Disease relevance of Radiation Injuries

• There was notable reduction in radiation-induced fibrosis in captopril-treated animals in this model, as in experimental lung radiation injury [1].
• Occlusion of the vasa vasorum by thrombosis, inflammation, neoplastic cells or radiation injury appears to be the cause of aortic necrosis and fistula formation [2].
• Histopathologic changes were assessed with a radiation injury scoring system (RIS), total TGF-beta immunoreactivity was quantified with computerized image analysis, and CTMC hyperplasia was assessed in toluidine blue-stained sections [3].
• Succinylcholine-induced hyperkalemia in the rat following radiation injury to muscle [4].
• Modification of radiation injury by ramipril, inhibitor of angiotensin-converting enzyme, on optic neuropathy in the rat [5].

High impact information on Radiation Injuries

• We conclude that radiation injury results in increased Cox-1 levels in crypt stem cells and their progeny, and that PGE2 produced through Cox-1 promotes crypt stem cell survival and proliferation [6].
• Apobec-1 protects intestine from radiation injury through posttranscriptional regulation of cyclooxygenase-2 expression [7].
• This study assessed whether in vivo administration of a soluble TGF-beta type II receptor (TbetaR-II) protein ameliorates intestinal radiation injury (radiation enteropathy) [8].
• Intracolonic WR 2721 protection of the rat colon from acute radiation injury [9].
• We extend our hypothesis here to include consideration of respiration, tricarboxylic acid cycle activity, peptide transport and metal reduction, which together with Mn(II) transport represent potential new targets to control recovery from radiation injury [10].

Chemical compound and disease context of Radiation Injuries

• Radiation injury also induced dose-dependent increases in serum luteinizing hormone (LH) concentration, with the maximal median difference from baseline level occurring at 6 months [11].
• Role of ornithine decarboxylase in diallyl sulfide inhibition of colonic radiation injury in the mouse [12].
• If the activities of these enzymes are important in the protection of the intestine from radiation injury, then the addition of extra glutamine may provide no benefit [13].
• Results of studies pertaining to successful uses of bioavailable essential metalloelement chelates and combinations of them as well as aminothiols, Ca-channel blockers, acyl Melatonin homologs, substituted anilines, and curcumin radioprotectants are included in this review to suggest their use as chelates in overcoming radiation injury [14].
• Measurement of hydroxyl radical (*OH) in living animals irradiated with ionizing radiation should be required to clarify the mechanisms of radiation injury and the in vivo assessment of radiation protectors, because generation of *OH is believed to be one of the major triggers of radiation injury [15].

Biological context of Radiation Injuries

• These results suggest that dipyridamole has a protective effect on animal survival 30 days after 60Co gamma-irradiation and inhibits lipid peroxidation - which is thought to play a part in the radiation injury in mouse liver and spleen [16].
• The findings that both staurosporine and caffeine treatments reverse the depression in cyclin B1 expression suggest that these two compounds may act on a common pathway of cell cycle control in response to radiation injury [17].
• Radiation effects on testes. XII. Monovalent electrolytes in relation to radiation injury of germinal epithelium [18].
• We designed a study to evaluate the effects of supplemental dietary arginine on intestinal mucosal recovery and bacterial translocation and bacterial clearance after induction of radiation injury in rats [19].
• Procarbazine (501 mg/kg) injected intraperitoneally enhanced the effect of the gastrointestinal radiation syndrome in whole-body lethality studies by reducing the 7-day LD50 by 269 rads [20].

Anatomical context of Radiation Injuries

• Prostaglandins as biochemical markers of radiation injury to the salivary glands after iodine-131 therapy [21]?
• Effect of misonidazole on radiation injury to mouse spinal cord [22].
• The topical use of estrogen, which promotes proliferation of epithelium, is generally described in connection with treatment and prophylaxis of late radiation injuries [23].
• Does misonidazole enhance radiation injury to the central nervous system [24]?
• Protection of microcirculation in rat brain against late radiation injury by gammaphos [25].

Gene context of Radiation Injuries

• This study investigated whether SC-'236, a selective inhibitor of COX-2, potentiates antitumor efficacy of radiation without increasing radiation injury to normal tissue [26].
• Transforming growth factor-beta (TGF-beta) has been proposed to be critical in tissue repair mechanisms resulting from radiation injury [27].
• To assess the role of 8-oxoguanine glycosylase (OGG1) in the cell defense against radiation injury, the radiation-induced cytotoxicities were compared between the mutant type KG-1 featuring a loss of OGG1 activity due to a homozygous mutation of Arg 229 Gln, and the wild type U937 [28].
• Furthermore, MCF-7 cells underwent apoptosis in response to radiation injury, which was also reversed by CUGBP2 siRNAs [29].
• CONCLUSIONS: The increase in the density of NPY-, SP- and TH-immunoreactive nerves in the irradiated bladders may be due to axonal sprouting which contributes to the symptoms of radiation injury [30].

Analytical, diagnostic and therapeutic context of Radiation Injuries

• Endothelium-directed interventions ameliorate intestinal radiation injury (radiation enteropathy) in animal models, and anecdotal reports also suggest a beneficial effect of heparin [31].
• Subgroup analysis revealed this trend to be attributable to a decreased incidence of severe late radiation injury in cervical cancer patients who consumed higher levels of caffeine at the time of their radiotherapy (p = 0.02) [32].
• There was one case of symptomatic radiation injury that resolved with steroid therapy, and no patient required repeat craniotomy for parenchymal necrosis [33].
• The results of this study support the hypothesis that cranial irradiation in children can lead to hypothalamic GRF deficiency secondary to radiation injury of hypothalamic GRF-secreting neurons [34].
• Comparison of autologous cell therapy and granulocyte-colony stimulating factor (G-CSF) injection vs. G-CSF injection alone for the treatment of acute radiation syndrome in a non-human primate model [35].

References