Browsing by Subject "Radiation"

Now showing 1 - 3 of 3
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    Morphometric analysis of bromodeoxyuridine distribution and cell density in the rat Dunning prostate tumor R3327-AT1 following treatment with radiation andtor hyperthermia
    (Murcia : F. Hernández, 1999) Peschke, P.; Klein, V.; Wolber, G.; Friedrich, E.; Hahn, E.W.
    To monitor cellular response to single doses of radiation (RT) andlor local tumor hyperthermia (LTH) proliferation kinetics were determined in the anaplastic prostate adenocarcinoma R3327-AT1 grown in Copenhagen rats. Tumor-bearing animals were injected i.v. with a bolus of bromodeoxyuridine (BrdUrd), and at defined times after treatment the tumors were surgically removed, fixed and embedded in paraffin. BrdUrd incorporated into the DNA of S-Phase nuclei was detected on 4-6 pm-thick tissue sections using a monoclonal anti-BrdUrd antibody followed by streptavidinbiotin and alkaline phosphatase as a reporter system. Cell nuclei were stained with the fluorescence dye DAPI (Diaminophenylindole). Morphometric analysis was performed using a computer-assisted Leitz-TASIplus system. Depending on tumor size, up to 18,000 nuclei were routinely analyzed. Untreated tumors of standardized size (8-10 mm) exhibited a BrdUrdlabeling index (LI) of (6.921.6)%. In general, the L1 was higher in the periphery than in the center, being more pronounced in larger tumors. After 6 Gy y-rays, the mean L1 decreased to 1.8% (24 h) and rose afterwards to 5.4% by 168 h. Following LTH (43.5 "C, 35 min water bath), the mean L1 rapidly decreased to 2% (8 h), rose to 9.8% (48 h), and plateaued at 6% after 168 h. A combined treatment consisting of irradiation (6 Gy) followed by LTH yielded smallest L1 (2.4+0.18%) and lowest cell density (111+0.6 nuclei per field) by 168 h. The morphometric procedure was reliable and reproducible and can be used to characterize and compare the effects of different therapies on cell kinetics. Of particular value is that these analyses are done on an Offprint requests to: Dr. Peter Peschke. Deutsches Krebsforschungszentrum, Forschungsschwerpunkt Radiologie. Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. Fax:+ 6221-422572. e mail: P.Peschke@DKFZ-HeideIberg.de intact tissue architecture and hence enable a better interpretation of flow cytometric results of treatmentinduced alterations within different topohistological regions in solid tumors. Moreover, the technique provides the basis for 3D reconstruction of the cellular activity and heterogeneity of experimental neoplasms.
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    Neurobiological toxicity of radiation in hippocampal cells
    (2013) Kim, Joong-Sun; Yang, Miyoung; Kim, Sung-Ho; Shin, Taekyun; Moon, Changjong
    Worldwide radiation exposure is increasing due to recent nuclear accidents, space travel, atomic weapons testing and use, and medical treatments. In adult animals, ionizing radiation can significantly impact hippocampal neurogenesis and negatively affect hippocampal functions such as cognition. However, there is considerable uncertainty regarding the mechanisms underlying these effects. This article reviews in vivo and in vitro studies on the effects of irradiation on hippocampal neurogenesis and function in order to gain new mechanistic insights. This information will provide complementary views of our understanding of the normal brain’s tolerance to radiation exposure, the potentially serious implications of radiation exposure to cognition, and lead to a discussion of potential strategies for pharmacotherapy and behavioral intervention.
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    Phosphatidylinositide 3-kinase AKT in radiation responses
    (Murcia : F. Hernández, 2004) Zhan, M.; Han, Z.C.
    Ionizing or ultraviolet radiation-induced cellular survival signaling pathways induce development of cancer and insensitivity of tumor cells to radiation therapy. Accumulating evidence suggests that the phosphatidylinositide 3-kinase (PI3K)/AKT signal pathway is a major contributor to radioresistance. In many cell types PI3K/AKT signaling is a key cytoprotective response downstream of the EGFR family receptors and mediated carcinogenesis. Cytokines, such as HGF, IGF-I, and IL-6 also protects cells against apoptosis induced by radiation through PI3K/AKT pathway. The mechanics by which PI3K/AKT signaling functions in radiation responses may include its regulation of mitochondrial proteins, transcription factors, translation machinery, and cell-cycle progression. In addition, cross-talk between the PI3K/AKT pathway and mitogen-activated protein kinases, protein kinase A, and protein kinase C signal pathway may also play an important role.