Relevant bibliographies by topics / Interferon

Academic literature on the topic 'Interferon'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Interferon"

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Simpson, S. "Interfering with Interferon." Science's STKE 2007, no. 376 (February 28, 2007): tw81. http://dx.doi.org/10.1126/stke.3762007tw81.

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Polyak, Stephen J. "Interfering with interferon." Trends in Microbiology 7, no. 10 (October 1999): 401. http://dx.doi.org/10.1016/s0966-842x(99)01592-9.

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Bucci, Mirella. "Interfering with Interferon." Nature Chemical Biology 10, no. 5 (April 17, 2014): 324. http://dx.doi.org/10.1038/nchembio.1511.

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Martz, Lauren. "Interfering with interferon." Science-Business eXchange 6, no. 16 (April 2013): 381. http://dx.doi.org/10.1038/scibx.2013.381.

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Harris, Bethany D., Srilalitha Kuruganti, Ashlesha Deshpande, Paul A. Goepfert, W. Winn Chatham, and Mark R. Walter. "Characterization of Type-I IFN subtype autoantibodies and activity in SLE serum and urine." Lupus 29, no. 9 (July 1, 2020): 1095–105. http://dx.doi.org/10.1177/0961203320935976.

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Background/objective Type-I interferons contribute to pathogenesis in systemic lupus erythematosus, including nephritis. Interferons consist of a family of 16 proteins yet are often characterized in patients without knowledge of the specific interferon subtypes involved. Different interferons may function in the kidneys, and other organs, relative to what is often measured in patient blood. Moreover, antibodies to interferons may potentially modulate systemic or organ-specific interferon activity. The aim of this study was to characterize global interferon activity levels and identify autoantibodies to the 12 interferon α subtypes in patient serum and urine. Methods Interferon activity levels in serum and urine were measured using an interferon bioassay. Anti-interferon and anti-cytokine autoantibodies were measured by ELISA. Serum and urine samples were also characterized for their ability to neutralize the biological activity of exogenously added interferons. Results Serum interferon activity was increased in 62% of systemic lupus erythematosus patient samples, relative to healthy donor controls, whereas binding interferon α autoantibodies to at least one interferon α subtype were found in 68% of the samples evaluated. High Systemic Lupus Erythematosus Disease Activity Index scores were significantly ( p = 0.001) associated with patient samples containing interferon α autoantibodies to three or more interferon α subtypes in their serum. Interferon α autoantibodies that potently block interferon activity were rare (∼5% of samples), but collectively bound to all 12 interferon α subtypes. Urine interferon activity and interferon α autoantibody profiles did not correlate with their serum counterparts, suggesting immune responses in systemic lupus erythematosus kidneys can be distinct from those measured in serum. Analysis of autoantibodies to 15 additional cytokines in serum identified higher frequencies of granulocyte-macrophage colony-stimulating factor and interleukin 17A autoantibodies, suggesting these signaling pathways may potentially contribute, with interferons, to systemic lupus erythematosus pathogenesis. Conclusions The measurement of autoantibodies to multiple interferon subtypes in serum and urine may provide an alternative method for following interferon-mediated systemic lupus erythematosus disease activity. The results suggest autoantibodies might be used for patient monitoring and/or identifying additional cytokine signaling pathways that are functioning in different systemic lupus erythematosus patients.
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Barinaga, M. "Immunology. Interfering with interferon." Science 259, no. 5102 (March 19, 1993): 1693–94. http://dx.doi.org/10.1126/science.8456294.

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Smith, Geoffrey L., Julian A. Symons, and Antonio Alcamı́. "Poxviruses: Interfering with Interferon." Seminars in Virology 8, no. 5 (April 1998): 409–18. http://dx.doi.org/10.1006/smvy.1997.0145.

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REVEL, MICHEL, ASHER ZILBERSTEIN, ROSE MARIA RUGGIERI, MENACHEM RUBINSTEIN, and LUISA CHEN. "Autocrine Interferons and Interferon-β2." Journal of Interferon Research 7, no. 5 (October 1987): 529–36. http://dx.doi.org/10.1089/jir.1987.7.529.

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MENKES, DAVID B., and JAMES A. MacDONALD. "Interferons, serotonin and neurotoxicity." Psychological Medicine 30, no. 2 (March 2000): 259–68. http://dx.doi.org/10.1017/s0033291799001774.

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Background. Interferons are a class of cytokines profoundly affecting immune function. Several interferons are now synthesized and used clinically, notably for viral diseases and cancer. In addition to their desired immune effects, interferons cause a number of toxicities, including prominent effects on the nervous system.Methods. This literature review focused on the incidence of depression associated with interferon treatment. Possible neurochemical mechanisms and remedial strategies were also considered.Results. Interferon treatment, particularly with the alpha subtype, is unquestionably linked with depression, but the strength of association is uncertain because of erratic ascertainment and pre- treatment co-morbidity. A likely pathogenic mechanism has been described, involving interferon suppression of serotonin synthesis. Controlled treatment trials of interferon-induced depression are not yet available.Conclusions. Neurotoxicity substantially limits the use of interferons. At least some of the risk of depression appears to derive from their anti-serotonergic effects, consistent with the large body of evidence pointing to a general link between serotonin and affective illness. Vigilant detection and aggressive treatment of depression is necessary to optimize interferon treatment of many patients.
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de Lemos, Livia Pires, Augusto Guerra, Ramon Pereira, Rosangela Gomes, Isabella Godói, Isabela Diniz, Ivan Zimmermann, et al. "OP40 First Case Of Disinvestment Using Real-World Evidence In Brazil." International Journal of Technology Assessment in Health Care 33, S1 (2017): 18–19. http://dx.doi.org/10.1017/s0266462317001349.

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INTRODUCTION:Beta-interferons are used as first-line therapy for relapsing-remitting multiple sclerosis in Brazil. In order to evaluate the possible inferiority of one of the beta-interferons available and support a guideline update, we conducted an eleven-year (January 2000 to December 2010) nationwide real-world performance assessment using the Unified Health System (SUS) databases.METHODS:We assessed whether patients using subcutaneous beta-interferon switched treatment, relapsed or died (composite event) earlier than patients using intramuscular beta-interferons. Patients without a dispensing registry longer than three months were censored. We used the Kaplan-Meier method to estimate the cumulative probability of persistence on initial treatment, and compared groups with the Log-rank test. The influence of the drug on the occurrence of event was assessed with Cox proportional hazards analysis.RESULTS:The number of patients included was 12,154, and the majority started treatment with subcutaneous beta-interferon-1a (45.7 percent), followed by subcutaneous beta-interferon-1b (27.7 percent) and by intramuscular beta-interferon (26.6 percent). Women represented 73.1 percent and the mean age was 38.93±11.34 years old. The group of patients who used intramuscular beta-interferon switched treatment, relapsed or died earlier (median 47 months; 95 percent Confidence Interval, CI 44–52) than patients using the subcutaneous beta-interferons, (69 months (95 percent CI 64–76) for beta- interferon 1a and 73 (95 percent CI 66–84) months for beta-interferon 1b) (p< .0001 for both comparisons). Accordingly, the use of intramuscular beta-interferon was associated with a higher probability of event (Hazard ratio, HR 1.38; 95 percent CI 1.29-1.48), while the use of the other beta-interferons had a protective effect (1a: HR .86; 95 percent CI .81-.92; 1b: HR .89; 95 percent CI .83-.95).CONCLUSIONS:The inferiority of intramuscular beta-interferon found in the real-world corroborates findings from head-to-head studies and systematic reviews conducted by Cochrane and the National Commission for Technology Incorporation in SUS (CONITEC/Brazil). This result led to disinvestment in intramuscular beta-interferon and was the first case of clinical guideline update using real-world evidence in Brazil.
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Dissertations / Theses on the topic "Interferon"

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Short, John A. L. "Defective interfering particles of parainfluenza virus subtype 5 and interferon induction." Thesis, University of St Andrews, 2015. http://hdl.handle.net/10023/7036.

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The innate immune response is the first line of defence against virus infection. Cells contain a diverse array of pathogen recognition receptors (PRRs) that are able to recognise multiple pathogen associated molecular patterns (PAMPS) that present themselves during virus infection. The RIG-I (Retinoic acid inducible–gene-I) and MDA5 (melanoma differentiation- associated gene 5) PRRs detect specific viral RNA ligands and subsequently induce the expression of the cytokine Interferon-β(IFN-β). IFN-βis secreted, acting on the infected cell and neighbouring uninfected cells to generate an antiviral state that is hostile to virus transcription, replication and dissemination, whilst also orchestrating adaptive immune responses. Given IFN-βs crucial cellular antiviral role, understanding its induction is of great importance to developing future antiviral drugs and vaccine strategies. Using A549 reporter cells in which GFP expression is under the control of the IFN-βpromoter, we show that there is a heterocellular response to parainfluenza virus 5 (PIV5) and infection with other negative sense RNA viruses. Only a limited number of infected cells are responsible for IFN-βinduction. Using PIV5 as a model, this thesis addresses the nature of the PAMPs that are responsible for inducing IFN-βfollowing PIV5 infection. The previous work has shown that PIV5 Defective Interfering particle (DI) rich virus preparations acted as a better inducer of IFN-βcompared to DI poor stocks. DIs are incomplete virus genomes produced during wild-type virus replication as a result of errors in the viral polymerase. To investigate this further, A549 Naïve, MDA5/RIG-I/LGP2 Knock down reporter cells were infected with PIV5 W3 at a low MOI to examine the inverse correlation of NP and GFP of DIs generated during virus replication and not from the initial infection. GFP+ve cells were cell sorted, and using QPCR it was found that cells that have the IFN-βpromoter activated contain large amounts of DIs relative to GFP-ve cells. This data supports the Randall group's findings that DIs generated during errors of wild-type replication by the viral RNA polymerase are the primary PAMPs that induce of IFN-β, as opposed to PAMPs being generated during normal wild-type virus replication.
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Jones, Meleri. "Interfering with interferon : developing a reporter system to study the interaction between hepatitus C viral proteins and the interferon signalling pathway." Thesis, Queen Mary, University of London, 2008. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1530.

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The aim of the project was to investigate the mechanism by which HCV evades therapeutic IFN treatment. This involved the development of novel testing systems and their application to patient samples. Initial experiments focused on flavivirus replicons and novel observations on effects of one of these replicons (dengue virus) on interferon signalling were made. The dengue replicon system was demonstrated to inhibit IFNa signalling by reducing the expression of STAT2, an essential component of the type I IFN signalling pathway. This phenomenom was then further examined in dengue virus infected human cells and again it was observed that the expression of STAT2 was reduced. The mechanism of STAT2 degradation was further explored and STAT2 expression was found to be restored using a proteasomal inhibitor. A second flavivirus replicon system involving BVDV was also developed as a reporter system, again with novel observations. The BVDV replicon system was shown to be sensitive to the antiviral effects of I FNa and was not shown to inhibit the IFNa signalling pathway. The BVDV replicon was tested as a reporter system using a well-known viral inhibitor of I FNa. The viral inhibitor, inhibited the antiviral action of IFNa on the BVDV reporter. Having developed and validated this system, the effects of a small number of patient derived samples were assessed and it was demonstrated that NS5a derived from a patient who failed to respond to IFNa treatment inhibited the effects of IFNa on the BVDV reporter. To increase the senstitivity of the assay the reporter cassette was then changed to a destabilised GFP for use in a FACS based assay.
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Busche, Andreas. "Identifizierung und Charakterisierung von Modulatoren der Interferon-[gamma]-Antwort [Interferon-Gamma-Antwort]." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96971954X.

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Migliorini, Adriana. "Role of interferon-α and interferon-β in glomerular injury and repair." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168014.

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Obwohl die immunstimulatorischen Effekte viraler Nukleinsäursen, wie auch IFN -α und IFN-β, während Virusinfektionen eine wichtige Rolle spielen, ist wenig über ihre Funktion bei viraler Glomerulonephritis, wie beispielsweise HIV Nephropathie, bekannt. Virusinfektionen aktivieren, vor allem mittels IFN-α und IFN-β Produktion eine systemische antivirale Immunantwort. Es wurde gezeigt, dass diese inflammatorischen Zytokine einen pleiotropen immunmodulatorischen Effekt auf renale Mesangialzellen ausüben, was direkt zu glomerulären Krankheiten führt. Aber es ist bisher nicht bekannt, ob die viralen Nukleinsäuren und Typ I IFN einen Effekt auf die glomerulären Epithelzellen haben. (z.B. Podozyten und PECs). Um den Effekt von Nukleinsäuren auf Podozyten und PECs zu erforschen, stimulierten wir diese Zellen mit synthetischen dsDNA-(poly-dAdT) Komplexen mit lipofectamine, um eine virale Infektion zu imitieren. Wir haben herausgefunden, dass dsDNA stetig viele IFN-stimulierte Gene in Podozyten und PECs induziert. Desweitern haben wir herausgefunden, dass dsDNA die PECs Proliferation mindert und die CD24+/CD133+PECs Differenzierung zu ausgereiften Podozyten inhibiert. Um unsere Hypothese, dass deis aufgrund von der Sekretion von IFN-α und IFN-β passiert ist, zu bestätigen, haben wir den Effekt von diesen anitviralen Zytokinen auf PECs- und Podozyten-Homöostase etabliert. Wir haben herausgefunden, dass beide IFNs stetig Podozyten und PECs dazu anregen, stetig mehrere IFN-stimulierte Gene zu exprimieren. Trotzdem hat nur IFN-β das Podozytensterben induziert und die Permeabilität der Podozyten-Monolayer erhöht. In der Adriamycin-induzierter Nephropathie bei SCID Mäusen haben Injektionen mit IFN-α oder IFN-β die Proteinurie, den Makrophagen Influx und die Glomerulosklerose verstärkt. Trotzdem induziert nur IFN-β das mitotische Podozytensterben (katastrophale Mitose), welches zu einer reduzierten Podozytenanzahl führt. Wir haben führt, dass IFN-α einen Zellzyklusarrest in-vivo bei PECs induziert, der zur glomerulären Schädigung führt. Balb/c Mäuse, die Adriamycin gespritzt bekommen haben und täglich mit IFN-α und IFN-β behandelt wurden zeigten einen aggravierten Phänotyp mit vermehrter Proteinurie. Im Gegensatz zu dem, was an Studien in SCID Mausen gezeigt wurde, war der Effekt auf die Proteinurie nach IFN-α Behandlung prominenter bei Balb/c Mäusen, verglichen mit IFN-β. Deshalb haben Typ I IFNs einen deutlichen Effekt auf Podozyten und Parietalzellen. Zusammen fördern die Typ I IFNs die Glomerulosklerose durch verstärkten Untergang der Podozyten sowie durch Unterdrückung ihrer Regeneration aus Vorläuferzellen.
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Bazzigher, Luigi G. "Interferon-induced Mx proteins /." Zürich, 1992. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=9650.

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Hosana, Barreto de Oliveira Francisca. "Interferon gama versus asma." Universidade Federal de Pernambuco, 2004. https://repositorio.ufpe.br/handle/123456789/9728.

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Made available in DSpace on 2014-06-12T23:15:52Z (GMT). No. of bitstreams: 2 arquivo8706_1.pdf: 1817930 bytes, checksum: f2ac6cbb0fce841bf670e49e6225a371 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2004
Objetivo: Revisar a literatura científica acerca do papel do interferon gama (IFN-y) na doença atópica, especificamente asma. Métodos: Pesquisados dados do Medline e Lilacs nos últimos 10 anos. Resultados: Vários autores discutem a importância da relação entre a secreção de IFN-y e o componente atópico per se, por outro lado é questionado se esta citocina tem relação direta com a doença asmática, independente do estado atópico. Foi verificada a existência de várias pesquisas relacionando asma e IFN-y; entretanto, os resultados destas pesquisas se apresentam controversos. Conclusão: Ainda não se chegou a uma conclusão definitiva do verdadeiro mecanismo de atuação desempenhado pelo IFN-y na doença asmática, é indiscutível a importância de novas pesquisas esclarecedoras sobre este assunto
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Barbulescu, Karina. "Transkriptionelle Regulation des humanen Interferon-[gamma]-Promotors [Interferon-gamma-Promotors] in T-Lymphocyten." [S.l.] : [s.n.], 1999. http://deposit.ddb.de/cgi-bin/dokserv?idn=959887458.

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Carlton-Smith, Charles. "Impact of interferon β and interferon stimulated gene induction on Bunyamwera virus replication." Thesis, University of St Andrews, 2012. http://hdl.handle.net/10023/3179.

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The first line of defence against viral infection is the interferon (IFN) response, which must be overcome by a virus for successful replication. Pattern recognition receptors detect virus which triggers induction of IFNβ. Secreted IFNβ stimulates the JAK/STAT signal transduction pathway and the upregulation of IFN stimulated genes (ISGs) culminating with expression of hundreds of antiviral proteins. Bunyamwera virus (BUNV) is the prototype virus for the genus Orthobunyavirus and the family Bunyaviridae. BUNV is a trisegmented single stranded negative sense RNA virus whose genome comprises the Large (L), Medium (M) and Small (S) RNA segments. The L segment encodes the RNA polymerase, the M segment the two glycoproteins Gn and Gc and a non-structural protein NSm, and the S segment the nucleoprotein and a non-structural protein NSs in overlapping reading frames. The NSs protein interferes with RNA polymerase II mediated transcription thereby inhibiting cellular mRNA production, including IFN mRNA, and hence it is the primary IFN antagonist. A recombinant virus, rBUNdelNSs, that is unable to express the NSs protein, does not inhibit cellular transcription and is thus a strong IFN inducer. The aim of this thesis was to understand how IFN inhibits BUNV replication. Cells stimulated into the antiviral state by IFN treatment were protected against BUNV infection but addition of IFN 6 hours (or later) post infection had little effect on the replication cycle. However, addition of IFN immediately following infection conferred restriction on BUNV replication by initially increasing viral protein synthesis and then by blocking translation of positive sense viral RNA. To identify ISGs with anti-BUNV activity, I screened a panel of 26 cell lines that inducibly express individual ISGs. To aid screening, recombinant BUNV that expressed green fluorescent protein (GFP) were employed, including an NSs deletion virus with GFP fused to the Gc, rBUNGceGFPdelNSs, that I created and characterised. By a combination of virus yield assays, Western blotting and fluorescence techniques, three cell lines that inducibly express PKR, viperin or MTAP44 were shown to restrict BUNV replication. More detailed studies revealed PKR to restrict BUNV RNA and protein synthesis, but when PKR was knocked-down in IFN competent A549 cells viral replication was not blocked in cells pre-treated with IFN. Viperin inhibited viral protein synthesis and virally-induced host cell protein synthesis shut-off. Additionally, viral RNA synthesis was restricted by viperin and this was dependent on the CX₃CX₂C motif 1 of viperin. Taken together, these data show that the restriction of BUNV replication mediated by IFN is an accumulated effect of several different ISGs acting on different stages of the viral life cycle.
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Shearer, M. A. "Monoclonal antibodies to human interferon-#alpha# applied to the study of interferon-receptor interaction." Thesis, Open University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379866.

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Burkhart, Margi Anne. "Biological activity and therapeutic applications of intracellular interferon gamma and interferon gamma mimetic peptides." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0001180.

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Books on the topic "Interferon"

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Ferdinando, Dianzani, Rossi G. B, International Society for Interferon Research., and International Ares-Serono Symposium on the Interferon System (1985 : Rome, Italy), eds. The Interferon system. New York: Raven Press, 1985.

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Joyce, Taylor-Papadimitriou, ed. Interferons: Their impact in biology and medicine. Oxford: Oxford University Press, 1985.

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The story of interferon: The ups and downs in the life of a scientist. Singapore: World Scientific, 1998.

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Ion, Gresser, ed. Interferon. London: Academic, 1986.

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Ion, Gresser, ed. Interferon. London: Academic, 1987.

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Ion, Gresser, ed. Interferon. London: Academic Press, 1985.

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1940-, Stewart William E., and Schellekens Huub, eds. The biology of the interferon system 1985: Proceedings of the 1985 TNO-ISIR Meeting on the Interferon System, held in Clearwater Beach, Florida, USA on 13-18 October, 1985. Amsterdam: Elsevier Science, 1986.

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E, Stewart William, Schellekens Huub, International Society for Interferon Research., and Nederlandse Centrale Organisatie voor Toegepast-Natuurwetenschappelijk Onderzoek., eds. The biology of the interferon system 1985: Proceedings of the 1985 TNO-ISIR Meeting on the Interferon System held in Clearwater Beech, Florida, USA on 13-18 October, 1985. Amsterdam: Elsevier Science, 1986.

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Holger, Kirchner, Schellekens Huub, Nederlandse Centrale Organisatie voor Toegepast-Natuurwetenschappelijk Onderzoek., and International Society for Interferon Research., eds. The biology of the interferon system 1984: Proceedings of the 1984 TNO-ISIR Meeting on the Interferon System, held in Heidelberg, Federal Republic of Germany, on 21-25 October 1984. Amsterdam: Elsevier Science, 1985.

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Obert, Hans-Joachim. Beta-Interferon. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-97641-4.

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Book chapters on the topic "Interferon"

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Falke, D. "Interferon." In Springer-Lehrbuch, 680–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-08626-1_85.

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Gooch, Jan W. "Interferon." In Encyclopedic Dictionary of Polymers, 902. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14040.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Interferone — eine unsystematische Substanzgruppe." In Beta-Interferon, 1–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_1.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Interferon-beta — eine Substanz stellt sich vor." In Beta-Interferon, 17–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_2.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Die klinischen Studien." In Beta-Interferon, 93–164. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_3.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Dosierungsschemata für IFN-β." In Beta-Interferon, 165–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_4.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Andere Therapieansätze bei MS." In Beta-Interferon, 187–201. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_5.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Pharmakologie — Schlüssel zu manchem Verständnis." In Beta-Interferon, 202–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_6.

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Obert, Hans-Joachim, and Dieter Pöhlau. "Grundlagen der Immunologie." In Beta-Interferon, 245–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59764-0_7.

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Obert, Hans-Joachim. "Interferone in Deutschland." In Beta-Interferon, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-97641-4_1.

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Conference papers on the topic "Interferon"

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Lau, Eric, Giuseppina Claps, David S. Hoon, and Ze'ev A. Ronai. "Abstract 4091: Interfering with interferon: An axis of ATF2-mediated chemoresistance." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4091.

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Borisov, Valery Alexandrovich, Boris Ivanovich Sanin, Svetlana Evgenievna Samsonova, Nikolaevna Harutyunyan Elena, and Borisovna Golubeva Dina. "THE EXPERIENCE OF DOMESTIC ANTIVIRAL AGENTS, AND SOME OF OWN APPROACHES IN THE TREATMENT OF CHRONIC HEPATITIS C IN ADULTS." In Themed collection of papers from Foreign intemational scientific conference «Joint innovation - joint development». Medical sciences . Part 2. Ьу НNRI «National development» in cooperation with PS of UA. June 2023. Crossref, 2023. http://dx.doi.org/10.37539/230629.2023.19.61.022.

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In the management of 148 adult patients with chronic hepatitis C (CHC) of both sexes without special selection (taken into account only absolute contraindications to its performance) there were used domestic basic antiviral drugs - BAD| (short-living interferons (IFN) α, interferon inducers and nucleoside analogues) in parallel with additional antiviral drugs (drug glycyrrhizinic acid or amantadine) and maintenance therapy (stimulators of T-cell immunity and means of correction of side effects). Treatment was carried out in the framework of the developed complex of principles and approaches including in part, the formation of the starting average weekly dose of interferon IFN with accounting of the character of interferon status of the patient, a gradual increase in the average weekly dose of interferon IFN during the course of therapy, the delayed use of nucleoside analogs and others. As a result, against the background of a significant reduction in financial expenses and the aggressiveness of treatment the stable positive therapeutic outcome in the general population of patients occurred in 92.6%, with 87.2% in patients with genotype (G) 1.
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Jordan, Jarrat, Matteo Cesaroni, Jessica Schreiter, Chichi Huang, Marc Chevrier, and Jacqueline Benson. "II-21 Interfering with interferon in lupus: hitting the sweet spot with CNTO 6358." In Abstracts of the Third Biannual Scientific Meeting of the North and South American Lupus Community, Armonk, New York, USA, September 29 – October 1, 2016. Lupus Foundation of America, 2016. http://dx.doi.org/10.1136/lupus-2016-000179.51.

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Tsai, Yu-Chen, Sidney Pestka, Lu-Hai Wang, Loren W. Runnels, and Leroy F. Liu. "Abstract 3438: Oncogenes-induced interferon-beta: modulation of tranformation phenotypes through interferon-ISG15 autocrine signaling." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3438.

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"401 Type I interferon in NPSLE." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.13.

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Bauer, Eileen, and Philip M. Bauer. "A Novel Role For Interferon Response Factor 3 And Interferon Alpha In The Development Of Pulmonary Hypertension." 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.a4754.

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Skums, P., D. S. Campo, Z. Dimitrova, G. Vaughan, D. T. Lau, and Y. Khudyakov. "Modelling differential interferon resistance of HCV quasispecies." In 2011 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2011. http://dx.doi.org/10.1109/bibmw.2011.6112367.

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Odajima, Nao, John C. Gomez, Stephanie L. King, Jessica R. Martin, and Claire M. Doerschuk. "S. Pneumoniae Induces Interferon-³ Production By Neutrophils." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2793.

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Rönnblom, L. "SP0047 Type i interferon system in autoimmunity." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7134.

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Xue, Z., Y. Tang, M. Dai, S. Chen, and N. Shen. "121 Interferon stimulated long noncoding rna lncrna-cmpk2 facilitates neutrophils interferon production by tlr7/8 agonist in sle." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.121.

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Reports on the topic "Interferon"

1

Bello, Jake, and Judith O'Malley. Interferon Inducers against Infectious Diseases. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/adb134571.

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Bello, Jake, and Judith O'Malley. Interferon Inducers against Infectious Diseases. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada231360.

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Sastre, Adolfo G., and Connie S. Schmaljohn. Interferon Antagonism as a Common Virulence Factor of Hemorrhagic Fever Viruses. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada494593.

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Johnson, Howard M. Interferon Agonists/Mimetics as Therapeutics for Smallpox and Other Respiratory Viruses. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada455389.

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Ivanova, Sonya, Raliza Skrobanska, Vera Kolyovska, Ivan Milanov, Valentina Dimitrova, and Veneta Bojinova. Neutralizing Antibodies against Interferon‑beta in Bulgarian Adolescent Multiple Sclerosis Patients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, September 2018. http://dx.doi.org/10.7546/crabs.2018.09.15.

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Kozina, Carol L., Matthew Wallace Moorman, Catherine Branda, Meiye Wu, Ronald Paul Manginell, James Bryce Ricken, Conrad D. James, Oscar A. Negrete, Milind Misra, and Bryan D. Carson. Investigation of type-I interferon dysregulation by arenaviruses : a multidisciplinary approach. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1029825.

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Sastre, Adolfo G., and Connie S. Schmaljohn. Interferon Antagonism as a Common Virulence Factor of Hemorrhagic Fever Viruses. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada479293.

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Monath, Thomas P. Ribavirin, Interferon, and Antibody Approaches to Prophylaxis and Therapy for Viral Hemorrhagic Fevers. Fort Belvoir, VA: Defense Technical Information Center, January 1990. http://dx.doi.org/10.21236/ada233097.

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Mitchell, David P. Analyzing the Utilization of Interferon-Gamma Screening for Tuberculosis at Recruit Training Command, Great Lakes. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada476199.

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Chakraborty, Sanchita, Vignesh Mariappan, Shalinda Adikari, Lokesh Shanmugam, Joshy M. Easow, and Agieshkumar Balakrishna Pillai. Differential expression of interferon inducible protein: guanylate binding protein (GBP1 & GBP2) in severe dengue. Peeref, June 2023. http://dx.doi.org/10.54985/peeref.2306p1644622.

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