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Relevant bibliographies by topics / T-dependent

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Academic literature on the topic 'T-dependent'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "T-dependent"

1

Andersen, Mads Hald. "T-cell dependent immunoselection." OncoImmunology 1, no. 7 (2012): 1003. http://dx.doi.org/10.4161/onci.20927.

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Khanolkar, Aaruni, Michael J. Fuller, and Allan J. Zajac. "CD4 T Cell-Dependent CD8 T Cell Maturation." Journal of Immunology 172, no. 5 (2004): 2834–44. http://dx.doi.org/10.4049/jimmunol.172.5.2834.

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Burattini, Laura, Wojciech Zareba, and Roberto Burattini. "Is T-wave alternans T-wave amplitude dependent?" Biomedical Signal Processing and Control 7, no. 4 (2012): 358–64. http://dx.doi.org/10.1016/j.bspc.2011.06.009.

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BOHM, ADAM, ARNOLD PINTER, and ISTVAN PREDA. "QT Dependent T Wave Sensing." Pacing and Clinical Electrophysiology 21, no. 7 (1998): 1490–91. http://dx.doi.org/10.1111/j.1540-8159.1998.tb00226.x.

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Maruyama, Toru. "Rate-Dependent Repolarization Dynamics: Correlation between Electrocardiographic T Wave and U Wave." Rate-Dependent Repolarization Dynamics: Correlation between Electrocardiographic T Wave and U Wave 01, no. 01 (2018): 1–5. http://dx.doi.org/10.31546/jcccvt.1007.

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El Shikh, Mohey Eldin M., Rania M. El Sayed, Andras K. Szakal, and John G. Tew. "T-Independent Antibody Responses to T-Dependent Antigens: A Novel Follicular Dendritic Cell-Dependent Activity." Journal of Immunology 182, no. 6 (2009): 3482–91. http://dx.doi.org/10.4049/jimmunol.0802317.

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Yuntao Wu, Margaret H. Beddall, and Jon W. Marsh. "Rev-Dependent Indicator T Cell Line." Current HIV Research 5, no. 4 (2007): 394–402. http://dx.doi.org/10.2174/157016207781024018.

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Jeurissen, Axel, and Xavier Bossuyt. "T Cell-Dependent and -Independent Responses." Journal of Immunology 172, no. 5 (2004): 2728. http://dx.doi.org/10.4049/jimmunol.172.5.2728.

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Ketland, J. "Conservativeness and translation-dependent T-schemes." Analysis 60, no. 4 (2000): 319–28. http://dx.doi.org/10.1093/analys/60.4.319.

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Cascalho, M., and JL Platt. "B cell-dependent T cell development." Acta Paediatrica 93 (January 2, 2007): 52–53. http://dx.doi.org/10.1111/j.1651-2227.2004.tb03057.x.

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Dissertations / Theses on the topic "T-dependent"

1

Pido, Jeffrey. "Factors affecting thymic-dependent T cell reconstitution." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406587.

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Cobb, Dustin. "T-bet-dependent regulation of T cell responses during Trypanosoma cruzi infection." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/372.

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The human pathogen Trypanosoma cruzi is an intracellular parasite and the etiological agent of Chagas disease. Protective immune responses to T. cruzi are highly dependent on T helper 1 and CD8+ T cells which produce interferon-gamma. A deficiency in these responses has severe consequences on the ability to control infection. Our investigation into the role of the Th1 transcription factor, T-bet, during murine T. cruzi infection revealed that T-bet is required for resistance. Contrary to our expectations, T-bet was not required for the development of Th1 immunity during infection, as T-bet-deficient mice still developed interferon-gamma-producing T cells. However, T-bet was required to suppress the differentiation of Th17 cells and for the expansion of T. cruzi-specific CD8+ T cells. We first sought to determine the cause of reduced numbers of T. cruzi-specific CD8+ T cells in infected T-bet-deficient mice. First, we found that impaired migration or survival did not contribute to the low number of T. cruzi-specific CD8+ T cells. Secondly, we determined that reduced numbers of CD8+ T cells was not secondary to a defect in antigen-presenting cell activation or priming of CD8+ T cells. A recapitulation of defective expansion in mice with normal T-bet-expressing antigen-presenting cells demonstrated that T-bet expression in T cells was required. Thus, we determined that T-bet regulates the expansion of antigen-specific CD8+ T cells during T. cruzi infection in a T cell-intrinsic manner. Although it was evident T-bet had an integral role in suppressing the development of Th17 cells in response to infection with T. cruzi, several issues remained unclear. The first was the apparent lack of a negative regulatory effect of IFN-g/IFN-g-signaling on Th17 cells, which contradicted published reports. To clarify the role of IFN-g, we investigated the effect of IFN-g- or Stat-1-deficiency during T. cruzi infection. Surprisingly, IFN-g did not have a major role in up-regulating T-bet or for suppressing the development of Th17 responses, whereas Stat-1 was necessary for both. This was unexpected as Stat-1 is an IFN-g-inducible transcription factor, and its activation leads to T-bet induction. Thus, the T-bet-mediated inhibition of Th17 responses during T. cruzi infection is dependent on Stat-1, but not IFN-g. The final aim of this project was to identify the cytokines that negatively regulate Th17 differentiation in response to T. cruzi. We focused on the IL-12-family cytokines, IL-12 and IL-27, which are known to regulate T cell responses. Indeed, IL-12-deficient mice infected with T. cruzi developed a significant increase in Th17 cells similar to that observed in T-bet-deficient mice. Surprisingly, and in contrast to published results in other models, IL-27-deficient mice did not exhibit an increase in Th17 development. Our results demonstrate that IL-12, but not IL-27, is necessary for optimal T-bet expression and regulation of Th17 responses during T. cruzi infection.

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Long, Tianying. "Autoaggressive T cells in insulin-dependent diabetes mellitus." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60429.

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Considerable evidence suggests that insulin-dependent diabetes mellitus (IDDM) is a T cell-mediated autoimmune process that is directed against antigenic target(s) on pancreatic $ beta$ cells. To better understand T cell involvement in the pathogenesis of IDDM, a panel of T cell hybridomas were produced from pancreas-derived T cells of spontaneously diabetic NOD mice. A total of 119 hybridomas were constructed from 8 fusions and 94 of these were tested. Twelve hybridomas were found to be islet-reactive since they produced high level of interleukin-2 (IL-2) in the presence of NOD islet cells and NOD antigen-presenting cells (APC's). The responses could also be detected against islet cells of other strains (i.e. C3H/Hej or C57B1/6), but only in the presence of the NOD APC's. Phenotyping of these islet-reactive hybridomas showed that all of them were CD3$ sp{+}$CD4$ sp{+}$. Furthermore, a high frequency (39%) of CD4$ sp{+}$ T hybridomas in the panel were found to be islet reactive. In addition, analysis of T-cell receptor (TCR) V$ sb{ beta}$ expression of these islet-reactive T-cell hybridomas revealed that TCR V$ sb{ beta}$ element usage is heterogeneous unlike findings in some experimentally induced autoimmune diseases.

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Zarozinski, Christopher C. "T Cell Receptor-Dependent and Independent Events During Potent Anti-Viral T Cell Responses." eScholarship@UMMS, 1998. http://escholarship.umassmed.edu/gsbs_diss/175.

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The relative contribution of T cell receptor-dependent stimulation versus TcR-independent bystander stimulation in the massive increase in the number of activated proliferating CD8+ T cells seen during acute many acute viral infections is unclear. To determine if this increase was the result of TcR-independent bystander activation and proliferation, anti-viral cytotoxic T lymphocytes were induced in vivo via DNA immunization so that the anti-viral immune response could be examined in the absence of the high levels of cytokines generated during acute infection. After a single immunization with a plasmid encoding the nucleoprotein of the lymphocytic choriomeningitis virus (LCMV) a nearly 2 log10 reduction in viral titers in the spleen was observed 3 days after LCMV infection. After 2 or 3 immunizations a greater that 3 log10 inhibition of viral titers in the spleen was observed, with most animals having no detectable virus. After intracerebral challenge vaccinated animals displayed either protection or enhanced immunopathology leading to accelerated kinetics of death. By limiting dilution analysis LCMV-specific CTL precursors were detected in both the spleen and lymph nodes of vaccinated animals. C57BL/6 mice inoculated with DNA demonstrated an anamnestic CTL response detectable at days 4 after LCMV challenge. However, the numbers of CTL precursors elicited by DNA vaccination was too low to determine if cytokine-mediated TcR-independent bystander activation and proliferation had taken place. HY-specific TcR-transgenic mice, which have a restricted TcR repertoire, and LCMV-carrier mice, which are tolerant to LCMV, were used to determine the extent of TcR-independent bystander activation and proliferation during acute LCMV infection. LCMV infection of C57BL/6 mice induced CTL that lysed uninfected H-2k and H-2d allogeneic targets, but, LCMV-induced CTL from HY- transgenic mice lysed only the H-2k-expressing cells. The HY-mice generated both anti-H-2k and anti-H-2d CTL in mixed lymphocyte cultures, strongly suggesting that the generation of allospecific CTL during acute LCMV-infection is antigen specific. During the LCMV infection there was blastogenesis of the CDB+ T cell population, but the HY-specific T cells remained small in size, and did not alter their expression of the activation molecules CD44 and MEL-14. In order to examine the potential for bystander stimulation under conditions of a very strong CTL response, T cell chimeras were made between normal and HY-transgenic mice. Even in the context of a normal vicus-induced CTL response, no stimulation of HY -specific T cells was observed, and HY-specific cells were diluted in number by day 9 post-infection. In LCMV-carrier mice in which donor and host T cells could be distinguished by Thy 1 allotypic markers, adoptive transfer of LCMV-immune T cells into LCMV-carrier mice, whose T cells were tolerant to LCMV, resulted in activation and proliferation of donor CDB cells but little or no activation of host CDB+ T cells. These results show that TcR-independent bystander activation of non virus-specific T cells is not a significant component of an anti-viral T cell response and support the hypothesis that the massive polyclonal CTL response to LCMV infection is virus-specific. T cells activated during potent anti-viral immune responses are sensitized to undergo apoptosis after strong TcR-stimulation in a process known as activation-induced cell death (AICD). To determine if T cells, not participating in the immune response were also subject to AICD, LCMV-carrier mice were used. Using TUNEL flow cytometry, it was shown that after reconstitution of Thy 1.2+ LCMV-carrier mice with spleen cells from Thy 1.1+ LCMV-immune mice, the Thy 1.2+ host T cells which were not specific for the virus and did not proliferate in a bystander fashion, were rendered sensitive to TcR-induced apoptosis in vitro. This bystander sensitization to AICD was shown not to be dependent on the continued presence of activated proliferating donor cells during the in vitro culture period. Bystander sensitization to AICD was not the result of an antigen presenting cell defect, but rather was the result of an in vivo conditioning of the T cells themselves. The mechanism of this sensitization was, at least, partially dependent on the ability of host T cells to respond to IFNγ, and on the expression of Fas ligand on the activated, proliferating donor cells. This bystander sensitization to AICD may explain why memory T cell responses are so poor during acute viral infection and can serve as a potential mechanism for virus-induced immunosuppression.

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English, Kieran. "Deciphering the cellular mechanisms promoting CD4+ T cell-dependent intrahepatic CD8+ T cell immunity." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/27735.

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The liver is the body’s largest internal organ and assumes many important physiological and metabolic functions. It is also well-established that the liver possesses unique immunological properties and a delicate balance between tolerance and immunity exists within this large organ. CD4 T cell help to CD8 T cells has emerged as a critical factor involved in promoting robust CD8 T cell responses against viral and tumour antigens. Studies in humans and chimpanzees indicate that CD4 T cells are critical for strong intrahepatic CD8 T cell responses and the spontaneous control of hepatitis C virus and hepatitis B virus infections. However, due to limitations of current small animal models, the precise role of CD4 help in orchestrating intrahepatic CD8 T cell responses, and the mechanisms by which CD4 help is transferred to intrahepatic CD8 T cells remains poorly understood. Using an rAAV based approach to express model antigens containing both CD4 and CD8 T cell epitopes specifically in hepatocytes, we first demonstrate that CD4 help enhances the primary expansion of CD8 T cells responding to hepatocyte expressed antigens, which is critical for the generation of a large pool of memory CD8 T cells in the liver, blood and lymphoid tissues. Importantly, we decipher a novel mechanism facilitating the transfer of CD4 help to intrahepatic CD8 T cells: cognate CD40-CD40L licensing of hepatic XCR1 cDC1s in situ within portal tracts and central veins. In deciphering this mechanism, we also uncovered a previously unrecognised interconnected myeloid cell network contained within portal tracts in the steady state and following antigen expression in the liver. Together, these discoveries yield important insights into the mechanisms governing the outcome of intrahepatic immune responses, and suggest avenues for future work, with the possibility of translational research to explore novel therapies to manipulate intrahepatic immunity and hence beneficially alter outcomes in human liver diseases.

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Camoglio, Luisa. "IL-12 and T-lymphocyte dependent mucosal immune responses." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/82609.

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Wang, Shu-Fang. "Development of Notch-dependent T-cell leukemia by deregulated Rap1 signaling." 京都大学 (Kyoto University), 2008. http://hdl.handle.net/2433/137035.

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Macintyre, Andrew Neil. "Phosphoinositide dependent kinase 1 maintains T-Cell metabolism during proliferactive stress." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510626.

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Hertweck, Arnulf. "Dicer-dependent regulation of gene expression and development in T lymphocytes." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501208.

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Martin, Matthew David. "Time-dependent alterations in memory CD8 T cell function after infection." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3138.

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CD8 T cells play a critical role in the clearance of pathogenic bacteria, viruses, and protozoan parasites. Upon encountering their cognate antigen through either infection or vaccination, naïve CD8 T cells undergo robust proliferative expansion, which is followed by contraction and the formation of a memory population. Memory CD8 T cells are long-lived, and because they persist in increased numbers and possess enhanced functional abilities compared to naïve CD8 T cells, they are able to provide the host with increased protection following re-infection. Because of these properties, vaccines designed to elicit memory CD8 T cells have the potential to reduce health care burdens related to infection with pathogens including human immuno deficiency virus (HIV), malaria, influenza, and hepatitis virus. However, stimulating protective CD8 T cell responses against these pathogens through vaccination has proven challenging. Therefore, a better understanding of the properties of memory CD8 T cells generated following vaccination, and the characteristics of memory CD8 T cells best suited for providing protection against diverse pathogens is needed. While memory CD8 T cells can be maintained for as long as the life of the host, evidence suggests that their properties change with time after infection. Because CD8 T cell-mediated protection is based upon both the numbers and quality or functional abilities of memory cells present at the time of re-infection, changes in memory CD8 T cell function over time could impact their ability to provide protection upon re-infection. Therefore, a better understanding of how memory CD8 T cells change with time after infection is needed. As part of the studies presented in this thesis, I found that the phenotype and function of memory CD8 T cells including localization, interleukin (IL)-2 cytokine production, responsiveness to homeostatic cytokines, metabolic capabilities, and proliferation and secondary memory generation potential change with time after infection. Interestingly functional changes could not be completely explained by changes in subset composition that occur with time, as changes over time were also seen in defined CD62Lhi subsets. Importantly, functional changes of memory CD8 T cells that occurred with time led to an increased ability to provide protection against a chronic viral infection. These data improve our knowledge of the capabilities of memory CD8 T cells generated following infection, and suggests that the outcome of vaccination strategies designed to elicit protective memory CD8 T cells using single or prime-boost immunizations will depend upon the timing between antigen encounters. Following re-infection, memory CD8 T cells become activated and produce effector cytokines and cytolytic molecules that aid the host in clearing invading microbes. Activation can be triggered not only through cognate antigen recognition, but also by antigen-independent cytokine driven signals. However, our knowledge of how antigen-dependent and –independent signals contribute to CD8 T cell activation and protection following infection is incomplete. In the second part of my thesis, I show that the ability of memory CD8 T cells to become activated in response to inflammation decreases with time after infection, that antigen and inflammation act synergistically to induce activation of memory CD8 T cells, that the presence of cognate antigen enhances activation of memory CD8 T cells that contribute to clearance of infection, and that bystander memory CD8 T cell responses following unrelated bacterial infection do not provide the host with a protective benefit. Together, the data in this thesis further our understanding of memory CD8 T cells generated following infection and/or vaccination, and the properties of memory CD8 T cells important for providing protection upon re-infection with invading pathogens.

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Books on the topic "T-dependent"

1

Charles, Snow E., ed. T-cell dependent and independent B-cell activation. CRC Press, 1991.

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1955-, Suttles Jill, ed. T-cell signaling of macrophage activation: Cell contact-dependent and cytokine signals. R.G. Landes, 1995.

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Saoulli, Catherine. CD28-independent, TRAF2-dependent costimulation of resting T cells by 4-1BB ligand. National Library of Canada, 1998.

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Thaumaturgic prowess: Autonomous and dependent miracle-working in Mark's Gospel and the Second Temple period. Mohr Siebeck, 2019.

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Chen, Liane. Regulation and mechanism of perforin-dependent activation-induced T cell death. 2006.

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Nau, Gerard Joseph. Regulation of interleukin 2-dependent prolifration of cloned murine T lymphocytes. 1989.

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Levinsky, Yuri V. P-T-X Handbook, Pressure Dependent Phase Diagrams of Binary Alloys. Asm Intl, 1998.

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Fox, Casey John. Genetic regulation of contingent macrophage- and T cell-dependent steps in islet inflammation. 1999.

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Stout, Robert D. T-Cell Signaling of Macrophage Activation: Cell Contact-Dependent and Cytokine Signals (Archives of Toxicology). Springer, 1996.

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A. Bócsai, Zs. Ancsin, Cs. Fernye, et al. Dose-dependent short-term effects of T-2 toxin exposure on lipid peroxidation and antioxidant parameters of laying hens. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.115.

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Book chapters on the topic "T-dependent"

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Gooch, Jan W. "T-Dependent Antigen." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14929.

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Yockey, Ronald D. "The Dependent-Samples t Test." In SPSS® Demystified. Routledge, 2018. http://dx.doi.org/10.4324/9781315268545-9.

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Yockey, Ronald D. "The Dependent-Samples t Test." In SPSS Demystified, 4th ed. Routledge, 2023. http://dx.doi.org/10.4324/9781003028154-9.

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Holcomb, Zealure C., and Keith S. Cox. "t-Test for Dependent Groups I." In Interpreting Basic Statistics. Routledge, 2017. http://dx.doi.org/10.4324/9781315225647-42.

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Holcomb, Zealure C., and Keith S. Cox. "t-Test for Dependent Groups II." In Interpreting Basic Statistics. Routledge, 2017. http://dx.doi.org/10.4324/9781315225647-43.

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Piccotti, Joseph R. "T Cell-Dependent Antibody Response Tests." In Immunotoxicology Strategies for Pharmaceutical Safety Assessment. John Wiley & Sons, Inc., 2008. http://dx.doi.org/10.1002/9780470386385.ch6.

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Cox, Keith S., and Zealure C. Holcomb. "t-Test for Dependent Groups I." In Interpreting Basic Statistics, 9th ed. Routledge, 2021. http://dx.doi.org/10.4324/9781003096764-41.

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Cox, Keith S., and Zealure C. Holcomb. "t-Test for Dependent Groups II." In Interpreting Basic Statistics, 9th ed. Routledge, 2021. http://dx.doi.org/10.4324/9781003096764-42.

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Ladics, Gregory S. "The Sheep Erythrocyte T-Dependent Antibody Response (TDAR)." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8549-4_6.

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White, Kimber L., Deborah L. Musgrove, and Ronnetta D. Brown. "The Sheep Erythrocyte T-Dependent Antibody Response (TDAR)." In Methods in Molecular Biology. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-401-2_12.

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Conference papers on the topic "T-dependent"

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Christmann, BS, JL Werner, AR Fowlkes, AE Metz, and C. Steele. "STAT4-Dependent, T-Bet Independent Lung Immune Responses toPneumocystis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5547.

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Ghosh, Shirsendu. "Microvilli: The ERM Dependent Activation Hubs of T-Cells." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.482.

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Park, Jeong J., Shaoping Bian, and Mark G. Kuzyk. "Dynamics of intensity dependent refractive index using T-Scan." In International Symposium on Optical Science and Technology, edited by Manfred Eich and Mark G. Kuzyk. SPIE, 2002. http://dx.doi.org/10.1117/12.453855.

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Kauranen, Martti, Hannu Husu, Brian K. Canfield, et al. "Gap-dependent chiral coupling in T-shaped gold nanodimers." In Photonics Europe, edited by David L. Andrews, Jean-Michel Nunzi, and Andreas Ostendorf. SPIE, 2008. http://dx.doi.org/10.1117/12.780513.

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Tsai, Shun-Hung, Siou-An Jian, Yu-An Chen, H. K. Lam, and Yuandi Li. "Delay-dependent stabilization condition for T-S fuzzy neutral systems." In 2015 IEEE International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2015. http://dx.doi.org/10.1109/fuzz-ieee.2015.7337896.

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Shalapour, Shabnam, and Michael Karin. "Abstract B045: Immunosuppressive plasmocytes impede T-cell-dependent immunogenic chemotherapy." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b045.

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Zhang, Simon M. F., Johannes P. Seif, Thomas G. Allen, et al. "Temperature- and Illumination-Dependent Characterization of Solar Cells Using Suns-VOC(T) and I-V(T)." In 2021 IEEE 48th Photovoltaic Specialists Conference (PVSC). IEEE, 2021. http://dx.doi.org/10.1109/pvsc43889.2021.9518959.

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Bell, H., S. Lalnunhlimi, M. Green, F. Van Delft, and A. Krippner-Heidenreich. "Tumour Necrosis Factor receptor (TNFR)-signalling dependent killing in T-cell acute lymphoblastic leukaemia (T-ALL)." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687172.

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Yang, Xiaozhan, Hak-Keung Lam, and Ligang Wu. "Novel membership-function-dependent stability condition for T-S fuzzy systems." In 2016 IEEE International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2016. http://dx.doi.org/10.1109/fuzz-ieee.2016.7737966.

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Garibaldi, Brian T., Franco R. D'Alessio, Daniel C. Files, et al. "Regulatory T Cell Depletion Increases CXCL12-Dependent Fibroproliferation After LPS Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3982.

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Reports on the topic "T-dependent"

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Stritzinger, Laurel Elaine Winter, Y. Lai, Ross David Mcdonald, and R. E. Baumbach. Temperature Dependent Magnetoresistance of CeCu2Si2 up to 60 T [Proposal: P14728]. Office of Scientific and Technical Information (OSTI), 2017. http://dx.doi.org/10.2172/1351217.

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Zheng, Dao-Chen, L. Zamick, and H. Muether. Energy difference of T=1 and T=0 J{sup {pi}}=0{sup {minus}} states in {sup 16}O: Effects of the tensor interaction, configuration mixing, and density-dependent Dirac spinors. Office of Scientific and Technical Information (OSTI), 1992. http://dx.doi.org/10.2172/10141970.

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Zheng, Dao-Chen, L. Zamick, and H. Muether. Energy difference of T=1 and T=0 J[sup [pi]]=0[sup [minus]] states in [sup 16]O: Effects of the tensor interaction, configuration mixing, and density-dependent Dirac spinors. Office of Scientific and Technical Information (OSTI), 1992. http://dx.doi.org/10.2172/6606534.

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Levy, Maggie, Raymond Zielinski, and Anireddy S. Reddy. IQD1 Function in Defense Responses. United States Department of Agriculture, 2012. http://dx.doi.org/10.32747/2012.7699842.bard.

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The main objective of the proposed research was to study IQD1's mechanism of action and elucidate its role in plant protection. Preliminary experiments suggest that IQD1 binds CaM in a Ca²⁺-dependent manner and functions in general defense responses. We propose to identify proteins and genes that interact with IQD1, which may provide some clues to its mechanism of action. We also plan to dissect IQD1's integration in defense pathways and to study and modulate its binding affinity to CaM in order to enhance crop resistance. Our specific objectives were: (1) Analysis of IQD1's CaM-binding properties; (2) Identification of IQD1 targets;(3) Dissection of IQD1 integration into defense signaling pathways. Analysis of IQD1's CaM-binding properties defined four potential classes of sequences that should affect CaM binding: one is predicted to raise the affinity for Ca²⁺-dependent interaction but have no effect on Ca²⁺-independent binding; a second is predicted to act like the first mutation but eliminate Ca²⁺-independent binding; a third has no predicted effect on Ca²⁺-dependent binding but eliminates Ca²⁺-independent binding; and the fourth is predicted to eliminate or greatly reduce both Ca²⁺-dependent and Ca²⁺-independent binding. Following yeast two hybrid analysis we found that IQD1 interact with AtSR1 (Arabidopsis thalianaSIGNALRESPONSIVE1), a calcium/calmodulin-binding transcription factor, which has been shown to play an important role in biotic and abiotic stresses. We tested IQD1 interaction with both N-terminal or C-terminal half of SR1. These studies have uncovered that only the N-terminal half of the SR1 interacts with the IQD1. Since IQD1 has an important role in herbivory, its interaction with SR1 suggests that it might also be involved in plant responses to insect herbivory. Since AtSR1, like IQD1, is a calmodulin-binding protein and the mutant showed increased sensitivity to a herbivore, we analyzed WT, Atsr1 and the complemented line for the levels of GS to determine if the increased susceptibility of Atsr1 plants to T. ni feeding is associated with altered GS content. In general, Atsr1 showed a significant reduction in both aliphatic and aromatic GS levels as compared to WT. In order to study IQD1's molecular basis integration into hormone-signaling pathways we tested the epistatic relationships between IQD1 and hormone-signaling mutants. For that purpose we construct double mutants between IQD1ᴼXᴾ and mutants defective in plant-hormone signaling and GS accumulation. Epitasis with SA mutant NahG and npr1-1 and JA mutant jar1-1 suggested IQD1 function is dependent on both JA and SA as indicated by B. cinerea infection assays. We also verified the glucosinolate content in the crosses siblings and found that aliphatic GSL content is reduced in the double transgenic plants NahG:IQD1ᴼXᴾ as compare to parental lines while the aliphatic GSL content in the npr1-1:IQD1ᴼXᴾ and jar1-1: IQD1ᴼXᴾ double mutants was intimidated to the parental lines. This suggests that GSL content dependency on SA is downstream to IQD1. As a whole, this project should contribute to the development of new defense strategies that will improve crop protection and reduce yield losses and the amount of pesticides required; these will genuinely benefit farmers, consumers and the environment.

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Casey, D. P. p{sub T} dependence of inclusive Z boson production. Office of Scientific and Technical Information (OSTI), 1996. http://dx.doi.org/10.2172/618794.

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Harman, Gary E., and Ilan Chet. Enhancement of plant disease resistance and productivity through use of root symbiotic fungi. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7695588.bard.

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The objectives of the project were to (a) compare effects ofT22 and T-203 on growth promotion and induced resistance of maize inbred line Mol7; (b) follow induced resistance of pathogenesis-related proteins through changes in gene expression with a root and foliar pathogen in the presence or absence of T22 or T-203 and (c) to follow changes in the proteome of Mol? over time in roots and leaves in the presence or absence of T22 or T-203. The research built changes in our concepts regarding the effects of Trichoderma on plants; we hypothesized that there would be major changes in the physiology of plants and these would be reflected in changes in the plant proteome as a consequence of root infection by Trichoderma spp. Further, Trichoderma spp. differ in their effects on plants and these changes are largely a consequence of the production of different elicitors of elicitor mixtures that are produced in the zone of communication that is established by root infection by Trichoderma spp. In this work, we demonstrated that both T22 and T-203 increase growth and induce resistance to pathogens in maize. In Israel, it was shown that a hydrophobin is critical for root colonization by Trichoderma strains, and that peptaibols and an expansin-like protein from Ttrichoderma probably act as elicitors of induced resistance in plants. Further, this fungus induces the jasmonate/ethylene pathway of disease resistance and a specific cucumber MAPK is required for transduction of the resistance signal. This is the first such gene known to be induced by fungal systems. In the USA, extensive proteomic analyses of maize demonstrated a number of proteins are differentially regulated by T. harzianum strain T22. The pattern of up-regulation strongly supports the contention that this fungus induces increases in plant disease resistance, respiratory rates and photosynthesis. These are all very consistent with the observations of effects of the fungus on plants in the greenhouse and field. In addition, the chitinolytic complex of maize was examined. The numbers of maize genes encoding these enzymes was increased about 3-fold and their locations on maize chromosomes determined by sequence identification in specific BAC libraries on the web. One of the chitinolytic enzymes was determined to be a heterodimer between a specific exochitinase and different endochitinases dependent upon tissue differences (shoot or root) and the presence or absence of T. harzianum. These heterodimers, which were discovered in this work, are very strongly antifungal, especially the one from shoots in the presence of the biocontrol fungus. Finally, RNA was isolated from plants at Cornell and sent to Israel for transcriptome assessment using Affymetrix chips (the chips became available for maize at the end of the project). The data was sent back to Cornell for bioinformatic analyses and found, in large sense, to be consistent with the proteomic data. The final assessment of this data is just now possible since the full annotation of the sequences in the maize Affy chips is just now available. This work is already being used to discover more effective strains of Trichoderma. It also is expected to elucidate how we may be able to manipulate and breed plants for greater disease resistance, enhanced growth and yield and similar goals. This will be possible since the changes in gene and protein expression that lead to better plant performance can be elucidated by following changes induced by Trichoderma strains. The work was in, some parts, collaborative but in others, most specifically transcriptome analyses, fully synergistic.

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Strycker, Glenn Loyd. Measurement of the inclusive forward-backward t$\bar{t}$ production asymmetry and its rapidity dependence dA_fb/d(Δy). Office of Scientific and Technical Information (OSTI), 2010. http://dx.doi.org/10.2172/988435.

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Zeman, J., G. Martinez, P. Y. Yu, and K. Uchida. Magnetic field dependence of up-converted photoluminescence in partially ordered GaInP{sub 2}/GaAs up to 23 T. Office of Scientific and Technical Information (OSTI), 1996. http://dx.doi.org/10.2172/446412.

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Epel, Bernard L., Roger N. Beachy, A. Katz, et al. Isolation and Characterization of Plasmodesmata Components by Association with Tobacco Mosaic Virus Movement Proteins Fused with the Green Fluorescent Protein from Aequorea victoria. United States Department of Agriculture, 1999. http://dx.doi.org/10.32747/1999.7573996.bard.

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The coordination and regulation of growth and development in multicellular organisms is dependent, in part, on the controlled short and long-distance transport of signaling molecule: In plants, symplastic communication is provided by trans-wall co-axial membranous tunnels termed plasmodesmata (Pd). Plant viruses spread cell-to-cell by altering Pd. This movement scenario necessitates a targeting mechanism that delivers the virus to a Pd and a transport mechanism to move the virion or viral nucleic acid through the Pd channel. The identity of host proteins with which MP interacts, the mechanism of the targeting of the MP to the Pd and biochemical information on how Pd are alter are questions which have been dealt with during this BARD project. The research objectives of the two labs were to continue their biochemical, cellular and molecular studies of Pd composition and function by employing infectious modified clones of TMV in which MP is fused with GFP. We examined Pd composition, and studied the intra- and intercellular targeting mechanism of MP during the infection cycle. Most of the goals we set for ourselves were met. The Israeli PI and collaborators (Oparka et al., 1999) demonstrated that Pd permeability is under developmental control, that Pd in sink tissues indiscriminately traffic proteins of sizes of up to 50 kDa and that during the sink to source transition there is a substantial decrease in Pd permeability. It was shown that companion cells in source phloem tissue export proteins which traffic in phloem and which unload in sink tissue and move cell to cell. The TAU group employing MP:GFP as a fluorescence probe for optimized the procedure for Pd isolation. At least two proteins kinases found to be associated with Pd isolated from source leaves of N. benthamiana, one being a calcium dependent protein kinase. A number of proteins were microsequenced and identified. Polyclonal antibodies were generated against proteins in a purified Pd fraction. A T-7 phage display library was created and used to "biopan" for Pd genes using these antibodies. Selected isolates are being sequenced. The TAU group also examined whether the subcellular targeting of MP:GFP was dependent on processes that occurred only in the presence of the virus or whether targeting was a property indigenous to MP. Mutant non-functional movement proteins were also employed to study partial reactions. Subcellular targeting and movement were shown to be properties indigenous to MP and that these processes do not require other viral elements. The data also suggest post-translational modification of MP is required before the MP can move cell to cell. The USA group monitored the development of the infection and local movement of TMV in N. benthamiana, using viral constructs expressing GFP either fused to the MP of TMV or expressing GFP as a free protein. The fusion protein and/or the free GFP were expressed from either the movement protein subgenomic promoter or from the subgenomic promoter of the coat protein. Observations supported the hypothesis that expression from the cp sgp is regulated differently than expression from the mp sgp (Szecsi et al., 1999). Using immunocytochemistry and electron microscopy, it was determined that paired wall-appressed bodies behind the leading edge of the fluorescent ring induced by TMV-(mp)-MP:GFP contain MP:GFP and the viral replicase. These data suggest that viral spread may be a consequence of the replication process. Observation point out that expression of proteins from the mp sgp is temporary regulated, and degradation of the proteins occurs rapidly or more slowly, depending on protein stability. It is suggested that the MP contains an external degradation signal that contributes to rapid degradation of the protein even if expressed from the constitutive cp sgp. Experiments conducted to determine whether the degradation of GFP and MP:GFP was regulated at the protein or RNA level, indicated that regulation was at the protein level. RNA accumulation in infected protoplast was not always in correlation with protein accumulation, indicating that other mechanisms together with RNA production determine the final intensity and stability of the fluorescent proteins.

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