovenii︠a︡ Adolʹfa Gitlera (1945-1949). Moskva: Modest Kolerov i "Tri kvadrata", 2003.

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Kozlov, Vladimir Aleksandrovich. " Gde Gitler?" Povtornoe rassledovanie NKVD-MVD SSSR obstoi︠a︡telʹstv ischeznovenii︠a︡ Adolʹfa Gitlera (1945-1949). Moskva: Modest Kolerov & "Tri kvadrata", 2003.

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Hoffnung auch hinter Gittern. München: Verlag Neue Stadt, 1987.

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Eckart, Ulrike. Walter - Liebe hinter Gittern. Stuttgart: Panini-Verl.-GmbH, 2000.

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Book chapters on the topic "Gitern"

1

Wolfart, Jürgen. "Gitter." In Einführung in die Zahlentheorie und Algebra, 227–86. Wiesbaden: Vieweg+Teubner, 2011. http://dx.doi.org/10.1007/978-3-8348-9833-3_8.

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Ochmann, Nadine. "Einleitung." In Gesundheit hinter Gittern, 1–5. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_1.

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Ochmann, Nadine. "Intramurale Gesundheit und gesundheitliche Versorgung." In Gesundheit hinter Gittern, 7–82. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_2.

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Ochmann, Nadine. "Methode." In Gesundheit hinter Gittern, 83–94. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_3.

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Ochmann, Nadine. "Beschreibung der Stichprobe." In Gesundheit hinter Gittern, 95–99. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_4.

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Ochmann, Nadine. "Ergebnisse." In Gesundheit hinter Gittern, 101–202. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_5.

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Ochmann, Nadine. "Zusammenfassung und Diskussion der Ergebnisse." In Gesundheit hinter Gittern, 203–31. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_6.

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Ochmann, Nadine. "Fazit und Handlungsempfehlungen." In Gesundheit hinter Gittern, 233–37. Wiesbaden: Springer Fachmedien Wiesbaden, 2018. http://dx.doi.org/10.1007/978-3-658-20777-9_7.

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Weipert, Thomas. "„Als Rechter hinter Gittern“." In Beiträge zu Kriminologie und Strafrecht, 82–83. Herbolzheim: Centaurus Verlag & Media, 2003. http://dx.doi.org/10.1007/978-3-86226-828-3_20.

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Kowalsky, Wolfgang. "Reziprokes Gitter." In Dielektrische Werkstoffe der Elektronik und Photonik, 35–36. Wiesbaden: Vieweg+Teubner Verlag, 1994. http://dx.doi.org/10.1007/978-3-322-84838-3_3.

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Conference papers on the topic "Gitern"

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Guggino, G., D. di liberto, A. Rizzo, M. La Manna, A. Ferrante, L. saieva, R. Alessandro, G. Sireci, and F. ciccia. "FRI0161 Role of gitr/gitrl in modulating th9 response in psoriatic arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6449.

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Wang, Min, Fiore Cattaruzza, Pete Yeung, Alayne Brunner, Erwan LeScolan, Yuwang Liu, Jennifer Cain, et al. "Abstract 5621: Prevalence of GITR expression and pharmacodynamic (PD) biomarkers in syngeneic tumor models treated by a GITR agonist (GITRL-Fc)." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5621.

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Schröder, Matthias, Viola Marshall, Meinolf Thiemann, David M. Richards, Christian Merz, Jaromir Sykora, Julian P. Sefrin, et al. "Abstract 4143: The novel hexavalent human GITR agonist HERA-GITRL promotes anti-tumor efficacy independent of Fc-functionality and shows superior activity compared with the monoclonal anti-GITR antibody TRX518." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4143.

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Schröder, Matthias, Viola Marshall, Meinolf Thiemann, David M. Richards, Christian Merz, Jaromir Sykora, Julian P. Sefrin, et al. "Abstract 4143: The novel hexavalent human GITR agonist HERA-GITRL promotes anti-tumor efficacy independent of Fc-functionality and shows superior activity compared with the monoclonal anti-GITR antibody TRX518." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4143.

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Romero, Ricardo, Esteban Parra, and Sonia Haiduc. "Experiences Building an Answer Bot for Gitter." In ICSE '20: 42nd International Conference on Software Engineering. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3387940.3391505.

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Shi, Lin, Xiao Chen, Ye Yang, Hanzhi Jiang, Ziyou Jiang, Nan Niu, and Qing Wang. "A first look at developers’ live chat on Gitter." In ESEC/FSE '21: 29th ACM Joint European Software Engineering Conference and Symposium on the Foundations of Software Engineering. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3468264.3468562.

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Gonzalez, Ana M., Mariana L. Manrique, Lukasz Swiech, Thomas Horn, Jeremy Waight, Yuqi Liu, Shiwen Lin, et al. "Abstract 3643: INCAGN1876, a unique GITR agonist antibody that facilitates GITR oligomerization." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3643.

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Melnikov, Denis. "Preparatory Numerical Analysis of Future Space Experiments Influenced by j-gitter." In 54th International Astronautical Congress of the International Astronautical Federation, the International Academy of Astronautics, and the International Institute of Space Law. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2003. http://dx.doi.org/10.2514/6.iac-03-j.2.04.

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Morrow, Michelle, Rebecca Leyland, James Hair, Ross Stewart, Natalie Tigue, Lisa Bamber, Samantha Ireland, et al. "Abstract 4604: MEDI1873, a GITR ligand fusion protein (GITRL FP), induces effector T-cell proliferation, modulates T-regulatory cell function and has the potential to combine with checkpoint inhibitors." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4604.

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Argast, Gretchen M., Belinda Cancilla, Fiore Cattaruzza, Pete Yeung, Reyhaneh Lahmy, Erwan Le Scolan, Rose Harris, et al. "Abstract 3826: GITRL-Fc biomarker and mechanism study: GITRL-Fc reduces Treg frequency in tumors and requires effector function for inhibition of tumor growth." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3826.

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Reports on the topic "Gitern"

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Lamothe, D. Indices et gites de minéraux. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2007. http://dx.doi.org/10.4095/223375.

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Auclair, M., and M. Gauthier. Eastern Metals Un Gite a Ni - Cu - Zn - Co - Au Au Sein D'une Serpentinite Alteree [Listwaenite]. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1990. http://dx.doi.org/10.4095/130892.

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