Effects of 50 Roentgens and 25 Roentgens Fractional Daily Total-Body γ-Irradiation in the Burro

1955 ◽  
Vol 2 (5) ◽  
pp. 475 ◽  
Author(s):  
John H. Rust ◽  
Bernard F. Trum ◽  
John J. Lane ◽  
U. S. Grant Kuhn ◽  
John R. Paysinger ◽  
...  
Keyword(s):  
Γ Irradiation ◽  
Total Body ◽  
Daily Total

Changes in Respiratory Gases of Burros after Prolonged Fractionated Total-Body γ-Irradiation

1955 ◽  
Vol 2 (1) ◽  
pp. 64 ◽  
Author(s):  
John J. Lane ◽  
James L. Wilding ◽  
John H. Rust ◽  
Bernard F. Trum ◽  
Joseph C. Schoolar
Keyword(s):  
Γ Irradiation ◽  
Total Body ◽  
Respiratory Gases

Ionizing radiation stimulates muscarinic regulation of rat intestinal mucosal function

1998 ◽  
Vol 275 (6) ◽  
pp. G1333-G1340 ◽  
Author(s):  
F. Lebrun ◽  
A. Francois ◽  
M. Vergnet ◽  
L. Lebaron-Jacobs ◽  
P. Gourmelon ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Enzyme Activities ◽  
Plasma Membranes ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Marker Enzyme ◽  
Γ Irradiation ◽  
Ussing Chambers ◽  
Radiation Induced ◽  
Total Body

The aim of this study was to determine whether ionizing radiation modifies muscarinic regulation of intestinal mucosal function. Rats exposed to total body 8-Gy γ-irradiation or sham irradiated were studied up to 21 days after irradiation. Basal and carbachol-stimulated short-circuit current ( I sc) and transepithelial conductance ( G t) of stripped ileum were determined in Ussing chambers. Muscarinic receptor characteristics using the muscarinic antagonist [3H]quinuclidinyl benzilate and three unlabeled antagonists were measured in small intestinal plasma membranes together with two marker enzyme activities (sucrase, Na+-K+-ATPase). Enzyme activities were decreased 4 days after irradiation ( day 4). Basal electrical parameters were unchanged. Maximal carbachol-induced changes in I sc and G t were increased at day 4 (maximal Δ I sc = 195.8 ± 14.7 μA/cm2, n = 19, vs. 115.4 ± 8.2 μA/cm2, n = 63, for control rats) and unchanged at day 7. Dissociation constant was decreased at day 4 (0.73 ± 0.29 nM, n = 10, vs. 2.14 ± 0.39 nM, n = 13, for control rats) but unchanged at day 7, without change in binding site number. Thus total body irradiation induces a temporary stimulation of cholinergic regulation of mucosal intestinal function that may result in radiation-induced diarrhea.

scholarly journals Radiation Impacts Early Atherosclerosis by Suppressing Intimal LDL Accumulation

2021 ◽  
Author(s):  
Jiro Ikeda ◽  
Corey A Scipione ◽  
Sharon Hyduk ◽  
Marwan G Althagafi ◽  
Jawairia Atif ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Single Cell ◽  
Neutral Lipid ◽  
Aortic Arch ◽  
Myeloid Cell ◽  
Transcript Abundance ◽  
Γ Irradiation ◽  
Transport Pathways ◽  
Total Body ◽  
Aortic Intima

Rationale: Bone marrow transplantation (BMT) is used frequently to study the role of hematopoietic cells in atherosclerosis, but aortic arch lesions are smaller in mice after BMT. Objective: To identify the earliest stage of atherosclerosis inhibited by BMT and elucidate potential mechanisms. Methods and Results: Ldlr -/- mice underwent total body γ-irradiation, bone marrow reconstitution and 6-week recovery. Atherosclerosis was studied in the ascending aortic arch and compared to mice without BMT. In BMT mice neutral lipid and myeloid cell topography were lower in lesions after feeding a cholesterol-rich diet (CRD) for 3, 6 and 12 weeks. Lesion coalescence and height were suppressed dramatically in mice post-BMT, whereas lateral growth was inhibited minimally. Targeted radiation to the upper thorax alone reproduced the BMT phenotype. Classical monocyte recruitment, intimal myeloid cell proliferation and apoptosis did not account for the post-BMT phenotype. Neutral lipid accumulation was reduced in 5-day lesions, thus we developed quantitative assays for LDL accumulation and paracellular leakage using DiI-labeled human LDL and rhodamine B-labeled 70kD dextran. LDL accumulation was dramatically higher in the intima of Ldlr -/- relative to Ldlr +/+ mice, and was inhibited by injection of HDL mimics, suggesting a regulated process. LDL, but not dextran, accumulation was lower in mice post-BMT both at baseline and in 5-day lesions. Since the transcript abundance of molecules implicated in LDL transcytosis was not significantly different in the post-BMT intima, transcriptomics from whole aortic arch intima, and at single cell resolution, was performed to give insights into pathways modulated by BMT. Conclusions: Radiation exposure inhibits LDL entry into the aortic intima at baseline and the earliest stages of atherosclerosis. Single cell transcriptomic analysis suggests that LDL uptake by endothelial cells is diverted to lysosomal degradation and reverse cholesterol transport pathways. This reduces intimal accumulation of lipid and impacts lesion initiation and growth.

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

2012 ◽  
Vol 177 (3) ◽  
pp. 251-264 ◽  
Author(s):  
Xian Luo-Owen ◽  
Michael J. Pecaut ◽  
Asma Rizvi ◽  
Daila S. Gridley
Keyword(s):  
Immune Response ◽  
Low Dose ◽  
Proton Radiation ◽  
Γ Irradiation ◽  
Total Body

Regenerative Effects of Tetrachlorodecaoxide in BD IX Rats after Total-Body γ Irradiation

1988 ◽  
Vol 115 (1) ◽  
pp. 115 ◽  
Author(s):  
Stan Ivankovic ◽  
Susanne R. Kempf
Keyword(s):  
Γ Irradiation ◽  
Total Body

scholarly journals Krüppel-like factor 4 is a radioprotective factor for the intestine following γ-radiation-induced gut injury in mice

2015 ◽  
Vol 308 (2) ◽  
pp. G121-G138 ◽  
Author(s):  
Daniel Talmasov ◽  
Xinjun Zhang ◽  
Bing Yu ◽  
Mandayam O. Nandan ◽  
Agnieszka B. Bialkowska ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
Morphological Changes ◽  
Γ Irradiation ◽  
Γ Radiation ◽  
Proliferative Zone ◽  
Acute Response ◽  
Radiation Induced ◽  
Total Body

Gut radiation-induced injury is a concern during treatment of patients with cancer. Krüppel-like factor 4 (KLF4) is expressed in differentiated villous epithelial cells of the small intestine. We previously showed that KLF4 protects cells from apoptosis following γ-irradiation in vitro. We sought to determine whether KLF4 mediates the small intestinal response to γ-irradiation in vivo. Mice with intestinal epithelium-specific deletion of Klf4 ( Klf4 ΔIS) and control ( Klf4 fl/fl) mice were irradiated with total-body γ-radiation. Following irradiation, the Klf4 ΔIS mice had significantly increased mortality compared with irradiated Klf4 fl/fl mice. Immunohistochemistry and immunofluorescence staining were used to assess the morphological changes, levels of proliferation, and apoptosis in the intestinal epithelium. At 96 h following irradiation, there was a regenerative response manifested by an expansion of the proliferative zone in both mouse groups, with the control mice having a higher proliferative activity than the Klf4 ΔIS group. In addition, there was a significant increase in the number of Klf4/Ki67-copositive cells in the irradiated control mice compared with unirradiated mice. Also, the irradiated Klf4 ΔIS mice had a significantly higher number of crypt cells positive for apoptosis, p53, and p21 compared with irradiated Klf4 fl/fl mice. Taken together, our data suggest that Klf4 may function as a radioprotective factor against gastrointestinal syndrome in mice following γ-irradiation by inhibiting apoptosis in the acute response to irradiation and contributing to crypt regeneration.

Mpl ligand prevents lethal myelosuppression by inhibiting p53-dependent apoptosis

Blood ◽  
2001 ◽  
Vol 98 (7) ◽  
pp. 2084-2090 ◽  
Author(s):  
Tamara I. Pestina ◽  
John L. Cleveland ◽  
Chunying Yang ◽  
Gerard P. Zambetti ◽  
Carl W. Jackson
Keyword(s):  
Bone Marrow ◽  
Autologous Bone Marrow Transplantation ◽  
Constitutive Expression ◽  
Autologous Bone Marrow ◽  
Wild Type ◽  
Γ Irradiation ◽  
Development Factor ◽  
Proapoptotic Protein ◽  
Exogenous Cytokine ◽  
Total Body

A single dose of Mpl ligand (Mpl-L) given immediately after lethal DNA-damaging regimens prevents the death of mice. However, the mechanism of this myeloprotection is unknown. The induction of p53-dependent apoptosis in response to DNA damage signals suggests that immediate administration of Mpl-L may inhibit p53-dependent apoptosis. This hypothesis was tested by administering a single injection of pegylated murine Megakaryocyte Growth and Development Factor (PEG-rmMGDF, a truncated recombinant Mpl-L) top53−/−and wild-type mice immediately after carboplatin (80 mg/kg) and 7.5 Gy total body γ-irradiation. PEG-rmMGDF was required to prevent the death of wild-type mice, whereas p53−/−mice survived with or without the exogenous cytokine. The degree of platelet depression and subsequent recovery was comparable in p53−/−mice to wild-type animals given PEG-rmMGDF. Hence, either Mpl-L administration or p53-deficiency protected multipotent hematopoietic progenitors and committed megakaryocyte precursors. The myelosuppressive regimen induced expression of p53 and the p53 target, p21Cipl in wild-type bone marrow, indicating that Mpl-L acts downstream of p53 to prevent apoptosis. Constitutive expression of the proapoptotic protein Bax, was not further increased. Bax−/− mice survived the lethal regimen only when given PEG-rmMGDF; however, these Bax−/−mice showed more rapid hematopoietic recovery than did identically-treated wild-type mice. Therefore, administration of Mpl-L immediately after myelosuppressive chemotherapy or preparatory regimens for autologous bone marrow transplantation should prevent p53-dependent apoptosis, decrease myelosuppression, and reduce the need for platelet transfusions.

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