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  1. Book ; Online: Current Topics on Military Medicine

    Gorbunov, Nikolai V

    2021  

    Keywords Occupational medicine ; ptsd, biomarker, botulinum toxin, telemedicine, cytokine, posttraumatic stress disorder
    Language English
    Size 1 electronic resource (80 pages)
    Publisher IntechOpen
    Document type Book ; Online
    Note English
    HBZ-ID HT030646328
    ISBN 9781839689963 ; 183968996X
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book ; Online: Traumatic Brain Injury

    Gorbunov, Nikolai V / Long, Joseph B

    Pathobiology, Advanced Diagnostics and Acute Management

    2018  

    Keywords Neurology & clinical neurophysiology ; concussion, neurodegeneration, neuroinflammation, acupuncture, herbal medicine, biomechanics
    Language English
    Size 1 electronic resource (242 pages)
    Publisher IntechOpen
    Document type Book ; Online
    Note English
    HBZ-ID HT030647791
    ISBN 9781838813376 ; 1838813373
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Book ; Online: Autophagy in Current Trends in Cellular Physiology and Pathology

    Gorbunov, Nikolai V / Schneider, Marion

    2016  

    Keywords Cytology ; cancer, apoptosis, aging, hepatocellular carcinoma, glucose metabolism, breast cancer
    Language English
    Size 1 electronic resource (526 pages)
    Publisher IntechOpen
    Document type Book ; Online
    Note English
    HBZ-ID HT030646299
    ISBN 9789535141525 ; 953514152X
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  4. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Protracted Oxidative Alterations in the Mechanism of Hematopoietic Acute Radiation Syndrome.

    Gorbunov, Nikolai V / Sharma, Pushpa

    Antioxidants (Basel, Switzerland)

    2015  Volume 4, Issue 1, Page(s) 134–152

    Abstract: The biological effects of high-dose total body ionizing irradiation [(thereafter, irradiation (IR)] are attributed to primary oxidative breakage of biomolecule targets, mitotic, apoptotic and necrotic cell death in the dose-limiting tissues, clastogenic ... ...

    Abstract The biological effects of high-dose total body ionizing irradiation [(thereafter, irradiation (IR)] are attributed to primary oxidative breakage of biomolecule targets, mitotic, apoptotic and necrotic cell death in the dose-limiting tissues, clastogenic and epigenetic effects, and cascades of functional and reactive responses leading to radiation sickness defined as the acute radiation syndrome (ARS). The range of remaining and protracted injuries at any given radiation dose as well as the dynamics of post-IR alterations is tissue-specific. Therefore, functional integrity of the homeostatic tissue barriers may decline gradually within weeks in the post-IR period culminating with sepsis and failure of organs and systems. Multiple organ failure (MOF) leading to moribundity is a common sequela of the hemotapoietic form of ARS (hARS). Onset of MOF in hARS can be presented as "two-hit phenomenon" where the "first hit" is the underlying consequences of the IR-induced radiolysis in cells and biofluids, non-septic inflammation, metabolic up-regulation of pro-oxidative metabolic reactions, suppression of the radiosensitive hematopoietic and lymphoid tissues and the damage to gut mucosa and vascular endothelium. While the "second hit" derives from bacterial translocation and spread of the bacterial pathogens and inflammagens through the vascular system leading to septic inflammatory, metabolic responses and a cascade of redox pro-oxidative and adaptive reactions. This sequence of events can create a ground for development of prolonged metabolic, inflammatory, oxidative, nitrative, and carbonyl, electrophilic stress in crucial tissues and thus exacerbate the hARS outcomes. With this perspective, the redox mechanisms, which can mediate the IR-induced protracted oxidative post-translational modification of proteins, oxidation of lipids and carbohydrates and their countermeasures in hARS are subjects of the current review. Potential role of ubiquitous, radioresistant mesenchymal stromal cells in the protracted responses to IR and IR-related septicemia is also discussed.
    Language English
    Publishing date 2015-02-27
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox4010134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Bone Marrow Mesenchymal Stem Cells Increase Survival after Ionizing Irradiation Combined with Wound Trauma: Characterization and Therapy.

    Kiang, Juliann G / Gorbunov, Nikolai V

    Journal of cell science & therapy

    2014  Volume 5, Issue 6

    Abstract: The aim of this study was to investigate whether treatment with mesenchymal stem cells (MSCs) could improve survival after radiation combined injury. Bone marrow MSCs (BMSCs) were isolated from femurs of B6D2F1/J female mice and were expanded and ... ...

    Abstract The aim of this study was to investigate whether treatment with mesenchymal stem cells (MSCs) could improve survival after radiation combined injury. Bone marrow MSCs (BMSCs) were isolated from femurs of B6D2F1/J female mice and were expanded and cultivated in hypoxic conditions (5% O
    Language English
    Publishing date 2014-11-24
    Publishing country United States
    Document type Journal Article
    ISSN 2157-7013
    ISSN 2157-7013
    DOI 10.4172/2157-7013.1000190
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Thrombopoietin Receptor Agonist Mitigates Hematopoietic Radiation Syndrome and Improves Survival after Whole-Body Ionizing Irradiation Followed by Wound Trauma.

    Kiang, Juliann G / Zhai, Min / Liao, Pei-Jun / Ho, Connie / Gorbunov, Nikolai V / Elliott, Thomas B

    Mediators of inflammation

    2017  Volume 2017, Page(s) 7582079

    Abstract: Ionizing radiation combined with trauma tissue injury (combined injury, CI) results in greater mortality and H-ARS than radiation alone (radiation injury, RI), which includes thrombocytopenia. The aim of this study was to determine whether increases in ... ...

    Abstract Ionizing radiation combined with trauma tissue injury (combined injury, CI) results in greater mortality and H-ARS than radiation alone (radiation injury, RI), which includes thrombocytopenia. The aim of this study was to determine whether increases in numbers of thrombocytes would improve survival and mitigate H-ARS after CI. We observed in mice that WBC and platelets remained very low in surviving RI animals that were given 9.5 Gy
    MeSH term(s) Animals ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Body Weight/drug effects ; Body Weight/radiation effects ; Female ; Gamma Rays ; Mice ; Radiation Injuries/drug therapy ; Radiation Injuries/therapy ; Receptors, Thrombopoietin/antagonists & inhibitors ; Receptors, Thrombopoietin/metabolism ; Whole-Body Irradiation/methods ; Wound Healing/drug effects ; Wound Healing/radiation effects ; Wounds and Injuries/drug therapy
    Chemical Substances ALXN4100 ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Receptors, Thrombopoietin
    Language English
    Publishing date 2017-03-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2017/7582079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3575: Show issues Location:
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  10. Article ; Online: Up-regulation of autophagy in small intestine Paneth cells in response to total-body gamma-irradiation.

    Gorbunov, Nikolai V / Kiang, Juliann G

    The Journal of pathology

    2009  Volume 219, Issue 2, Page(s) 242–252

    Abstract: Macroautophagy (mAG) is a lysosomal mechanism of degradation of cell self-constituents damaged due to variety of stress factors, including ionizing irradiation. Activation of mAG requires expression of mAG protein Atg8 (LC3) and conversion of its form I ( ...

    Abstract Macroautophagy (mAG) is a lysosomal mechanism of degradation of cell self-constituents damaged due to variety of stress factors, including ionizing irradiation. Activation of mAG requires expression of mAG protein Atg8 (LC3) and conversion of its form I (LC3-I) to form II (LC3-II), mediated by redox-sensitive Atg4 protease. We have demonstrated upregulation of this pathway in the innate host defense Paneth cells of the small intestine (SI) due to ionizing irradiation and correlation of this effect with induction of pro-oxidant inducible nitric oxide synthase (iNOS). CD2F1 mice were exposed to 9.25 Gy gamma-ionizing irradiation. Small intestinal specimens were collected during 7 days after ionizing irradiation. Assessment of ionizing irradiation-associated alterations in small intestinal crypt and villus cells and activation of the mAG pathway was conducted using microscopical and biochemical techniques. Analysis of iNOS protein and the associated formation of nitrites and lipid peroxidation products was performed using immunoblotting and biochemical analysis, and revealed increases in iNOS protein, nitrate levels and oxidative stress at day 1 following ionizing irradiation. Increase in immunoreactivity of LC3 protein in the crypt cells was observed at day 7 following ionizing irradiation. This effect predominantly occurred in the CD15-positive Paneth cells and was associated with accumulation of LC3-II isoform. The formation of autophagosomes in Paneth cells was confirmed by transmission electron microscopy (TEM). Up-regulation of LC3 pathway in the irradiated SI was accompanied by a decreased protein-protein interaction between LC3 and chaperone heat shock protein 70. A high-level of LC3-immunoreactivity in vacuole-shaped structures was spatially co-localized with immunoreactivity of 3-nitro-tyrosine. The observed effects were diminished in iNOS knockout B6.129P2-NOS2(tm1Lau)/J mice subjected to the same treatments. We postulate that the observed up-regulation of mAG in the irradiated small intestine is at least in part mediated by the iNOS signalling mechanism.
    MeSH term(s) Animals ; Autophagy/radiation effects ; Gamma Rays ; In Situ Nick-End Labeling ; Intestine, Small/radiation effects ; Intestine, Small/ultrastructure ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Nitric Oxide Synthase Type II/physiology ; Oxidative Stress/radiation effects ; Paneth Cells/radiation effects ; Paneth Cells/ultrastructure ; Up-Regulation/radiation effects ; Whole-Body Irradiation
    Chemical Substances Nitric Oxide Synthase Type II (EC 1.14.13.39)
    Language English
    Publishing date 2009-10
    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 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.2591
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.12: Show issues Location:
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