Academic literature on the topic 'IP-10'

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Journal articles on the topic "IP-10"

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Ruffilli, I., S. Ferrari, M. Colaci, C. Ferri, P. Fallahi, and A. Antonelli. "IP-10 in Autoimmune Thyroiditis." Hormone and Metabolic Research 46, no. 09 (June 30, 2014): 597–602. http://dx.doi.org/10.1055/s-0034-1382053.

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Yamashita, T., H. Akamatsu, A. Tomitaka, Y. Ogawa, N. Sugawara, and K. Matsunaga. "IP-10 in atopic dermatitis." Allergy 58, no. 3 (March 2003): 261. http://dx.doi.org/10.1034/j.1398-9995.2003.00062_2.x.

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Bai, Xiyuan, Kathryn Chmura, Alida R. Ovrutsky, Russell P. Bowler, Robert I. Scheinman, Rebecca E. Oberley-Deegan, Haiying Liu, Shaobin Shang, Diane Ordway, and Edward D. Chan. "Mycobacterium tuberculosis increases IP-10 and MIG protein despite inhibition of IP-10 and MIG transcription." Tuberculosis 91, no. 1 (January 2011): 26–35. http://dx.doi.org/10.1016/j.tube.2010.11.005.

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Cornberg, Markus, and Steffen B. Wiegand. "ImPortance of IP-10 in hepatitis B." Antiviral Therapy 21, no. 2 (2015): 93–96. http://dx.doi.org/10.3851/imp3014.

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Nadimi, A. E. "477 IP-10 AND ACUTE MYOCARDIAL INFARCTION." Atherosclerosis Supplements 12, no. 1 (June 2011): 101–2. http://dx.doi.org/10.1016/s1567-5688(11)70478-0.

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Uruha, A., S. Noguchi, W. Sato, H. Nishimura, S. Mitsuhashi, T. Yamamura, and I. Nishino. "Plasma IP-10 level distinguishes inflammatory myopathy." Neuromuscular Disorders 25 (October 2015): S249. http://dx.doi.org/10.1016/j.nmd.2015.06.234.

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Uruha, Akinori, Satoru Noguchi, Wakiro Sato, Hiroaki Nishimura, Satomi Mitsuhashi, Takashi Yamamura, and Ichizo Nishino. "Plasma IP-10 level distinguishes inflammatory myopathy." Neurology 85, no. 3 (July 1, 2015): 293–94. http://dx.doi.org/10.1212/wnl.0000000000001767.

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Jabeen, Talat, Philip Leonard, Haryati Jamaluddin, and K. Ravi Acharya. "Structure of mouse IP-10, a chemokine." Acta Crystallographica Section D Biological Crystallography 64, no. 6 (May 14, 2008): 611–19. http://dx.doi.org/10.1107/s0907444908007026.

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Yang, Chun-Kang, Dao-Da Chen, Yuan Tian, and Jing-Hui Zhang. "Chemokine IP-10 produced by colorectal carcinoma." World Chinese Journal of Digestology 11, no. 11 (November 15, 2003): 1703–5. http://dx.doi.org/10.11569/wcjd.v11.i11.1703.

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TAKAKU, Y., T. KOBAYASHI, T. SOMA, K. HAGIWARA, M. KANAZAWA, and M. NAGATA. "IP-10 Induces Eosinophil Superoxide Anion Generation." Journal of Allergy and Clinical Immunology 121, no. 2 (February 2008): S46. http://dx.doi.org/10.1016/j.jaci.2007.12.186.

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Dissertations / Theses on the topic "IP-10"

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Muñoz, Roldan Melba Lucia. "Interferon gamma inducible protein 10 (IP-10) and regulatory T Cells in leishmaniasis." College Park, Md.: University of Maryland, 2007. http://hdl.handle.net/1903/7336.

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Thesis (M.S.) -- University of Maryland, College Park, 2007.
Thesis research directed by: Dept. of Cell Biology and Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Beier, Stefanie [Verfasser]. "Entwicklung eines IP-10 Bioassays zur Bestimmung der Interferon Sensitivität / Stefanie Beier." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2007. http://d-nb.info/1022580183/34.

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Campos, Mauricio de Souza. "Níveis de citocinas plasmáticas em indivíduos com hepatite b crônica naive e sob tratamento antiviral." Instituto de Ciências da Saúde, 2014. http://repositorio.ufba.br/ri/handle/ri/17932.

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Submitted by ROBERTO PAULO CORREIA DE ARAÚJO (ppgorgsistem@ufba.br) on 2015-07-17T18:21:40Z No. of bitstreams: 1 CAMPOS, Maurício de Souza.pdf: 2732552 bytes, checksum: 0aae28f6faaa3ad7fd787acbca547eea (MD5)
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PRONEX e CAPES
Introdução: A infecção pelo vírus da hepatite B (HBV) compreende um amplo espectro de quadros clínicos que vai desde a manifestação aguda e autolimitada até a forma crônica, com possibilidade de desenvolvimento de cirrose hepática e carcinoma hepatocelular. A proteína 10 induzida por INF-γ (IP-10) é uma quimiocina CXC que pode ser secretada pelos hepatócitos e endotélio sinusoidal no fígado de pacientes com hepatite viral. Por ligação ao receptor CXCR3, IP-10 exerce efeito quimiotático em células NK, células T ativadas e células dendríticas, modulando, dessa forma, a resposta imunológica. Sabe-se que o IFN-γ estimula a secreção de IP-10 por células infectadas pelo vírus da hepatite C, mas no contexto da infecção pelo HBV, essa relação ainda é pouco conhecida. Objetivo: descrever os níveis das citocinas e quimiocinas séricas em pacientes com hepatite B crônica naive e sob tratamento antiviral. Material e métodos: foi realizada a dosagem de citocinas séricas de 24 voluntários com hepatite B crônica em tratamento e 33 voluntários com hepatite B crônica naive, utilizando o kit de CBA (Citokine Beads Array) da eBioscience e análise em FACScalibur BD. A citocina IP-10 foi quantificada utilizando o kit CBA da empresa BD conforme padronização prévia e recomendação do fabricante, e também analisada em FACScalibur BD. Os softwares SPSS versão 18 e GraphPad versão 6 foram utilizados para análise estatística. Resultados: foram encontradas diferenças estatísticas na comparação dos níveis de IP-10, IL-5 e TGF – β entre indivíduos com hepatite B crônica tratados e naive. Foram encontrados valores mais elevados de citocinas Th1 no soro de pacientes naive, quando comparados aos pacientes tratados. Os níveis séricos de IP-10 nos pacientes tratados e não tratados são mais elevados que os de INF-γ. Conclusão: os níveis séricos de citocinas Th1 entre pacientes não tratados estavam mais elevados do que em pacientes tratados. A amplitude dos níveis de INFγ foi maior nas amostras dos indivíduos com hepatite B sem tratamento. A correlação entre os níveis de INFγ e IL- 10 foi inversa em amostras de indivíduos não tratados. O tratamento pareceu modular a produção de INFγ sem interferir nos níveis de IP-10 e IL-10. A correlação entre os níveis de IP-10 e IL-10 também foi inversa em amostras de indivíduos não tratados. A IP-10 pode ser um marcador de maior sensibilidade que o INF-gama anteriormente descrito como a citocina chave no processo inflamatório na HBV
Background: infection with the hepatitis B virus(HBV) comprises a broad spectrum of clinical presentations ranging from acute and self-limited to the chronic form, with the possibility of development of liver cirrhosis and hepatocellular carcinoma. The protein10 induced by INF-γ(IP-10) is a CXC chemokine that can be secreted by hepatocytes and sinusoidal endothelium in the liver of patients with viral hepatitis. By binding to CXCR3 receptor, IP-10 exerts a chemotactic effect on NK cells, activated T cells and dendritic cells, potentializing, thus, the immune response. It is known that IFN-γ stimulates IP-10 secretion by cells infected with hepatitis C, but in the context of HBV infection, this relationship is still poorly known. Aim: to describe the levels of cytokines and chemokines in serum patients with chronic hepatitis B naïve and under antiviral treatment. Methods: the dosage of serum cytokines of 24 volunteers with chronic hepatitis B treatment and 33 volunteers with chronic hepatitis B naïve was performed using the CBA kit (Citokine Beads Array) from eBioscience and analyzed using FACScalibur BD. IP-10 cytokine was quantified using the CBA kit from BD company as previous standardization and recommendation of the manufacturer and also analyzed using FACScalibur BD. The SPSS software version 18 and GraphPad version 6 were used for statistical analysis. Results: statistical differences were found when comparing the IP-10 levels, IL-5 and TGF-β among individuals with chronic hepatitis B treated and naive. Higher values of Th1cytokines were found in the serum of treated patients when compared to naïve patients. The IP-10 serum levels in treated and untreated patients are higher than those of INF-γ. Conclusion: the serum levels of Th1cytokines from untreated patients were higher than in patients treated. The breadth of the INFγ levels were higher in samples of individuals without hepatitis B treatment. The correlation between the levels of INFγ and IL-10 was reverse on samples from untreated individuals. The treatment appeared to modulate INFγ production without interfering on IP-10and IL-10 production levels. The correlation between the IP-10 and IL-10 levels was also reverse in samples of untreated individuals. IP-10 may be a higher sensibility marker than the INFγ priorly described as a key cytokine in the inflammatory process in hepatitis B.
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Alsleben, Neele. "Der Biomarker IP-10 für die Diagnose der aktiven Tuberkulose und der latenten Tuberkuloseinfektion im Kindesalter." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168313.

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Einleitung: Zur in-vitro Diagnostik der Tuberkulose (TB) und latenten TB Infektion (LTBI) im Kindesalter werden derzeit zunehmend „Interferon-gamma (IFN-γ) release assays“ (IGRA) verwendet. Die Sensitivität der IGRA insbesondere im Kindesalter ist umstritten. Auch eine diagnostische Unterscheidung zwischen TB und LTBI ist mittels IGRA und anderen bisherigen basierten Testverfahren nicht möglich. In vorangegangen Studien zeigte sich der Biomarker „IFN-γ-inducible-protein-10“ (IP-10) als viel versprechend zur Diagnose der TB und LTBI. Ziele: In der vorliegenden Dissertationsschrift wurden die IP-10-Plasmakonzentrationen von Kindern mit TB, LTBI, Atemwegsinfektion (AWI) oder nicht-tuberkulöse Mykobakterien (NTM)-Erkrankung ohne Stimulation der Proben, nach unspezifischer Mitogen-Stimulation und nach spezifischer Mycobacterium tuberculosis (M. tuberculosis)-Antigen-Stimulation bestimmt. Die Antigen-stimulierten IP-10-Plasmakonzentrationen der TB- und LTBI-Gruppe wurden mit denen der NTM- und AWI-Gruppe verglichen. Darüberhinaus wurde beurteilt, ob eine Unterscheidung zwischen TB und LTBI anhand der IP-10-Plasmakonzentration möglich ist. Außerdem wurde die Konkordanz und Korrelation zwischen dem IP-10-ELISA und QuantiFERON® -TB Gold In-Tube (QFT-IT) Test beurteilt und untersucht, ob der Biomarker IP-10 altersabhängig sezerniert wird. Material & Methoden: 48 Kinder wurden in die Studie eingeschlossen. Das mittlere Alter der Studienteilnehmer war 54 Monate. Alle Studienteilnehmer wurden zuvor in Deutschland entweder mit einer TB (n=11), LTBI (n=14), NTM (n=8) oder AWI (n=15) diagnostiziert. Unabhängig von der vorliegenden Studie wurden bei allen teilnehmenden Kindern IFN-γ-Werte mittels des QFT-IT-Testes bestimmt. Im Rahmen des QFT-IT wurden die für den Test notwendigen Blutproben entweder nicht stimuliert, mit einer unspezifischen Mitogenen-Substanz oder mit spezifischen M.tuberculosis-Antigenen stimuliert. Die jeweiligen Plasma-Überstände wurden asserviert und zur Bestimmung von IP-10 verwendet. Die IP-10-Konzentrationen wurden, in Zusammenarbeit mit dem Klinischen Forschungszentrums der Universität von Kopenhagen, mittels einem zu Forschungszwecken entwickelten ELISAs gemessen. Ergebnisse: Die IP-10-Plasmakonzentrationen ohne Stimulation, mit unspezifischer Mitogen- und spezifischer Antigen-Stimulation betrug für die TB-Gruppe 704 pg/ml, 12.966 pg/ml und 12.702 pg/ml; für die LTBI-Gruppe 366,5 pg/ml, 10.232 pg/ml und 9.109 pg/ml; für die NTM-Gruppe 309 pg/ml, 11.197 pg/ml und 97 pg/ml; und für die AWI-Gruppe 694 pg/ml, 5.401 pg/ml und 84 pg/ml. Es konnte kein signifikanter Unterschied zwischen der IP-10-Konzentration der TB- und LTBI-Gruppe festgestellt werden (p-Wert= 0,24). Die IP-10- und IFN-γ- Plasmakonzentrationen der Kinder mit TB und LTBI korrelierten stark miteinander (rsp=0,65; p-Wert = 0,03 und rsp=0,79; p-Wert < 0,001). Der IP-10-ELISA und QFT-IT Test zeigten ebenso eine hohe Konkordanz (κ =0,96). Die IP-10-Sekretion war 18fach höher im Vergleich zur IFN-γ-Sekretion. Es konnte keine Korrelation zwischen dem Alter und der Mitogen-stimulierten IP-10-Konzentration nachgewiesen werden. Schlussfolgerungen: Die IP-10-Plasmakonzentration von Kindern mit TB und LTBI im Vergleich zu Kindern mit NTM und AWI ist signifikant nach spezifischer M.tuberculosis-Antigen-Stimulation erhöht (p-Wert > 0,001). Die qualitativen und quantitativen Testergebnisse des IP-10-ELISAs korrelieren stark mit denen des QFT-IT-Testes. Im Vergleich zu IFN-γ scheint IP-10 in höheren Konzentrationen und möglicherweise unabhängig vom Alter sezerniert zu werden. Das legt die Vermutung nahe, dass IP-10 zur Diagnose der TB und LTBI im Kindesalter in Zukunft Verwendung finden könnte.
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Enderlin, Marta. "Evaluation of IP-10 and TNFalpha-transducing parvoviral vectors as antitumoral agents in animal glioblastoma models." [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11759090.

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Carew, Jennifer S., Claudia M. Espitia, Weiguo Zhao, Monica M. Mita, Alain C. Mita, and Steffan T. Nawrocki. "Oncolytic reovirus inhibits angiogenesis through induction of CXCL10/IP-10 and abrogation of HIF activity in soft tissue sarcomas." IMPACT JOURNALS LLC, 2017. http://hdl.handle.net/10150/625966.

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The tumor-selective viral replication capacity and pro-apoptotic effects of oncolytic reovirus have been reported to be dependent on the presence of an activated RAS pathway in several solid tumor types. However, the mechanisms of selective anticancer efficacy of the reovirus-based formulation for cancer therapy (Reolysin, pelareorep) have not been rigorously studied in soft tissue sarcomas (STS). Here we report that Reolysin triggered a striking induction of the anti-angiogenic chemokine interferon-gamma-inducible protein 10 (IP-10)/CXCL10 (CXC chemokine ligand 10) in both wild type and RAS mutant STS cells. Further analysis determined that Reolysin treatment possessed significant anti-angiogenic activity irrespective of RAS status. In addition to CXCL10 induction, Reolysin dramatically downregulated the expression of hypoxia inducible factor (HIF)-1 alpha, HIF-2 alpha and inhibited vascular endothelial growth factor (VEGF) secretion. CXCL10 antagonism significantly diminished the anti-angiogenic effects of Reolysin indicating that it is a key driver of this phenomenon. Xenograft studies demonstrated that Reolysin significantly improved the anticancer activity of the anti-angiogenic agents sunitinib, temsirolimus, and bevacizumab in a manner that was associated with increased CXCL10 levels. This effect was most pronounced following treatment with Reolysin in combination with temsirolimus. Further analysis in additional sarcoma xenograft models confirmed the significant increase in CXCL10 and increased anticancer activity of this combination. Our collective results demonstrate that Reolysin possesses CXCL10-driven anti-angiogenic activity in sarcoma models, which can be harnessed to enhance the anticancer activity of temsirolimus and other agents that target the tumor vasculature.
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Hubel, Silvia [Verfasser]. "Untersuchung der Biomarker Interferon-gamma induziertes Protein 10 (IP-10) und CXC-Motiv-Chemokinrezeptor 3 (CXCR3) im Plasma nierentransplantierter Patienten in den ersten fünfzehn Monaten nach Transplantation / Silvia Hubel." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1218073640/34.

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Rose, Thomas [Verfasser]. "IFNα and its response proteins, IP-10 and SIGLEC-1, are biomarkers of disease activity in systemic lupus erythematosus / Thomas Rose." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1052222056/34.

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Alsleben, Neele [Verfasser], and Holger [Akademischer Betreuer] Rüssmann. "Der Biomarker IP-10 für die Diagnose der aktiven Tuberkulose und der latenten Tuberkuloseinfektion im Kindesalter / Neele Alsleben. Betreuer: Holger Rüssmann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1050647890/34.

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Su, Yung-Chang University of New South Wales &amp Garvan Institute of Medical Research St Vincent's Clinical School UNSW. "Immune regulation in mouse models of allergic asthma." Awarded by:University of New South Wales & Garvan Institute of Medical Research. St. Vincent's Clinical School, 2006. http://handle.unsw.edu.au/1959.4/26978.

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Allergic asthma is an immunological disease, mediated by CD4+ Th2 cells, and its prevalence has increased over recent decades. Features of allergic asthma include airway hyperresponsiveness (AHR), airway eosinophilia, excessive airway mucus production, and increased IgE and Th2 cytokine levels. Airway remodeling with pulmonary fibrosis is noted in the progress of asthma. In this thesis, a murine model of allergic asthma was used to investigate the effect of cyclophosphamide (CY) on asthma and the involvement of regulatory T cells (Treg), and the role of Granulocyte-macrophage colony stimulating-factor (GM-CSF) in allergic asthma by using GM-CSF knockout mice. CY is a cytotoxic agent, which paradoxically augments several immune responses. The first part of this thesis was aimed to study the effects of CY in a murine model of allergic airway inflammation. BALB/c mice were immunized with ovalbumin (OVA) on days 0 and 14, and challenged with aerosolized OVA from days 21 to 27. Some mice additionally received CY on days -2 and 12. In the CY-treated animals, pronounced worsening of inflammatory features was noted, including increases in eosinophil infiltration, epithelial thickness, mucus occlusion and eosinophil numbers in bronchoalveolar lavage fluid (BALF). Increased total and OVA-specific serum IgE were also noted in the CY-treated animals. In cell cultures from peritracheal lymph nodes, the Th2 cytokines IL-4 and IL-5 were elevated in animals treated with CY. It was hypothesized that the effects of CY could be caused by reduced immunosuppression mediated by Treg. mRNA expression of the immunosuppressive cytokines IL-10 and TGF-beta was reduced in the lungs of CY-treated mice. The expression of FoxP3, a marker of naturally occurring Treg, was significantly reduced in spleens, thymuses and peritracheal lymph nodes after the second injection of CY, and in the lung tissue after allergen challenge in CY-treated mice. Furthermore, lung IL-10-producing CD4+ T cells and CTLA-4+-bearing CD4+ T cells were reduced after allergen aerosol challenge in CY-treated mice. Thus CY worsened the features of allergic pulmonary inflammation in this model, in association with increased production of IgE and Th2 cytokines. The reduction in expression of FoxP3 and immunosuppressive cytokines by CY suggests that toxicity to Treg may contribute to the increased inflammation. GM-CSF plays a role in the growth, development, and maturation of bone marrow hemopoietic cells into mature blood cells, and has been proposed to be involved in potentiating the function of inflammatory cells in allergic inflammation. In the second part of this thesis, GM-CSF knockout (KO) mice were used to investigate the role of GM-CSF. In allergic KO mice, airway eosinophils were only shown in the perivascular, but not peribronchial areas in the lung, compared to the allergic wild-type (WT) mice in which eosinophil infiltration appeared in both areas. Eosinophil numbers were drastically reduced in the bronchoalveolar lavage fluid (BALF) of KO mice. IL-5 production in the lung tissue and BALF in allergic KO mice was reduced; similar results were also found in peritracheal draining lymph nodes after in vitro stimulation assays. However, IL-4 and IL-13 production, airway hyperresponsiveness (AHR), and serum IgE production were not affected in allergic KO mice. Surprisingly, lung IFN-gamma mRNA and BALF levels were increased in allergic KO mice. Lung mRNA levels of CCR3, a key chemokine receptor on eosinophils, were significantly reduced in allergic KO mice, whereas expression of the chemokines eotaxin and RANTES were at similar levels in allergic KO and WT mice. Lung mRNA levels of the IFN-gamma-inducible chemokines Mig (CXCL9) and IP-10 (CXCL10), which are antagonists of CCR3, and their receptor CXCR3 were increased in allergic KO mice, compared with allergic WT mice. Data obtained from flow cytometry showed more eosinophils survived in the lung of WT mice than KO mice. Another allergy model, a peritoneal allergy model was performed to investigate inflammation in a different model. Leukocyte subpopulations such as neutrophils, eosinophils, macrophages, and lymphocytes were reduced in the peritoneal lavage fluid of allergic KO mice. The findings revealed that GM-CSF is essential for IL-5 production, pulmonary airway eosinophilia and eosinophil survival. In the absence of GM-CSF, over-production of IFN-???? may induce chemokines, including Mig and IP-10, which are antagonists for CCR3 and may reduce airway eosinophil infiltration. In this thesis, a murine model of allergic asthma has been used to obtain novel findings on the regulation of allergic inflammation. The results with CY are relevant to the treatment of asthma patients with CY and other cytotoxic agents. The findings in the GM-CSF KO mice suggest that GM-CSF is a potential therapeutic target in asthma, and that in assessment of new therapeutic agents for asthma, effects on GM-CSF should be considered.
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Books on the topic "IP-10"

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Martini, Frederic H. Anatomy and Physiology with IP-10. Pearson Education, Limited, 2008.

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Choraś, Ryszard S., and Michał Choraś. Image Processing and Communications Challenges 10: 10th International Conference, IP&C’2018 Bydgoszcz, Poland, November 2018, Proceedings. Springer, 2018.

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Jones, Alison, and Brenda Sufrin. 12. Licensing Agreements and other Agreements Involving Intellectual Property Rights. Oxford University Press, 2016. http://dx.doi.org/10.1093/law/9780198723424.003.0012.

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All books in this flagship series contain carefully selected substantial extracts from key cases, legislation, and academic debate, providing able students with a stand-alone resource. This chapter examines some of the different types of intellectual property rights (IPRs) before outlining the relationship between intellectual property and both EU competition law and the EU free movement rules. It focuses, however, on IP licensing agreements and their treatment under Article 101. The chapter is organized as follows. Section 3 traces the development of EU competition policy to IP licensing agreements. Sections 4 and 5 examine the current Technology Transfer Block Exemption, Regulation 772/2004 (TTBER) and the Guidelines in detail (noting where significant changes might occur in 2014). Sections 6, 7, and 8 deal with trade mark licences, trade mark delimitation agreements, and copyright (other than software) licences not covered by the TTBER and Guidelines. Section 9 outlines issues arising in cases involving IPRs under Article 102, while Section 10 concludes.
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Claudio, Chiarolla. Part II Commercial Aspects of the Marine Environment, 10 The Work of WIPO and Its Possible Relevance for Global Ocean Governance. Oxford University Press, 2018. http://dx.doi.org/10.1093/law/9780198823964.003.0010.

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This chapter focuses on the work of the World Intellectual Property Organization (WIPO) and its possible relevance for global ocean governance. It first provides a background on WIPO and its activities, legal foundations and mandate before asking whether there is a place for intellectual property (IP) considerations in regard to global ocean governance. It then considers what role, if any, WIPO should play, as the competent UN agency responsible for the development of a balanced and effective international IP system, in strengthening the contribution of IP to the global governance of oceans, in line with Sustainable Development Goals 14 (Life below water). It also describes some key areas of overlap and possible interrelationships between global ocean governance and the work of WIPO from both normative and practical standpoints. Finally, it reflects on WIPO’s future role in the context of the evolving sustainable ocean governance.
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Book chapters on the topic "IP-10"

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Appleton, Kathryn M., Ian Cushman, Yuri K. Peterson, Balachandran Manavalan, Shaherin Basith, Sangdun Choi, Akihiro Kimura, et al. "IP-10." In Encyclopedia of Signaling Molecules, 972. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100667.

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Drabe, Camilla Heldbjerg, Thomas Blauenfeldt, and Morten Ruhwald. "ELISA-Based Assay for IP-10 Detection from Filter Paper Samples." In Cytokine Bioassays, 27–37. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0928-5_3.

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Hallevy, Gabriel. "AI vs. IP." In Artificial Intelligence and the Law, 222–46. Milton Park, Abingdon, Oxon ; New York, NY : Routledge, 2021.: Routledge, 2020. http://dx.doi.org/10.4324/9780429344015-10.

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Brandacher, Gerald, S. Schneeberger, R. Öllinger, W. Steurer, R. Margreiter, E. R. Werner, and G. Werner-Felmayer. "Chemokinexpression von I-TAC, IP-10 und MIG in murinen Herztransplantaten wird nicht beeinflusst durch Cyclosporin-A." In Deutsche Gesellschaft für Chirurgie, 373–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_103.

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Brandacher, G., S. Schneeberger, R. Öllinger, W. Steurer, R. Margreiter, E. R. Werner, and G. Werner-Felmayer. "Chemokinexpression von I-TAC, IP-10 und MIG in murinen Herztransplantaten wird nicht beeinflusst durch Cyclosporin-A." In Zurück in die Zukunft, 517–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_335.

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Liu, M. T., B. P. Chen, P. Oertel, M. J. Buchmeier, T. A. Hamilton, D. A. Armstrong, and T. E. Lane. "The CXC Chemokines IP-10 and Mig are Essential in Host Defense Following Infection with a Neurotropic Coronavirus." In Advances in Experimental Medicine and Biology, 323–27. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_48.

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Nematollahi, Mohammad Ali, Chalee Vorakulpipat, and Hamurabi Gamboa Rosales. "Hardware IP Watermarking." In Digital Watermarking, 181–90. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-2095-7_12.

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Belabas, K., and Henri Cohen. "Binary cubic forms and cubic number fields." In AMS/IP Studies in Advanced Mathematics, 191–219. Providence, Rhode Island: American Mathematical Society, 1997. http://dx.doi.org/10.1090/amsip/007/10.

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Bhardwaj, Anshu, and Subir Kumar Roy. "Defeating HaTCh: Building Malicious IP Cores." In Communications in Computer and Information Science, 345–53. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-7470-7_34.

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Mandhar, Vipul, and Virender Ranga. "IP Traceback Schemes for DDoS Attack." In Networking Communication and Data Knowledge Engineering, 37–50. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4585-1_4.

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Conference papers on the topic "IP-10"

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Hong, Ji Young, Gyeong Seo Jung, Young Mi Kim, Sang Nae Cho, Ji Ye Jung, Byung Hoon Park, Moo Suk Park, et al. "Efficacy Of IP-10 For The Diagnosis Of Tuberculosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4732.

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Petrone, Linda, Elisa Petruccioli, Valentina Vanini, Teresa Chiacchio, Gilda Cuzzi, Fabrizio Palmieri, Giuseppe Ippolito, and Delia Goletti. "Evaluation of IP-10 in IGRA for LTBI diagnosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5271.

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Bai, Xiyuan, Kathryn Chmura, Alida Ovrutsky, Russell P. Bowler, Robert Scheinman, Rebecca E. Oberley-Deegan, Shaobin Shang, Diane Ordway, and Edward D. Chan. "Mycobacterium Tuberculosis Increases Interferon-Gamma Inducible Protein-10 (Ip-10) And Monokine Induced By Interferon-Gamma (MIG) Protein Despite Inhibition Of Ip-10 And Mig Gene Transcription." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3344.

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Ragchaa, Byambajav, Liji Wu, Xiangmin Zhang, and Honghao Chu. "Analog sub-circuits for 10 bit, 2.5Msps ADC IP core." In 2018 14th IEEE International Conference on Solid-State and Integrated Circuit Technology (ICSICT). IEEE, 2018. http://dx.doi.org/10.1109/icsict.2018.8564890.

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Rao, Nageswara S. V., Stephen W. Poole, Susan E. Hicks, Chris Kemper, Steve Hodson, Greg Hinkel, and Josh Lothian. "Experimental study of wide-area 10 Gbps IP transport technologies." In MILCOM 2009 - 2009 IEEE Military Communications Conference. IEEE, 2009. http://dx.doi.org/10.1109/milcom.2009.5379777.

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Mazumdar, Kaushik, and Ananya Ghorai. "Power Optimized 10 Bit ADC IP Design in Transistor Level." In 2021 Devices for Integrated Circuit (DevIC). IEEE, 2021. http://dx.doi.org/10.1109/devic50843.2021.9455816.

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Strzelak, Agnieszka, Anna Komorowska-Piotrowska, Agnieszka Borowa, Maria Krasińska, Wojciech Feleszko, and Marek Kulus. "IP-10 decreases during antituberculous treatment in children with active tuberculosis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.5302.

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Gueble, Matthew, Carole Holm, Nicole Grant, Lois Ravage-Mass, Terri-Dawn Levesh, Jean Estrom, Eleni Kapagiannidou, et al. "Proinflammatory cytokines and IP-10 differentiate neutrophilic and eosinophilic asthma subgroups." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa908.

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Wang, Li, Yun Niu, Liji Wu, and Xiangmin Zhang. "Design of an IPSec IP-Core for 10 Gigabit Ethernet Security Processor." In 2010 10th IEEE International Conference on Solid-State and Integrated Circuit Technology (ICSICT). IEEE, 2010. http://dx.doi.org/10.1109/icsict.2010.5667343.

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Yoshino, Takeshi, Yutaka Sugawara, Katsushi Inagami, Junji Tamatsukuri, Mary Inaba, and Kei Hiraki. "Performance optimization of TCP/IP over 10 Gigabit Ethernet by precise instrumentation." In 2008 SC - International Conference for High Performance Computing, Networking, Storage and Analysis. IEEE, 2008. http://dx.doi.org/10.1109/sc.2008.5215913.

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