Relevant bibliographies by topics / Radiation Induced Activation

Academic literature on the topic 'Radiation Induced Activation'

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Published: 14 March 2023

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Journal articles on the topic "Radiation Induced Activation"

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TAKAMASA, Tomoji, Koji OKAMOTO, Kaichiro MISHIMA, and Masahiro FURUYA. "Radiation Induced Surface Activation." Journal of the Atomic Energy Society of Japan / Atomic Energy Society of Japan 45, no. 2 (2003): 112–17. http://dx.doi.org/10.3327/jaesj.45.112.

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KIKUCHI, Takayoshi, Yoshinori HIROSE, Tatsuya HAZUKU, and Tomoji TAKAMASA. "ICONE15-10316 EFFECT OF RADIATION INDUCED SURFACE ACTIVATION ON SURFACE WETTABILITY IN HIGH-TEMPERATURE CONDITION." Proceedings of the International Conference on Nuclear Engineering (ICONE) 2007.15 (2007): _ICONE1510. http://dx.doi.org/10.1299/jsmeicone.2007.15._icone1510_160.

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Yang, Nong, Xican Gao, Xiaofei Qu, Ruiguang Zhang, Fan Tong, Qian Cai, Jihua Dong, Yu Hu, Gang Wu, and Xiaorong Dong. "PIDD Mediates Radiation-Induced Microglia Activation." Radiation Research 186, no. 4 (October 2016): 345–59. http://dx.doi.org/10.1667/rr14374.1.

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Dong, X., M. Luo, J. Dong, and G. Wu. "The Mechanism of Radiation-induced Microglia Activation." International Journal of Radiation Oncology*Biology*Physics 78, no. 3 (November 2010): S632—S633. http://dx.doi.org/10.1016/j.ijrobp.2010.07.1473.

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Redd, Priscilla S., Kankana Bardhan, May R. Chen, Amy V. Paschall, Chunwan Lu, Roni J. Bollag, Fengchong Kong, et al. "NF-κB acts as a molecular link between tumor cells and Th1/Tc1 T cells in the tumor microenvironment to exert radiation-mediated tumor suppression." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 213.3. http://dx.doi.org/10.4049/jimmunol.196.supp.213.3.

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Abstract Radiation is a local treatment for many types of solid cancers. About two thirds of cancer patients require radiation during the course of their disease treatment. Radiation modulates both tumor cells and immune cells in the tumor microenvironment to exert anti-tumor activity, but the molecular connection between tumor cells and immune cells that mediates radiation-exerted tumor suppression activity is largely unknown. We report here that radiation induces rapid activation of the p65/p50 and p50/p50 NF-κB complexes in human soft tissue sarcoma (STS) cells. Radiation-activated p65/p50 and p50/p50 bind to the TNFα promoter to activate its transcription in STS cells. Radiation-induced TNFα then induces tumor cell death in an autocrine manner. Smac mimetic BV6 induces cIAP1 and cIAP2 degradation to increase tumor cell sensitivity to radiation-induced cell death in vitro and to enhance radiation-mediated suppression of STS xenografts in vivo. Inhibition of caspases, RIP1, or RIP3 blocks radiation/TNFα-induced cell death, whereas inhibition of RIP1 blocks TNFα-induced caspase activation, suggesting that caspases and RIP1 act sequentially to mediate the non-compensatory cell death pathways. We determined in a syngeneic sarcoma mouse model that radiation up-regulates the NF-κB target genes IRF3, IFNβ, and the T cell chemokines CCL2 and CCL5 in the tumor microenvironment, which is associated with activation and increased infiltration of Th1/Tc1 T cells in the tumor microenvironment. Consequently, combined BV6 and radiation completely suppressed tumor growth in vivo. Radiation-induced NF-κB functions as a molecular link between tumor cells and immune cells in the tumor microenvironment for radiation mediated tumor suppression.
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Judge, J. L., K. M. Owens, S. J. Pollock, C. F. Woeller, T. H. Thatcher, J. P. Williams, R. P. Phipps, P. J. Sime, and R. M. Kottmann. "Ionizing radiation induces myofibroblast differentiation via lactate dehydrogenase." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 8 (October 15, 2015): L879—L887. http://dx.doi.org/10.1152/ajplung.00153.2015.

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Pulmonary fibrosis is a common and dose-limiting side-effect of ionizing radiation used to treat cancers of the thoracic region. Few effective therapies are available for this disease. Pulmonary fibrosis is characterized by an accumulation of myofibroblasts and excess deposition of extracellular matrix proteins. Although prior studies have reported that ionizing radiation induces fibroblast to myofibroblast differentiation and collagen production, the mechanism remains unclear. Transforming growth factor-β (TGF-β) is a key profibrotic cytokine that drives myofibroblast differentiation and extracellular matrix production. However, its activation and precise role in radiation-induced fibrosis are poorly understood. Recently, we reported that lactate activates latent TGF-β through a pH-dependent mechanism. Here, we wanted to test the hypothesis that ionizing radiation leads to excessive lactate production via expression of the enzyme lactate dehydrogenase-A (LDHA) to promote myofibroblast differentiation. We found that LDHA expression is increased in human and animal lung tissue exposed to ionizing radiation. We demonstrate that ionizing radiation induces LDHA, lactate production, and extracellular acidification in primary human lung fibroblasts in a dose-dependent manner. We also demonstrate that genetic and pharmacologic inhibition of LDHA protects against radiation-induced myofibroblast differentiation. Furthermore, LDHA inhibition protects from radiation-induced activation of TGF-β. We propose a profibrotic feed forward loop, in which radiation induces LDHA expression and lactate production, which can lead to further activation of TGF-β to drive the fibrotic process. These studies support the concept of LDHA as an important therapeutic target in radiation-induced pulmonary fibrosis.
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Yacoub, Adly, Anna Miller, Ruben W. Caron, Liang Qiao, David A. Curiel, Paul B. Fisher, Michael P. Hagan, Steven Grant, and Paul Dent. "Radiotherapy-induced signal transduction." Endocrine-Related Cancer 13, Supplement_1 (December 2006): S99—S114. http://dx.doi.org/10.1677/erc.1.01271.

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Exposure of tumor cells to ionizing radiation causes compensatory activation of multiple intracellular survival signaling pathways to maintain viability. In human carcinoma cells, radiation exposure caused an initial rapid inhibition of protein tyrosine phosphatase function and the activation of ERBB receptors and downstream signaling pathways. Radiation-induced activation of extracellular regulated kinase (ERK)1/2 promoted the cleavage and release of paracrine ligands in carcinoma cells which caused re-activation of ERBB family receptors and intracellular signaling pathways. Blocking ERBB receptor phosphorylation or ERK1/2 pathway activity using small-molecule inhibitors of kinases for a short period of time following exposure (3 h) surprisingly protected tumor cells from the toxic effects of ionizing radiation. Prolonged exposure (48–72 h) of tumor cells to inhibition of ERBB receptor/ERK1/2 function enhanced radiosensitivity. In addition to ERBB receptor signaling, expression of activated forms of RAS family members and alterations in p53 mutational status are known to regulate radiosensitivity apparently independent of ERBB receptor function; however, changes in RAS or p53 mutational status, in isogenic HCT116 cells, were also noted to modulate the expression of ERBB receptors and ERBB receptor paracrine ligands. These alterations in receptor and ligand expression correlated with changes in the ability of HCT116 cells to activate ERK1/2 and AKT after irradiation, and to survive radiation exposure. Collectively, our data in multiple human carcinoma cell lines argues that tumor cells are dynamic and rapidly adapt to any single therapeutic challenge, for example, radiation and/or genetic manipulation e.g. loss of activated RAS function, to maintain tumor cell growth and viability.
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FURUYA, Masahiro, Tomoji TAKAMASA, Koji OKAMOTO, David T. YASUNAGA, and Susumu UEMATSU. "Corrosion Control Based on Radiation Induced Surface Activation." Journal of The Japan Institute of Marine Engineering 41, no. 2 (2006): 278–84. http://dx.doi.org/10.5988/jime.41.2_278.

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XUE, JUN, JI-HUA DONG, GUO-DONG HUANG, XIAO-FEI QU, GANG WU, and XIAO-RONG DONG. "NF-κB signaling modulates radiation-induced microglial activation." Oncology Reports 31, no. 6 (April 23, 2014): 2555–60. http://dx.doi.org/10.3892/or.2014.3144.

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HONJO, Yoshio, Masahiro FURUYA, Tomoji TAKAMASA, and Koji OKAMOTO. "Mechanism of Hydrophilicity by Radiation-Induced Surface Activation." Journal of Power and Energy Systems 3, no. 1 (2009): 216–27. http://dx.doi.org/10.1299/jpes.3.216.

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Dissertations / Theses on the topic "Radiation Induced Activation"

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Sander, David [Verfasser]. "Radiation-Induced Activation of the Epidermal Growth Factor Receptor in Lung Cancer / David Sander." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1010749641/34.

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Meziani, Lydia. "Study of Interaction Between the Inflammatory Response and Radiation-Induced Fibrosis." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T041.

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La fibrose radio-induite (FRI) est une complication tardive de la radiothérapie souvent associée à une réponse inflammatoire chronique et à un infiltrat de macrophages. Aujourd’hui, les macrophages sont pressentis comme des médiateurs cellulaires important dans le processus de fibrose mais leur rôle n’a jamais été étudié dans le contexte de la FRI. Dans une précédente étude nous avions montré que l’irradiation (IR) induit une polarisation M1 des macrophages cardiaques après irradiation de souris ApoE-/- et est associée un score de fibrose élevé, ce qui suggérait que la polarisation des macrophages pourrait contribuer à la fibrogénèse radio-induite. Afin de valider cette hypothèse, nous avons cherché à caractériser le rôle des macrophages dans la FRI en utilisant un modèle classique de fibrose pulmonaire chez la souris C57Bl/6 induit après IR thoracique à 16Gy. Nous avons caractérisé les phénotypes et la fonction des macrophages alvéolaires (MA) et interstitiels (MI). Durant la phase précoce, les résultats montrent une déplétion des MA accompagnée de la sécrétion de CXCL1, MCP-1 et de MCSF. Cette déplétion est suivie d’une repopulation suite au recrutement et à la prolifération des monocytes/macrophages d’origine médullaire. La nouvelle population de MA présente une polarisation hybride accompagnée d’une augmentation simultanée de la sécrétion de cytokines Th1 et Th2. Durant la phase tardive les MI présentent une polarisation de type M2 accompagnée d’une diminution des cytokines Th1 et d’une augmentation de cytokines Th2 dans le lysat tissulaire. Nous avons ensuite cherché à caractériser la contribution des MA hybrides vs MI M2 dans le processus de fibrose. Nous avons montré que contrairement au MA hybrides, les MI M2 étaient capables d’induire l’activation des fibroblastes in vitro et l’expression de TGF-β1. De plus, la déplétion des MA hybrides avec une administration intranasale de clodronate exacerbe la FRI et induit l’augmentation de l’infiltrat de MI M2. Ensuite, nous nous somme interrogés à la contribution du processus de fibrose dans la polarisation des macrophages. Après 24h de coculture entre fibroblastes irradiés et macrophages pulmonaires non irradiés, une sécrétion de cytokines telles que M-CSF et TIMP-1 qui pourraient stimuler l’activation des fibroblastes est observée. De plus, l’inhibition de la FRI avec de la pravastatine montre que l’inhibition de la fibrose est accompagnée d’une augmentation des MI M1 et d’une diminution des MI M2 dans le poumon. En résumé, nos résultats montrent une contribution opposée des Macrophages Alvéolaires et des Macrophages Interstitiels dans le processus de fibrose radio-induite ainsi qu’une contribution du processus de fibrose dans le type d’activation des Macrophages interstitiels formant ainsi une boucle d’activation fibrogénique chronique
Radiation-induced fibrosis (RIF) is a delayed complication of radiotherapy often associated with chronic inflammatory process and macrophage infiltration. Nowadays, macrophages are suggested to be important cellular contributors to fibrogenic process, but their implication in the context of RIF has never been investigated. In a previous study we have shown that irradiation (IR) induced the polarization of cardiac macrophages into M1 in ApoE-/- mice and was associated with a high fibrosis score in ApoE-/- mice, suggesting that macrophage polarization could drive tissue sensitivity to ionizing radiation. This observation prompted us to investigate the role of macrophages in RIF using a classical experimental model of lung fibrosis developed in C57Bl/6 mice after 16Gy thorax-IR. We profiled both alveolar macrophages (AM) and interstitial macrophages (IM). During the acute phase we found AM depletion associated with CXCL1, MCP-1 and M-CSF secretion, followed by a repopulation phase mediated by recruitment and proliferation of monocytes/macrophages from the bone marrow. Interestingly, the newly recruited AM exhibited a yet never described hybrid polarization (M1/M2), associated with the up-regulation of both Th1 and Th2 cytokines. At delayed times points, IM were M2-polarized and associated with downregulation of Th1 cytokines and upregulation of Th2 cytokines in tissue lysates. These results suggest a differential contribution of hybrid AM vs M2 IM to fibrogenesis. Interestingly, in contrast to activated hybrid AM, activated M2 IM were able to induce fibroblast activation in vitro mediated by an enhanced TGF-β1 expression. Therefore, specific depletion of hybrid AM using intranasal administration of clodrosome increased RIF score and enhanced M2 IM infiltration. We next evaluated if the fibrogenic process can in turn affect macrophage polarization. Interestingly, after coculture of irradiated fibroblast with non-irradiated pulmonary macrophages, secretion of cytokines such as M-CSF and TIMP-1, which can stimulate macrophage activation, was observed. Furthermore, RIF inhibition using pravastatin treatment showed that fibrosis inhibition was associated with a decrease in M2 IM accompanied by an increase in M1 IM, but had no effect on polarization of AM. These present study shows a dual and opposite contribution of alevolar versus intertitial macrophages in RIF and the contribution of the fibrogenic process to IM polarization, resulting thereby in a chronical fibrogenic loop
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Gibhardt, Christine S. [Verfasser], Gerhard [Akademischer Betreuer] Thiel, and Marco [Akademischer Betreuer] Durante. "Radiation induced activation of potassium-channels: The role of ROS and calcium / Christine S. Gibhardt. Betreuer: Gerhard Thiel ; Marco Durante." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2014. http://d-nb.info/1110979487/34.

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Chishti, Arif Ali [Verfasser]. "The role of linear energy transfer in modulating radiation- induced NF-kB activation and its down-stream target genes / Arif Ali Chishti." Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1057915106/34.

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Sheridan, Andrew Keith. "Kinetics and temperature- and pressure-induced polymorphic phase transformations in molecular crystals." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322597.

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Fahy, Katherine Erin. "Thermal Burn Injury Induced Microvesicle Particle Release." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright149383031006972.

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Liu, Langni. "Ultraviolet-B radiation induces release of bioactive microvesicle particles in keratinocytes via platelet-activating factor and acid sphingomyelinase." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598672100210086.

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Gibhardt, Christine S. "Radiation induced activation of potassium-channels: The role of ROS and calcium." Phd thesis, 2014. https://tuprints.ulb.tu-darmstadt.de/4227/1/Doktorarbeit_Endversion.pdf.

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Ionizing radiation (IR), in particular photons, is a quasi-universal tool in medical diagnostics and in tumor therapy. The negative side effects of this high-energy photon irradiation, which often cause secondary cancers or cell invasiveness, are well documented. The classical paradigm still is that all these effects can be traced back to irradiation induced DNA damage. Damage to other cellular compartments has been neglected for a long time. Recent research, however, has demonstrated that a calcium-activated K+-channel (hIK-channel) is activated by different types of ionizing radiation, e.g. γ-irradiation (Kuo et al., 1993), X-ray, α-particles and heavy-ion irradiation (Roth, 2013). The elevated K+ conductance results in a membrane hyperpolarization; the latter is a known signal for cell cycle progression. In the present thesis I elucidate the signal cascade, which is activated by IR and which finally activates hIK channels. In order to examine whether excursion in the concentration of cellular hydrogen peroxide (H2O2), or of the free concentration of Ca2+ ([Ca2+]cyt) are involved in signaling after IR, I employed several genetically encoded fluorescence sensors. The generation of reactive oxygen species (ROS), especially H2O2, was measured before and immediately after cells were challenged with either 405 nm UV laser micro-irradiation, X-rays or heavy-ion irradiation with a sensor for H2O2 (HyPer) and a sensor for the glutathione redox-buffer (Grx1-roGFP2). The latter is a sink for all ROS, which are eliminated in a cell by the oxidation of glutathione. These measurements provide for the first time robust quantitative data on the generation of ROS directly after irradiation in single living cells with a high temporal and spatial resolution. The data show that ROS molecules are generated immediately after the irradiation stress. They are rapidly buffered by an efficient redox-buffer system, which involves glutathione. When the buffer is exhausted the concentration of ROS is increasing throughout the cell; the latter could be monitored directly by an increase in the concentration of H2O2, a known second messenger in the cell. This general pattern is observed with some variations after exposing cells to X-ray stress (1-10 Gy) and 405 nm UV-irradiation (0.5-4.5 mJ/µm2). The latter micro-irradiation experiments of the cells with laser light provide the additional information that the ROS response is maximal in the compartment, which is directly irradiated and that an irradiation of the nucleus generates about 2 to 3 times more H2O2 than the equivalent irradiation of the cytosol. Also an irradiation of cells with heavy-ions causes an increase in H2O2 concentration, but the response is more variable and not all cells reveal an increase in H2O2. Further experiments suggest that the rise in H2O2, which is generated in cells as a responds to irradiation stress, is sufficient to trigger a signal cascade, involving an increase in [Ca2+]cyt. The latter hypothesis is supported by the finding that an incubation of A549 cells and HEK293 cells in a buffer with H2O2 is triggering an elevation in [Ca2+]cyt. This was measured with a FRET based Ca2+ sensor (YC3.60). The fact that challenging the same cells with the identical amount of H2O2 is sufficient to stimulate the Ca2+-activated hIK channel suggests that channel activation is mediated via a H2O2 induced increase in [Ca2+]cyt. This upstream part of the signaling cascade is independent of the cell type and found in HEK293 cells and A549 cells. The increase in membrane conductance, which is downstream of these events, is only elevated in cells like A549 cells, which express the hIK channel. When hIK channels are transiently expressed in HEK293 cells, also these cells, which are in their native form insensitive to IR, respond to the radiation stress with an increase in membrane conductance. Collectively the data show that cells, which functionally express hIK channels, are sensitive to ionizing irradiation. The activation of these Ca2+ sensitive channels, which can have severe impacts on the differentiation of cells, is based on an elevation in [Ca2+]cyt in these cells; the latter gain is the result of a rapid elevation of ROS molecules in the nucleus but also in the cytosol of cells, which under went an exposure to ionizing irradiation.
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Liu, Kuang-Hsin, and 柳光欣. "Curcumin Enhances Radiation-induced Cytotoxicity Via Suppression of NF-kB Activation in Breast Cancer MCF-7 Cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/87548230918557977897.

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碩士
中臺科技大學
醫學影像暨放射科學系暨研究所
102
Breast cancer is the most common malignancy in women around the world. Radiotherapy is one of the treatment modality used in multidisciplinary strategy against breast cancer nowadays. Recurrence after radiotherapy is not uncommon and it may be resulted from induced radioresistance. Radiation-induced NF-B activity can upregulate anti-apoptotic genes in irradiated breast cancer cells. Curcumin is plant phytochemical derived from the root of Curcuma longa and known for the inhibitory effect on NF-B activity. The main goal of this study is to investigate whether curcumin is able to radiosensitize breast cancer cells through suppression of radiation-induced NF-B activity. In this study, the effects of curcumin combined with radiation on cell proliferation in MCF-7 cells were evaluated with clonogenic formation assay. Whether curcumin can increase radiation-induced apoptosis was investigated by using DNA fragmentation assay. We also determined the effects of curcumin on radiation-induced NF-B activity and increased the expression of NF-B regulated gene products with Western blotting assay. To confirm whether NF-B inhibition can sensitize breast cancer to radiation, the effects of NF-B inhibitor combined with radiation in MCF-7 cell were evaluated in this study. These results showed that curcumin can significantly increase radiation-inhibited cell proliferation as compared to radiation alone. Curcumin also enhanced radiation-induced cell apoptosis via dependent and independent mitochondrial pathways. We also found curcumin decreased radiation activated NF-B activity and increased the expression of NF-B regulated gene products (Bcl-2 and C-FLIP) from Western blotting assay. In addition, the results also showed NF-B inhibitor can increase radiosensitivity in MCF-7 cell.
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Books on the topic "Radiation Induced Activation"

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Sobolev. Role of Cyclic Nucleotides in Radiobiology/The Functional Role of Radiation-induced Activation of Cholesterol and Lipogenesis in the Animal Body. Routledge, 1997.

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Henriksen, Niels Engholm, and Flemming Yssing Hansen. Unimolecular Reactions. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198805014.003.0007.

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This chapter considers unimolecular reactions; photo-induced reactions, that is, true unimolecular reactions; and reactions initiated by collisional activation, that is, apparent unimolecular reactions where it is assumed that the time scales for activation and subsequent reaction are well separated. Elements of classical and quantum dynamical descriptions are discussed, including Slater theory and the quantum mechanical description of photo-induced reactions. Statistical theories aiming at the calculation of micro-canonical as well as canonical rate constants are discussed, including a detailed discussion of RRKM theory. It concludes with a discussion of femtochemistry, that is, the observation and control of chemical dynamics using femtosecond pulses of electromagnetic radiation, focusing on the control of unimolecular reactions via the interaction with coherent light; that is, laser control.
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Book chapters on the topic "Radiation Induced Activation"

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Busi, F. "Redox Properties of Radiation Induced Free Radicals." In Selective Activation of Drugs by Redox Processes, 63–78. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3768-7_6.

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Kemp, C. J., R. Bremner, and A. Balmain. "Molecular Genetics of Oncogene Activation and Gene Loss in Carcinogen-Induced Animal Tumours." In Anticarcinogenesis and Radiation Protection 2, 117–22. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3850-9_17.

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Tang, D. G., C. A. Diglio, and K. V. Honn. "12(S)-Hete-Induced Microvascular Endothelial Cell Retraction is Mediated by Cytoskeletal Rearrangement Dependent on PKC Activation." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 219–29. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_44.

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Frohns, A., and F. Frohns. "Safety of Water-Filtered Infrared A (wIRA) on the Eye as a Novel Treatment Option for Chlamydial Infections." In Water-filtered Infrared A (wIRA) Irradiation, 259–69. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_22.

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AbstractwIRA has been shown to reduce chlamydial infections in vitro and in vivo and might therefore offer an innovative therapeutic approach for fighting trachoma. However, since the eye is a highly temperature- and radiation-sensitive organ, a safety assessment of the ocular structures affected by wIRA treatment is required to establish wIRA as a potentially successful treatment option for clinical application. A prerequisite for this is to demonstrate that wIRA does not have adverse side-effects such as inducing a non-physiological temperature increase which causes cell stress and damage to ocular tissues and which, in turn, is ultimately associated with impaired vision. Likewise, the potential negative impact of non-thermal photochemical effects of wIRA irradiation needs to be investigated. Data from our ex vivo studies in pig and mouse models, as well as in vivo data in a guinea pig model, provide good evidence for the safe use of wIRA to treat chlamydial infections. These studies have excluded a non-physiological temperature rise as well as the activation of heat and stress-induced proteins after wIRA irradiation with therapy-relevant irradiances. Nevertheless, additional detailed in vitro and in vivo studies are needed to further advance the clinical use of wIRA.
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Sola, J., and L. Vila. "Platelet-Activating Factor Induces Receptor Mediated Leukocyte 5 Lipoxygenase Activation Through its Translocation to the Membrane." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 35–38. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_8.

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Hanahan, D. J., L. Gregory, A. Tokumura, T. Nouchi, and M. S. Olson. "Some Novel Observations on Inhibitors of Platelet Activating Factor Induced Reactions." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 731–33. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_141.

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"Photochemical and Radiation-Induced Activation of CO2 in Homogeneous Media." In Greenhouse Gas Carbon Dioxide Mitigation, 411–30. CRC Press, 1998. http://dx.doi.org/10.1201/9781482227833-17.

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ZHIVOTOVSKY, B. D., and A. A. SEILIEV. "ROLE OF GENOME ACTIVATION PRODUCTS IN RADIATION-INDUCED INTERPHASE DEATH OF LYMPHOID CELLS." In Radiation Research: A Twentieth-century Perspective, 216. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-12-168561-4.50774-5.

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SARASIN, A., C. ROBERT, C. DROUGARD, and L. DAYA-GROSJEAN. "ONCOGENE ACTIVATION IN ULTRAVIOLET-INDUCED SKIN TUMORS FROM NORMAL INDIVIDUALS AND XERODERMA PIGMENTOSUM PATIENTS." In Radiation Research: A Twentieth-century Perspective, 42. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-12-168561-4.50068-8.

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Sloan, Steven R., and Angel Pellicer. "ras ONCOGENE ACTIVATION IN GAMMA- AND NEUTRON-RADIATION INDUCED MURINE THYMIC LYMPHOMAS." In Congress Proceedings, 353–57. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-12-168562-1.50065-3.

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Conference papers on the topic "Radiation Induced Activation"

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Honjo, Yoshio, Masahiro Furuya, Tomoji Takamasa, and Koji Okamoto. "Interfacial Phenomena of Radiation-Induced and Photo-Induced." In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48320.

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When a metal oxide is irradiated by gamma rays, the irradiated surface becomes hydrophilic. This surface phenomenon is called as radiation induced surface activation (RISA). In order to investigate radiation-induced and photo-induced hydrophilicity, the contact angles of water droplets on a titanium dioxide surface were measured in terms of irradiation intensity and time for gamma rays of cobalt-60 and for ultraviolet rays. Reciprocals of the contact angles increased in proportion to irradiation time before the contact angles reached their super-hydrophilicity state. The reciprocals of contact angles correlate well with integrated intensity by a straight line, regardless of the irradiation intensity and time. Radiation-induced and photo-induced hydrophilicity phenomena are identical to each other in this regard. In addition, an effect of ambient gas was investigated. In pure argon gas, the contact angle remains the same against the irradiation time. This clearly shows that a certain humidity in ambient gas is required to take the place of RISA hydrophilicity. A single crystal titanium dioxide (100) surface was analyzed by X-ray photoelectron spectrometry (XPS). After irradiation with gamma rays, a peak was found in the O 1s spectrum, indicating the adsorption of dissociative water to a surface 5-fold coordinate titanium site, and the formation of a surface hydroxyl group. We conclude that the RISA hydrophilicity is caused by chemisorption of the hydroxyl group on the surface.
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Wennerberg, Erik, Noriko Kawashima, and Sandra Demaria. "Abstract A21: Adenosine is a rheostat for radiation therapy-induced immune activation." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a21.

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Tamura, Naohisa, Tatsuya Hazuku, Tomoji Takamasa, Kaichiro Mishima, Toru Mitsutake, and Sinichi Morooka. "Effect of Wall Surface Wettability Due to Radiation Induced Surface Activation on Quenching Process." In 12th International Conference on Nuclear Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/icone12-49420.

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This report presents an experimental result on quenching which affected by the Radiation Induced Surface Activation. Increasing of quenching velocity requires that the cooling liquid can contact the heated surface, or a high wettability of the surface when quenching initiates. From this point of view, an experimental study to investigate the relationship between surface wettability and quenching was performed by use of an oxide semiconductor-coated material after γ-ray irradiation. The results showed that highly surface wettability or highly hydrophilic condition of a simulated fuel rod made of SUS was achieved, and the quenching velocities were increased up to 15% after 300 kGy 60Co γ-ray irradiation.
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Abernathy, Lisa M., Matthew D. Fountain, John M. David, Christopher K. Yunker, Michael C. Joiner, and Gilda G. Hillman. "Abstract 277: Radioprotection of lung tissue involves modulation of radiation-induced macrophage activation by soy isoflavones." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-277.

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5

Gasparyan, Levon, Grigory Brill, and Anu Makela. "Activation of VEGF and FGF induced angiogenesis under influence of low level laser radiation in vitro." In Biomedical Optics 2006, edited by Michael R. Hamblin, Ronald W. Waynant, and Juanita Anders. SPIE, 2006. http://dx.doi.org/10.1117/12.645936.

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Chen, Genwen, Qianqian Zhao, Baoying Yuan, and Zhaochong Zeng. "PWE-1 ALKBH5-modified HMGB1-STING activation contributes to radiation induced liver disease via innate immune response." In Abstracts of the BSG Annual Meeting, 8–12 November 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-bsg.191.

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Zhang, Jian, Kaichiro Mishima, Naoki Sugitani, Masahiro Hino, and Tomoji Takamasa. "Radiation Induced Surface Activation on SUS304 Rod Surface Coated With Thin Film Layer Formed by Vacuum Evaporation Method." In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48192.

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In this study, the effect of film layer deposited on a metal surface by vacuum evaporation method on the RISA phenomenon was investigated from the view points of surface wettability and quenching velocity. Test rods were made of SUS304 with the outer diameter of 24mm and the length of 150mm. Four kinds of materials, i.e. titanium, zircaloy-II, germanium and silicon, were deposited separately on the half-circumference surface of a SUS304 rod with thickness of 200 nm. It was concluded that the RISA effect was observed on the film-coated surfaces after gamma-ray irradiation, which is similar to that on an oxide layer of SUS304 surface. It was also found that the quenching velocity on film-coated surfaces was much faster than that on an un-coated surface.
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Veeraraghavan, Jamunarani, Mohan Natarajan, Vibhudutta Awasthi, Terence S. Herman, and Natarajan Aravindan. "Abstract 4203: EF24, a novel curcumin analogue inhibits oncogenic activation induced by radiation abscopal effect in distant mice lungs." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4203.

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Brannon, James H. "Chemical Etching of Silicon by CO2 Laser Induced Dissociation of NF3." In Microphysics of Surfaces, Beams, and Adsorbates. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/msba.1987.mb3.

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Surface studies have established that radicals frequently react with surfaces which are inert to the parent molecule. Dissociation of the parent molecule provides a reaction channel which avoids the often large activation barrier inherent in parent molecule-surface interactions. The interaction of gaseous NF3 with amorphous silicon is an excellent example of this type of behavior. While NF3 does not measurably chemically react with silicon at ambient temperatures, the fluorine containing radicals produced from laser dissociated NF3 readily do so. Some fraction of the fluorosilyl reaction products spontaneously desorb, resulting in silicon removal (etching). In this study parallel incident dissociating radiation did not contact the silicon surface, indicating that the observed etching reactions result from purely chemical effects. Effects due to transient surface heating or physical ablation can be discounted.
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Walker, Joshua M., Diego M. Barragan, Melissa J. Kasiewicz, Charles R. Thomas, and William L. Redmond. "Abstract 1664: Alpha-tocopheryloxyacetic acid (aTEA) induced immune activation synergizes with radiation therapy to treat primary and metastatic murine mammary carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1664.

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