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Article ; Online: Combined radiation injury and its impacts on radiation countermeasures and biodosimetry.

Kiang, Juliann G / Blakely, William F

International journal of radiation biology

2023 Volume 99, Issue 7, Page(s) 1055–1065

Abstract: Purpose: Preparedness for medical responses to major radiation accidents and the increasing threat of nuclear warfare worldwide necessitates an understanding of the complexity of combined radiation injury (CI) and identifying drugs to treat CI is ... ...

Abstract	Purpose: Preparedness for medical responses to major radiation accidents and the increasing threat of nuclear warfare worldwide necessitates an understanding of the complexity of combined radiation injury (CI) and identifying drugs to treat CI is inevitably critical. The vital sign and survival after CI were presented. The molecular mechanisms, such as microRNA pathways, NF-κB-iNOS-IL-18 pathway, C3 production, the AKT-MAPK cross-talk, and TLR/MMP increases, underlying CI in relation to organ injury and mortality were analyzed. At present, no FDA-approved drug to protect, mitigate, or treat CI is available. The development of CI-specific medical countermeasures was reviewed. Because of the worsened acute radiation syndrome resulting from CI, diagnostic triage can be problematic. Therefore, biodosimetry and CI are bundled together with the need to establish effective triage methods with CI. Conclusions: CI mouse model studies at AFRRI are reviewed addressing molecular responses, findings from medical countermeasures, and a proposed plasma proteomic biodosimetry approach based on a panel of radiation-responsive biomarkers (i.e., CD27, Flt-3L, GM-CSF, CD45, IL-12, TPO) negligibly influenced by wounding in an algorithm used for dose predictions is described.
MeSH term(s)	Animals ; Mice ; Proteomics ; Radioactive Hazard Release ; Acute Radiation Syndrome ; MicroRNAs ; Triage/methods
Chemical Substances	MicroRNAs
Language	English
Publishing date	2023-03-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.1080/09553002.2023.2188933
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Article ; Online: Effects of Hemorrhage on Hematopoietic Cell Depletion after a Combined Injury with Radiation: Role of White Blood Cells and Red Blood Cells as Biomarkers.

Kiang, Juliann G / Woods, Akeylah K / Cannon, Georgetta

International journal of molecular sciences

2024 Volume 25, Issue 5

Abstract: Combined radiation with hemorrhage (combined injury, CI) exacerbates hematopoietic acute radiation syndrome and mortality compared to radiation alone (RI). We evaluated the effects of RI or CI on blood cell depletion as a biomarker to differentiate the ... ...

Abstract	Combined radiation with hemorrhage (combined injury, CI) exacerbates hematopoietic acute radiation syndrome and mortality compared to radiation alone (RI). We evaluated the effects of RI or CI on blood cell depletion as a biomarker to differentiate the two. Male CD2F1 mice were exposed to 8.75 Gy γ-radiation (
MeSH term(s)	Male ; Animals ; Mice ; Hemorrhage ; Erythrocytes ; Gamma Rays ; Monocytes ; Biomarkers
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-03-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25052988
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Article ; Online: Brain Damage and Patterns of Neurovascular Disorder after Ionizing Irradiation. Complications in Radiotherapy and Radiation Combined Injury.

Gorbunov, Nikolai V / Kiang, Juliann G

Radiation research

2021 Volume 196, Issue 1, Page(s) 1–16

Abstract: Exposure to ionizing radiation, mechanical trauma, toxic chemicals or infections, or combinations thereof (i.e., combined injury) can induce organic injury to brain tissues, the structural disarrangement of interactive networks of neurovascular and glial ...

Abstract	Exposure to ionizing radiation, mechanical trauma, toxic chemicals or infections, or combinations thereof (i.e., combined injury) can induce organic injury to brain tissues, the structural disarrangement of interactive networks of neurovascular and glial cells, as well as on arrays of the paracrine and systemic destruction. This leads to subsequent decline in cognitive capacity and decompensation of mental health. There is an ongoing need for improvement in mitigating and treating radiation- or combined injury-induced brain injury. Cranial irradiation per se can cause a multifactorial encephalopathy that occurs in a radiation dose- and time-dependent manner due to differences in radiosensitivity among the various constituents of brain parenchyma and vasculature. Of particular concern are the radiosensitivity and inflammation susceptibility of: 1. the neurogenic and oligodendrogenic niches in the subependymal and hippocampal domains; and 2. the microvascular endothelium. Thus, cranial or total-body irradiation can cause a plethora of biochemical and cellular disorders in brain tissues, including: 1. decline in neurogenesis and oligodendrogenesis; 2. impairment of the blood-brain barrier; and 3. ablation of vascular capillary. These changes, along with cerebrovascular inflammation, underlie different stages of encephalopathy, from the early protracted stage to the late delayed stage. It is evident that ionizing radiation combined with other traumatic insults such as penetrating wound, burn, blast, systemic infection and chemotherapy, among others, can exacerbate the radiation sequelae (and vice versa) with increasing severity of neurogenic and microvascular patterns of radiation brain damage.
MeSH term(s)	Animals ; Brain/blood supply ; Brain/pathology ; Brain/radiation effects ; Brain Injuries/etiology ; Cerebrovascular Circulation/radiation effects ; Dose-Response Relationship, Radiation ; Humans ; Radiation Injuries/etiology ; Radiation, Ionizing ; Radiotherapy/adverse effects
Language	English
Publishing date	2021-05-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RADE-20-00147.1
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Article ; Online: Exacerbation of Mild Hypoxia on Acute Radiation Syndrome and Subsequent Mortality.

Kiang, Juliann G

Adaptive medicine

2017 Volume 9, Issue 1, Page(s) 28–33

Abstract: Mild hypoxia induced by 20% hemorrhage results in increases in few cytokine concentrations and sclerostin levels in blood, but shows no changes in bone formation, bone marrow cellularity, and gastrointestinal (GI) integrity and no systemic bacterial ... ...

Abstract	Mild hypoxia induced by 20% hemorrhage results in increases in few cytokine concentrations and sclerostin levels in blood, but shows no changes in bone formation, bone marrow cellularity, and gastrointestinal (GI) integrity and no systemic bacterial infection as well as no subsequent mortality. On the other hand, severe hypoxia induced by 40% hemorrhage causes significant increases in most cytokine concentrations, GI injury, lung injury, systemic bacterial infection, cellular ATP reduction and subsequent mortality. The severe hypoxia drastically damages GI and lung morphology, elevates cytokine concentrations in blood and increases inducible nitric oxide synthase (iNOS) expression in cells that is mediated by transcription factors NF-κB/NF-IL6, subsequently producing free radicals that disrupt mitochondria. ATP depletion, p53 phosphorylation, and caspase-3 activation are found, suggesting cell apoptosis. As a result, mortality occurs. However, when mild hypoxia follows ionizing radiation, the mild hypoxia significantly enhances radiation-induced mortality and acute radiation syndrome, including injury of bone marrow, GI, kidney, and lung. The synergism also occurs at the molecular level, resulting in alteration of microRNAs, amplification of iNOS expression, cytokine increases, sepsis, and ATP depletion. This is the first demonstration of synergistic effects between mild hypoxia and ionizing radiation.
Language	English
Publishing date	2017-03-31
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ISSN	2218-340X
ISSN (online)	2218-340X
DOI	10.4247/am.2017.abg170
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Article ; Online: A review of the impact on the ecosystem after ionizing irradiation: wildlife population.

Cannon, Georgetta / Kiang, Juliann G

International journal of radiation biology

2020 Volume 98, Issue 6, Page(s) 1054–1062

Abstract: Purpose: On 26 April 1986, reactor 4 at the Chernobyl power plant underwent a catastrophic failure leading to core explosions and open-air fires. On 11 March 2011, a combination of earthquake and tsunami led to a similar disaster at the Fukushima ... ...

Abstract	Purpose: On 26 April 1986, reactor 4 at the Chernobyl power plant underwent a catastrophic failure leading to core explosions and open-air fires. On 11 March 2011, a combination of earthquake and tsunami led to a similar disaster at the Fukushima Daiichi power plant. In both cases, radioactive isotopes were released and contaminated the air, soil and water in a substantial area around the power plants. Humans were evacuated from the immediate regions but the wildlife stayed and continued to be affected by the ongoing high radiation exposure initially and later decayed amounts of fallout dusts with time. In this review, we will examine the significant effects of the increased radiation on vegetation, insects, fish, birds and mammals. Conclusions: The initial intense radiation in these areas has gradually begun to decrease but still remains high. Adaptation to radiation is evident and the ecosystems have dynamically changed from the periods immediately after the accidents to the present day. Understanding the molecular mechanisms that allow the adaptation and recovery of wildlife to chronic radiation challenges would aid in future attempts at ecosystem remediation in the wake of such incidents.
MeSH term(s)	Animals ; Animals, Wild ; Ecosystem ; Fukushima Nuclear Accident ; Mammals ; Nuclear Power Plants ; Radiation Monitoring ; Tsunamis
Language	English
Publishing date	2020-07-24
Publishing country	England
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.1080/09553002.2020.1793021
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Article ; Online: Adult Mesenchymal Stem Cells and Radiation Injury.

Kiang, Juliann G

Health physics

2016 Volume 111, Issue 2, Page(s) 198–203

Abstract: Recent understanding of the cellular and molecular signaling activations in adult mesenchymal stem cells (MSCs) has provided new insights into their potential clinical applications, particularly for tissue repair and regeneration. This review focuses on ... ...

Abstract	Recent understanding of the cellular and molecular signaling activations in adult mesenchymal stem cells (MSCs) has provided new insights into their potential clinical applications, particularly for tissue repair and regeneration. This review focuses on these advances, specifically in the context of self-renewal for tissue repair and recovery after radiation injury. Thus far, MSCs have been characterized extensively and shown to be useful in mitigation and therapy for acute radiation syndrome and cognitive dysfunction. Use of MSCs for treating radiation injury alone or in combination with additional trauma is foreseeable.
MeSH term(s)	Animals ; Brain Injuries/pathology ; Brain Injuries/therapy ; Evidence-Based Medicine ; Humans ; Mesenchymal Stem Cell Transplantation/methods ; Mesenchymal Stem Cells/cytology ; Mice ; Radiation Injuries/pathology ; Radiation Injuries/therapy ; Recovery of Function ; Treatment Outcome
Language	English
Publishing date	2016-06-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2406-5
ISSN	1538-5159 ; 0017-9078
ISSN (online)	1538-5159
ISSN	0017-9078
DOI	10.1097/HP.0000000000000459
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Article ; Online: Radiation Combined Injury: DNA Damage, Apoptosis, and Autophagy.

Kiang, Juliann G / Garrison, Bradley R / Gorbunov, Nikolai V

Adaptive medicine

2021 Volume 2, Issue 1, Page(s) 1–10

Abstract: Radiation combined injury is defined as an ionizing radiation exposure received in combination with other trauma or physiological insults. The range of radiation threats we face today includes everything from individual radiation exposures to mass ... ...

Abstract	Radiation combined injury is defined as an ionizing radiation exposure received in combination with other trauma or physiological insults. The range of radiation threats we face today includes everything from individual radiation exposures to mass casualties resulting from a terrorist nuclear incident, and many of these exposure scenarios include the likelihood of additional traumatic injury. Radiation combined injury sensitizes target organs and cells and exacerbates acute radiation syndrome. Organs and cells with high sensitivity to combined injury are the skin, the hematopoietic system, the gastrointestinal tract, spermatogenic cells, and the vascular system. Among its many effects, radiation combined injury results in decreases in lymphocytes, macrophages, neutrophils, platelets, stem cells, and tissue integrity; activation of the iNOS/NF-κB/NF-IL6 and p53/Bax pathways; and increases in DNA single and double strand breaks, TLR signaling, cytokine concentrations, bacterial infection, and cytochrome c release from mitochondria to cytoplasm. These alterations lead to apoptosis and autophagy and, as a result, increased mortality. There is a pressing need to understand more about the body's response to combined injury in order to be able to develop effective countermeasures, since few currently exist. In this review, we summarize what is known about how combined injury modifies the radiation response, with a special emphasis on DNA damage/repair, signal transduction pathways, apoptosis, and autophagy. We also describe current and prospective countermeasures relevant to the treatment and prevention of combined injury.
Language	English
Publishing date	2021-09-25
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ISSN	2218-340X
ISSN (online)	2218-340X
DOI	10.4247/AM.2010.ABA004
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Article: Radiation: a poly-traumatic hit leading to multi-organ injury.

Kiang, Juliann G / Olabisi, Ayodele O

Cell & bioscience

2019 Volume 9, Page(s) 25

Abstract: The range of radiation threats we face today includes everything from individual radiation exposures to mass casualties resulting from a terrorist incident, and many of these exposure scenarios include the likelihood of additional traumatic injury as ... ...

Abstract	The range of radiation threats we face today includes everything from individual radiation exposures to mass casualties resulting from a terrorist incident, and many of these exposure scenarios include the likelihood of additional traumatic injury as well. Radiation injury is defined as an ionizing radiation exposure inducing a series of organ injury within a specified time. Severity of organ injury depends on the radiation dose and the duration of radiation exposure. Organs and cells with high sensitivity to radiation injury are the skin, the hematopoietic system, the gastrointestinal (GI) tract, spermatogenic cells, and the vascular system. In general, acute radiation syndrome (ARS) includes DNA double strand breaks (DSB), hematopoietic syndrome (bone marrow cells and circulatory cells depletion), cutaneous injury, GI death, brain hemorrhage, and splenomegaly within 30 days after radiation exposure. Radiation injury sensitizes target organs and cells resulting in ARS. Among its many effects on tissue integrity at various levels, radiation exposure results in activation of the iNOS/NF-kB/NF-IL6 and p53/Bax pathways; and increases DNA single and double strand breaks, TLR signaling, cytokine concentrations, bacterial infection, cytochrome c release from mitochondria to cytoplasm, and possible PARP-dependent NAD and ATP-pool depletion. These alterations lead to apoptosis and autophagy and, as a result, increased mortality. In this review, we summarize what is known about how radiation exposure leads to the radiation response with time. We also describe current and prospective countermeasures relevant to the treatment and prevention of radiation injury.
Language	English
Publishing date	2019-03-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2593367-X
ISSN	2045-3701
ISSN	2045-3701
DOI	10.1186/s13578-019-0286-y
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Article ; Online: Ghrelin Therapy Decreases Incidents of Intracranial Hemorrhage in Mice after Whole-Body Ionizing Irradiation Combined with Burn Trauma.

Gorbunov, Nikolai V / Kiang, Juliann G

International journal of molecular sciences

2017 Volume 18, Issue 8

Abstract: Nuclear industrial accidents and the detonation of nuclear devices cause a variety of damaging factors which, when their impacts are combined, produce complicated injuries challenging for medical treatment. Thus, trauma following acute ionizing ... ...

Abstract	Nuclear industrial accidents and the detonation of nuclear devices cause a variety of damaging factors which, when their impacts are combined, produce complicated injuries challenging for medical treatment. Thus, trauma following acute ionizing irradiation (IR) can deteriorate the IR-induced secondary reactive metabolic and inflammatory impacts to dose-limiting tissues, such as bone marrow/lymphatic, gastrointestinal tissues, and vascular endothelial tissues, exacerbating the severity of the primary injury and decreasing survival from the exposure. Previously we first reported that ghrelin therapy effectively improved survival by mitigating leukocytopenia, thrombocytopenia, and bone-marrow injury resulting from radiation combined with burn trauma. This study was aimed at investigating whether radiation combined with burn trauma induced the cerebro-vascular impairment and intracranial hemorrhage that could be reversed by ghrelin therapy. When B6D2F1 female mice were exposed to 9.5 Gy Cobalt-60 γ-radiation followed by 15% total skin surface burn, cerebro-vascular impairment and intracranial hemorrhage as well as platelet depletion were observed. Ghrelin treatment after irradiation combined with burn trauma significantly decreased platelet depletion and brain hemorrhage. The results suggest that ghrelin treatment is an effective therapy for ionizing radiation combined with burn trauma.
Language	English
Publishing date	2017-08-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms18081693
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Article ; Online: Skin Wound following Irradiation Aggravates Radiation-Induced Brain Injury in a Mouse Model.

Xiao, Mang / Li, Xianghong / Wang, Li / Lin, Bin / Zhai, Min / Hull, Lisa / Zizzo, Alex / Cui, Wanchang / Kiang, Juliann G

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Radiation injury- and radiation combined with skin injury-induced inflammatory responses in the mouse brain were evaluated in this study. Female B6D2F1/J mice were subjected to a sham, a skin wound (SW), 9.5 ... ...

Abstract	Radiation injury- and radiation combined with skin injury-induced inflammatory responses in the mouse brain were evaluated in this study. Female B6D2F1/J mice were subjected to a sham, a skin wound (SW), 9.5 Gy
MeSH term(s)	Mice ; Female ; Animals ; Chemokine CXCL10 ; Endothelial Cells ; Radiation Injuries/etiology ; Disease Models, Animal ; Brain ; Brain Injuries/etiology ; Skin/radiation effects
Chemical Substances	Chemokine CXCL10
Language	English
Publishing date	2023-06-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241310701
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