SU-E-T-356: Dose Response of a 2D Diode Array for Non-Primary Photon Radiation from a Dynamic MLC

2012 ◽  
Vol 39 (6Part15) ◽  
pp. 3786-3786
Author(s):  
A Chu ◽  
W Feng ◽  
Z Chen ◽  
R Nath
2018 ◽  
Author(s):  
Ricciotti Emanuela ◽  
Dimitra Sarantopoulou ◽  
Gregory R. Grant ◽  
Jenine K. Sanzari ◽  
Gabriel S. Krigsfeld ◽  
...  

AbstractPurpose. The cardiovascular biology of proton radiotherapy is not well understood. We aimed to compare the genomic dose-response to proton and gamma radiation of the mouse aorta to assess whether their vascular effects may diverge.Materials and methods.We performed comparative RNA sequencing of the aorta following (4 hrs) total-body proton and gamma irradiation (0.5 - 200 cGy whole body dose, 10 dose levels) of conscious mice. A trend analysis identified genes that showed a dose response.Results.While fewer genes were dose-responsive to proton than gamma radiation (29 vs. 194 genes;q-value ≤ 0.1), the magnitude of the effect was greater. Highly responsive genes were enriched for radiation response pathways (DNA damage, apoptosis, cellular stress and inflammation;p-value ≤ 0.01). Gamma, but not proton radiation induced additionally genes in vasculature specific pathways. Genes responsive to both radiation types showed almost perfectly superimposable dose-response relationships.Conclusions.Despite the activation of canonical radiation response pathways by both radiation types, we detected marked differences in the genomic response of the murine aorta. Models of cardiovascular risk based on photon radiation may not accurately predict the risk associated with proton radiation.


Dose-Response ◽  
2005 ◽  
Vol 3 (4) ◽  
pp. dose-response.0 ◽  
Author(s):  
Bobby R. Scott

New research data for low-dose, low- linear energy transfer (LET) radiation-induced, stochastic effects (mutations and neoplastic transformations) are modeled using the recently published NEOTRANS3 model. The model incorporates a protective, stochastic threshold (StoThresh) at low doses for activating cooperative protective processes considered to include presumptive p53-dependent, high-fidelity repair of nuclear DNA damage in competition with presumptive p53-dependent apoptosis and a novel presumptive p53-independent protective apoptosis mediated (PAM) process which selectively removes genomically compromised cells (mutants, neoplastic transformants, micronucleated cells, etc.). The protective StoThresh are considered to fall in a relatively narrow low-dose zone (Transition Zone A). Below Transition Zone A is the ultra-low-dose region where it is assumed that only low-fidelity DNA repair is activated along with presumably apoptosis. For this zone there is evidence for an increase in mutations with increases in dose. Just above Transition Zone A, a Zone of Maximal Protection (suppression of stochastic effects) arises and is attributed to maximal cooperation of high-fidelity, DNA repair/apoptosis and the PAM process. The width of the Zone of Maximal Protection depends on low-LET radiation dose rate and appears to depend on photon radiation energy. Just above the Zone of Maximal Protection is Transition Zone B, where deleterious StoThresh for preventing the PAM process fall. Just above Transition Zone B is a zone of moderate doses where complete inhibition of the PAM process appears to occur. However, for both Transition Zone B and the zone of complete inhibition of the PAM process, high-fidelity DNA repair/apoptosis are presumed to still operate. The indicated protective and deleterious StoThresh lead to nonlinear, hormetic-type dose-response relationships for low-LET radiation-induced mutations, neoplastic transformation and, presumably, also for cancer.


2015 ◽  
Vol 42 (2) ◽  
pp. 856-865 ◽  
Author(s):  
Maegan Gargett ◽  
Brad Oborn ◽  
Peter Metcalfe ◽  
Anatoly Rosenfeld

1963 ◽  
Vol 45 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Donald H. Hanscom ◽  
Armand Littman ◽  
Jack V. Pinto

1999 ◽  
Vol 1 ◽  
pp. S47-S47
Author(s):  
N PAYNE ◽  
R GROCOTTMASON ◽  
A IONESCU ◽  
B SJOBERG ◽  
I SANDBLOM ◽  
...  

2002 ◽  
Author(s):  
N. B. Hansen ◽  
M. J. Lambert ◽  
E. M. Forman
Keyword(s):  

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