The Gottingen minipig is a model of the hematopoietic acute radiation syndrome: G-colony stimulating factor stimulates hematopoiesis and enhances survival from lethal total-body γ-irradiation.
The Gottingen minipig is a model of the hematopoietic acute radiation syndrome: G-colony stimulating factor stimulates hematopoiesis and enhances survival from lethal total-body γ-irradiation.
复制标题
DOI:
10.1016/j.ijrobp.2013.04.041
复制
发表时间:
2013-08-01
影响因子:
7
通讯作者:
Whitnall, Mark H.
中科院分区:
文献类型:
--
作者:
Moroni, Maria;Ngudiankama, Barbara F.;Christensen, Christine;Olsen, Cara H.;Owens, Rossitsa;Lombardini, Eric D.;Holt, Rebecca K.;Whitnall, Mark H.
We are characterizing the Gottingen minipig as an additional large animal model for advanced drug testing for the Acute Radiation Syndrome (ARS), to enhance discovery and development of novel radiation countermeasures. Among the advantages provided by this model, the similarities to human hematological parameters and dynamics of cell loss/recovery following irradiation provide a convenient means to compare efficacy of drugs known to affect bone marrow cellularity and hematopoiesis. Male Gottingen minipigs, 4–5 months old and weighing 9–11 kg were used for this study. We tested the standard off-label treatment for ARS, rhG-CSF (Neupogen®, 10 μg/kg/day for 17 days), at the estimated LD70/30 total-body gamma-irradiation (TBI) radiation dose for the hematopoietic syndrome, starting 24 hours after irradiation. Results indicate G-CSF enhanced survival, stimulated recovery from neutropenia, and induced mobilization of hematopoietic progenitor cells. In addition, administration of G-CSF resulted in maturation of monocytes/macrophages. These results support continuing efforts toward validation of the minipig as a large animal model for advanced testing of radiation countermeasures and characterization of the pathophysiology of ARS, and suggest that the efficacy of G-CSF in improving survival after total body irradiation may involve mechanisms other than increasing numbers of circulating granulocytes.
登录
查看更多内容
影响因子:
3.7
作者:
Forcheron F;Agay D;Scherthan H;Riccobono D;Herodin F;Meineke V;Drouet M
通讯作者:
Drouet M
影响因子:
20.3
作者:
MacVittie, TJ;Farese, AM;McKearn, JP
通讯作者:
McKearn, JP
影响因子:
3.4
作者:
Moroni, Maria;Coolbaugh, Thea V.;Whitnall, Mark H.
通讯作者:
Whitnall, Mark H.
影响因子:
2
作者:
Grace MB;Singh VK;Rhee JG;Jackson WE 3rd;Kao TC;Whitnall MH
通讯作者:
Whitnall MH
影响因子:
2
作者:
Yu, Zu-Yin;Li, Ming;Luo, Qing-Liang
通讯作者:
Luo, Qing-Liang