scholarly journals In Situ Micro-Pillar Compression to Examine Radiation-Induced Hardening Mechanisms of FeCrAl Alloys

2021 ◽  
Vol 202 ◽  
pp. 255-265
Author(s):  
Yuchi Cui ◽  
Eda Aydogan ◽  
Jonathan G. Gigax ◽  
Yongqiang Wang ◽  
Amit Misra ◽  
...  
2020 ◽  
Author(s):  
Yuchi Cui ◽  
Eda Aydogan ◽  
Jonathan G. Gigax ◽  
Stuart A. Maloy ◽  
Yongqiang Wang ◽  
...  

Author(s):  
Charles W. Allen

Irradiation effects studies employing TEMs as analytical tools have been conducted for almost as many years as materials people have done TEM, motivated largely by materials needs for nuclear reactor development. Such studies have focussed on the behavior both of nuclear fuels and of materials for other reactor components which are subjected to radiation-induced degradation. Especially in the 1950s and 60s, post-irradiation TEM analysis may have been coupled to in situ (in reactor or in pile) experiments (e.g., irradiation-induced creep experiments of austenitic stainless steels). Although necessary from a technological point of view, such experiments are difficult to instrument (measure strain dynamically, e.g.) and control (temperature, e.g.) and require months or even years to perform in a nuclear reactor or in a spallation neutron source. Consequently, methods were sought for simulation of neutroninduced radiation damage of materials, the simulations employing other forms of radiation; in the case of metals and alloys, high energy electrons and high energy ions.


2021 ◽  
Author(s):  
Nathan J. Madden ◽  
Samuel A. Briggs ◽  
Diana Perales ◽  
Timothy J. Boyle ◽  
Khalid Hattar ◽  
...  

2003 ◽  
Vol 792 ◽  
Author(s):  
Michael I. Ojovan ◽  
William E. Lee

ABSTRACTThe kinetics of alkali ion exchange of irradiated glasses were investigated using the structural energy barrier model for ion exchange of glasses. Derived rates of alkali ion exchange depend both on irradiation dose D(Gy) and dose rate q(Gy/s) illustrating that some effects cannot be simulated by external irradiation and require in-situ measurements. Higher D and q lead to increased ion exchange rates. Significant changes occur in the activation energies demonstrating a 4 – 6 times decrease depending on glass composition. Radiation-induced changes are higher at relatively low temperatures and are diminished by increased glass temperature. Numerical estimations show that changes in alkali ion exchange kinetics occur at D far below damaging doses.


1995 ◽  
Vol 219 ◽  
pp. 169-175 ◽  
Author(s):  
J.D. Hunn ◽  
R.E. Stoller ◽  
S.J. Zinkle

2019 ◽  
Vol 20 (13) ◽  
pp. 3212 ◽  
Author(s):  
Magdalena Jarosz-Biej ◽  
Ryszard Smolarczyk ◽  
Tomasz Cichoń ◽  
Natalia Kułach

Radiotherapy (RT), besides cancer cells, also affects the tumor microenvironment (TME): tumor blood vessels and cells of the immune system. It damages endothelial cells and causes radiation-induced inflammation. Damaged vessels inhibit the infiltration of CD8+ T lymphocytes into tumors, and immunosuppressive pathways are activated. They lead to the accumulation of radioresistant suppressor cells, including tumor-associated macrophages (TAMs) with the M2 phenotype, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). The area of tumor hypoxia increases. Hypoxia reduces oxygen-dependent DNA damage and weakens the anti-cancer RT effect. It activates the formation of new blood vessels and leads to cancer relapse after irradiation. Irradiation may also activate the immune response through immunogenic cell death induction. This leads to the “in situ” vaccination effect. In this article, we review how changes in the TME affect radiation-induced anticancer efficacy. There is a very delicate balance between the activation of the immune system and the immunosuppression induced by RT. The effects of RT doses on immune system reactions and also on tumor vascularization remain unclear. A better understanding of these interactions will contribute to the optimization of RT treatment, which may prevent the recurrence of cancer.


Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 4011-4013 ◽  
Author(s):  
Robert Hromas ◽  
Rinah Shopnick ◽  
Hani George Jumean ◽  
Charles Bowers ◽  
Marileila Varella-Garcia ◽  
...  

Abstract AML1 is a transcriptional activator that is essential for normal hematopoietic development. It is the most frequent target for translocations in acute leukemia. We recently identified 3 patients in whom pancytopenia developed almost 50 years after high-level radiation exposure from nuclear explosions during or after World War II. In all 3 patients, acute myeloid leukemia (AML) eventually developed that had similar characteristics and clinical courses. Cytogenetics from the 3 patients revealed a t(1;21)(p36;q22), a t(18;21)(q21;q22), and a t(19;21)(q13.4;q22). By fluorescent in situ hybridization (FISH), all 3 translocations disrupted the AML1 gene. Two of theseAML1 translocations, the t(18;21) and the t(19;21), have not been reported previously. It is possible that the AML1 gene is a target for radiation-induced AML.


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