1
40
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Text
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URL Address
<a href="http://doi.org/10.1093/toxsci/kfaa144" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfaa144</a>
ISSN
1096-0929
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1093/toxsci/kfaa144" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1093/toxsci/kfaa144</a>
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Update Year & Number
September 2020 List
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
NEOMED Student Publications
Department of Pharmaceutical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Deltamethrin exposure inhibits adult hippocampal neurogenesis and causes deficits in learning and memory in mice.
Publisher
An entity responsible for making the resource available
Toxicological Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-09-25
Subject
The topic of the resource
mice; pyrethroid; cognition; adult neurogenesis
Creator
An entity primarily responsible for making the resource
Hossain MM;Belkadi A;Al-Haddad S;Richardson JR
Description
An account of the resource
Deficits in learning and memory are often associated with disruption of hippocampal neurogenesis, which is regulated by numerous processes, including precursor cell proliferation, survival, migration, and differentiation to mature neurons. Recent studies demonstrate that adult born neurons in the dentate gyrus (DG) in the hippocampus can functionally integrate into the existing neuronal circuitry and contribute to hippocampal-dependent learning and memory. Here, we demonstrate that relatively short-term deltamethrin exposure (3 mg/kg every 3 days for 1 month) inhibits adult hippocampal neurogenesis and causes deficits in learning and memory in mice. Hippocampal-dependent cognitive functions were evaluated using two independent hippocampal-dependent behavioural tests, the novel object recognition task and Morris water maze. We found that deltamethrin-treated mice exhibited profound deficits in novel object recognition and learning and memory in water maze. Deltamethrin exposure significantly decreased bromodeoxyuridine (BrdU)-positive cells (39%) and Ki67+ cells (47%) in the dentate gyrus (DG) of the hippocampus, indicating decreased cellular proliferation. In addition, deltamethrin-treated mice exhibited a 44% decrease in nestin-expressing neural progenitor cells and a 38% reduction in the expression of doublecortin (DCX), an early neuronal differentiation marker. Furthermore, deltamethrin exposed mice exhibited a 25% reduction in total number of granule cells in the DG. These findings indicate that relatively short-term exposure to deltamethrin causes significant deficits in hippocampal neurogenesis that is associated with impaired learning and memory. (© The Author(s) 2020. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/toxsci/kfaa144" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfaa144</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
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journalArticle
2020
adult neurogenesis
Al-Haddad S
Belkadi A
Cognition
Department of Pharmaceutical Sciences
Hossain MM
journalArticle
Mice
NEOMED College of Pharmacy
NEOMED Student Publications
Pyrethroid
Richardson JR
September 2020 List
Toxicological Sciences
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1093/toxsci/kfy031" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfy031</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
265-278
Issue
1
Volume
163
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Bile Acid Sequestration by Cholestyramine Mitigates FGFR4 Inhibition-Induced ALT Elevation
Publisher
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Toxicological Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-05
Subject
The topic of the resource
7alpha-hydroxy-4-cholesten-3-one; aminotransferase; aspartate-aminotransferase isozymes; bile acids; Cyp7a1; FGF19; fibroblast-growth-factor; fibroblast-growth-factor; hepatocellular carcinoma; identification; induced liver-injury; Klotho beta; lipophilicity; liver injury; mitigation; nuclear receptor; serum; sinusoidal endothelial-cells; suppression; tgr5; Toxicology
Creator
An entity primarily responsible for making the resource
Schadt H S; Wolf A; Mahl J A; Wuersch K; Couttet P; Schwald M; Fischer A; Lienard M; Emotte C; Teng C H; Skuba E; Richardson T A; Manenti L; Weiss A; Porta D G; Fairhurst R A; Kullak-Ublick G A; Chibout S D; Pognan F; Kluwe W; Kinyamu-Akunda J
Description
An account of the resource
The FGF19- fibroblast growth factor receptor (FGFR4)-beta Klotho (KLB) pathway plays an important role in the regulation of bile acid (BA) homeostasis. Aberrant activation of this pathway has been described in the development and progression of a subset of liver cancers including hepatocellular carcinoma, establishing FGFR4 as an attractive therapeutic target for such solid tumors. FGF401 is a highly selective FGFR4 kinase inhibitor being developed for hepatocellular carcinoma, currently in phase I/II clinical studies. In preclinical studies in mice and dogs, oral administration of FGF401 led to induction of Cyp7a1., elevation of its peripheral marker 7alpha-hydroxy-4-cholesten-3-one, increased BA pool size, decreased serum cholesterol and diarrhea in dogs. FGF401 was also associated with increases of serum aminotransferases, primarily alanine aminotransferase (ALT), in the absence of any observable adverse histopathological findings in the liver, or in any other organs. We hypothesized that the increase in ALT could be secondary to increased BAs and conducted an investigative study in dogs with FGF401 and coadministration of the BA sequestrant cholestyramine (CHO). CHO prevented and reversed FGF401-related increases in ALT in dogs in parallel to its ability to reduce BAs in the circulation. Correlation analysis showed that FGF401-mediated increases in ALT strongly correlated with increases in taurolithocholic acid and taurodeoxycholic acid, the major secondary BAs in dog plasma, indicating a mechanistic link between ALT elevation and changes in BA pool hydrophobicity. Thus, CHO may offer the potential to mitigate elevations in serum aminotransferases in human subjects that are caused by targeted FGFR4 inhibition and elevated intracellular BA levels.
Identifier
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<a href="http://doi.org/10.1093/toxsci/kfy031" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfy031</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2018
7alpha-hydroxy-4-cholesten-3-one
aminotransferase
aspartate-aminotransferase isozymes
BILE acids
Chibout S D
Couttet P
CYP7A1
Emotte C
Fairhurst R A
FGF19
fibroblast-growth-factor
Fischer A
Hepatocellular carcinoma
identification
induced liver-injury
Journal Article
Kinyamu-Akunda J
Klotho beta
Kluwe W
Kullak-Ublick G A
Lienard M
lipophilicity
Liver injury
Mahl J A
Manenti L
mitigation
Nuclear Receptor
Pognan F
Porta D G
Richardson T A
Schadt H S
Schwald M
serum
sinusoidal endothelial-cells
Skuba E
suppression
Teng C H
TGR5
Toxicological Sciences
Toxicology
Weiss A
Wolf A
Wuersch K