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Article: "Workfare" or active social inclusion

Simonyi, Agnes

Global crossroads in social welfare : emergent issues, debates and innovations across the globe , p. 165-178

2010 , Page(s) 165–178

Author's details	By Agnes Simonyi
Keywords	Aktivierende Arbeitsmarktpolitik ; EU-Sozialpolitik ; Soziale Integration ; EU-Staaten
Language	English
Publisher	Europäischer Hochschulverl.
Publishing place	Bremen
Document type	Article
ISBN	978-3-941482-77-7 ; 3-941482-77-7
Database	ECONomics Information System

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Article ; Online: TNFα alters occludin and cerebral endothelial permeability: Role of p38MAPK.

Ni, Yawen / Teng, Tao / Li, Runting / Simonyi, Agnes / Sun, Grace Y / Lee, James C

PloS one

2017 Volume 12, Issue 2, Page(s) e0170346

Abstract: Occludin is a key tight junction (TJ) protein in cerebral endothelial cells (CECs) playing an important role in modulating blood-brain barrier (BBB) functions. This protein (65kDa) has been shown to engage in many signaling pathways and phosphorylation ... ...

Abstract	Occludin is a key tight junction (TJ) protein in cerebral endothelial cells (CECs) playing an important role in modulating blood-brain barrier (BBB) functions. This protein (65kDa) has been shown to engage in many signaling pathways and phosphorylation by both tyrosine and threonine kinases. Despite yet unknown mechanisms, pro-inflammatory cytokines and endotoxin (lipopolysaccharides, LPS) may alter TJ proteins in CECs and BBB functions. Here we demonstrate the responses of occludin in an immortalized human cerebral endothelial cell line (hCMEC/D3) to stimulation by TNFα (10 ng/mL), IL-1β (10 ng/mL) and LPS (100 ng/mL). Exposing cells to TNFα resulted in a rapid and transient upward band-shift of occludin, suggesting of an increase in phosphorylation. Exposure to IL-1β produced significantly smaller effects and LPS produced almost no effects on occludin band-shift. TNFα also caused transient stimulation of p38MAPK and ERK1/2 in hCMEC/D3 cells, and the occludin band-shift induced by TNFα was suppressed by SB202190, an inhibitor for p38MAPK, and partly by U0126, the MEK1/2-ERK1/2 inhibitor. Cells treated with TNFα and IL-1β but not LPS for 24 h resulted in a significant (p < 0.001) decrease in the expression of occludin, and the decrease could be partially blocked by SB202190, the inhibitor for p38MAPK. Treatment with TNFα also altered cell morphology and enhanced permeability of the CEC layer as measured by the FITC-dextran assay and the trans-endothelial electrical resistances (TEER). However, treatment with SB202190 alone could not effectively reverse the TNFα -induced morphology changes or the enhanced permeability changes. These results suggest that despite effects of TNFα on p38MAPK-mediated occludin phosphorylation and expression, these changes are not sufficient to avert the TNFα-induced alterations on cell morphology and permeability.
MeSH term(s)	Blood-Brain Barrier/metabolism ; Cell Line ; Cell Survival/drug effects ; Cerebral Cortex/metabolism ; Electrophysiological Phenomena ; Endothelial Cells/metabolism ; Gene Expression ; Humans ; Interleukin-1beta/metabolism ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/immunology ; MAP Kinase Signaling System/drug effects ; Occludin/genetics ; Occludin/metabolism ; Permeability ; Phosphorylation ; Signal Transduction/drug effects ; Tight Junctions/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Interleukin-1beta ; Lipopolysaccharides ; Occludin ; Tumor Necrosis Factor-alpha ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2017-02-07
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0170346
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Der Arbeitsmarkt und lokale Interventionen - neue Akteure greifen in die Beschäftigungskrise ein

Simonyi, Agnes

Steuerungsebenen der Arbeitsmarktpolitik : [proceedings der Internationalen Konferenz 2001 in Graz zum Thema "Steuerungsebenen der Arbeitsmarktpolitik"; im Auftr. des Arbeitsmarktservice Steiermark] , p. 166-175

2002 , Page(s) 166–175

Author's details	Agnes Simonyi
Keywords	Arbeitsmarktpolitik ; Aktivierende Arbeitsmarktpolitik ; Gemeinde ; Vergleich ; Ungarn ; Frankreich
Language	German
Publisher	Hampp
Publishing place	München [u.a.]
Document type	Article
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Article ; Online: Botanical Polyphenols Mitigate Microglial Activation and Microglia-Induced Neurotoxicity: Role of Cytosolic Phospholipase A2.

Chuang, Dennis Y / Simonyi, Agnes / Cui, Jiankun / Lubahn, Dennis B / Gu, Zezong / Sun, Grace Y

Neuromolecular medicine

2016 Volume 18, Issue 3, Page(s) 415–425

Abstract: Microglia play a significant role in the generation and propagation of oxidative/nitrosative stress, and are the basis of neuroinflammatory responses in the central nervous system. Upon stimulation by endotoxins such as lipopolysaccharides (LPS), these ... ...

Abstract	Microglia play a significant role in the generation and propagation of oxidative/nitrosative stress, and are the basis of neuroinflammatory responses in the central nervous system. Upon stimulation by endotoxins such as lipopolysaccharides (LPS), these cells release pro-inflammatory factors which can exert harmful effects on surrounding neurons, leading to secondary neuronal damage and cell death. Our previous studies demonstrated the effects of botanical polyphenols to mitigate inflammatory responses induced by LPS, and highlighted an important role for cytosolic phospholipase A2 (cPLA2) upstream of the pro-inflammatory pathways (Chuang et al. in J Neuroinflammation 12(1):199, 2015. doi: 10.1186/s12974-015-0419-0 ). In this study, we investigate the action of botanical compounds and assess whether suppression of cPLA2 in microglia is involved in the neurotoxic effects on neurons. Differentiated SH-SY5Y neuroblastoma cells were used to test the neurotoxicity of conditioned medium from stimulated microglial cells, and WST-1 assay was used to assess for the cell viability of SH-SY5Y cells. Botanicals such as quercetin and honokiol (but not cyanidin-3-O-glucoside, 3CG) were effective in inhibiting LPS-induced nitric oxide (NO) production and phosphorylation of cPLA2. Conditioned medium from BV-2 cells stimulated with LPS or IFNγ caused neurotoxicity to SH-SY5Y cells. Decrease in cell viability could be ameliorated by pharmacological inhibitors for cPLA2 as well as by down-regulating cPLA2 with siRNA. Botanicals effective in inhibition of LPS-induced NO and cPLA2 phosphorylation were also effective in ameliorating microglial-induced neurotoxicity. Results demonstrated cytotoxic factors from activated microglial cells to cause damaging effects to neurons and potential use of botanical polyphenols to ameliorate the neurotoxic effects.
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-016-8419-5
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Article ; Online: Subchronic apocynin treatment attenuates methamphetamine-induced dopamine release and hyperactivity in rats.

Miller, Dennis K / Oelrichs, Clark E / Sun, Grace Y / Simonyi, Agnes

Life sciences

2014 Volume 98, Issue 1, Page(s) 6–11

Abstract: Aims: The effects of methamphetamine are linked to stimulation of dopaminergic neurons, which can be accompanied by production of reactive oxygen species (ROS). Apocynin (4-hydroxy-3-methoxy-acetophenone) is a nicotinamide adenine dinucleotide phosphate ...

Abstract	Aims: The effects of methamphetamine are linked to stimulation of dopaminergic neurons, which can be accompanied by production of reactive oxygen species (ROS). Apocynin (4-hydroxy-3-methoxy-acetophenone) is a nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase (NOX) inhibitor shown to mitigate oxidative stress in a number of models. The present study aimed at testing whether apocynin suppresses the dopamine-releasing and locomotor-activating properties of methamphetamine. Main methods: (1) Apocynin (0.01-100μM) was applied to rat striatal slices preloaded with [(3)H]dopamine and its efficacy to evoke [(3)H]overflow and to alter methamphetamine (3μM)-evoked [(3)H]overflow was measured. (2) Groups of rats received apocynin (15 or 50mg/kg/day) or vehicle injection for seven consecutive days, and the efficacy and potency of methamphetamine to evoke [(3)H]overflow were determined. (3) Groups of apocynin-treated rats were administered methamphetamine (0.5 or 1mg/kg) or saline to determine the effect of apocynin on stimulant-induced hyperactivity. Key findings: (1) Apocynin applied to striatal slices did not evoke [(3)H]overflow or alter methamphetamine-evoked [(3)H]overflow. (2) However, subchronic apocynin treatment significantly and dose-dependently decreased methamphetamine's potency and efficacy to evoke [(3)H]overflow. (3) Subchronic apocynin treatment also decreased the locomotor activity evoked by methamphetamine. Significance: Subchronic apocynin treatment diminished methamphetamine induced dopamine-release and its locomotor-activating properties. The pattern of results indicates that apocynin is more effective after repeated, rather than after acute, treatment. The findings also suggest that NOX inhibitors or agents suppressing oxidative stress may constitute a new area for research to understand how methamphetamine produces its deleterious and neurotoxic outcomes in the brain.
MeSH term(s)	Acetophenones/administration & dosage ; Acetophenones/pharmacology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/administration & dosage ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Dopamine/metabolism ; Dose-Response Relationship, Drug ; Hyperkinesis/drug therapy ; Male ; Methamphetamine/pharmacology ; Motor Activity/drug effects ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Acetophenones ; Anti-Inflammatory Agents, Non-Steroidal ; Methamphetamine (44RAL3456C) ; acetovanillone (B6J7B9UDTR) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2014-03-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2013.12.031
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TNFα alters occludin and cerebral endothelial permeability

Yawen Ni / Tao Teng / Runting Li / Agnes Simonyi / Grace Y Sun / James C Lee

PLoS ONE, Vol 12, Iss 2, p e

Role of p38MAPK.

2017 Volume 0170346

Abstract	Occludin is a key tight junction (TJ) protein in cerebral endothelial cells (CECs) playing an important role in modulating blood-brain barrier (BBB) functions. This protein (65kDa) has been shown to engage in many signaling pathways and phosphorylation by both tyrosine and threonine kinases. Despite yet unknown mechanisms, pro-inflammatory cytokines and endotoxin (lipopolysaccharides, LPS) may alter TJ proteins in CECs and BBB functions. Here we demonstrate the responses of occludin in an immortalized human cerebral endothelial cell line (hCMEC/D3) to stimulation by TNFα (10 ng/mL), IL-1β (10 ng/mL) and LPS (100 ng/mL). Exposing cells to TNFα resulted in a rapid and transient upward band-shift of occludin, suggesting of an increase in phosphorylation. Exposure to IL-1β produced significantly smaller effects and LPS produced almost no effects on occludin band-shift. TNFα also caused transient stimulation of p38MAPK and ERK1/2 in hCMEC/D3 cells, and the occludin band-shift induced by TNFα was suppressed by SB202190, an inhibitor for p38MAPK, and partly by U0126, the MEK1/2-ERK1/2 inhibitor. Cells treated with TNFα and IL-1β but not LPS for 24 h resulted in a significant (p < 0.001) decrease in the expression of occludin, and the decrease could be partially blocked by SB202190, the inhibitor for p38MAPK. Treatment with TNFα also altered cell morphology and enhanced permeability of the CEC layer as measured by the FITC-dextran assay and the trans-endothelial electrical resistances (TEER). However, treatment with SB202190 alone could not effectively reverse the TNFα -induced morphology changes or the enhanced permeability changes. These results suggest that despite effects of TNFα on p38MAPK-mediated occludin phosphorylation and expression, these changes are not sufficient to avert the TNFα-induced alterations on cell morphology and permeability.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway.

Chuang, Dennis Y / Simonyi, Agnes / Kotzbauer, Paul T / Gu, Zezong / Sun, Grace Y

Journal of neuroinflammation

2015 Volume 12, Page(s) 199

Abstract: Background: Oxidative stress and inflammation are important factors contributing to the pathophysiology of numerous neurological disorders, including Alzheimer's disease, Parkinson's disease, acute stroke, and infections of the brain. There is well- ... ...

Abstract	Background: Oxidative stress and inflammation are important factors contributing to the pathophysiology of numerous neurological disorders, including Alzheimer's disease, Parkinson's disease, acute stroke, and infections of the brain. There is well-established evidence that proinflammatory cytokines and glutamate, as well as reactive oxygen species (ROS) and nitric oxide (NO), are produced upon microglia activation, and these are important factors contributing to inflammatory responses and cytotoxic damage to surrounding neurons and neighboring cells. Microglial cells express relatively high levels of cytosolic phospholipase A2 (cPLA2), an enzyme known to regulate membrane phospholipid homeostasis and release of arachidonic acid (AA) for synthesis of eicosanoids. The goal for this study is to elucidate the role of cPLA2IV in mediating the oxidative and inflammatory responses in microglial cells. Methods: Experiments involved primary microglia cells isolated from transgenic mice deficient in cPLA2α or iPLA2β, as well as murine immortalized BV-2 microglial cells. Inhibitors of cPLA2/iPLA2/cyclooxygenase (COX)/lipoxygenase (LOX) were used in BV-2 microglial cell line. siRNA transfection was employed to knockdown cPLA2 expression in BV-2 cells. Griess reaction protocol was used to determine NO concentration, and CM-H2DCF-DA was used to detect ROS production in primary microglia and BV-2 cells. WST-1 assay was used to assess cell viability. Western blotting was used to assess protein expression levels. Immunocytochemical staining for phalloidin against F-actin was used to demonstrate cell morphology. Results: In both primary and BV-2 microglial cells, stimulation with lipopolysaccharide (LPS) or interferon gamma (IFNγ) resulted in a time-dependent increase in phosphorylation of cPLA2 together with ERK1/2. In BV-2 cells, LPS- and IFNγ-induced ROS and NO production was inhibited by arachidonyl trifluoromethyl ketone (AACOCF3) and pyrrophenone as well as RNA interference, but not BEL, suggesting a link between cPLA2, and not iPLA2, on LPS/IFNγ-induced nitrosative and oxidative stress in microglial cells. Primary microglial cells isolated from cPLA2α-deficient mice generated significantly less NO and ROS as compared with the wild-type mice. Microglia isolated from iPLA2β-deficient mice did not show a decrease in LPS-induced NO and ROS production. LPS/IFNγ induced morphological changes in primary microglia, and these changes were mitigated by AACOCF3. Interestingly, despite that LPS and IFNγ induced an increase in phospho-cPLA2 and prostaglandin E2 (PGE2) release, LPS- and IFNγ-induced NO and ROS production were not altered by the COX-1/2 inhibitor but were suppressed by the LOX-12 and LOX-15 inhibitors instead. Conclusions: In summary, the results in this study demonstrated the role of cPLA2 in microglial activation with metabolic links to oxidative and inflammatory responses, and this was in part regulated by the AA metabolic pathways, namely the LOXs. Further studies with targeted inhibition of cPLA2/LOX in microglia during neuroinflammatory conditions can be valuable to investigate the therapeutic potential in ameliorating neurological disease pathology.
MeSH term(s)	Actins/metabolism ; Animals ; Cell Line ; Cytosol/enzymology ; Female ; Inflammation/enzymology ; Inflammation/pathology ; Lipoxygenase/metabolism ; MAP Kinase Signaling System/drug effects ; Macrophage Activation/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microglia/drug effects ; Microglia/enzymology ; Nitric Oxide/metabolism ; Phospholipases A2/genetics ; Phospholipases A2/metabolism ; Primary Cell Culture ; Prostaglandin-Endoperoxide Synthases/physiology ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects
Chemical Substances	Actins ; Reactive Oxygen Species ; Nitric Oxide (31C4KY9ESH) ; Lipoxygenase (EC 1.13.11.12) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Phospholipases A2 (EC 3.1.1.4)
Language	English
Publishing date	2015-10-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-015-0419-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Metabotropic glutamate receptor subtype 5 antagonism in learning and memory.

Simonyi, Agnes / Schachtman, Todd R / Christoffersen, Gert R J

European journal of pharmacology

2010 Volume 639, Issue 1-3, Page(s) 17–25

Abstract: The role of the metabotropic glutamate receptor 5 (mGlu(5) receptor) in learning and memory and other behaviors are reviewed by examining the influence of selective antagonists and genetic knockout on performance. This receptor is involved in spatial ... ...

Abstract	The role of the metabotropic glutamate receptor 5 (mGlu(5) receptor) in learning and memory and other behaviors are reviewed by examining the influence of selective antagonists and genetic knockout on performance. This receptor is involved in spatial learning, contextual fear conditioning, inhibitory avoidance, fear potentiated startle, and conditioned taste aversion. However, mGlu(5) receptor antagonists have proven to be ineffective in other learning tasks, such as the delayed-match-to-position test and a three-hole spatial learning task. Locomotion is often decreased by mGlu(5) receptor antagonists; and other behaviors such as social interaction and consummatory responses can also be affected. In mGlu(5) receptor knockout mice, performance in contextual fear conditioning and spatial water maze tasks is impaired. Although the available evidence is suggestive of an important contribution of mGlu(5) receptors to cognitive functions, further studies are needed, particularly those with in vivo evaluation of the role of mGlu(5) receptors in selective brain regions in different stages of memory formation.
MeSH term(s)	Animals ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Learning/drug effects ; Learning/physiology ; Locomotion/drug effects ; Locomotion/physiology ; Memory/drug effects ; Memory/physiology ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/antagonists & inhibitors ; Receptors, Metabotropic Glutamate/metabolism
Chemical Substances	Excitatory Amino Acid Antagonists ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate
Language	English
Publishing date	2010-04-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2009.12.039
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Article ; Online: Withania somnifera and Its Withanolides Attenuate Oxidative and Inflammatory Responses and Up-Regulate Antioxidant Responses in BV-2 Microglial Cells.

Sun, Grace Y / Li, Runting / Cui, Jiankun / Hannink, Mark / Gu, Zezong / Fritsche, Kevin L / Lubahn, Dennis B / Simonyi, Agnes

Neuromolecular medicine

2016 Volume 18, Issue 3, Page(s) 241–252

Abstract: Withania somnifera (L.) Dunal, commonly known as Ashwagandha, has been used in Ayurvedic medicine for promoting health and quality of life. Recent clinical trials together with experimental studies indicated significant neuroprotective effects of ... ...

Abstract	Withania somnifera (L.) Dunal, commonly known as Ashwagandha, has been used in Ayurvedic medicine for promoting health and quality of life. Recent clinical trials together with experimental studies indicated significant neuroprotective effects of Ashwagandha and its constituents. This study is aimed to investigate anti-inflammatory and anti-oxidative properties of this botanical and its two withanolide constituents, namely, Withaferin A and Withanolide A, using the murine immortalized BV-2 microglial cells. Ashwagandha extracts not only effectively inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) and reactive oxygen species (ROS) production in BV-2 cells, but also stimulates the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway, leading to induction of heme oxygenase-1 (HO-1), both in the presence and absence of LPS. Although the withanolides were also capable of inhibiting LPS-induced NO production and stimulating Nrf2/HO-1 pathway, Withaferin A was tenfold more effective than Withanolide A. In serum-free culture, LPS can also induce production of long thin processes (filopodia) between 4 and 8 h in BV-2 cells. This morphological change was significantly suppressed by Ashwagandha and both withanolides at concentrations for suppressing LPS-induced NO production. Taken together, these results suggest an immunomodulatory role for Ashwagandha and its withanolides, and their ability to suppress oxidative and inflammatory responses in microglial cells by simultaneously down-regulating the NF-kB and upregulating the Nrf2 pathways.
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-016-8411-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Linking blast physics to biological outcomes in mild traumatic brain injury: Narrative review and preliminary report of an open-field blast model.

Song, Hailong / Cui, Jiankun / Simonyi, Agnes / Johnson, Catherine E / Hubler, Graham K / DePalma, Ralph G / Gu, Zezong

Behavioural brain research

2016 Volume 340, Page(s) 147–158

Abstract: Blast exposures are associated with traumatic brain injury (TBI) and blast-induced TBIs are common injuries affecting military personnel. Department of Defense and Veterans Administration (DoD/VA) reports for TBI indicated that the vast majority (82.3%) ... ...

Abstract	Blast exposures are associated with traumatic brain injury (TBI) and blast-induced TBIs are common injuries affecting military personnel. Department of Defense and Veterans Administration (DoD/VA) reports for TBI indicated that the vast majority (82.3%) has been mild TBI (mTBI)/concussion. mTBI and associated posttraumatic stress disorders (PTSD) have been called "the invisible injury" of the current conflicts in Iraq and Afghanistan. These injuries induce varying degrees of neuropathological alterations and, in some cases, chronic cognitive, behavioral and neurological disorders. Appropriate animal models of blast-induced TBI will not only assist the understanding of physical characteristics of the blast, but also help to address the potential mechanisms. This report provides a brief overview of physical principles of blast, injury mechanisms related to blast exposure, current blast animal models, and the neurological behavioral and neuropathological findings related to blast injury in experimental settings. We describe relationships between blast peak pressures and the observed injuries. We also report preliminary use of a highly reproducible and intensity-graded blast murine model carried out in open-field with explosives, and describe physical and pathological findings in this experimental model. Our results indicate close relationships between blast intensities and neuropathology and behavioral deficits, particularly at low level blast intensities relevant to mTBI.
MeSH term(s)	Animals ; Biomechanical Phenomena ; Blast Injuries/physiopathology ; Blast Injuries/therapy ; Brain Concussion/etiology ; Brain Concussion/physiopathology ; Brain Concussion/therapy ; Disease Models, Animal ; Humans ; Mice ; War-Related Injuries/physiopathology ; War-Related Injuries/therapy
Language	English
Publishing date	2016-08-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2016.08.037
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