The Experts below are selected from a list of 138777 Experts worldwide ranked by ideXlab platform
Julian J. Lum - One of the best experts on this subject based on the ideXlab platform.
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WE‐C‐BRA‐09: Towards Treatment Monitoring of Tumour Radiation Response with Raman Spectroscopy
Medical Physics, 2012Co-Authors: Q. Matthews, Andrew Jirasek, Alexandre G. Brolo, Julian J. LumAbstract:Purpose: To use single‐cell Raman spectroscopy (RS) and principal component analysis (PCA) for early treatment monitoring of Radiation Response. Methods: Two human tumourcell lines, one known to be radioresistant (H460, SF2 = 0.64) and one radiosensitive (LNCaP, SF2 = 0.27), were treated with daily 2 Gy fractions of 6 MV photons, up to a maximum total dose of 10 Gy. Irradiated and unirradiated cultures were harvested and analyzed with RS each day after the previous daily fraction, and also at 2 and 3 days after the final fraction. Single‐cell Raman spectra were acquired from 20 cells per sample with a Raman microscope utilizing a 785 nm excitation laser. All spectra (280 per cell line) were post‐processed, and the total data set for each cell line was analyzed with PCA using standard algorithms. Results: One Radiation‐induced PCA component was detected for each cell line by identification of statistically significant changes in the PCA score distributions for irradiated samples, as compared to unirradiated samples, at time points after the start of Radiation treatment. The radioresistant cells (H460) exhibit a strong RS molecular Radiation Response signature, detectable as early as 2 days after the start of treatment, of which Radiation‐induced glycogen synthesis is a significant contributor. The radiosensitive cells (LNCaP) exhibit a weak molecular Radiation Response signature that is not correlated with the radioresistant cell Response, with no contributions from glycogen. The glycogen synthesis observed in the radioresistant cells is confirmed via Western blotting to be the result of Radiation‐induced activation of the phosphatidylinositol‐3‐kinase/Akt (PI3K/Akt) signalling pathway, a molecular Radiation Response known to promote cell survival and confer Radiation resistance. Conclusions: This work supports the feasibility of using RS for early treatment monitoring of tumour Radiation Response, leading to personalized therapy.
C.f. Hawkins - One of the best experts on this subject based on the ideXlab platform.
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Modeling of the transient ionizing Radiation Response of an inductively-loaded power MOSFET
[1991] Proceedings of the 3rd International Symposium on Power Semiconductor Devices and ICs, 1Co-Authors: A.a. Keshavarz, G.a. Franz, C.f. HawkinsAbstract:The authors present a two-dimensional computer simulation of the Radiation Response of a power MOSFET device that uses the effect of the external load circuit in calculations. It makes it possible to observe the effects of the device structure, external circuitry, and biasing voltage on the transient Radiation Response of the device. The method is used to find important parameters such as the maximum induced current in the device or the maximum power dissipation under ionizing Radiation. Based on the results, it can be decided if the device will be operating within its safety operating region when irradiated by a specific Radiation pulse. The simulation can replace expensive and time-consuming laboratory testing with short-duration pulses. >
Ralph P. Mason - One of the best experts on this subject based on the ideXlab platform.
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A role for dynamic contrast-enhanced magnetic resonance imaging in predicting tumour Radiation Response.
British journal of cancer, 2016Co-Authors: Rami R. Hallac, Heling Zhou, R. Pidikiti, K. Song, Timothy D. Solberg, Vikram D. Kodibagkar, Peter Peschke, Ralph P. MasonAbstract:A role for dynamic contrast-enhanced magnetic resonance imaging in predicting tumour Radiation Response
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Correlations of noninvasive BOLD and TOLD MRI with pO2 and relevance to tumor Radiation Response
Magnetic resonance in medicine, 2013Co-Authors: Rami R. Hallac, Heling Zhou, R. Pidikiti, K. Song, Timothy D. Solberg, Peter Peschke, Strahinja Stojadinovic, Dawen Zhao, Ralph P. MasonAbstract:Purpose To examine the potential use of BOLD (Blood Oxygenation Level Dependent) and TOLD (Tissue Oxygenation Level Dependent) contrast MRI to assess tumor oxygenation and predict Radiation Response.
Eric C Holland - One of the best experts on this subject based on the ideXlab platform.
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in vivo Radiation Response of proneural glioma characterized by protective p53 transcriptional program and proneural mesenchymal shift
Proceedings of the National Academy of Sciences of the United States of America, 2014Co-Authors: John Halliday, Karim Helmy, Siobhan S Pattwell, Kenneth L Pitter, Quincey Laplant, Tatsuya Ozawa, Eric C HollandAbstract:Glioblastoma is the most common adult primary brain tumor and has a dismal median survival. Radiation is a mainstay of treatment and significantly improves survival, yet recurrence is nearly inevitable. Better understanding the Radiation Response of glioblastoma will help improve strategies to treat this devastating disease. Here, we present a comprehensive study of the in vivo Radiation Response of glioma cells in a mouse model of proneural glioblastoma. These tumors are a heterogeneous mix of cell types with differing Radiation sensitivities. To explicitly study the gene expression changes comprising the Radiation Response of the Olig2+ tumor bulk cells, we used translating ribosome affinity purification (TRAP) from Olig2-TRAP transgenic mice. Comparing both ribosome-associated and total pools of mRNA isolated from Olig2+ cells indicated that the in vivo gene expression Response to Radiation occurs primarily at the total transcript level. Genes related to apoptosis and cell growth were significantly altered. p53 and E2F were implicated as major regulators of the Radiation Response, with p53 activity needed for the largest gene expression changes after Radiation. Additionally, Radiation induced a marked shift away from a proneural expression pattern toward a mesenchymal one. This shift occurs in Olig2+ cells within hours and in multiple genetic backgrounds. Targets for Stat3 and CEBPB, which have been suggested to be master regulators of a mesenchymal shift, were also up-regulated by Radiation. These data provide a systematic description of the events following Radiation and may be of use in identifying biological processes that promote glioma radioresistance.
Q. Matthews - One of the best experts on this subject based on the ideXlab platform.
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WE‐C‐BRA‐09: Towards Treatment Monitoring of Tumour Radiation Response with Raman Spectroscopy
Medical Physics, 2012Co-Authors: Q. Matthews, Andrew Jirasek, Alexandre G. Brolo, Julian J. LumAbstract:Purpose: To use single‐cell Raman spectroscopy (RS) and principal component analysis (PCA) for early treatment monitoring of Radiation Response. Methods: Two human tumourcell lines, one known to be radioresistant (H460, SF2 = 0.64) and one radiosensitive (LNCaP, SF2 = 0.27), were treated with daily 2 Gy fractions of 6 MV photons, up to a maximum total dose of 10 Gy. Irradiated and unirradiated cultures were harvested and analyzed with RS each day after the previous daily fraction, and also at 2 and 3 days after the final fraction. Single‐cell Raman spectra were acquired from 20 cells per sample with a Raman microscope utilizing a 785 nm excitation laser. All spectra (280 per cell line) were post‐processed, and the total data set for each cell line was analyzed with PCA using standard algorithms. Results: One Radiation‐induced PCA component was detected for each cell line by identification of statistically significant changes in the PCA score distributions for irradiated samples, as compared to unirradiated samples, at time points after the start of Radiation treatment. The radioresistant cells (H460) exhibit a strong RS molecular Radiation Response signature, detectable as early as 2 days after the start of treatment, of which Radiation‐induced glycogen synthesis is a significant contributor. The radiosensitive cells (LNCaP) exhibit a weak molecular Radiation Response signature that is not correlated with the radioresistant cell Response, with no contributions from glycogen. The glycogen synthesis observed in the radioresistant cells is confirmed via Western blotting to be the result of Radiation‐induced activation of the phosphatidylinositol‐3‐kinase/Akt (PI3K/Akt) signalling pathway, a molecular Radiation Response known to promote cell survival and confer Radiation resistance. Conclusions: This work supports the feasibility of using RS for early treatment monitoring of tumour Radiation Response, leading to personalized therapy.
