Готові списки джерел за темами / Brain irradiation

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Добірка наукової літератури з теми "Brain irradiation"

Автор: Grafiati
Опубліковано: 26 жовтня 2024

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Статті в журналах з теми "Brain irradiation"

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Shirato, Hiroki, Akio Takamura, Masayoshi Tomita, Keishiro Suzuki, Takashi Nishioka, Toyohiko Isu, Tsutomu Kato, et al. "Stereotactic irradiation without whole-brain irradiation for single brain metastasis." International Journal of Radiation Oncology*Biology*Physics 37, no. 2 (January 1997): 385–91. http://dx.doi.org/10.1016/s0360-3016(96)00488-9.

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Feng, Xi, Sonali Gupta, David Chen, Zoe Boosalis, Sharon Liu, Nalin Gupta, and Susanna Rosi. "SCIDOT-04. REPLACEMENT OF MICROGLIA BY BRAIN-ENGRAFTED MACROPHAGES PREVENTS MEMORY DEFICITS AFTER THERAPEUTIC WHOLE-BRAIN IRRADIATION." Neuro-Oncology 21, Supplement_6 (November 2019): vi273. http://dx.doi.org/10.1093/neuonc/noz175.1145.

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Abstract Microglia have a distinct origin compared to blood circulating myeloid cells. Under normal physiological conditions, microglia are maintained by self-renewal, independent of hematopoietic progenitors. Following genetic or pharmacologic depletion, newborn microglia derive from the local residual pool and quickly repopulate the entire brain. The depletion of brain resident microglia during therapeutic whole-brain irradiation fully prevents irradiation-induced synaptic loss and recognition memory deficits but the mechanisms driving these protective effects are unknown. Here, we demonstrate that after CSF-1R inhibitor-mediated microglia depletion and therapeutic whole-brain irradiation, circulating monocytes engraft into the brain and replace the microglia pool. These monocyte-derived brain-engrafted macrophages have reduced phagocytic activity compared to microglia from irradiated brains, but similar to locally repopulated microglia without brain irradiation. Transcriptome comparisons reveal that brain-engrafted macrophages have both monocyte and embryonic microglia signatures. These results suggest that monocyte-derived brain-engrafted macrophages represent a novel therapeutic avenue for the treatment of brain radiotherapy-induced cognitive deficits.
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Feng, Xi, Sonali Gupta, David Chen, Zoe Boosalis, Sharon Liu, Nalin Gupta, and Susanna Rosi. "EXTH-08. REPLACEMENT OF MICROGLIA BY BRAIN-ENGRAFTED MACROPHAGES PREVENTS MEMORY DEFICITS AFTER THERAPEUTIC WHOLE-BRAIN IRRADIATION." Neuro-Oncology 21, Supplement_6 (November 2019): vi83—vi84. http://dx.doi.org/10.1093/neuonc/noz175.342.

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Abstract Microglia have a distinct origin compared to blood circulating myeloid cells. Under normal physiological conditions, microglia are maintained by self-renewal, independent of hematopoietic progenitors. Following genetic or pharmacologic depletion, newborn microglia derive from the local residual pool and quickly repopulate the entire brain. The depletion of brain resident microglia during therapeutic whole-brain irradiation fully prevents irradiation-induced synaptic loss and recognition memory deficits but the mechanisms driving these protective effects are unknown. Here, we demonstrate that after CSF-1R inhibitor-mediated microglia depletion and therapeutic whole-brain irradiation, circulating monocytes engraft into the brain and replace the microglia pool. These monocyte-derived brain-engrafted macrophages have reduced phagocytic activity compared to microglia from irradiated brains, but similar to locally repopulated microglia without brain irradiation. Transcriptome comparisons reveal that brain-engrafted macrophages have both monocyte and embryonic microglia signatures. These results suggest that monocyte-derived brain-engrafted macrophages represent a novel therapeutic avenue for the treatment of brain radiotherapy-induced cognitive deficits.
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Yuan, Hong, Judith N. Rivera, Jonathan E. Frank, Jonathan Nagel, Colette Shen, and Sha X. Chang. "Mini-Beam Spatially Fractionated Radiation Therapy for Whole-Brain Re-Irradiation—A Pilot Toxicity Study in a Healthy Mouse Model." Radiation 4, no. 2 (May 8, 2024): 125–41. http://dx.doi.org/10.3390/radiation4020010.

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Анотація:
For patients with recurrent brain metastases, there is an urgent need for a more effective and less toxic treatment approach. Accumulating evidence has shown that spatially fractionated radiation therapy (SFRT) is able to provide a significantly higher therapeutic ratio with lower toxicity compared to conventional radiation using a uniform dose. The purpose of this study was to explore the potential low toxicity benefit of mini-beam radiotherapy (MBRT), a form of SFRT, for whole-brain re-irradiation in a healthy mouse model. Animals first received an initial 25 Gy of uniform whole-brain irradiation. Five weeks later, they were randomized into three groups to receive three different re-irradiation treatments as follows: (1) uniform irradiation at 25 Gy; (2) MBRT at a 25 Gy volume-averaged dose (106.1/8.8 Gy for peak/valley dose, 25 Gy-MBRT); and (3) MBRT at a 43 Gy volume-averaged dose (182.5/15.1 Gy for peak/valley dose, 43 Gy-MBRT). Animal survival and changes in body weight were monitored for signs of toxicity. Brains were harvested at 5 weeks after re-irradiation for histologic evaluation and immunostaining. The study showed that 25 Gy-MBRT resulted in significantly less body weight loss than 25 Gy uniform irradiation in whole-brain re-irradiation. Mice in the 25 Gy-MBRT group had a higher level of CD11b-stained microglia but also maintained more Ki67-stained proliferative progenitor cells in the brain compared to mice in the uniform irradiation group. However, the high-dose 43 Gy-MBRT group showed severe radiation toxicity compared to the low-dose 25 Gy-MBRT and uniform irradiation groups, indicating dose-dependent toxicity. Our study demonstrates that MBRT at an appropriate dose level has the potential to provide less toxic whole-brain re-irradiation. Future studies investigating the use of MBRT for brain metastases are warranted.
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OKAMOTO, Shinichiro, Hajime HANDA, Junkoh YAMASHITA, Yasuhiko TOKURIKI, and Mitsuyuki ABE. "Post-irradiation Brain Tumors." Neurologia medico-chirurgica 25, no. 7 (1985): 528–33. http://dx.doi.org/10.2176/nmc.25.528.

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Wurm, R. E., L. Schlenger, A. Kaiser, M. Kömer, M. Fitzek, L. Röschel, D. Böhmer, G. Matnjani, M. Stuschke, and V. Budach. "Brain metastases — Radiosurgery or whole brain irradiation?" European Journal of Cancer 35 (September 1999): S129. http://dx.doi.org/10.1016/s0959-8049(99)80896-x.

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7

Natsuko, Kondo, Sakurai Yoshinori, Takayuki Kajihara, Takushi Takada, Nobuhiko Takai, Kyo Kume, Shinichi Miyatake, Shoji Oda, and Minoru Suzuki. "ET-13 CONTROL OF ACTIVATED MICROGLIA THROUGH P2X4 RECEPTOR IN RADIATION BRAIN NECROSIS." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii10. http://dx.doi.org/10.1093/noajnl/vdz039.043.

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Abstract INTRODUCTION Brain radiation necrosis (RN) is severe adverse event after radiation therapy for brain tumor patients, especially in case of re-irradiation. Although corticosteroids or vitamin E, etc. are clinically used for RN, the effect is limited and underlying mechanism is to be cleared. Therefore, we established RN mouse model with irradiating right hemisphere of mouse brain using proton beam at dose of 60 Gy [Kondo et al., 2015]. In this study, we investigated change of phospholipids and lipid mediators after irradiation using this RN model in correlation with microglia activation. METHODS After irradiation, change of phospholipids and lipid mediators in mouse brain was investigated using imaging mass spectrometry and LC-MS. Immunohistochemistry on microglia and P2X4 receptor, a receptor for lysophosphatidylcholine (LPC) was performed. RESULTS In imaging mass spectrometry, 1 and 4 months after irradiation, phosphatidylcholine (PC): (16:0/20:4), (18:0/20:4) decreased in irradiated area compared non-irradiated area. On the other hand, LPC: (16:0) increased in irradiated area compared to non-irradiated area after 1 month and 4 months irradiation. PC (16:0/20:4) is a precursor of LPC (16:0) and arachidonic acid (20:4). By LC-MS, LPC was twice higher in irradiated area compared to non-irradiated, 6 months after irradiation. Microglia was highly activated in irradiated area compared to non-irradiated from 3 months after irradiation to 8 months and strongly co-expressed P2X4 receptor was confirmed in irradiated area after 6 months. Preliminary P2X4 receptor agonist administration test prolonged the RN to 12 months after irradiation. CONCLUSION In RN, LPC may continuously activated microglia through P2X4 receptor and cause chronic inflammation after irradiation. P2X4 agonist administration test including action resolution and immunohistochemistry is ongoing.
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Crvenkova, S., and C. Tolevska. "314 Partial brain irradiation (PBI) or whole brain irradiation (WBI), the justified solution." European Journal of Cancer Supplements 1, no. 5 (September 2003): S96. http://dx.doi.org/10.1016/s1359-6349(03)90347-8.

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9

Romano, Mariele, Alberto Bravin, Alberto Mittone, Alicia Eckhardt, Giacomo E. Barbone, Lucie Sancey, Julien Dinkel, et al. "A Multi-Scale and Multi-Technique Approach for the Characterization of the Effects of Spatially Fractionated X-ray Radiation Therapies in a Preclinical Model." Cancers 13, no. 19 (October 1, 2021): 4953. http://dx.doi.org/10.3390/cancers13194953.

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Анотація:
The purpose of this study is to use a multi-technique approach to detect the effects of spatially fractionated X-ray Microbeam (MRT) and Minibeam Radiation Therapy (MB) and to compare them to seamless Broad Beam (BB) irradiation. Healthy- and Glioblastoma (GBM)-bearing male Fischer rats were irradiated in-vivo on the right brain hemisphere with MRT, MB and BB delivering three different doses for each irradiation geometry. Brains were analyzed post mortem by multi-scale X-ray Phase Contrast Imaging–Computed Tomography (XPCI-CT), histology, immunohistochemistry, X-ray Fluorescence (XRF), Small- and Wide-Angle X-ray Scattering (SAXS/WAXS). XPCI-CT discriminates with high sensitivity the effects of MRT, MB and BB irradiations on both healthy and GBM-bearing brains producing a first-time 3D visualization and morphological analysis of the radio-induced lesions, MRT and MB induced tissue ablations, the presence of hyperdense deposits within specific areas of the brain and tumor evolution or regression with respect to the evaluation made few days post-irradiation with an in-vivo magnetic resonance imaging session. Histology, immunohistochemistry, SAXS/WAXS and XRF allowed identification and classification of these deposits as hydroxyapatite crystals with the coexistence of Ca, P and Fe mineralization, and the multi-technique approach enabled the realization, for the first time, of the map of the differential radiosensitivity of the different brain areas treated with MRT and MB. 3D XPCI-CT datasets enabled also the quantification of tumor volumes and Ca/Fe deposits and their full-organ visualization. The multi-scale and multi-technique approach enabled a detailed visualization and classification in 3D of the radio-induced effects on brain tissues bringing new essential information towards the clinical implementation of the MRT and MB radiation therapy techniques.
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Lissoni, P., S. Meregalli, S. Curreri, G. Messina, F. Brivio, L. Fumagalli, M. Colciago, and G. Gardani. "Brain Irradiation-Induced Lymphocytosis Predicts Response in Cancer Patients with Brain Metastases." International Journal of Biological Markers 23, no. 2 (April 2008): 111–14. http://dx.doi.org/10.1177/172460080802300207.

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Lymphocytopenia is one of the main toxicities of radiotherapy and its severity is related to the irradiation dose. The occurrence of lymphocytopenia depends on the body site of radiotherapy; it is most pronounced with pelvic irradiation, whereas the effect of brain irradiation on the lymphocyte count is to be elucidated. This preliminary study was performed to evaluate changes in lymphocyte number occurring during brain irradiation in cancer patients with brain metastases. The study included 50 patients who received brain radiotherapy for single or multiple brain metastases at a total dose of 30 Gy. Overall, no significant changes in mean lymphocyte number occurred during brain radiotherapy. However, when lymphocyte variations were assessed in relation to the clinical response of brain metastases, a significant increase in the mean number of lymphocytes was found in patients who achieved objective regression of brain metastases on brain irradiation. The mean lymphocyte number decreased in nonresponding patients, albeit without a statistically significant difference with respect to the pretreatment values. The results of this study show that the efficacy of radiotherapy in the treatment of brain metastases is associated with a significant increase in mean lymphocyte number. Therefore, evidence of brain irradiation-induced lymphocytosis may predict the efficacy of radiotherapy.
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Більше джерел

Дисертації з теми "Brain irradiation"

1

Madhoo, Jitesh. "Continuous low dose rate irradiation of the rat brain." Doctoral thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/26785.

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The reported median survival time for patients who are diagnosed with high grade astrocytomas and who undergo postoperative radiotherapy is of the order of 24 to 40 weeks. The course of radiotherapy administered to these patients takes up a considerable portion of their expected survival time. Therefore, any means of reducing the treatment time may contribute to an enhanced quality of life for these patients. A potentially useful method for the reduction of the treatment time may be achieved with the use of continuous low dose rate external beam radiotherapy, where the treatment is administered over a 12 to 24 hour period. A relationship between fractionated and continuous low dose rate irradiation has been reported for skin, however, no such relationship has been reported for the brain. Low dose rate protocols that are equivalent in effect to fractionated (conventional) protocols can be derived using the linear quadratic theory, provided that quantitative radiobiological data for normal tissue (brain) is known. Thus, the aim of the current study is to test the radiation tolerance of the rat brain to low dose rate and fractionated radiation in order to establish the values for the parameters of the linear quadratic model.
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2

Wedlock, Pauline Margaret. "Behavioural effects of low intensity laser irradiation of the rodent brain." Thesis, University of Ulster, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339311.

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3

Lee, Won Hee. "Molecular mechanisms of radiation-induced brain injury." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/77254.

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Radiation therapy has been most commonly used modality in the treatment of brain tumors. About 200,000 patients with brain tumors are treated with either partial large field or whole brain irradiation every year in the United States. The use of radiation therapy for treatment of brain tumor, however, can subsequently lead to devastating functional deficits several months to years after treatment. Unfortunately, there are no known successful treatments and effective strategies for mitigating radiation-induced brain injury. In addition, the specific mechanisms by which irradiation causes brain injury in normal tissues are not fully understood. A deeper understanding of the molecular mechanisms underlying these phenomena could enable the development of more effective therapies to contribute to long-term disease suppression or even cure. Therefore,the primary goal of this research project was to determine the molecular mechanisms responsible for radiation-induced brain injury in normal tissues. In the first study, the effects of whole brain irradiation on pro-inflammatory pathways in the brain were examined. Results demonstrated that brain irradiation induces regionally specific alterations in pro-inflammatory environments through activation of pro-inflammatory transcription factors (e.g., activator protein-1 (AP-1),nuclear factor-κB (NF-κB), and cAMP response element-binding protein (CREB)) and overexpression of pro-inflammatory mediators (e.g., tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and monocyte chemoattractant protein-1 (MCP-1)) in brain. This study provides evidence for a differential induction of pro-inflammatory mediators in specific brain regions that have importance for the neurological/neuropathological consequences of irradiation. In the second study, a mathematical model describing radiation-induced mRNA and protein expression kinetics of TNF-α in hippocampus was reconstructed. This study demonstrated that the reaction kinetic model could predict protein expression levels of TNF-α in cortex, suggesting that this model could be used to predict protein expression levels of pro-inflammatory mediators in other parts of the brain. In the third study, the effects of aging on radiation-mediated impairment of immune responses in brain were examined. Results showed that radiation-induced acute inflammatory responses, such as overexpression of pro-inflammatory cytokines (e.g., TNF-α, IL-1β, and IL-6),adhesion molecules (e.g., intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin), chemokine MCP-1, and matrix metalloproteinase-9 (MMP-9), are significantly impaired in aged brain. This study suggests that reduced production of pro-inflammatory mediators in response to irradiation compromises the normal host defense mechanisms in damaged brain tissue and subsequently leads to impaired repair/remodeling responses in old individuals. In the fourth study, the effects of irradiation on MMPs/tissue inhibitor of metalloproteinases (TIMPs) and extracellular matrix (ECM) degradation in brain were examined. Results demonstrated that whole brain irradiation induces an imbalance between MMPs and TIMPs expression, increases gelatinase activity, and degrades collagen type IV in the brain. This study suggests that a radiation-induced imbalance between MMP-2 and TIMP-2 expression may have an important role in the pathogenesis of brain injury by degrading ECM components of the blood-brain barrier (BBB) basement membrane. In the fifth study, the effects of irradiation on angiogenic factors and vessel rarefaction in brain were examined. Results demonstrated that whole brain irradiation decreases endothelial cell (EC) proliferation, increases EC apoptosis, and differentially regulates the expression of angiogenic factors such as angiopoietin-1 (Ang-1), Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) in brain. This study suggests that radiation-induced differential regulation of angiogenic factors may be responsible for vessel rarefaction. In summary, the results from these studies demonstrated that whole brain irradiation induces brain injury by triggering pro-inflammatory pathways, degrading extracellular matrix, and altering physiologic angiogenesis. Therefore, this work may be beneficial in defining a new cellular and molecular basis responsible for radiation-induced brain injury. Furthermore, it may provide new opportunities for prevention and treatment of brain tumor patients who are undergoing radiotherapy.
Ph. D.
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4

Pike, G. Bruce (Gilbert Bruce). "Three dimensional stereotaxic intracavitary and external beam isodose calculation for treatment of brain lesions." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=65439.

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Pontén, Emeli. "Astrocyte response after irradiation of the juvenile brain : -­‐ a study on C57BL/6 strain mice (p21)." Thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-55163.

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Kasahara, Seiko. "Hyperintense dentate nucleus on unenhanced T1-weighted MR images is associated with a history of brain irradiation." Kyoto University, 2011. http://hdl.handle.net/2433/151912.

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Spoudeas, Helen Alexandra. "The evolution of growth hormone neurosecretory disturbance during high dose cranial irradiation and chemotherapy for childhood brain tumours." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261873.

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Pham, Thao Nguyen. "Biοmathematical insights intο radiatiοn-induced systemic immune effects in brain and head & neck cancer using preclinical and clinical mοdels". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC407.

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Анотація:
La radiothérapie, bien qu'efficace contre les tumeurs, peut perturber le système immunitaire et provoquer une lymphopénie, ce qui impacte négativement les résultats du traitement. Des radiothérapies plus ciblées, telles que la protonthérapie, offrent des perspectives prometteuses pour réduire la lymphopénie. Au-delà de la lymphopénie, les sous-populations de leucocytes dans les lignées lymphoïde et myéloïde ont un impact significatif sur la réponse immunitaire antitumorale. Cette thèse examine l'impact de l'irradiation cérébrale sur le système immunitaire en utilisant la modélisation biomathématique. Des données provenant de diverses sources, y compris des essais cliniques, des études animales et des études in vitro sont utilisées pour construire le modèle. L'analyse de la littérature montre un lien quantitatif entre une diminution du nombre de lymphocytes et une survie réduite des patients. De plus, un nouveau modèle de radiosensibilité (modèle de saturation) des lymphocytes est proposé, prouvant une précision supérieure aux modèles linéaires-quadratiques existants. Les études comparant la radiothérapie par rayons X et la protonthérapie chez les souris ont révélé que les rayons X réduisent significativement le nombre de lymphocytes de plusieurs sous-populations et induit une inflammation persistante. La protonthérapie, en revanche, a un impact minimal sur les sous-populations de lymphocytes grâce à son effet balistique épargnant, entre autres, les ganglions lymphatiques cervicaux. La modélisation a également montré que bien que les lymphocytes B et T puissent se rétablir après une déplétion induite par les rayons X, les tumeurs peuvent retarder de manière significative la récupération des cellules B. En outre, les tumeurs affaiblissent elles-mêmes le système immunitaire en diminuant les lymphocytes T circulants. Les données de l'essai clinique CYRAD suggèrent que des doses élevées de radiation aux ganglions lymphatiques lors du traitement du cancer de la tête et du cou affectent de manière significative le nombre de lymphocytes circulants, indépendamment de la dose reçue par le sang lui-même. Ces résultats soulignent l'importance de prendre en compte l'irradiation à la fois du sang mais aussi des ganglions lymphatiques pour préserver le système immunitaire pendant la radiothérapie
Radiotherapy, while effective against tumors, can disturb the immune system and cause lymphopenia, which negatively impacts patient outcomes. Beyond lymphopenia, leukocyte subpopulations of lymphoid and myeloid lineages also have a significant impact on antitumor immune response. More targeted radiation therapies like proton therapy offer promise in reducing lymphopenia. We investigated the impact of brain irradiation on the immune system using biomathematical modeling. Data from various published sources, i.e., clinical trials in humans, animal studies and in vitro data, were used to build the models. A quantitative link between low lymphocyte count and poor patient survival was confirmed using the linear-quadratic model. Modelling accuracy was improved by integrating saturation effects on lymphocyte radiosensitivity (as conceptualized by a new “saturation model” of our own). Modeling based on mice data showed that X-ray therapy significantly reduced lymphocyte counts of multiple subpopulations and induced persistent inflammation while proton therapy had minimal impact on lymphocyte subpopulations, mostly by its ballistic sparing of cervical lymph nodes. Non-linear mixed-effect modeling also showed that while both B and T-lymphocytes recovered after X-ray-induced depletion, tumors could significantly delay B-cell recovery and reduce circulating T cell counts in mice. Additionally, data from a clinical trial in humans suggested that therapeutic radiation doses to lymph nodes significantly affected circulating lymphocyte counts, regardless of the dose to the blood. These findings highlight the importance of considering blood but also lymph node irradiation for preserving the circulating immune cells during and after radiotherapy
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Martigne, Patrick. "Neuropathologie radio-induite : des effets précoces aux séquelles tardives : études comportementales et métaboliques chez le rat après irradiation globale sublétale." Grenoble, 2010. http://www.theses.fr/2010GRENS012.

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Анотація:
Le dogme relatif à la radiorésistance du Système Nerveux Central (SNC) a vécu. Les progrès en neurosciences permettent aujourd'hui de reconsidérer les dysfonctionnements cognitifs radio-induits observés au décours des radiothérapies ou après un accident d'irradiation, et d'envisager des moyens diagnostiques et thérapeutiques adaptés. Nous avons développé un modèle Rat afin d'étudier les effets d'une irradiation gamma corps entier à dose sublétale (4,5 Gy). Celle-ci induit des troubles de l'apprentissage et de la mémorisation d'une tâche en cours d'acquisition durant le premier mois – lesquels sont prévenus par l'administration d'une molécule radioprotectrice de référence (amifostine) – tandis qu'elle ne semble pas perturber la mémoire rétrograde. Précocement, une vague apoptotique survient 5 à 9 heures après exposition dans la zone sous-ventriculaire avec, en parallèle, une neurogenèse anéantie. Deux jours après irradiation, l'étude métabolique ex vivo réalisée par RMN HRMAS (High Resolution Magic Angle Spinning) suggère la présence d'un œdème cérébral tandis que l'étude des lipides cérébraux en RMN liquide confirme l'atteinte membranaire (élévation du cholestérol et des phospholipides). Le profil lipidique se normalise ensuite tandis qu'une réaction gliale apparait. Enfin, 1 mois post-irradiation, l'élévation du GABA, neurotransmetteur inhibiteur du SNC, dans 2 structures cérébrales distinctes, s'accompagne d'une diminution de la taurine dans l'hippocampe qui persiste 6 mois. Notre modèle intégré permet ainsi de valider des biomarqueurs quantifiables en spectroscopie RMN in vivo – prochaine étape expérimentale – et de tester de nouvelles thérapeutiques radioprotectrices
The radioresistance dogma of Central Nervous System (CNS) is now obsolete. Recent progress in neuroscience allow us to reconsider the radiation-induced cognitive dysfunctions observed after radiation therapy or after a nuclear accident, and to devise appropriate diagnostic and therapeutic means. We have developed a Rat model to study the effects of total body irradiation at a sublethal dose (4. 5 Gy). This leads to impaired learning and memory of a task being acquired during the first month – which is prevented by administration of a radioprotector (amifostine) – while it does not appear to affect retrograde memory. Early, an apoptotic wave occurs in the sub-ventricular zone, 5 to 9 hours after exposure, while neurogenesis is suppressed. Two days after irradiation, the metabolic study conducted by NMR HRMAS (High Resolution Magic Angle Spinning) suggests the presence of cerebral oedema and the study of brain lipids in liquid NMR confirms the membrane damages (elevated cholesterol and phospholipids). The lipid profile is then normalized while a gliosis appears. Finally, 1 month post-irradiation, the elevation of GABA, an inhibitory neurotransmitter, in 2 separate brain structures, occurs simultaneously with a taurine decrease in the hippocampus that lasts 6 months. Our integrated model allows validating biomarkers measurable in vivo NMR spectroscopy – the next experimental stage – and testing new radiation-protective agents
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Dwiri, Fatima azzahra. "Impacts de l'irradiation ciblée sur le tissu cérébral et les déficits cognitifs : études multiparamétriques et longitudinales chez le rat." Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMC411.

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Bien que la radiothérapie, traitement incontournable en neuro-oncologie, améliore la survie des patients, elle affecte de manière considérable le tissu cérébral sain avoisinant la tumeur conduisant à des déficits cognitifs qui sont retrouvés chez 50 à 90 % des patients. Les avancées technologiques réalisées lors de la dernière décennie ont permis de concevoir de nouvelles techniques d’irradiation avec des propriétés balistiques prometteuses. Cependant, leurs intérêts pour prévenir la radiotoxicité cérébrale reste à démontrer, en s’appuyant notamment sur des recherches précliniques pour lesquelles l’utilisation de ces techniques de radiothérapie est fragmentaire à ce jour. L’objectif de ces travaux de thèse a été de caractériser, chez le rat adulte sain ou porteur d’une tumeur cérébrale, les effets de l’irradiation cérébrale ciblée sur l’intégrité tissulaire et les déficits cognitifs, d’une part de manière multiparamétrique via l’utilisation de l’imagerie IRM, de différents tests comportementaux ainsi que des analyses immunohistologiques, et d’autre part de manière longitudinale avec un suivi des animaux jusqu’à 6 mois après irradiation. Collectivement, nos données montrent, comme attendu et en accord avec la littérature, que l’irradiation du cerveau sain entier engendre des déficits dans les processus d’apprentissage, de mémorisation et d’émotion, et ceci pendant les phases aiguës et chroniques. De même, ce paradigme d’irradiation est associé à des altérations du tissu cérébral. Cependant, et d’une manière un peu surprenante par rapport à notre hypothèse de départ, l’irradiation d’un seul hémisphère n’a pas modifié de façon significative les performances cognitives évaluées et n’a pas altéré l’intégrité du tissu cérébral. Les résultats obtenus dans le modèle de tumeur cérébrale montrent des déficits cognitifs suite à une irradiation cerveau entier, lesquels sont aussi observés avec l’irradiation hémisphérique mais avec des effets moindres. Malheureusement, du fait des effectifs faibles au sein des groupes expérimentaux, il est difficile de conclure sur le fait que les déficits cognitifs radio-induits observés soient exacerbés en présence de tumeur
Although radiotherapy, an essential treatment in neuro-oncology, improves the survival of patients, it significantly affects the surrounding healthy brain tissue, leading to cognitive deficits found in 50 to 90% of patients. Technological advancements made in the last decade have allowed the development of new irradiation techniques with promising ballistic properties. However, their potential for preventing cerebral radiotoxicity remains to be demonstrated, relying mainly on preclinical research, for which the use of these radiotherapy techniques is currently fragmented. The objective of this thesis work was to characterize the effects of targeted brain irradiation on tissue integrity and cognitive deficits in healthy adult rats and rats bearing brain tumor. This characterization was done through multiparametric imaging using MRI, various behavioral tests, as well as immunohistological analyses. Furthermore, a longitudinal approach was employed, with the animals being monitored up to 6 months after irradiation. Collectively, our data demonstrate, as expected and in accordance with the literature, that whole-brain irradiation leads to deficits in learning, memory, and emotion processes, both during acute and chronic phases. Similarly, this irradiation paradigm is associated with alterations in brain tissue. However, somewhat surprisingly compared to our initial hypothesis, irradiation of a single hemisphere did not significantly modify the evaluated cognitive performances or compromise tissue integrity. In the brain tumor model, cognitive deficits were observed following whole-brain irradiation, which were also present with hemispheric irradiation but with lesser effects. Unfortunately, due to low sample sizes within the experimental groups, it is difficult to conclude whether the observed radio-induced cognitive deficits are exacerbated in the presence of a tumor
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Книги з теми "Brain irradiation"

1

Wedlock, Pauline Margaret. Behavioural effects of low intesity laser irradiation of the rodent brain. [s.l: The Author], 1995.

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2

International Commission on Radiological Protection. Committee 1., ed. Developmental effects of irradiation on the brain of the embryo and fetus: A report. Oxford: Pergamon Press, 1986.

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Shvarts, Shifra, and Siegal Sadetzki. Ringworm and Irradiation. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197568965.001.0001.

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The practice of using x-rays for the medical treatment of benign diseases began in the 1920s and peaked in the 1940s and 1950s. Radiation therapy was considered good medical practice during the first decades of the 20th century and was very effective at controlling and eliminating ringworm (tinea capitis), an epidemic that was spread mainly among children. Results were often immediate. In the United States, Canada, Europe, Australia, the Middle East, and North Africa, hundreds of thousands of children were treated with radiation therapy for ringworm of the scalp. X-ray treatment gradually came to an end in the 1960s when other effective oral treatments were developed (e.g., griseofulvin for ringworm). In parallel, studies started to suggest that radiation exposure, especially in childhood, might increase the risk for developing blood malignancies, benign and malignant tumors of the thyroid gland, and leukemia. This volume discusses the use of irradiation for the treatment of ringworm in different countries in the first half of the 20th century; the latent risk for the development of tumors, malignancies, thyroid cancer, brain tumors, and other health effects among the exposed population; media coverage; and the initiatives of the National Cancer Institute to launch a nationwide campaign warning the medical community and public about the late health effects of ionizing radiation
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Jo, Jasmin, and David Schiff. Brain Metastases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0141.

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In the past, detection of brain metastases signaled the conclusion of aggressive systemic treatment and shifted the focus of care toward palliation. The median survival for patients with single brain metastasis without brain-directed treatment is about a month. Whole brain radiation therapy was the traditional palliative treatment utilized, offering an additional 2 to 5 months. More recently, in addition to whole brain irradiation, the roles of surgery, stereotactic radiosurgery, chemotherapy, and targeted therapies in the definitive management of brain metastases have been investigated in numerous studies. In selected patients, the use of aggressive local therapies can be associated with long survival and good quality of life. This chapter discusses the current state of the art therapeutic options for brain metastases.
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5

Thorne, M. ICRP Publication 49: Developmental Effects of Irradiation on the Brain of the Embryo and Fetus. Elsevier Science & Technology, 1987.

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Developmental effects of irradiation on the brain of the embryo and fetus: A report of a task group of committee 1 of the International Commission on Radiological Protection : adopted by the Commission in July 1986. Oxford: Pergamon for the International Commission on Radiological Protection, 1986.

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7

Jalali, Rakesih, Patrick Y. Wen, and Takamitsu Fujimaki. Meningiomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0011.

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Meningiomas are the most common type of primary brain tumour, comprising approximately one-third of all intracranial neoplasms. It is therefore important for all neuro-oncologists to understand the biology and optimal managements of these tumours. The majority of meningiomas are World Health Organization grade I benign tumours, but grade II (atypical) or grade III (anaplastic) tumours are not uncommon. Total surgical removal is the standard of care but may not be feasible if the tumour involves critical structures such as cranial nerves or important blood vessels. Conventional radiation therapy, stereotactic radiosurgery, or particle irradiation is used for residual or recurrent tumours. To date, medical treatments have had a limited role, except for controlling seizures. However, there are ongoing clinical trials with molecularly targeted drugs and immunotherapies based on improved understanding of the molecular pathogenesis of these tumours. In this chapter, the clinical presentation, biology, and therapy for these tumours are discussed.
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Hodgkiss, Andrew. Biological Psychiatry of Cancer and Cancer Treatment. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.001.0001.

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As long-term cancer survival becomes a widely shared experience, the quality of life of people living with and beyond a cancer diagnosis is increasingly important. Optimizing the prevention and treatment of any psychiatric consequences of certain tumours and treatments is now central to high-quality cancer care. This book—a rather original addition to the oncology and psycho-oncology literature—aims to equip oncology clinicians with the knowledge to more expertly prevent, detect, and manage the ‘organic’ psychiatric disorders experienced by people with cancer. It will also serve as a valuable introduction to contemporary oncology for psychiatrists.The psychiatry of cancer is a distinct subject within the wider field of psycho-oncology. Psychiatric disorders arising through direct biological mechanisms from particular tumours or cancer treatments is a narrower topic still, but one in which oncologists are required to have expertise. This book considers in detail the psychiatric aspects of pro-inflammatory cytokines, endocrine paraneoplastic syndromes, onconeuronal antibodies, brain irradiation, hormone deprivation, glucocorticoid treatment, conventional chemotherapies, and molecularly targeted agents.
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Частини книг з теми "Brain irradiation"

1

Nieder, Carsten, Anca L. Grosu, and Minesh P. Mehta. "Brain Metastases." In Re-irradiation: New Frontiers, 209–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/174_2010_66.

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2

Gains, Jennifer E., and Susan C. Short. "Brain Tumors." In Re-irradiation: New Frontiers, 85–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/174_2010_68.

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Nieder, Carsten, Anca L. Grosu, and Minesh P. Mehta. "Brain Metastases." In Re-Irradiation: New Frontiers, 337–56. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/174_2016_58.

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4

Palmer, Joshua D., Colin Champ, Susan C. Short, and Shannon E. Fogh. "Brain Tumours." In Re-Irradiation: New Frontiers, 127–42. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/174_2016_66.

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5

Alesch, François, R. Hawliczek, and W. Th Koos. "Interstitial Irradiation of Brain Metastases." In Stereotactic Neuro-Radio-Surgery, 29–34. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-9399-0_7.

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6

Korinthenberg, R. "Irradiation-Induced Brain Dysfunction in Children." In Acute and Long-Term Side-Effects of Radiotherapy, 199–207. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84892-6_17.

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Tarbell, Nancy J., James Wallman, Patricia Eifel, and J. Robert Cassady. "Results of definitive irradiation for optic gliomas." In Biology of Brain Tumour, 375–79. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_50.

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8

Oppel, F., H. W. Pannek, J. Voges, and M. Brock. "Interstitial Irradiation of Inoperable Brain Stem Tumors." In Surgery in and around the Brain Stem and the Third Ventricle, 526–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71240-1_69.

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9

Lafuente, J. V., J. Cervós-Navarro, and E. Gutierrez Argandoña. "Evaluation of BBB Damage in an UV Irradiation Model by Endogenous Protein Tracers." In Brain Edema IX, 139–41. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_37.

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Salcman, Michael, Wilfred Sewchand, Pradip P. Amin, and Edwin H. Bellis. "Technique and preliminary results of interstitial irradiation for recurrent glial tumors." In Biology of Brain Tumour, 367–72. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_49.

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Тези доповідей конференцій з теми "Brain irradiation"

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Filatov, P. V., E. S. Polovnikov, K. Yu Orlov, A. V. Krutko, I. A. Kirilova, A. V. Moskalev, E. V. Filatova, and A. A. Zheravin. "Multiple brain metastases irradiation with Eleka Axesse stereotactic system." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS: Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications (PC IPCA’17). Author(s), 2017. http://dx.doi.org/10.1063/1.5001597.

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Moore, Elizabeth, Mitra Kooshki, Lance Miller, and Mike Robbins. "Abstract 78: Fractionated whole brain irradiation modulates Homer1a expression in a brain region specific manner." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-78.

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Ojeda, Abril Damaris Iglesias, Monserrat Llaguno Munive, Efrén Hernández Ramirez, and Luis Alberto Medina Velázquez. "Dosimetry in fractionated irradiation of rat brain to evaluate radiobiological response." In PROCEEDINGS OF THE XVI MEXICAN SYMPOSIUM ON MEDICAL PHYSICS. AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0051374.

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Kolesnikova, Inna, Natalia Budennaya, Yurii Severiukhin, Kristina Lyakhova, Dina Utina, Maria Lalkovičova, and Аlexander Ivanov. "THE EFFECT OF PROTON IRRADIATION ON THE MORPHOFUNCTIONAL STATE OF THE RAT BRAIN." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m430.sudak.ns2019-15/226-227.

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5

Stoica, Roberta, Mihai Radu, and Beatrice Mihaela Radu. "Functional changes in brain microvascular endothelial cells upon low-energy accelerated proton-irradiation." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.32.17.

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Moskaleva, Elizaveta, Alla Rodina, Alexander Zhirnik, Oksana Smirnova, Anna Parfenova, Alexander Strepetov, and Yuia Semochkina. "STATE OF BRAIN CELLS AND COGNITIVE FUNCTIONS IN MICE AFTER NEUTRON HEAD IRRADIATION." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2854.sudak.ns2022-18/238-239.

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Chernikova, Sophia, G.-One Ahn, Shie-Chau Liu, Jason Stafford, and J. Martin Brown. "Abstract C291: Targeting SDF-1 (CXCL12) pathway to inhibit the recurrence of breast cancer brain metastases after whole-brain irradiation." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c291.

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Momiyama, Masashi, Yukihiko Hiroshima, Atsushi Suetsugu, Yasunori Tome, Sumiyuki Mii, Shuya Yano, Takashi Chishima, Michael Bouvet, Itaru Endo, and Robert M. Hoffman. "Abstract 5546: UVC irradiation inhibits superficial tumor growth in the brain of nude mice." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5546.

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Xiao, Xue-Chang, Jia-Zheng Dong, Xiao-Fan Chu, Shao-Wei Jia, Timon C. Liu, Jian-Ling Jiao, Xi-Yuan Zheng, and Ci-Xiong Zhou. "SPECT study of low intensity He-Ne laser intravascular irradiation therapy for brain infarction." In Third International Conference on Photonics and Imaging in Biology and Medicine, edited by Qingming Luo, Valery V. Tuchin, Min Gu, and Lihong V. Wang. SPIE, 2003. http://dx.doi.org/10.1117/12.546102.

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Kopaeva, Marina, Anton Cherepov, Mikhail Nesterenko, and Irina Zarayskaya. "PROTECTIVE EFFECT OF LACTOFERRIN ON MOUSE BRAIN CELLS AFTER GAMMA IRRADIATION OF THE HEAD." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2796.sudak.ns2022-18/176-177.

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Звіти організацій з теми "Brain irradiation"

1

Manley, N. B., J. I. Fabrikant, and E. L. Alpen. Cell and tissue kinetics of the subependymal layer in mouse brain following heavy charged particle irradiation. Office of Scientific and Technical Information (OSTI), December 1988. http://dx.doi.org/10.2172/7191328.

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