scholarly journals PD20-01 VALIDATION OF AN ANIMAL MODEL OF PELVIC RADIATION INDUCED FEMALE SEXUAL AND URINARY DYSFUNCTION

2019 ◽  
Vol 201 (Supplement 4) ◽  
Author(s):  
Lindsey Burleson* ◽  
Shelby Powers ◽  
Michael Odom ◽  
Dillon Ellis ◽  
Jae Won Jung ◽  
...  
2019 ◽  
Vol 133 (1) ◽  
pp. 53S-51S
Author(s):  
Lindsey K. Burleson ◽  
Shelby A. Powers ◽  
Michael R. Odom ◽  
Dillon A. Ellis ◽  
Jae W. Jung ◽  
...  

2021 ◽  
Author(s):  
Halida Thanveer Asana Marican ◽  
Hongyuan Shen

Metaphase-based cytogenetic methods based on scoring of chromosome aberrations for the estimation of the radiation dose received provide a powerful approach for evaluating the associated risk upon radiation exposure and form the bulk of our current knowledge of radiation-induced chromosome damages. They mainly rely on inducing quiescent peripheral lymphocytes into proliferation and blocking them at metaphases to quantify the damages at the chromosome level. However, human organs and tissues demonstrate various sensitivity towards radiation and within them, self-proliferating progenitor/stem cells are believed to be the most sensitive populations. The radiation-induced chromosome aberrations in these cells remain largely unknown, especially in the context of an intact living organism. Zebrafish is an ideal animal model for research into this aspect due to their small size and the large quantities of progenitor cells present during the embryonic stages. In this study, we employ a novel metaphase-based cytogenetic approach on zebrafish embryos and demonstrate that chromosome-type and chromatid-type aberrations could be identified in progenitor cells at different cell-cycle stages at the point of radiation exposure. Our work positions zebrafish at the forefront as a useful animal model for studying radiation-induced chromosome structural changes in vivo.


2020 ◽  
Vol 40 (4) ◽  
pp. 1981-1988
Author(s):  
HIROSHI DOI ◽  
MIKOTO TAMURA ◽  
KIYOSHI NAKAMATSU ◽  
HAJIME MONZEN ◽  
YASUMASA NISHIMURA

Cytotherapy ◽  
2014 ◽  
Vol 16 (4) ◽  
pp. S88
Author(s):  
N. Mathieu ◽  
C. Durand ◽  
L. Moussa ◽  
C. Demarquay ◽  
R. Bessout ◽  
...  

2002 ◽  
Vol 43 (2) ◽  
pp. 135-135 ◽  
Author(s):  
KOUICHI YAMAMOTO ◽  
NORIAKI TAKEDA ◽  
ATSUSHI YAMATODANI

Author(s):  
Suzanne N. King ◽  
Justin Hurley ◽  
Zachary Carter ◽  
Nicholas Bonomo ◽  
Brian Wang ◽  
...  

Radiation based treatments for oropharyngeal and hypopharyngeal cancers result in impairments in swallowing mobility, but the mechanisms behind the dysfunction are not clear. The purpose of this study was to determine if we could establish an animal model of radiation-induced dysphagia in which mechanisms could be examined. We hypothesized that (1) radiation focused at the depth of the mylohyoid muscle would alter normal bolus transport and bolus size; and (2) that radiation to the mylohyoid muscle will induce an injury/stress-like response in trigeminal sensory neurons whose input might modulate swallow. Rats were exposed to 48 or 56 Gy of radiation to the mylohyoid given 8 Gy in 6 or 7 fractions. Swallowing function was evaluated by videofluoroscopy 2- and 4-weeks following treatment. Neuronal injury/stress was analyzed in trigeminal ganglion by assessing ATF3 and GAP-43 mRNA at 2-, 4- and 8-weeks post. Irradiated rats exhibited decreases in bolus movement through the pharynx and alterations in bolus clearance. Additionally, ATF3 and GAP-43 mRNAs were upregulated in trigeminal ganglion in irradiated rats, suggesting that radiation to mylohyoid muscle induced an injury/stress response in neurons with cell bodies that are remote from the irradiated tissue. These results suggest that radiation-induced dysphagia can be assessed in the rat, and that radiation induces injury/stress-like responses in sensory neurons.


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