Journal articles: 'Sendai'

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NA, Nancy Pe. "Sendai." Perspectives in the Arts and Humanities Asia 10, no. 2 (October 29, 2021): 287–88. http://dx.doi.org/10.13185/paha2020.10212.

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SATO, Yutaka. "Welcome to Sendai!" JOURNAL OF THE JAPAN WELDING SOCIETY 88, no. 3 (2019): 155–56. http://dx.doi.org/10.2207/jjws.88.155.

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Sasaki, Mutsuro. "Sendai Mediatheque, Japan." Structural Engineering International 12, no. 3 (August 2002): 146–48. http://dx.doi.org/10.2749/101686602777965315.

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Shoji, Tetsuo, and Masumi Saka. "Welcome to Sendai." Proceedings of the Asian Pacific Conference on Fracture and Strength and International Conference on Advanced Technology in Experimental Mechanics 1.01.203 (2001): A1. http://dx.doi.org/10.1299/jsmeatemapcfs.1.01.203.0_a1.

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Shoji, Tetsuo, and Masumi Saka. "Welcome to Sendai." Proceedings of the Asian Pacific Conference on Fracture and Strength and International Conference on Advanced Technology in Experimental Mechanics 2.01.03 (2001): A1. http://dx.doi.org/10.1299/jsmeatemapcfs.2.01.03.0_a1.

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OKADA, Satoru, Kouichi IIBUCHI, and Yasuo NAGAI. "GAIJIN-YA OF SENDAI 1N SENDAI-HAN DURING EDO-ERA." Journal of Architecture and Planning (Transactions of AIJ) 65, no. 527 (2000): 233–40. http://dx.doi.org/10.3130/aija.65.233_1.

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Kure, Shuichi, Taichi Tebakari, and Mamoru Miyamoto. "Review of Recent Water-Related Disasters and Scientific Activities in Southeast Asia: Lessons Learned and Future Challenges for Disaster Risk Reduction." Journal of Disaster Research 11, no. 3 (June 1, 2016): 394–401. http://dx.doi.org/10.20965/jdr.2016.p0394.

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This article reports on the public forum conducted by the authors at the Third United Nations World Conference on Disaster Risk Reduction, held in Sendai City, Miyagi Prefecture, Japan, from March 14 to 18, 2015. The conference included case studies of recent water-related disasters in the Southeast Asia region, reviews of academic research, and a description of the current situation about measures for risk reduction. This article also clarifies the relationship between the various recommendations proposed in the public forum and the Sendai Framework for Disaster Risk Reduction 2015–2030 (the Sendai framework), in order to identify the efforts that are necessary for the implementation of the Sendai framework.

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Kast, W. M., C. J. Boog, B. O. Roep, A. C. Voordouw, and C. J. Melief. "Failure or success in the restoration of virus-specific cytotoxic T lymphocyte response defects by dendritic cells." Journal of Immunology 140, no. 9 (May 1, 1988): 3186–93. http://dx.doi.org/10.4049/jimmunol.140.9.3186.

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Abstract C57BL/6 (B6, H-2b) mice are CTL responders to both Sendai virus and Moloney leukemia virus. In the former response the H-2Kb class I MHC molecule is used as CTL restriction element, in the latter response the H-2Db molecule. B6 dendritic cells (DC) are superior in the presentation of Sendai virus Ag to CTL in comparison with B6 normal spleen cells. Con A blasts have even less capacity to present viral Ag than NSC, and LPS blasts show an intermediate capacity to present viral Ag. H-2Kb mutant bm1 mice do not generate a CTL response to Sendai virus, but respond to Moloney leukemia virus, as demonstrated by undetectable CTL precursors to Sendai virus and a normal CTL precursor frequency to Moloney virus. Compared to B6 mice, other H-2Kb mutant mice show decreased Sendai virus-specific CTL precursor frequencies in a hierarchy reflecting the response in bulk culture. The Sendai virus-specific CTL response defect of bm1 mice was not restored by highly potent Sendai virus-infected DC as APC for in vivo priming and/or in vitro restimulation. In mirror image to H-2Kb mutant bm1 mice, H-2Db mutant bm14 mice do not generate a CTL response to Moloney virus, but respond normally to Sendai virus. This specific CTL response defect was restored by syngeneic Moloney virus-infected DC for in vitro restimulation. This response was Kb restricted indicating that the Dbm14 molecule remained largely defective and that a dormant Kb repertoire was aroused after optimal Ag presentation by DC. In conclusion, DC very effectively present viral Ag to CTL. However, their capacity to restore MHC class I determined specific CTL response defects probably requires at least some ability of a particular MHC class I/virus combination to associate and thus form an immunogenic complex.

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HOFFMANN, MICHAEL M., HUBERT SCHARNAGL, ELEFTHERIA PANAGIOTOU, WERNER T. BANGHARD, HEINRICH WIELAND, and WINFRIED MÄRZ. "Diminished LDL Receptor and High Heparin Binding of Apolipoprotein E2 Sendai Associated with Lipoprotein Glomerulopathy." Journal of the American Society of Nephrology 12, no. 3 (March 2001): 524–30. http://dx.doi.org/10.1681/asn.v123524.

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Abstract. Variants of apolipoprotein E (apoE) have been linked to lipoprotein glomerulopathy, a new glomerular disease characterized by the deposition of lipoproteins in mesangial capillaries. One third of affected patients are heterozygous for apoE2 Sendai (Arg145 Pro). Variants of apoE can also produce type III hyperlipoproteinemia (HLP). Recessive type III HLP is caused by apoE2 (Arg158 Cys), a mutant with diminished low-density lipoprotein (LDL) receptor binding but halfnormal heparin binding. Dominant type III HLP is caused by mutations that markedly alter heparin binding but modestly reduce receptor binding. This study examined whether apoE2 Sendai (Arg145 Pro) was functionally different from type III HLP-producing apoE variants by expressing apoE3, apoE2 (Arg158 Cys), apoE1 (Arg146 Glu), a dominant apoE variant, and apoE2 Sendai (Arg145 Pro) in the baculovirus system. LDL receptor binding was studied using recombinant apoE complexed to phospholipid vesicles and to very lowdensity lipoprotein from a patient with familiar apoE deficiency. Compared with apoE3, receptor-binding activities of apoE2 (Arg158 Cys), apoE1 (Arg146 Glu), and apoE2 Sendai (Arg145 Pro) all were less than 5%. Heparin-binding activities were 53%, 23%, and 66%, respectively, of apoE3. The distribution of apoE2 Sendai among the major plasma lipoprotein fractions was similar to that of apoE3 and apoE2 (Arg158 Cys). ApoE2 Sendai (Arg145 Pro) represents the only known mutation within the heparin-binding domain of apoE (residues 142 through 147), revealing diminished receptor binding and almost normal heparin binding. These unique characteristics of apoE2 Sendai (Arg145 Pro) may relate to the development of lipoprotein glomerulopathy.

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Percy, D. H., D. C. Auger, and B. A. Croy. "Signs and Lesions of Experimental Sendai Virus Infection in Two Genetically Distinct Strains of SCID/Beige Mice." Veterinary Pathology 31, no. 1 (January 1994): 67–73. http://dx.doi.org/10.1177/030098589403100109.

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The pathogenesis of Sendai virus infection was studied in genetically immunodeficient mice of genotype scid/scid.bg/bg (SCID-beige) using C.B-17 SCID-beige mice, a BALB/c-related strain that expresses the same major histocompatibility complex as the Sendai virus-susceptible DBA/2 (H-24). Mice were inoculated intranasals with isolate 771076 of Sendai virus, then killed at 2-day intervals beginning on day 4 post-inoculation. Clinical signs were evident beginning at 8 to 10 days post-inoculation, and all animals remaining were killed in extremis by 14 to 17 days post-inoculation. Lesions in inoculated mice were confined to the respiratory tract. In the nasal passages, a nonresolving rhinitis, with epithelial hyperplasia/metaplasia occurred. Cranioventral bronchopneumonitis was characterized by marked hyperplasia and necrosis of epithelial cells lining airways and with leukocytic infiltration. At the alveolar level, there was marked hypertrophy and hyperplasia of type II pneumocytes, mobilization of alveolar macrophages, and obliteration of the normal architecture in severely affected areas. Viral antigen was evident beginning at 4 days post-inoculation and persisted in affected areas throughout the duration of the study. Because immunocompetent C57BL/6 mice are known to be genetically resistant to Sendai virus, the susceptibility of C57B/6 SCID-beige to Sendai virus was then compared to that of C.B-17 SCID-beige mice. In age-matched animals of the two strains, there was no evidence of natural resistance to Sendai virus infection in the immunodeficient C57BL/6 strain compared to the C.B-17 mice. These studies indicate that the genetic differences in susceptibility of two strains of immunocompetent mice to Sendai virus infection are eliminated by expression of the mutations scid and beige.

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Cole, G. A., T. L. Hogg, M. A. Coppola, and D. L. Woodland. "Efficient priming of CD8+ memory T cells specific for a subdominant epitope following Sendai virus infection." Journal of Immunology 158, no. 9 (May 1, 1997): 4301–9. http://dx.doi.org/10.4049/jimmunol.158.9.4301.

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Abstract The relationship between the primary effector CTL response to viral infection and the subsequent pool of memory CTL precursors (CTLp) is poorly understood. Here, we have analyzed the induction of both effector CTL and memory CTLp to dominant and subdominant epitopes following Sendai virus infection of C57BL/6 mice. A single peptide derived from the Sendai virus nucleoprotein (NP(324-332)) binds to both H-2 Kb and Db MHC class I molecules, generating both immunodominant (NP(324-332)/Kb) and subdominant (NP(324-332)/Db) epitopes. Following intranasal Sendai virus infection, NP(324-332)/Kb-specific CTL dominated the primary effector CTL response in the lung and were present at high frequency in the memory CTLp pool. In contrast, NP(324-332)/Db-specific CTL were not a detectable component of the effector response to primary Sendai virus infection. However, memory CTLp specific for this subdominant epitope were induced at frequencies approaching those of CTLp specific for the immunodominant epitope. These data indicate that memory CTLp specific for subdominant epitopes can be primed by Sendai virus infection in the absence of a detectable effector response. To determine whether CTLp memory to subdominant epitopes is functional in the context of Sendai virus infection, memory CTLp specific for a subdominant epitope were selectively primed by vaccination. These cells dominated the subsequent effector CTL response to Sendai virus infection, demonstrating that memory CTLp primed against subdominant epitopes can participate in an immune response and effectively compete with T cells specific for immunodominant epitopes. These data have implications for the development of vaccines designed to emphasize cellular immunity.

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Liu, T., B. Chambers, A. D. Diehl, L. Van Kaer, M. Jondal, and H. G. Ljunggren. "TAP peptide transporter-independent presentation of heat-killed Sendai virus antigen on MHC class I molecules by splenic antigen-presenting cells." Journal of Immunology 159, no. 11 (December 1, 1997): 5364–71. http://dx.doi.org/10.4049/jimmunol.159.11.5364.

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Abstract Immunization of C57BL/6 (B6) mice with heat-killed Sendai virus generates a Sendai virus-specific CD8+ T cell response. This suggests that APC have the capacity to take up and present exogenous (nonreplicative) Sendai virus Ag on MHC class I molecules. Little is known about the intracellular requirements for processing of this form of Ag and its presentation on MHC class I. Therefore, we have studied the processing and presentation of heat-killed Sendai virus Ag on MHC class I molecules in splenic APC. Heat-killed Sendai virus Ags were efficiently processed by normal B6 as well as by TAP-1(-/-) splenic APC. Presentation was MHC class I restricted, since no presentation was seen by APC from TAP-1/beta2m-/- mice that lack expression of MHC class I. Presentation occurred even in the presence of brefeldin A, but was blocked by cytochalasin D as well as chloroquine. Finally, B6 as well as TAP-1(-/-) splenic APC, loaded with heat-killed Sendai virus Ag in vitro, primed naive CD8+ T cells in vivo. These studies suggest the existence of a TAP-independent pathway for Ag presentation on MHC class I in normal splenic APC, bearing many similarities with the MHC class II pathway for Ag presentation. The present results are discussed in relation to the events underlying the processing and presentation of exogenous Ag on MHC class I, the molecular basis for CD8+ T cell priming during viral infections, and prospects for vaccine development.

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Chen, Yongjin, Robert G. Webster, and David L. Woodland. "Induction of CD8+ T Cell Responses to Dominant and Subdominant Epitopes and Protective Immunity to Sendai Virus Infection by DNA Vaccination." Journal of Immunology 160, no. 5 (March 1, 1998): 2425–32. http://dx.doi.org/10.4049/jimmunol.160.5.2425.

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Abstract While recent studies have demonstrated that DNA vaccination induces potent CD8+ T cell memory in vivo, it is unclear whether this memory is qualitatively and quantitatively comparable with that induced by natural viral infection. In the current studies, we have investigated the induction of CD8+ memory CTL responses to Sendai virus nucleoprotein (NP) in C57BL/6 mice following gene gun vaccination. The data demonstrate that this mode of vaccination induces potent long-lived memory CTL precursors (CTLp) specific for both the dominant (NP324–332/Kb) and the subdominant (NP324–332/Db) epitopes of NP. The frequencies of T cells specific for each of these epitopes in the spleen is about 1:2000 CD8+ T cells, similar to those induced by intranasal infection with Sendai virus. Moreover, the induction of memory CTLp by DNA vaccination is independent of MHC class II molecules or Ab, as is the case for memory CTLp induction by live Sendai virus infection. CTLp specific for both epitopes are capable of migrating to the lung following Sendai virus infection and express potent cytotoxic activity at the site of infection. Consistent with this activity, DNA vaccination with Sendai virus NP induced a substantial degree of Ab-independent protection from a challenge with a lethal dose of Sendai virus. Taken together, these data demonstrate that for the parameters tested, DNA vaccination is indistinguishable from live virus infection in terms of priming functional memory CTLp with broad specificity for both dominant and subdominant T cell epitopes.

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Iida, Akihiro, and Atsushi Kato. "Sendai virus based vectors." Uirusu 53, no. 2 (2003): 171–75. http://dx.doi.org/10.2222/jsv.53.171.

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KAWAMATA, Masayuki. "Sendai Aobayama, Kawauchi Report." IEICE ESS Fundamentals Review 9, no. 1 (2015): 68–70. http://dx.doi.org/10.1587/essfr.9.68.

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Cutter, Susan L., and Melanie Gall. "Sendai targets at risk." Nature Climate Change 5, no. 8 (July 24, 2015): 707–9. http://dx.doi.org/10.1038/nclimate2718.

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Ariyaningsih, R. B. Sukmara, and L. Pradita. "The Sendai Framework for disaster risk reduction: Insight from Covid-19 in Balikpapan City, Indonesia." IOP Conference Series: Earth and Environmental Science 896, no. 1 (November 1, 2021): 012068. http://dx.doi.org/10.1088/1755-1315/896/1/012068.

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Abstract The Sendai Framework for Disaster Risk Reduction 2015-2030 (SFDRR) serves as the international standard for disaster risk reduction. The SFDRR places a new emphasis on risk reduction during the post-disaster recovery phase. Additionally, SFDRR encourages tangible and verifiable outcomes for catastrophe loss reduction, such as indicators for tracking progress toward seven global targets. The purpose of this article is to map the current response to the biological disaster (Covid-19) in the City of Balikpapan, Indonesia, for the Sendai Framework, using academic literature and publicly available data from governments and organizations. To provide timely responses to COVID-19 at the municipal level, this study conducted a rapid examination of newly available information from the Balikpapan government and other sources. According to the analysis’s findings, Covid 19 will have ramifications for the Sendai Framework unless the government adopts necessary legislation to keep the Sendai Framework on track. SDFRR was used to detect COVID-19 responses in Balikpapan City, although one target in the SFDRR is unclear or unidentified. Despite the fact that this goal, “Improving Disaster Preparedness for Effective Response and “Building Back Better” in Recovery, Rehabilitation, and Reconstruction,” is crucial to the Sendai Framework’s success.

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Hokkirigawa, Kazuo. "ITC Sendai 2019 Special Issue: Part 1 – Papers from ITC Sendai 2019 –." Tribology Online 14, no. 5 (December 15, 2019): ii. http://dx.doi.org/10.2474/trol.14.ii.

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Holmes, David E., and Sue A. Moyer. "The Phosphoprotein (P) Binding Site Resides in the N Terminus of the L Polymerase Subunit of Sendai Virus." Journal of Virology 76, no. 6 (March 15, 2002): 3078–83. http://dx.doi.org/10.1128/jvi.76.6.3078-3083.2002.

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ABSTRACT Sendai virus encodes an RNA-dependent RNA polymerase which is composed of the L and P proteins. Site-directed mutagenesis of the N terminus of L has identified amino acids important for binding P. Seven of nine mutants in amino acids 1 to 350 of Sendai L lost the ability to bind to Sendai P, although they were still able to bind the viral C protein. Loss of P binding correlated with the loss of all RNA synthesis activities. Two L mutants gave limited P-L complex formation and limited viral transcription and replication.

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Beklemisheva, V. R., and A. G. Menzorov. "Use of a Sendai virus-based vector for effcient transduction of pinniped fbroblasts." Vavilov Journal of Genetics and Breeding 22, no. 8 (January 3, 2019): 1020–25. http://dx.doi.org/10.18699/vj18.445.

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Generation of induced pluripotent stem (iPS) cells expanded possibilities of pluripotency and early development studies. Generation of order Carnivora iPS cells from dog (Canis lupus familiaris), snow leopard (Panthera uncia), and American mink (Neovison vison) was previously reported. The aim of the current study was to examine conditions of pinniped fbroblast reprogramming. Pinnipeds are representatives of the suborder Caniformia sharing conservative genomes. There are several ways to deliver reprogramming transcription factors: RNA, proteins, plasmids, viral vectors etc. The most eﬀective delivery systems for mouse and human cells are based on viral vectors. We compared a lentiviral vector which integrates into the genome and a Sendai virusbased vector, CytoTune EmGFP Sendai Fluorescence Reporter. The main advantage of Sendai virusbased vectors is that they do not integrate into the genome. We performed delivery of genetic constructions carrying ﬂuorescent proteins to fbroblasts of seven Pinnipeds: northern fur seal (Callorhinus ursinus), Steller sea lion (Eumetopias jubatus), walrus (Odobenus rosmarus), bearded seal (Erignathus barbatus), Baikal seal (Pusa sibirica), ringed seal (Phoca hispida), and spotted seal (Phoca largha). We also transduced American mink (N. vison), human (Homo sapiens), and mouse (Mus musculus) fbroblasts as a control. We showed that the Sendai virusbased transduction system provides transgene expression onetwo orders of magnitude higher than the lentiviral system at a comparable multiplicity of infection. Also, transgene expression after Sendai virusbased transduction is quite stable and changes only slightly at day four compared to day two. These data allow us to suggest that Sendai virusbased vectors are preferable for generation of Pinniped iPS cells.

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Nunes-Correia, Isabel, João Ramalho-Santos, and Maria C. Pedroso de Lima. "Sendai Virus Fusion Activity as Modulated by Target Membrane Components." Bioscience Reports 18, no. 2 (April 1, 1998): 59–68. http://dx.doi.org/10.1023/a:1020180109275.

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We have studied the differences between erythrocytes and erythrocyte ghosts as target membranes for the study of Sendai virus fusion activity. Fusion was monitored continuously by fluorescence dequenching of R18-labeled virus. Experiments were carried out either with or without virus/target membrane prebinding. When Sendai virus was added directly to a erythrocyte/erythrocyte ghost suspension, fusion was always lower than that obtained when experiments were carried out with virus already bound to the erythrocyte/erythrocyte ghost in the cold, since with virus prebinding fusion can be triggered more rapidly. Although virus binding to both erythrocytes and erythrocyte ghosts was similar, fusion activity was much more pronounced when erythrocyte ghosts were used as target membranes. These observations indicate that intact erythrocytes and erythrocyte ghosts are not equivalent as target membranes for the study of Sendai virus fusion activity. Fusion of Sendai virus with both target membranes was inhibited when erythrocytes or erythrocyte ghosts were pretreated with proteinase K, suggesting a role of target membrane proteins in this process. Treatment of both target membranes with neuraminidase, which removes sialic acid residues (the biological receptors for Sendai virus) greatly reduced viral binding. Interestingly, this treatment had no significant effect on the fusion reaction itself.

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Payvandi, Faribourz, Sheela Amrute, and Patricia Fitzgerald-Bocarsly. "Exogenous and Endogenous IL-10 Regulate IFN-α Production by Peripheral Blood Mononuclear Cells in Response to Viral Stimulation." Journal of Immunology 160, no. 12 (June 15, 1998): 5861–68. http://dx.doi.org/10.4049/jimmunol.160.12.5861.

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Abstract IL-10 is an important regulator of the production of proinflammatory cytokines. Its effect on IFN-α production, however, has not been reported. In this study, PBMC from healthy donors were stimulated with virus in the presence of IL-10. Human IL-10 (hIL-10) caused reductions in both the frequency of IFN-α-producing cells (IPC) and bulk IFN in response to herpes simplex virus type-1 (HSV-1), Sendai virus, Newcastle disease virus, and vesicular stomatitis virus. The inhibitory effect occurred when IL-10 was added 2 or 4 h before, or 2 h poststimulation with HSV or Sendai virus, but not when added 4 h postinduction. Unlike IL-10, IL-4 did not affect the IFN-α response to HSV. However, when PBMC were induced with Sendai virus, IFN-α production was also reduced by IL-4. IL-10 treatment of PBMC resulted in strong reductions in the steady state levels of both HSV- and Sendai virus-induced IFN-α1, -α2, and -β mRNA as determined by RT-PCR. IFN-α production to Sendai virus occurs predominantly by monocytes, whereas most enveloped viruses stimulate low frequency “natural IFN-producing cells (NIPC),” which are thought to be dendritic cells. Peripheral blood dendritic cells were found to express the IL-10 receptor, suggesting that IL-10 may directly act on the dendritic IPC. Addition of monoclonal anti-IL-10 to PBMC resulted in a significant increase in both the frequency of IPC and the amount of secreted IFN-α in response to HSV but not Sendai virus. We conclude that human IL-10 can serve as both an endogenous and exogenous regulator of IFN-α production.

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Kast, W. M., A. M. Bronkhorst, L. P. de Waal, and C. J. Melief. "Cooperation between cytotoxic and helper T lymphocytes in protection against lethal Sendai virus infection. Protection by T cells is MHC-restricted and MHC-regulated; a model for MHC-disease associations." Journal of Experimental Medicine 164, no. 3 (September 1, 1986): 723–38. http://dx.doi.org/10.1084/jem.164.3.723.

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The in vivo importance of class I MHC regulation of the Tc response to a natural pathogenic agent of high virulence was studied on the basis of our previous demonstration of a major difference in the capacity to generate a Sendai virus-specific Tc response between C57BL/6 (B6, H-2b) mice and H-2Kb mutant B6.C-H-2bm1 (bm 1) mice. These two mouse strains differ from each other only in three amino acids in the crucial H-2Kb restriction element for this response. bm 1 mice, in contrast to B6 mice, are Tc nonresponders against this virus, but show Sendai-specific T cell proliferation, antibody production, and DTH reactions, as well as NK cell activity, equal to those of B6 mice. B6, Sendai Tc-deficient bm 1 and T cell-deficient B6 nu/nu mice differ from each other in susceptibility to lethal pneumonia induced by i.n. inoculation of virulent Sendai virus. The lethal dose (LD50) in B6 mice averaged 152 TCID50, in bm 1 mice, 14 TCID50 and in B6 nu/nu mice 0.5 TCID50. The importance of Tc was also shown by the complete protection of B6 nu/nu mice against infection with a lethal virus dose by i.v. injection of a Sendai virus-specific, IL-2-dependent and H-2Kb-restricted B6 Tc clone. In vivo protection by this Tc clone was H-2Kb-restricted. Apart from Tc, an important role for virus-specific Th cells is evident from the difference in susceptibility between bm 1 and B6 nu/nu mice. This conclusion was supported by the demonstration that the mean survival time of B6 nu/nu and bm 1 nu/nu mice could be significantly prolonged, in an I-Ab-restricted manner, by the injection of in vitro-propagated, Sendai-specific B6 or bm 1 Th clones after a lethal dose of Sendai virus, and by the demonstration that inoculation of these Th clones provided help to virus-specific Tc by means of IL-2 production. Strikingly, Th and Tc cooperate in anti-Sendai virus immunity, since permanent survival of lethally infected nu/nu mice was only achieved by inoculation of a mixture of Tc and Th clones or a mixture of a Tc clone and rIL-2. This study provides a unique model for the study of MHC-disease associations.

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Smith, A. L., K. Bottomly, and D. F. Winograd. "Altered splenic T cell function of BALB/cByJ mice infected with mouse hepatitis virus or Sendai virus." Journal of Immunology 138, no. 10 (May 15, 1987): 3426–30. http://dx.doi.org/10.4049/jimmunol.138.10.3426.

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Abstract Mouse hepatitis virus and Sendai virus are among the most common viruses naturally infecting laboratory mice. Concanavalin A-stimulated in vitro proliferative responses of splenocytes were examined after infection of BALB/cByJ mice with the JHM strain of mouse hepatitis virus (MHV-JHM) or Sendai virus. Mice were exposed to these viruses by presumed natural routes (per os or intranasally). Immunodepression was marked but transient among BALB/cByJ mice exposed to MHV-JHM. Among mice exposed to Sendai virus and examined over a 21-day period, spleen cells from only one mouse, sacrificed 10 days postinoculation, exhibited a severely impaired ability to respond to concanavalin A. Lymphokine production by spleen cells from control and infected mice was then assessed. IL 2 was either absent or present at very low levels in culture supernates of concanavalin A-unresponsive spleen cells from MHV-JHM-infected mice. Spleen cells from the single Sendai virus-infected mouse also produced very low levels of IL 2. In contrast, IL 1 was detected in supernatants of all spleen cell cultures derived from control, MHV-JHM-infected, or Sendai virus-infected mice. There was not a clear correlation between concanavalin A responsiveness and the ability of spleen cells to produce interferon-gamma. These results stress the importance of using laboratory mice of known microbiological status for immunologic experiments.

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Ritphring, Sompratana, and Hitoshi Tanaka. "MORPHOLOGY VARIABILITY IN THE VICINITY OF COASTAL STRUCTURES." Coastal Engineering Proceedings 1, no. 32 (January 30, 2011): 69. http://dx.doi.org/10.9753/icce.v32.sediment.69.

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The morphology variability is carried out in this study by using the historical bathymetry data. Two study areas in which the vicinity of coastal structures are selected and make a comparative study, Sendai Port and Yuriage Port. Both are located in the Sendai Coast, northeast of Japan, with the similar incoming wave condition from SE and ESE direction. Sediment is trapped in front of Breakwater at Yuriage Port; on the contrary, the severe erosion occurs in the updrift side of Sendai Port. Consequently, these phenomena should be clarified by study on morphology variability. To overcome these aspects, it needs to analyze a long-term series data set and investigate the characteristics of morphological variability in order to well understand for the perspective of coastal management.

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Kast, W. M., J. A. Bluestone, M. H. Heemskerk, J. Spaargaren, A. C. Voordouw, J. D. Ellenhorn, and C. J. Melief. "Treatment with monoclonal anti-CD3 antibody protects against lethal Sendai virus infection by induction of natural killer cells." Journal of Immunology 145, no. 7 (October 1, 1990): 2254–59. http://dx.doi.org/10.4049/jimmunol.145.7.2254.

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Abstract C57BL/6 mice are protected from a lethal pneumonia caused by Sendai virus when treated with low doses of mAb directed to the CD3 Ag. The protective mechanism is not due to an accelerated Sendai virus-specific Th cell, CTL, or antibody response but to a strong NK cell response via the in vivo induction of lymphokines. Antibodies directed against the NK1.1 and asialo GM1 marker totally reversed the protective effect of anti-CD3 treatment. In vivo treatment with rIL-2 also induced NK activity and induced antiviral protection. Treatment with anti-CD3 protects when given in a narrow time window (1 day before until 1 day after Sendai virus inoculation), indicating that NK activity is protective in the early phase of virus infection.

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OHYAMA, Tugio, Yoshinori ITOH, Arashi KITAKAZE, Toshiro NAGASE, and Mizuhiko AKIZUKI. "Cristobalite from Taihakusan, Sendai City." JOURNAL OF MINERALOGY, PETROLOGY AND ECONOMIC GEOLOGY 93, no. 9 (1998): 344–46. http://dx.doi.org/10.2465/ganko.93.344.

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KUNITSU, Hiroaki, Toru KOBORI, and Mitsugu ASANO. "Sendai Airport Passenger Terminal Building." IABSE Congress Report 16, no. 13 (January 1, 2000): 915–22. http://dx.doi.org/10.2749/222137900796297923.

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Mogi, I., K. Takahashi, S. Awaji, K. Watanabe, and M. Motokawa. "Magnetic levitation experiments in Sendai." Journal of Physics: Conference Series 51 (November 1, 2006): 431–38. http://dx.doi.org/10.1088/1742-6596/51/1/100.

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Nakagawa, Y., G. Kido, A. Hoshi, K. Watanabe, S. Miura, and Y. Muto. "High field magnets at Sendai." Physica B: Condensed Matter 164, no. 1-2 (June 1990): 29–34. http://dx.doi.org/10.1016/0921-4526(90)90058-3.

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Kanda, H., B. Beckford, T. Fujii, Y. Fujii, K. Futatsukawa, Y. C. Han, O. Hashimoto, et al. "Strangeness photoproduction experiments at SENDAI." Nuclear Physics A 835, no. 1-4 (April 2010): 317–20. http://dx.doi.org/10.1016/j.nuclphysa.2010.01.208.

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Murao, Osamu, and Hiroko Sakaba. "Quantitative Text Analysis of Sendai Framework for Disaster Risk Reduction 2015–2030." Journal of Disaster Research 11, no. 3 (June 1, 2016): 459–69. http://dx.doi.org/10.20965/jdr.2016.p0459.

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Three UN world conferences held on reducing disaster damage – the 1994 World Conference on Natural Disaster Reduction held in Yokohama during the International Decade for Natural Disaster Reduction, the 2005 World Conference on Disaster Reduction held in Hyogo Prefecture, and the 2015 World Conference on Disaster Risk Reduction held in Sendai – resulted in the Yokohama Strategy and Plan of Action for a Safer World, the Hyogo Framework for Action 2005-2015 (HFA), and the Sendai Framework for Disaster Risk Reduction 2015-2030.The sections that follow clarify Sendai Framework features compared to the Yokohama Strategy and the HFA based on a three-stage review of the literature:1) Overviews of the three documents, including framework structures, are arranged with basic conference information and a comparative study.2) A quantitative text analysis is conducted using the KH Coder, which is free quantitative text analysis software. Words occurring frequently in the documents are extracted and compared and a co-occurrence network is analyzed to determine relationships among these words.3) Features of the three documents, mainly focusing on the Sendai Framework, are specified and clarified based on the result of quantitative text analysis.

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Priyo Mukti Pribadi Winoto, Nursalam, Iis Noventi, Sulistyorini, Ika Mardiyanti, and Ainul Rofik. "Implementing the Sendai Framework for Volunteers in Sidoarjo District." Bali Medical Journal 12, no. 2 (June 22, 2023): 1978–80. http://dx.doi.org/10.15562/bmj.v12i2.4337.

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Introduction: Indonesia has a myriad of potential natural disasters that will occur. In the last 10 years, for example, the same disasters have happened again in Indonesia every year. This study aimed to determine the Sendai framework implementation on volunteers in the Sidoarjo district. Methods: This study used an analytic design with a cross sectional design. A sample size of 35 from a population of 50 was obtained by simple random sampling at the Sidoarjo Tangguh Volunteer Forum (FOREST). The independent variable is Sendai Framework, while the dependent variable is natural disaster management. Data analysis using independent T test. Results: based on this study, most respondents showed an increase in skill after the intervention, which before intervention most respondents were having not have enough skill of disaster management (21 respondents; 60.0%) and turned into most of the respondents had good skills after the intervention (28 respondents; 80.0%). The Wilcoxon sign rank test with a significance level of = 0.05 obtained a value of = 0.01. Conclusion: Sendai framework effectively increased disaster risk reduction capacity. Further studies are needed to assess the effectiveness of Sendai Framework in improving someone's skill in disaster management, including compounding factors related to the outcome.

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Uddback, Ida Elin Maria, Cameron Mattingly, Jeronay Thomas, Kirsten Nicole Kost, Zheng-Rong Tiger Li, Allan R. Thomsen, Christopher D. Scharer, Jan Pravsgaard Christensen, and Jacob E. Kohlmeier. "Resident Memory CD8+ T cells in the respiratory tract prevent transmission of respiratory viruses." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 103.01. http://dx.doi.org/10.4049/jimmunol.206.supp.103.01.

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Abstract Tissue-resident memory CD8+ T cells (TRM) in the respiratory tract reduce viral replication and limit pathology following respiratory virus infections. In infection with heterosubtypic influenza viruses, where pre-existing antibodies does not proved sterilizing immunity, TRM are critical for protection. However, in addition to protecting the host against disease vaccine programs are also designed to limit viral spread in a population. Due to the lack of an animal model to study the effect of TRM on transmission through longitudinal tracking, and with immunological parameters easily identified and manipulated available, this hasn’t been studied before. To solve these issues, we used a luciferase expressing Sendai virus, a natural mouse parainfluenza virus that readily transmits via the aerosol and contact routes, as well as a recombinant influenza virus expressing the immunodominant Sendai NP324-332/Kb epitope to generate SenNP+ memory CD8+ T cells. By utilizing IVIS imaging to non-invasively measure Sendai virus infection over time, we found that mice with pre-existing SenNP+ TRM in the respiratory system don’t transmit Sendai virus to naïve mice when co-housed. In contrast, mice with pre-existing circulating SenNP+ effector memory CD8+ T cells, but no TRM, failed to prevent transmission of Sendai virus to naïve mice when co-housed. In addition, we found that the prevention of transmission was dependent on the production of IFNγ. These findings demonstrates notably that antigen specific lung TRM contributes to herd immunity by preventing respiratory virus transmission. This underscores the importance, and potential, of TRMs generated by vaccines for protection against respiratory viruses.

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Bianchi Azevedo, Adriana Aparecida, Alexandre Galvão Fernandes, Kellen Cristine Nunes Salles, Márcio Romano Corrêa Custódio, Marília Aparecida Coelho Fraia de Souza, and Wellington Silva de Oliveira. "I Jornada de Redução do Risco de Desastres – Rio de Janeiro – 2015: os desafios e experiências compartilhadas." Territorium, no. 25(II) (May 22, 2018): 179–84. http://dx.doi.org/10.14195/1647-7723_25-2_14.

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O Marco de Ação de Sendai estabelece o plano global de prevenção reafirmando a necessidade de comprometimento para se reduzir o risco. Este trabalho apresenta a I Jornada Fluminense de Redução do Risco de Desastres realizada pela SEDEC-RJ (Secretaria de Estado de Defesa Civil) em 2015 no Rio de Janeiro, na qual foram apresentadas ações realizadas pelas COMDECs (Coordenadorias Municipais de Defesa Civil) a partir do Marco de Sendai. A jornada proporcionou o compartilhamento de boas práticas estimulando a troca de experiências entre profissionais da Proteção e Defesa Civil, bem como a valorização dos esforços por parte desses profissionais e o fomento de iniciativas em educação, contribuindo na formação destes no que diz respeito à implementação das diretrizes do Marco de Sendai para Redução do Risco de Desastres no Estado do Rio de Janeiro.

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Hoekstra, Dick, and Karin Klappe. "Use of a fluorescence assay to monitor the kinetics of fusion between erythrocyte ghosts, as induced by sendai virus." Bioscience Reports 6, no. 11 (November 1, 1986): 953–60. http://dx.doi.org/10.1007/bf01114971.

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The kinetics of the fusion process between erythrocyte ghosts, as induced by Sendal virus, were readily revealed by a simple fluorescence procedure previously employed to characterize the fusion of viruses with biological membranes. The method relies on the relief of fluorescence selfquenching of the membrane-inserted probe octadecyl Rhodamine B chloride (R18) as occurs when labeled membranes fuse with unlabeled counterparts. The kinetics of R18 insertion into ghost membranes, the non-exchangeable properties of the fluorophore and the kinetics, and some characteristics of Sendai virus-induced fusion of ghosts, are described. We propose that the experimental approach may be particularly advantageous to obtain insight into the efficiency and mechanism of a wide range of fusogens, capable of inducing fusion of erythrocyte membranes.

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MacDonald, Fiona, Brett Woods, Carla Hall, Tim Corney, and Derm Ryan. "Joining the dots to reimagine community resilience: empowering young people." October 2023 10.47389/38, No 4 (October 2023): 85–89. http://dx.doi.org/10.47389/38.4.85.

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Historically, disaster response management for children and young people, people from linguistically diverse cultural backgrounds and Aboriginal and Torres Strait Islander peoples have been shaped by a vulnerability and risk discourse, informed by trauma-informed and risk mitigation strategies. These are vital, but the vulnerability discourse has moved into other areas of disaster prevention, preparedness, response, recovery and resilience. Vulnerability has been linked to pre-existing, socially produced inequalities and power structures. This has worked to homogenise, marginalise and diminish the capability of community members in resilience efforts. The United Nations Sendai Framework for Disaster Risk Reduction 2015-2030 [Sendai Framework] calls for governments and relevant stakeholders to ‘advocate for resilient communities and an inclusive and all-of-society disaster risk management’ (UNDRR 2015, p.23). This includes the meaningful engagement of people who are marginalised from resilience building. The Sendai Framework makes a specific argument for engaging children and young people, declaring they are agents of change who should be given the space to contribute to disaster risk reduction. The aim of this paper is to consider how the Sendai Framework has influenced the inclusion of young people in disaster resilience and to introduce emerging evidence of how young people are joining the dots to reimagine community resilience.

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Nishio, Machiko, Ai Nagata, Ayako Yamamoto, Masato Tsurudome, Morihiro Ito, Mitsuo Kawano, Hiroshi Komada, and Yasuhiko Ito. "The properties of recombinant Sendai virus having the P gene of Sendai virus pi strain derived from BHK cells persistently infected with Sendai virus." Medical Microbiology and Immunology 195, no. 3 (February 8, 2006): 151–58. http://dx.doi.org/10.1007/s00430-006-0012-3.

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Mysiak, Jaroslav, Swenja Surminski, Annegret Thieken, Reinhard Mechler, and Jeroen Aerts. "Brief communication: Sendai framework for disaster risk reduction – success or warning sign for Paris?" Natural Hazards and Earth System Sciences 16, no. 10 (September 30, 2016): 2189–93. http://dx.doi.org/10.5194/nhess-16-2189-2016.

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Abstract. In March 2015, a new international blueprint for disaster risk reduction (DRR) was adopted in Sendai, Japan, at the end of the Third UN World Conference on Disaster Risk Reduction (WCDRR, 14–18 March 2015). We review and discuss the agreed commitments and targets, as well as the negotiation leading the Sendai Framework for DRR (SFDRR) and discuss briefly its implication for the later UN-led negotiations on sustainable development goals and climate change.

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Archer, Frank, Caroline Spencer, and Dudley McArdle. "From Yokohama, Hyogo, and Sendai to the World: The Global Legacy of Kobe." Prehospital and Disaster Medicine 34, s1 (May 2019): s133. http://dx.doi.org/10.1017/s1049023x19002905.

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Introduction:The Hyogo and Sendai Frameworks for Disaster Reduction are well known and have been influential globally. However, less is known of their broader contexts.Aim:A recent opportunity to visit Kobe, Japan, provided an opportunity to experience the rich, and largely unknown tapestry behind the scenes of the Hyogo and Sendai Frameworks. This paper aims to illuminate the journey of the Kobe Legacy and its global influence.Methods:An experiential visit to Kobe and exploring its rich resources relating to disaster risk reduction.Results:The First World Conference on Natural Disasters, was held in Yokohama, Japan, in 1994. Almost immediately, Kobe experienced the Great Hanshin Earthquake, January 17, 1995, resulting in 6,434 dead, 43,792 injured, and 249,180 homes damaged. The United Nations International Strategy for Disaster Reduction (2000 – 2005) culminated in the Second World Conference on Disaster Reduction, Kobe, 2005 and the Hyogo Framework for Action 2005 – 2015. The Great East Japan Earthquake occurred on March 11, 2011, with 18,453 dead or missing, 6157 injured, 1.1M homes damaged, with a tsunami and nuclear accidents. The Third World Conference on Disaster Risk Reduction followed in Sendai in 2015 with the Sendai Framework for Disaster Risk Reduction 2015 – 2030 agreed on. Subsequently, the Sendai Framework has further evolved. However, behind the scenes, Kobe has developed a rich tapestry of insightful and valuable resources which will be outlined in this presentation.Discussion:In the words of the Mayor of Kobe, Mr. Tatsuo Yada in 2010, “I would like to reaffirm my determination to never allow our experiences of the disaster to fade away. It is our responsibility to make the utmost effort for disaster prevention and mitigation and keep passing on our experiences and the lessons learned to future generations”. This is the real legacy of Kobe.

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Kanzaki, Luis I. B. "Replicação de sendai virus em células epiteliais primárias de camundongo." Revista do Instituto de Medicina Tropical de São Paulo 29, no. 1 (February 1987): 33–36. http://dx.doi.org/10.1590/s0036-46651987000100005.

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Células epiteliais primárias obtidas do trato respiratório de camundongos jovens foram infectadas com o Vírus Hemaglutinante do Japão (HVJ, Sendai Virus) e, a progénie viral, tratada ou não com tripsina foi titulada através do método de Imunofluorescência Indireta. A progénie de Sendai Virus obtida de células epiteliais primárias de camundongo apresentou um título considerável, demonstrando-se que há ativação das partículas virais, capazes de infectar células LLC-MK 2, nas quais, a progénie viral foi titulada.

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Mysiak, J., S. Surminski, A. Thieken, R. Mechler, and J. Aerts. "Brief Communication: Sendai Framework for Disaster Risk Reduction – success or warning sign for Paris?" Natural Hazards and Earth System Sciences Discussions 3, no. 6 (June 16, 2015): 3955–66. http://dx.doi.org/10.5194/nhessd-3-3955-2015.

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Abstract. In March 2015, a new international blueprint for disaster risk reduction (DRR) has been adopted in Sendai, Japan, at the end of the Third UN World Conference on Disaster Risk Reduction (WCDRR, 14–18 March 2015). We review and discuss the agreed commitments and targets, as well as the negotiation leading to the Sendai Framework for DRR (SFDRR) and discuss briefly its implication for the later UN-led negotiations on sustainable development goals and climate change.

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Wei, Wesley, Mohammad Mojtahedi, Maziar Yazdani, and Kamyar Kabirifar. "The Alignment of Australia’s National Construction Code and the Sendai Framework for Disaster Risk Reduction in Achieving Resilient Buildings and Communities." Buildings 11, no. 10 (September 23, 2021): 429. http://dx.doi.org/10.3390/buildings11100429.

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The risks associated with extreme weather events induced by climate change are increasingly being recognized, and must be addressed through each country’s construction regulations, building codes, and standards. Ensuring that buildings and cities are resilient against disasters is becoming more important. Few studies have analyzed the impact of global polices and frameworks in reducing disaster risks and increasing resilience in built environments. This research reviews disasters associated with climate change in the Sendai Framework for Disaster Risk Reduction 2015–2030, analyzing how Australia’s National Construction Code is aligned with the framework and the potential implications for reducing disaster risk. Decision-makers in construction companies in Sydney, Australia, were surveyed. The results show there is a statistically significant link among the National Construction Code, the Sendai Framework, and building resilience. The Sendai Framework is an effective mediator in this three-pronged relationship that can further enhance building resilience in Australia. Stakeholders in the construction industry will need to incorporate disaster risk reduction practices, especially authorities, such as local governments, building commissioners, and building certifiers that are responsible for the approval, quality, and defects mitigation of development applications and best practices. Overall, implementation of the Sendai Framework will help develop more regulations and standards for resilient buildings, set targets, and make improvements over time in the Australian construction industry.

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Algarté, Michèle, Hannah Nguyen, Christophe Heylbroeck, Rongtuan Lin, and John Hiscott. "IκB-Mediated Inhibition of Virus-Induced Beta Interferon Transcription." Journal of Virology 73, no. 4 (April 1, 1999): 2694–702. http://dx.doi.org/10.1128/jvi.73.4.2694-2702.1999.

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ABSTRACT We have examined the consequences of overexpression of the IκBα and IκBβ inhibitory proteins on the regulation of NF-κB-dependent beta interferon (IFN-β) gene transcription in human cells after Sendai virus infection. In transient coexpression studies or in cell lines engineered to express different forms of IκB under tetracycline-inducible control, the IFN-β promoter (−281 to +19) linked to the chloramphenicol acetyltransferase reporter gene was differentially inhibited in response to virus infection. IκBα exhibited a strong inhibitory effect on virus-induced IFN-β expression, whereas IκBβ exerted an inhibitory effect only at a high concentration. Despite activation of the IκB kinase complex by Sendai virus infection, overexpression of the double-point-mutated (S32A/S36A) dominant repressors of IκBα (TD-IκBα) completely blocked IFN-β gene activation by Sendai virus. Endogenous IFN-β RNA production was also inhibited in Tet-inducible TD-IκBα-expressing cells. Inhibition of IFN-β expression directly correlated with a reduction in the binding of NF-κB (p50-RelA) complex to PRDII after Sendai virus infection in IκBα-expressing cells, whereas IFN-β expression and NF-κB binding were only slightly reduced in IκBβ-expressing cells. These experiments demonstrate a major role for IκBα in the regulation of NF-κB-induced IFN-β gene activation and a minor role for IκBβ in the activation process.

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Tapia, Karla, and Carolina López. "Do immunostimulatory defective viral genomes arise during natural infections? (49.16)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 49.16. http://dx.doi.org/10.4049/jimmunol.186.supp.49.16.

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Abstract The generation of defective viral genomes (DVGs) during the replication of viruses in vitro has been described for many different viruses including influenza, vesicular stomatitis and rabies. DVGs are truncated forms of the standard virus genome that are unable to replicate due to the lack of a functional viral polymerase. We have shown that DVGs have a potent ability to elicit the activation of dendritic cells in vitro demonstrating their exceptional capacity to trigger innate immunity. The presence of DVGs in viral preparations has been broadly correlated with protection against lethal doses of viruses. It was recently shown that RIG-I predominantly binds DVGs during infections with Sendai virus. The role of DVGs during natural infections is not known. Infection of bone marrow dendritic cells with different strains of Sendai virus showed that DVGs of different sizes are detected in all the viral preparations. In addition, infection with a Sendai virus strain that had been depleted of DVGs results in DVG generation at late points after infection correlating with the peak of viral replication. Interestingly, in mice infected with Sendai virus lacking DVGs we could also detect the appearance of DVGs at late times of infection. Together, these results show that DVGs can arise during the course of a natural virus infection stimulating exciting questions regarding their role stimulating anti-viral immune responses.

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Pietila, Taija E., Ville Veckman, Anne Lehtonen, Pamela Osterlund, and Ilkka Julkunen. "The Regulation of CCL19 Gene Expression in Human Antigen Presenting Cells (B49)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): LB10. http://dx.doi.org/10.4049/jimmunol.178.supp.b49.

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Abstract CCL19 chemokine plays an important role in regulating DC traffic and recruitment of naïve T cells to the vicinity of activated DCs and macrophages. We have analyzed the regulation of CCL19 gene expression in human monocyte-derived DCs/macrophages infected with Salmonella enterica or Sendai virus. Computer analysis of the CCL19 promoter identified two putative NF-κB binding sites and one interferon stimulated response element (ISRE). Transcription factor binding experiments demonstrated that Salmonella or Sendai virus infection increased the binding of NF-κB proteins (p50, p52, p65, and RelB) to both CCL19 promoter NF-κB elements. Salmonella or Sendai virus infection also increased the binding of multiple IRFs, as well as STAT1 and STAT2, to the ISRE site. The role of NF-κB and various IRF family members in transcriptional control of CCL19 gene was further studied in transfection experiments. The expression of NF-κB dimers readily activated CCL19 promoter. The expression of IRF1, IRF3, or IRF7 proteins was also able to activate the promoter in the presence of Sendai virus infection. CCL19 promoter constructs containing mutated NF-κB and/or ISRE sites were weakly activated. Our data also suggests that c-Jun and c-Fos proteins binding to target AP-1 elements in CCL19 promoter plays a role in transcriptional control of CCL19. Further work focuses on the regulation of CCL19 in human macrophages and myeloid DCs.

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Matveeva, O. V., G. V. Kochneva, S. V. Netesov, S. B. Onikienko, and P. M. Chumakov. "Mechanisms of Oncolysis by Paramyxovirus Sendai." Acta Naturae 7, no. 2 (June 15, 2015): 6–16. http://dx.doi.org/10.32607/20758251-2015-7-2-6-16.

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Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.

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Chandra, Sunandini, Raju Kalaivani, Manoj Kumar, Narayanaswamy Srinivasan, and Debi P. Sarkar. "Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes." Molecular Biology of the Cell 28, no. 26 (December 15, 2017): 3801–14. http://dx.doi.org/10.1091/mbc.e17-06-0400.

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Reconstituted Sendai viral envelopes (virosomes) are well recognized for their promising potential in membrane fusion–mediated delivery of bioactive molecules to liver cells. Despite the known function of viral envelope glycoproteins in catalyzing fusion with cellular membrane, the role of host cell proteins remains elusive. Here, we used two-dimensional differential in-gel electrophoresis to analyze hepatic cells in early response to virosome-induced membrane fusion. Quantitative mass spectrometry together with biochemical analysis revealed that villin, an actin-modifying protein, is differentially up-regulated and phosphorylated at threonine 206—an early molecular event during membrane fusion. We found that villin influences actin dynamics and that this influence, in turn, promotes membrane mixing through active participation of Sendai viral envelope glycoproteins. Modulation of villin in host cells also resulted in a discernible effect on the entry and egress of progeny Sendai virus. Taken together, these results suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor villin.

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Liang, X. P., M. E. Lamm, and J. G. Nedrud. "Oral administration of cholera toxin-Sendai virus conjugate potentiates gut and respiratory immunity against Sendai virus." Journal of Immunology 141, no. 5 (September 1, 1988): 1495–501. http://dx.doi.org/10.4049/jimmunol.141.5.1495.

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Abstract Successful oral immunization to prevent infectious diseases in the gastrointestinal tract as well as distant mucosal tissues may depend on the effectiveness of an Ag to induce gut immune responses. We and others have previously reported that cholera toxin possesses strong adjuvant effects on the gut immune response to co-administered Ag. To explore further adjuvant effects of cholera toxin, the holotoxin or its B subunit was chemically cross-linked to Sendai virus. The resulting conjugates, which were not infectious, were evaluated for their capacity to induce gut immune responses against Sendai virus after oral administration to mice. Conjugating cholera toxin to virus significantly enhanced the adjuvant activity of cholera toxin compared to simple mixing. Cholera toxin B subunit, however, did not show an adjuvant effect either by itself or conjugated with the virus. Oral administration of the Sendai virus-cholera toxin conjugate was also able to prime for protective anti-viral responses in the respiratory tract. Mice that were orally immunized with the conjugate and intra-nasally boosted with inactivated virus alone showed virus-specific IgA titers in nasal secretions that correlated with protection against direct nasal challenge with live Sendai virus. For comparison, s.c. immunization was also studied. Systemic immunization with the virus-cholera toxin conjugate induced virus-specific antibody responses in serum as well as in the respiratory tract but failed to protect the upper respiratory tract against virus challenge. Systemic immunization plus an intra-nasal boost did, however, confer a variable degree of protection to the upper respiratory tract, which correlated primarily with bronchoalveolar lavage (lung) antibody titers.

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Egawa, Takashi. "Niigata-Sendai natural gas pipeline project." Journal of the Japanese Association for Petroleum Technology 62, no. 2 (1997): 112–21. http://dx.doi.org/10.3720/japt.62.112.

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Journal articles on the topic 'Sendai'

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