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  1. Article ; Online: Diabetic ketoacidosis causes chronic elevation in renal C-C motif chemokine ligand 5.

    Glaser, Nicole / Fernandez, Luis / Chu, Steven / O'Donnell, Martha E

    Endocrine

    2021  Volume 75, Issue 2, Page(s) 650–653

    MeSH term(s) Chemokines ; Diabetes Mellitus ; Diabetic Ketoacidosis/etiology ; Kidney ; Ligands
    Chemical Substances Chemokines ; Ligands
    Language English
    Publishing date 2021-11-02
    Publishing country United States
    Document type Letter
    ZDB-ID 1194484-5
    ISSN 1559-0100 ; 1355-008X ; 0969-711X
    ISSN (online) 1559-0100
    ISSN 1355-008X ; 0969-711X
    DOI 10.1007/s12020-021-02928-2
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  2. Article ; Online: Blood-brain barrier Na transporters in ischemic stroke.

    O'Donnell, Martha E

    Advances in pharmacology (San Diego, Calif.)

    2014  Volume 71, Page(s) 113–146

    Abstract: Blood-brain barrier (BBB) endothelial cells form a barrier that is highly restrictive to passage of solutes between blood and brain. Many BBB transport mechanisms have been described that mediate transcellular movement of solutes across the barrier ... ...

    Abstract Blood-brain barrier (BBB) endothelial cells form a barrier that is highly restrictive to passage of solutes between blood and brain. Many BBB transport mechanisms have been described that mediate transcellular movement of solutes across the barrier either into or out of the brain. One class of BBB transporters that is all too often overlooked is that of the ion transporters. The BBB has a rich array of ion transporters and channels that carry Na, K, Cl, HCO3, Ca, and other ions. Many of these are asymmetrically distributed between the luminal and abluminal membranes, giving BBB endothelial cells the ability to perform vectorial transport of ions across the barrier between blood and brain. In this manner, the BBB performs the important function of regulating the volume and composition of brain interstitial fluid. Through functional coupling of luminal and abluminal transporters and channels, the BBB carries Na, Cl, and other ions from blood into brain, producing up to 30% of brain interstitial fluid in healthy brain. During ischemic stroke cerebral edema forms by processes involving increased activity of BBB luminal Na transporters, resulting in "hypersecretion" of Na, Cl, and water into the brain interstitium. This review discusses the roles of luminal BBB Na transporters in edema formation in stroke, with an emphasis on Na-K-Cl cotransport and Na/H exchange. Evidence that these transporters provide effective therapeutic targets for reduction of edema in stroke is also discussed, as are recent findings regarding signaling pathways responsible for ischemia stimulation of the BBB Na transporters.
    MeSH term(s) Adenylate Kinase/metabolism ; Animals ; Blood-Brain Barrier/metabolism ; Brain Ischemia/metabolism ; Humans ; Ion Channels/metabolism ; Ion Pumps/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Sodium/metabolism ; Stroke/metabolism
    Chemical Substances Ion Channels ; Ion Pumps ; Sodium (9NEZ333N27) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Adenylate Kinase (EC 2.7.4.3)
    Language English
    Publishing date 2014
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1557-8925
    ISSN (online) 1557-8925
    DOI 10.1016/bs.apha.2014.06.011
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  3. Article ; Online: High glucose-induced effects on Na

    Klug, Nicholas R / Chechneva, Olga V / Hung, Benjamin Y / O'Donnell, Martha E

    American journal of physiology. Cell physiology

    2021  Volume 320, Issue 4, Page(s) C619–C634

    Abstract: Hyperglycemia exacerbates edema formation and worsens neurological outcome in ischemic stroke. Edema formation in the early hours of stroke involves transport of ions and water across an intact blood-brain barrier (BBB), and swelling of astrocytes. We ... ...

    Abstract Hyperglycemia exacerbates edema formation and worsens neurological outcome in ischemic stroke. Edema formation in the early hours of stroke involves transport of ions and water across an intact blood-brain barrier (BBB), and swelling of astrocytes. We showed previously that high glucose (HG) exposures of 24 hours to 7 days increase abundance and activity of BBB Na
    MeSH term(s) Animals ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/enzymology ; Blood-Brain Barrier/pathology ; Cattle ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Endothelial Cells/pathology ; Enzyme Activation ; Glucose/toxicity ; Humans ; Immediate-Early Proteins/metabolism ; Phosphorylation ; Protein Kinase C beta/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Sodium-Hydrogen Exchanger 1/metabolism ; Sodium-Potassium-Chloride Symporters/metabolism ; Time Factors
    Chemical Substances Immediate-Early Proteins ; Sodium-Hydrogen Exchanger 1 ; Sodium-Potassium-Chloride Symporters ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Protein Kinase C beta (EC 2.7.11.13) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2021-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00177.2019
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  4. Article ; Online: Pathophysiology of stroke: what do cells of the neurovascular unit have to do with it?

    O'Donnell, Martha E / Yuan, Jason X-J

    American journal of physiology. Cell physiology

    2018  Volume 316, Issue 1, Page(s) C1

    MeSH term(s) Blood-Brain Barrier/pathology ; Blood-Brain Barrier/physiopathology ; Brain/pathology ; Brain/physiopathology ; Humans ; Neurovascular Coupling/physiology ; Stroke/pathology ; Stroke/physiopathology
    Language English
    Publishing date 2018-11-21
    Publishing country United States
    Document type Editorial
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00470.2018
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  5. Article ; Online: Pathophysiology of stroke: the many and varied contributions of brain microvasculature.

    O'Donnell, Martha E / Yuan, Jason X-J

    American journal of physiology. Cell physiology

    2018  Volume 315, Issue 3, Page(s) C341–C342

    MeSH term(s) Brain/blood supply ; Brain/pathology ; Brain Ischemia/pathology ; Humans ; Microvessels/pathology ; Stroke/pathology
    Language English
    Publishing date 2018-08-15
    Publishing country United States
    Document type Editorial
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00328.2018
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  6. Article ; Online: Histological and cognitive alterations in adult diabetic rats following an episode of juvenile diabetic ketoacidosis: Evidence of permanent cerebral injury.

    Glaser, Nicole / Sasaki-Russell, Jennifer / Cohen, Michael / Little, Christopher / O'Donnell, Martha / Sall, Jeffrey

    Neuroscience letters

    2017  Volume 650, Page(s) 161–167

    Abstract: Evidence suggests that diabetic ketoacidosis (DKA) may cause subtle cognitive alterations in children but the mechanisms are poorly understood. Acute DKA is associated with reactive astrogliosis and microglial activation in a rat model. Whether these ... ...

    Abstract Evidence suggests that diabetic ketoacidosis (DKA) may cause subtle cognitive alterations in children but the mechanisms are poorly understood. Acute DKA is associated with reactive astrogliosis and microglial activation in a rat model. Whether these inflammatory changes permanently alter brain histology is unknown. We aimed to determine whether DKA results in permanent alterations in brain histology and whether these changes are associated with cognitive deficits in a rat model. We induced diabetes in juvenile rats with streptozotocin at 4 weeks of age. We induced DKA in one group (n=21) at 5 weeks of age and compared this group to rats with diabetes without DKA episodes (n=13). Beginning at 7 weeks, rats underwent a series of cognitive tests to evaluate memory. At 15 weeks, rat brains were harvested and examined using immunohistochemistry (IHC). In tests of novel object recognition and social recognition, both groups performed similarly, however, the DKA group performed more poorly in object-place recognition tests, suggesting alterations in hippocampal function. IHC studies demonstrated increased glial fibrillary acidic protein staining intensity in the hippocampus of DKA rats suggesting astrogliosis, and decreased NeuN positive cell counts in the cortex suggesting neuron loss. These studies demonstrate that DKA results in permanent alterations in brain microstructure in a rat diabetes model. These structural changes are associated with deficits in hippocampal function.
    MeSH term(s) Animals ; Brain/pathology ; Brain/physiopathology ; Brain Injuries/etiology ; Brain Injuries/pathology ; Brain Injuries/physiopathology ; Chronic Disease ; Cognition ; Cognition Disorders/etiology ; Cognition Disorders/physiopathology ; Diabetes Complications/complications ; Diabetes Complications/pathology ; Diabetes Complications/physiopathology ; Diabetic Ketoacidosis/complications ; Diabetic Ketoacidosis/pathology ; Diabetic Ketoacidosis/physiopathology ; Female ; Male ; Rats ; Rats, Sprague-Dawley
    Language English
    Publishing date 2017-04-21
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2017.04.035
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    Zs.A 1166: Show issues Location:
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  7. Article ; Online: Ischemia-induced stimulation of Na-K-Cl cotransport in cerebral microvascular endothelial cells involves AMP kinase.

    Wallace, Breanna K / Foroutan, Shahin / O'Donnell, Martha E

    American journal of physiology. Cell physiology

    2011  Volume 301, Issue 2, Page(s) C316–26

    Abstract: Increased blood-brain barrier (BBB) Na-K-Cl cotransporter activity appears to contribute to cerebral edema formation during ischemic stroke. We have shown previously that inhibition of BBB Na-K-Cl cotransporter activity reduces edema and infarct in the ... ...

    Abstract Increased blood-brain barrier (BBB) Na-K-Cl cotransporter activity appears to contribute to cerebral edema formation during ischemic stroke. We have shown previously that inhibition of BBB Na-K-Cl cotransporter activity reduces edema and infarct in the rat middle cerebral artery occlusion (MCAO) model of ischemic stroke. We have also shown that the BBB cotransporter is stimulated by the ischemic factors hypoxia, aglycemia, and arginine vasopressin (AVP), although the mechanisms responsible are not well understood. AMP-activated protein kinase (AMPK), a key mediator of cell responses to stress, can be activated by a variety of stresses, including ischemia, hypoxia, and aglycemia. Previous studies have shown that the AMPK inhibitor Compound C significantly reduces infarct in mouse MCAO. The present study was conducted to evaluate the possibility that AMPK participates in ischemic factor-induced stimulation of the BBB Na-K-Cl cotransporter. Cerebral microvascular endothelial cells (CMEC) were assessed for Na-K-Cl cotransporter activity as bumetanide-sensitive (86)Rb influx. AMPK activity was assessed by Western blot analysis and immunofluorescence methods using antibodies that detect total versus phosphorylated (activated) AMPK. We found that hypoxia (7% and 2% O(2)), aglycemia, AVP, and oxygen-glucose deprivation (5- to 120-min exposures) increase activation of AMPK. We also found that Compound C inhibition of AMPK reduces hypoxia-, aglycemia-, and AVP-induced stimulation of CMEC Na-K-Cl cotransporter activity. Confocal immunofluorescence of perfusion-fixed rat brain slices revealed the presence of AMPK, both total and phosphorylated kinase, in BBB in situ of both control and ischemic brain. These findings suggest that ischemic factor stimulation of the BBB Na-K-Cl cotransporter involves activation of AMPK.
    MeSH term(s) Adenylate Kinase/metabolism ; Animals ; Arginine Vasopressin/metabolism ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/enzymology ; Blotting, Western ; Bumetanide/pharmacology ; Cattle ; Cell Hypoxia ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Enzyme Activation ; Fluorescent Antibody Technique ; Glucose/deficiency ; Infarction, Middle Cerebral Artery/enzymology ; Male ; Microvessels/drug effects ; Microvessels/enzymology ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Sodium Potassium Chloride Symporter Inhibitors/pharmacology ; Sodium-Potassium-Chloride Symporters/metabolism ; Time Factors ; Up-Regulation
    Chemical Substances Protein Kinase Inhibitors ; Pyrazoles ; Pyrimidines ; Sodium Potassium Chloride Symporter Inhibitors ; Sodium-Potassium-Chloride Symporters ; Bumetanide (0Y2S3XUQ5H) ; dorsomorphin (10K52CIC1Z) ; Arginine Vasopressin (113-79-1) ; Adenylate Kinase (EC 2.7.4.3) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2011-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00517.2010
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  8. Article ; Online: Diabetic ketoacidosis in juvenile rats is associated with reactive gliosis and activation of microglia in the hippocampus.

    Lo, Weei / O'Donnell, Martha / Tancredi, Daniel / Orgain, Myra / Glaser, Nicole

    Pediatric diabetes

    2015  Volume 17, Issue 2, Page(s) 127–139

    Abstract: Background: Type 1 diabetes may be associated with structural and functional alterations in the brain. The role of diabetic ketoacidosis (DKA) in causing these alterations has not been well explored.: Methods: We used immunohistochemical staining to ... ...

    Abstract Background: Type 1 diabetes may be associated with structural and functional alterations in the brain. The role of diabetic ketoacidosis (DKA) in causing these alterations has not been well explored.
    Methods: We used immunohistochemical staining to investigate cellular alterations in brain specimens from juvenile rats with DKA before, during, and after treatment with insulin and saline, and compared these to samples from diabetic rats and normal controls.
    Results: Glial fibrillary acidic protein (GFAP) staining intensity was increased in the hippocampus during DKA and increased further during insulin/saline treatment. Twenty-four and 72 h after treatment, hippocampal GFAP intensity declined but remained above control levels. There were no significant changes in GFAP intensity in the cortex or striatum. OX42 staining intensity was increased during untreated DKA and increased further during insulin/saline treatment in the hippocampus and cortex. NeuN staining intensity was decreased after DKA treatment in the striatum but not in other regions.
    Conclusions: DKA causes inflammatory changes in the brain including reactive gliosis and activation of microglia. These findings are present during untreated DKA, but intensify during insulin/saline treatment. The hippocampus was disproportionately affected, consistent with previous studies showing deficits in hippocampal functions in rats after DKA recovery and decreased memory capacity in children with a history of DKA.
    MeSH term(s) Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Antigens, Nuclear/metabolism ; CD11b Antigen/metabolism ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetic Ketoacidosis/complications ; Diabetic Ketoacidosis/metabolism ; Diabetic Ketoacidosis/pathology ; Glial Fibrillary Acidic Protein/metabolism ; Gliosis/etiology ; Gliosis/metabolism ; Gliosis/pathology ; Hippocampus/metabolism ; Hippocampus/pathology ; Microglia/metabolism ; Microglia/pathology ; Nerve Tissue Proteins/metabolism ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; Antigens, Nuclear ; CD11b Antigen ; CD68 antigen, human ; Glial Fibrillary Acidic Protein ; Nerve Tissue Proteins ; Rbfox3 protein, rat
    Language English
    Publishing date 2015-01-16
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1502504-4
    ISSN 1399-5448 ; 1745-1426 ; 1399-543X
    ISSN (online) 1399-5448
    ISSN 1745-1426 ; 1399-543X
    DOI 10.1111/pedi.12251
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    Zs.A 5422: Show issues Location:
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  9. Article ; Online: Ischemia-induced stimulation of cerebral microvascular endothelial cell Na-K-Cl cotransport involves p38 and JNK MAP kinases.

    Wallace, Breanna K / Jelks, Karen A / O'Donnell, Martha E

    American journal of physiology. Cell physiology

    2011  Volume 302, Issue 3, Page(s) C505–17

    Abstract: Previous studies have provided evidence that, in the early hours of ischemic stroke, a luminal membrane blood-brain barrier (BBB) Na-K-Cl cotransporter (NKCC) participates in ischemia-induced cerebral edema formation. Inhibition of BBB NKCC activity by ... ...

    Abstract Previous studies have provided evidence that, in the early hours of ischemic stroke, a luminal membrane blood-brain barrier (BBB) Na-K-Cl cotransporter (NKCC) participates in ischemia-induced cerebral edema formation. Inhibition of BBB NKCC activity by intravenous bumetanide significantly reduces edema and infarct in the rat permanent middle cerebral artery occlusion model of ischemic stroke. We demonstrated previously that the BBB cotransporter is stimulated by hypoxia, aglycemia, and AVP, factors present during cerebral ischemia. However, the underlying mechanisms have not been known. Ischemic conditions have been shown to activate p38 and JNK MAP kinases (MAPKs) in brain, and the p38 and JNK inhibitors SB-239063 and SP-600125, respectively, have been found to reduce brain damage following middle cerebral artery occlusion and subarachnoid hemorrhage, respectively. The present study was conducted to determine whether one or both of these MAPKs participates in ischemic factor stimulation of BBB NKCC activity. Cultured cerebral microvascular endothelial cell NKCC activity was evaluated as bumetanide-sensitive (86)Rb influx. Activities of p38 and JNK were assessed by Western blot and immunofluorescence methods using antibodies that detect total vs. phosphorylated (activated) p38 or JNK. We report that p38 and JNK are present in cultured cerebral microvascular endothelial cells and in BBB endothelial cells in situ and that hypoxia (7% O(2) and 2% O(2)), aglycemia, AVP, and O(2)-glucose deprivation (5- to 120-min exposures) all rapidly activate p38 and JNK in the cells. We also provide evidence that SB-239063 and SP-600125 reduce or abolish ischemic factor stimulation of BBB NKCC activity. These findings support the hypothesis that ischemic factor stimulation of the BBB NKCC involves activation of p38 and JNK MAPKs.
    MeSH term(s) Animals ; Anthracenes/pharmacology ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/physiopathology ; Brain/blood supply ; Brain Ischemia/metabolism ; Bumetanide/pharmacology ; Cattle ; Cell Hypoxia ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Imidazoles/pharmacology ; Infarction, Middle Cerebral Artery ; JNK Mitogen-Activated Protein Kinases/metabolism ; Microcirculation ; Microvessels ; Pyrimidines/pharmacology ; Rubidium/metabolism ; Signal Transduction ; Sodium-Potassium-Chloride Symporters/metabolism ; Stroke ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Anthracenes ; Imidazoles ; Pyrimidines ; Sodium-Potassium-Chloride Symporters ; Bumetanide (0Y2S3XUQ5H) ; pyrazolanthrone (1TW30Y2766) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; SB 239063 (HII3DC8CPI) ; Rubidium (MLT4718TJW)
    Language English
    Publishing date 2011-11-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00261.2011
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  10. Article ; Online: Treatment with the KCa3.1 inhibitor TRAM-34 during diabetic ketoacidosis reduces inflammatory changes in the brain.

    Glaser, Nicole / Little, Christopher / Lo, Weei / Cohen, Michael / Tancredi, Daniel / Wulff, Heike / O'Donnell, Martha

    Pediatric diabetes

    2016  Volume 18, Issue 5, Page(s) 356–366

    Abstract: Background: Diabetic ketoacidosis (DKA) causes brain injuries in children ranging from subtle to life-threatening. Previous studies suggest that DKA-related brain injury may involve both stimulation of Na-K-Cl cotransport and microglial activation. ... ...

    Abstract Background: Diabetic ketoacidosis (DKA) causes brain injuries in children ranging from subtle to life-threatening. Previous studies suggest that DKA-related brain injury may involve both stimulation of Na-K-Cl cotransport and microglial activation. Other studies implicate the Na-K-Cl cotransporter and the Ca-activated K channel KCa3.1 in activation of microglia and ischemia-induced brain edema. In this study, we determined whether inhibiting cerebral Na-K-Cl cotransport or KCa3.1 could reduce microglial activation and decrease DKA-related inflammatory changes in the brain.
    Methods: Using immunohistochemistry, we investigated cellular alterations in brain specimens from juvenile rats with DKA before, during and after insulin and saline treatment. We compared findings in rats treated with and without bumetanide (an inhibitor of Na-K-Cl cotransport) or the KCa3.1 inhibitor TRAM-34.
    Results: Glial fibrillary acidic protein (GFAP) staining intensity was increased in the hippocampus during DKA, suggesting reactive astrogliosis. OX42 staining intensity was increased during DKA in the hippocampus, cortex and striatum, indicating microglial activation. Treatment with TRAM-34 decreased both OX42 and GFAP intensity suggesting a decreased inflammatory response to DKA. Treatment with bumetanide did not significantly alter OX42 or GFAP intensity.
    Conclusions: Inhibiting KCa3.1 activity with TRAM-34 during DKA treatment decreases microglial activation and reduces reactive astrogliosis, suggesting a decreased inflammatory response.
    MeSH term(s) Animals ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Biomarkers/metabolism ; Brain/drug effects ; Brain/immunology ; Brain/metabolism ; Brain/pathology ; Bumetanide/therapeutic use ; CD11b Antigen/antagonists & inhibitors ; CD11b Antigen/metabolism ; Cerebral Cortex/drug effects ; Cerebral Cortex/immunology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Corpus Striatum/drug effects ; Corpus Striatum/immunology ; Corpus Striatum/metabolism ; Corpus Striatum/pathology ; Diabetic Ketoacidosis/drug therapy ; Diabetic Ketoacidosis/immunology ; Diabetic Ketoacidosis/metabolism ; Diabetic Ketoacidosis/pathology ; Encephalitis/etiology ; Encephalitis/prevention & control ; Female ; Glial Fibrillary Acidic Protein/antagonists & inhibitors ; Glial Fibrillary Acidic Protein/metabolism ; Gliosis/etiology ; Gliosis/prevention & control ; Hippocampus/drug effects ; Hippocampus/immunology ; Hippocampus/metabolism ; Hippocampus/pathology ; Male ; Microglia/drug effects ; Microglia/immunology ; Microglia/metabolism ; Microglia/pathology ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/metabolism ; Potassium Channel Blockers/therapeutic use ; Pyrazoles/therapeutic use ; Random Allocation ; Small-Conductance Calcium-Activated Potassium Channels/antagonists & inhibitors ; Small-Conductance Calcium-Activated Potassium Channels/metabolism ; Sodium Potassium Chloride Symporter Inhibitors/therapeutic use
    Chemical Substances Anti-Inflammatory Agents, Non-Steroidal ; Biomarkers ; CD11b Antigen ; GFAP protein, rat ; Glial Fibrillary Acidic Protein ; Kcnn3 protein, rat ; Nerve Tissue Proteins ; Potassium Channel Blockers ; Pyrazoles ; Small-Conductance Calcium-Activated Potassium Channels ; Sodium Potassium Chloride Symporter Inhibitors ; TRAM 34 ; Bumetanide (0Y2S3XUQ5H)
    Language English
    Publishing date 2016-05-13
    Publishing country Denmark
    Document type Comparative Study ; Journal Article
    ZDB-ID 1502504-4
    ISSN 1399-5448 ; 1745-1426 ; 1399-543X
    ISSN (online) 1399-5448
    ISSN 1745-1426 ; 1399-543X
    DOI 10.1111/pedi.12396
    Database MEDical Literature Analysis and Retrieval System OnLINE

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