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  1. Article ; Online: Repeated mild traumatic brain injury causes chronic neuroinflammation, changes in hippocampal synaptic plasticity, and associated cognitive deficits.

    Aungst, Stephanie L / Kabadi, Shruti V / Thompson, Scott M / Stoica, Bogdan A / Faden, Alan I

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

    2014  Volume 34, Issue 7, Page(s) 1223–1232

    Abstract: Repeated mild traumatic brain injury (mTBI) can cause sustained cognitive and psychiatric changes, as well as neurodegeneration, but the underlying mechanisms remain unclear. We examined histologic, neurophysiological, and cognitive changes after single ... ...

    Abstract Repeated mild traumatic brain injury (mTBI) can cause sustained cognitive and psychiatric changes, as well as neurodegeneration, but the underlying mechanisms remain unclear. We examined histologic, neurophysiological, and cognitive changes after single or repeated (three injuries) mTBI using the rat lateral fluid percussion (LFP) model. Repeated mTBI caused substantial neuronal cell loss and significantly increased numbers of activated microglia in both ipsilateral and contralateral hippocampus on post-injury day (PID) 28. Long-term potentiation (LTP) could not be induced on PID 28 after repeated mTBI in ex vivo hippocampal slices from either hemisphere. N-Methyl-D-aspartate (NMDA) receptor-mediated responses were significantly attenuated after repeated mTBI, with no significant changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated responses. Long-term potentiation was elicited in slices after single mTBI, with potentiation significantly increased in ipsilateral versus contralateral hippocampus. After repeated mTBI, rats displayed cognitive impairments in the Morris water maze (MWM) and novel object recognition (NOR) tests. Thus, repeated mTBI causes deficits in the hippocampal function and changes in excitatory synaptic neurotransmission, which are associated with chronic neuroinflammation and neurodegeneration.
    MeSH term(s) Animals ; Brain Injuries/complications ; Brain Injuries/physiopathology ; Cognition Disorders/etiology ; Cognition Disorders/physiopathology ; Disease Models, Animal ; Functional Laterality/physiology ; Hippocampus/physiopathology ; Immunohistochemistry ; Inflammation/etiology ; Inflammation/physiopathology ; Long-Term Potentiation/physiology ; Male ; Organ Culture Techniques ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/physiology
    Language English
    Publishing date 2014-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604628-9
    ISSN 1559-7016 ; 0271-678X
    ISSN (online) 1559-7016
    ISSN 0271-678X
    DOI 10.1038/jcbfm.2014.75
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1663: Show issues Location:
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  2. Article ; Online: FDA Approval Summary: Entrectinib for the Treatment of

    Marcus, Leigh / Donoghue, Martha / Aungst, Stephanie / Myers, Claire E / Helms, Whitney S / Shen, Guoxiang / Zhao, Hong / Stephens, Olen / Keegan, Patricia / Pazdur, Richard

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2020  Volume 27, Issue 4, Page(s) 928–932

    Abstract: The FDA-approved entrectinib on August 15, 2019, for the treatment of adult and pediatric patients 12 years of age and older with solid tumors that have a neurotrophic tyrosine receptor kinase ( ...

    Abstract The FDA-approved entrectinib on August 15, 2019, for the treatment of adult and pediatric patients 12 years of age and older with solid tumors that have a neurotrophic tyrosine receptor kinase (
    MeSH term(s) Benzamides/administration & dosage ; Benzamides/adverse effects ; Drug Approval ; Humans ; Indazoles/administration & dosage ; Indazoles/adverse effects ; Neoplasms/drug therapy ; Neoplasms/genetics ; Oncogene Proteins, Fusion/antagonists & inhibitors ; Oncogene Proteins, Fusion/genetics ; Protein Kinase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/adverse effects ; Receptor, trkA/antagonists & inhibitors ; Receptor, trkA/genetics ; Receptor, trkB/antagonists & inhibitors ; Receptor, trkB/genetics ; Receptor, trkC/antagonists & inhibitors ; Receptor, trkC/genetics ; United States ; United States Food and Drug Administration/legislation & jurisprudence
    Chemical Substances Benzamides ; Indazoles ; Oncogene Proteins, Fusion ; Protein Kinase Inhibitors ; Receptor, trkA (EC 2.7.10.1) ; Receptor, trkB (EC 2.7.10.1) ; Receptor, trkC (EC 2.7.10.1) ; entrectinib (L5ORF0AN1I)
    Language English
    Publishing date 2020-09-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-20-2771
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4223: Show issues Location:
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  3. Article: Sensory deafferentation transsynaptically alters neuronal GluR1 expression in the external plexiform layer of the adult mouse main olfactory bulb.

    Hamilton, Kathryn A / Parrish-Aungst, Stephanie / Margolis, Frank L / Erdélyi, Ferenc / Szabó, Gabor / Puche, Adam C

    Chemical senses

    2008  Volume 33, Issue 2, Page(s) 201–210

    Abstract: Altered distribution of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunit GluR1 has been linked to stimulation-dependent changes in synaptic efficacy, including long-term potentiation and depression. The main olfactory ... ...

    Abstract Altered distribution of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunit GluR1 has been linked to stimulation-dependent changes in synaptic efficacy, including long-term potentiation and depression. The main olfactory bulb (OB) remains plastic throughout life; how GluR1 may be involved in this plasticity is unknown. We have previously shown that neonatal naris occlusion reduces numbers of interneuron cell bodies that are immunoreactive for GluR1 in the external plexiform layer (EPL) of the adult mouse OB. Here, we show that immunoreactivity of mouse EPL interneurons for GluR1 is also dramatically reduced following olfactory deafferentation in adulthood. We further show that expression of glutamic acid decarboxylase (GAD) 65, 1 of 2 GAD isoforms expressed by adult gamma-aminobutyric acidergic interneurons, is reduced, but to a much smaller extent, and that in double-labeled cells, immunoreactivity for the Ca(2+)-binding protein parvalbumin (PV) is also reduced. In addition, GluR1 expression is reduced in presumptive tufted cells and interneurons that are negative for GAD65 and PV. Consistent with previous reports, sensory deafferentation resulted in little neuronal degeneration in the adult EPL, indicating that these differences were not likely due to death of EPL neurons. Together, these results suggest that olfactory input regulates expression of the GluR1 AMPA receptor subunit by tufted cells that may in turn regulate GluR1 expression by interneurons within the OB EPL.
    MeSH term(s) Animals ; Cell Count ; Glutamate Decarboxylase/metabolism ; Interneurons/metabolism ; Mice ; Mice, Transgenic ; Olfactory Bulb/metabolism ; Olfactory Receptor Neurons/cytology ; Olfactory Receptor Neurons/drug effects ; Olfactory Receptor Neurons/metabolism ; Receptors, AMPA/metabolism ; Smell/physiology ; Zinc Sulfate/pharmacology
    Chemical Substances Receptors, AMPA ; glutamate receptor ionotropic, AMPA 1 ; Zinc Sulfate (7733-02-0) ; Glutamate Decarboxylase (EC 4.1.1.15) ; glutamate decarboxylase 2 (EC 4.1.1.15)
    Language English
    Publishing date 2008-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 754122-3
    ISSN 1464-3553 ; 0379-864X
    ISSN (online) 1464-3553
    ISSN 0379-864X
    DOI 10.1093/chemse/bjm079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: FDA Approval Summary: Lenvatinib for Progressive, Radio-iodine-Refractory Differentiated Thyroid Cancer.

    Nair, Abhilasha / Lemery, Steven J / Yang, Jun / Marathe, Anshu / Zhao, Liang / Zhao, Hong / Jiang, Xiaoping / He, Kun / Ladouceur, Gaetan / Mitra, Amit K / Zhou, Liang / Fox, Emily / Aungst, Stephanie / Helms, Whitney / Keegan, Patricia / Pazdur, Richard

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2015  Volume 21, Issue 23, Page(s) 5205–5208

    Abstract: The FDA approved lenvatinib (Lenvima, Eisai Inc.) for the treatment of patients with locally recurrent or metastatic, progressive, radioactive iodine-refractory (RAI-refractory) differentiated thyroid cancer (DTC). In an international, multicenter, ... ...

    Abstract The FDA approved lenvatinib (Lenvima, Eisai Inc.) for the treatment of patients with locally recurrent or metastatic, progressive, radioactive iodine-refractory (RAI-refractory) differentiated thyroid cancer (DTC). In an international, multicenter, double-blinded, placebo-controlled trial (E7080-G000-303), 392 patients with locally recurrent or metastatic RAI-refractory DTC and radiographic evidence of disease progression within 12 months prior to randomization were randomly allocated (2:1) to receive either lenvatinib 24 mg orally per day (n = 261) or matching placebo (n = 131) with the option for patients on the placebo arm to receive lenvatinib following independent radiologic confirmation of disease progression. A statistically significant prolongation of progression-free survival (PFS) as determined by independent radiology review was demonstrated [HR, 0.21; 95% confidence interval (CI), 0.16-0.28; P < 0.001, stratified log-rank test], with an estimated median PFS of 18.3 months (95% CI, 15.1, NR) in the lenvatinib arm and 3.6 months (95% CI, 2.2-3.7) in the placebo arm. The most common adverse reactions, in order of decreasing frequency, observed in the lenvatinib-treated patients were hypertension, fatigue, diarrhea, arthralgia/myalgia, decreased appetite, decreased weight, nausea, stomatitis, headache, vomiting, proteinuria, palmar-plantar erythrodysesthesia syndrome, abdominal pain, and dysphonia. Adverse reactions led to dose reductions in 68% of patients receiving lenvatinib at the 24 mg dose and 18% of patients discontinued lenvatinib for adverse reactions leading to residual uncertainty regarding the optimal dose of lenvatinib.
    MeSH term(s) Adult ; Aged ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Disease Progression ; Drug Approval ; Female ; Humans ; Iodine Radioisotopes/therapeutic use ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Neoplasm Grading ; Neoplasm Metastasis ; Neoplasm Staging ; Phenylurea Compounds/pharmacology ; Phenylurea Compounds/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Quinolines/pharmacology ; Quinolines/therapeutic use ; Radiation Tolerance ; Randomized Controlled Trials as Topic ; Retreatment ; Thyroid Neoplasms/drug therapy ; Thyroid Neoplasms/mortality ; Thyroid Neoplasms/pathology ; Treatment Outcome ; United States ; United States Food and Drug Administration
    Chemical Substances Antineoplastic Agents ; Iodine Radioisotopes ; Phenylurea Compounds ; Protein Kinase Inhibitors ; Quinolines ; lenvatinib (EE083865G2)
    Language English
    Publishing date 2015-12-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-15-1377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4223: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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