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Molecular Mechanisms of Combined Radiation Injury and Its Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2020) | Viewed by 2204

Special Issue Editor


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Guest Editor
Armed Forces Radiobiology Research Institute, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
Interests: signal transduction; apoptosis; autophagy; cytokine/inflammation storm; acute radiation syndrome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Combined radiation injury (CI) is a serious problem as it is more likely to be encountered than radiation injury (RI) in the real world. CI is defined as radiation exposure that takes place before or after a form of trauma that can be a physical wound, burn, hemorrhage, infection, blasting, bone fracture, or total brain injury, to name but a few examples. It is evident that while RI causes acute radiation syndrome (ARS), CI compounds the effects of ARS, resulting in multiorgan dysfunction and increases in mortality. Although radiation-induced cataracts are not fatal, the subject receives little attention.

The molecular mechanisms of CI are complex and not fully understood. Moreover, there are no radioprotectants, radiomitigators, or therapeutics available for preventing or treating CI because of its complexity. For this Special Issue, we would like to invite original articles or reviews that report on the current progress of molecular mechanisms of CI, CI-induced ARS, delayed effects of CI, and prophylactic drugs and therapeutics for CI, including gene, cell, or combinational therapies targeting bone marrow, gastrointestinal system, endothelium, brain, skin, eye, lung, and kidney.

Dr. Juliann G. Kiang
Guest Editor

Manuscript Submission Information

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Keywords

  • hematopoietic syndrome
  • gastrointestinal syndrome
  • cutaneous syndrome
  • brain hemorrhage
  • infection
  • radiation combined injury
  • therapy for radiation combined injury
  • microRNA regulation
  • signal transduction
  • cytokine/inflammation/infection

Published Papers (1 paper)

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Research

14 pages, 2812 KiB  
Article
Wound Trauma Exacerbates Acute, but not Delayed, Effects of Radiation in Rats: Mitigation by Lisinopril
by Meetha Medhora, Tracy Gasperetti, Ashley Schamerhorn, Feng Gao, Jayashree Narayanan, Zelmira Lazarova, Elizabeth R. Jacobs, Sergey Tarima and Brian L. Fish
Int. J. Mol. Sci. 2020, 21(11), 3908; https://doi.org/10.3390/ijms21113908 - 30 May 2020
Cited by 6 | Viewed by 1973
Abstract
The goal of this study is to understand and mitigate the effects of wounds on acute radiation syndrome (ARS) and delayed effects of acute radiation exposure (DEARE), for preparedness against a radiological attack or accident. Combined injuries from concomitant trauma and radiation are [...] Read more.
The goal of this study is to understand and mitigate the effects of wounds on acute radiation syndrome (ARS) and delayed effects of acute radiation exposure (DEARE), for preparedness against a radiological attack or accident. Combined injuries from concomitant trauma and radiation are likely in these scenarios. Either exacerbation or mitigation of radiation damage by wound trauma has been previously reported in preclinical studies. Female WAG/RijCmcr rats received 13 Gy X-rays, with partial-body shielding of one leg. Within 2 h, irradiated rats and non-irradiated controls were given full-thickness skin wounds with or without lisinopril, started orally 7 days after irradiation. Morbidity, skin wound area, breathing interval and blood urea nitrogen were measured up to 160 days post-irradiation to independently evaluate wound trauma and DEARE. Wounding exacerbated morbidity in irradiated rats between 5 and 14 days post-irradiation (during the ARS phase), and irradiation delayed wound healing. Wounding did not alter delayed morbidities from radiation pneumonitis or nephropathy after 30 days post-irradiation. Lisinopril did not mitigate wound healing, but markedly decreased morbidity during DEARE from 31 through 160 days. The results derived from this unique model of combined injuries suggest different molecular mechanisms of injury and healing of ARS and DEARE after radiation exposure. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Combined Radiation Injury and Its Therapies)
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