1
40
40
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2018.12.019</a>
Pages
36–42
Volume
66
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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Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
Publisher
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Environmental toxicology and pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; Oxygen consumption; Reactive oxygen species
Creator
An entity primarily responsible for making the resource
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Description
An account of the resource
Glyphosate-based herbicides, such as Touchdown (TD) and Roundup, are among the most heavily-used herbicides in the world. While the active ingredient is generally considered non-toxic, the toxicity resulting from exposure to commercially-sold formulations is less clear. In many cases, cell cultures or various model organisms exposed to glyphosate formulations show toxicity and, in some cases, lethality. Using Caenorhabditis elegans, we assessed potential toxic mechanisms through which a highly-concentrated commercial formulation of TD promotes neurodegeneration. Following a 30-min treatment, we assayed mitochondrial electron transport chain function and reactive oxygen species (ROS) production. Initial oxygen consumption studies indicated general mitochondrial inhibition compared to controls ((*)p \textless 0.05). When Complex II activity was further assessed, inhibition was observed in all TD-treated groups ((*)p \textless 0.05). Complex IV activity, however, was not adversely affected by TD. This electron transport chain inhibition also resulted in reduced ATP levels ((*)p \textless 0.05). Furthermore, hydrogen peroxide levels, but not other ROS, were increased ((*)p \textless 0.05). Taken together, these data indicate that commercially-available formulations of TD may exert neurotoxicity through Complex II (succinate dehydrogenase) inhibition, decreased ATP levels, and increased hydrogen peroxide production.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2018.12.019</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).
2019
Bailey Denise C
Burchfield Shelbie L
C. elegans
Denney Rachel D
Department of Pharmaceutical Sciences
Environmental toxicology and pharmacology
Fitsanakis Vanessa A
Glyphosate
Hydrogen peroxide
Mitochondrial inhibition
Negga Rekek
NEOMED College of Pharmacy
Oxygen Consumption
reactive oxygen species
Todt Callie E
-
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/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2018.12.019</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
36-42
Volume
66
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
A name given to the resource
Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
Publisher
An entity responsible for making the resource available
Environmental toxicology and pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
C. elegans; Glyphosate; *hydrogen peroxide; Mitochondrial inhibition; Oxygen Consumption; *Reactive oxygen species; Animals; Reactive Oxygen Species/metabolism; Adenosine Triphosphate/metabolism; Herbicides/*toxicity; Caenorhabditis elegans/*drug effects/metabolism; Electron Transport Complex II/*antagonists & inhibitors/metabolism; Glycine/*analogs & derivatives/toxicity
Creator
An entity primarily responsible for making the resource
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Description
An account of the resource
Glyphosate-based herbicides, such as Touchdown (TD) and Roundup, are among the most heavily-used herbicides in the world. While the active ingredient is generally considered non-toxic, the toxicity resulting from exposure to commercially-sold formulations is less clear. In many cases, cell cultures or various model organisms exposed to glyphosate formulations show toxicity and, in some cases, lethality. Using Caenorhabditis elegans, we assessed potential toxic mechanisms through which a highly-concentrated commercial formulation of TD promotes neurodegeneration. Following a 30-min treatment, we assayed mitochondrial electron transport chain function and reactive oxygen species (ROS) production. Initial oxygen consumption studies indicated general mitochondrial inhibition compared to controls ((*)p < 0.05). When Complex II activity was further assessed, inhibition was observed in all TD-treated groups ((*)p < 0.05). Complex IV activity, however, was not adversely affected by TD. This electron transport chain inhibition also resulted in reduced ATP levels ((*)p < 0.05). Furthermore, hydrogen peroxide levels, but not other ROS, were increased ((*)p < 0.05). Taken together, these data indicate that commercially-available formulations of TD may exert neurotoxicity through Complex II (succinate dehydrogenase) inhibition, decreased ATP levels, and increased hydrogen peroxide production.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2018.12.019</a>
*hydrogen peroxide
*Reactive oxygen species
2019
Adenosine Triphosphate/metabolism
Animals
Bailey Denise C
Burchfield Shelbie L
C. elegans
Caenorhabditis elegans/*drug effects/metabolism
Denney Rachel D
Department of Pharmaceutical Sciences
Electron Transport Complex II/*antagonists & inhibitors/metabolism
Environmental toxicology and pharmacology
Fitsanakis Vanessa A
Glycine/*analogs & derivatives/toxicity
Glyphosate
Herbicides/*toxicity
Mitochondrial inhibition
Negga Rekek
NEOMED College of Pharmacy
Oxygen Consumption
Reactive Oxygen Species/metabolism
Todt Callie E
-
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/10.1208/s12249-019-1333-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1208/s12249-019-1333-z</a>
Pages
116–116
Issue
3
Volume
20
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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Delivery Systems as Vital Tools in Drug Repurposing.
Publisher
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AAPS PharmSciTech
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
combination drugs; drug delivery systems; drug development; nanocarriers; nanoparticles
Creator
An entity primarily responsible for making the resource
Czech Tori; Lalani Reza; Oyewumi Moses O
Description
An account of the resource
The process of developing an old drug for new indications is now a widely accepted strategy of shortening drug development time, reducing drug costs, and improving drug availability, especially for rare and neglected diseases. In this mini-review, we highlighted the impact of drug delivery systems in the fulfillment of crucial aspects of drug repurposing such as (i) maximizing the repurposed drug effects on a new target, (ii) minimizing off-target effects, (iii) modulating the release profiles of drug at the site of absorption, (iv) modulating the pharmacokinetics/in vivo biodistribution of the repurposed drug, (v) targeting/modulating drug retention at the sites of action, and (vi) providing a suitable platform for therapeutic application of combination drugs.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1208/s12249-019-1333-z" target="_blank" rel="noreferrer noopener">10.1208/s12249-019-1333-z</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).
2019
AAPS PharmSciTech
combination drugs
Czech Tori
Department of Pharmaceutical Sciences
Drug Delivery Systems
drug development
Lalani Reza
nanocarriers
Nanoparticles
NEOMED College of Pharmacy
Oyewumi Moses O
-
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/10.1208/s12249-019-1333-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1208/s12249-019-1333-z</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
116-116
Issue
3
Volume
20
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
A name given to the resource
Delivery Systems as Vital Tools in Drug Repurposing.
Publisher
An entity responsible for making the resource available
AAPS PharmSciTech
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Humans; Nanoparticles; *Drug Delivery Systems; Nanoparticles; Tissue Distribution; combination drugs; *Drug Delivery Systems; drug development; nanocarriers; *Drug Repositioning; Drug Carriers
Creator
An entity primarily responsible for making the resource
Czech Tori; Lalani Reza; Oyewumi Moses O
Description
An account of the resource
The process of developing an old drug for new indications is now a widely accepted strategy of shortening drug development time, reducing drug costs, and improving drug availability, especially for rare and neglected diseases. In this mini-review, we highlighted the impact of drug delivery systems in the fulfillment of crucial aspects of drug repurposing such as (i) maximizing the repurposed drug effects on a new target, (ii) minimizing off-target effects, (iii) modulating the release profiles of drug at the site of absorption, (iv) modulating the pharmacokinetics/in vivo biodistribution of the repurposed drug, (v) targeting/modulating drug retention at the sites of action, and (vi) providing a suitable platform for therapeutic application of combination drugs.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1208/s12249-019-1333-z" target="_blank" rel="noreferrer noopener">10.1208/s12249-019-1333-z</a>
*Drug Delivery Systems
*Drug Repositioning
2019
AAPS PharmSciTech
combination drugs
Czech Tori
Department of Pharmaceutical Sciences
Drug Carriers
drug development
Humans
Lalani Reza
nanocarriers
Nanoparticles
NEOMED College of Pharmacy
Oyewumi Moses O
Tissue Distribution
-
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/10.18632/aging.101828" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/aging.101828</a>
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
A name given to the resource
Shared mechanisms: osteoporosis and Alzheimer's disease?
Publisher
An entity responsible for making the resource available
Aging
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Alzheimer's disease; dementia; osteoporosis; serotonin; Wnt
Creator
An entity primarily responsible for making the resource
Dengler-Crish Christine M; Elefteriou Florent
Identifier
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<a href="http://doi.org/10.18632/aging.101828" target="_blank" rel="noreferrer noopener">10.18632/aging.101828</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).
2019
Aging
Alzheimer's disease
dementia
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Elefteriou Florent
NEOMED College of Pharmacy
Osteoporosis
serotonin
WNT
-
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/10.18632/aging.101828" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/aging.101828</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
1317-1318
Issue
5
Volume
11
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
A name given to the resource
Shared mechanisms: osteoporosis and Alzheimer's disease?
Publisher
An entity responsible for making the resource available
Aging
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Alzheimer's disease; dementia; osteoporosis; serotonin; Wnt
Creator
An entity primarily responsible for making the resource
Dengler-Crish Christine M; Elefteriou Florent
Identifier
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<a href="http://doi.org/10.18632/aging.101828" target="_blank" rel="noreferrer noopener">10.18632/aging.101828</a>
2019
Aging
Alzheimer's disease
dementia
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Elefteriou Florent
NEOMED College of Pharmacy
Osteoporosis
serotonin
WNT
-
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/10.1080/03008207.2019.1624734" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/03008207.2019.1624734</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
1-15
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
A name given to the resource
Mechanistic complexities of bone loss in Alzheimer's disease: a review
Publisher
An entity responsible for making the resource available
Connective Tissue Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Aging; Alzheimer’s; bone density; dementia; Osteoporosis
Creator
An entity primarily responsible for making the resource
Frame Gabrielle; Bretland Katie A; Dengler-Crish Christine M
Description
An account of the resource
Purpose/Aim: Alzheimer's disease (AD), the primary cause of dementia in the elderly, is one of the leading age-related neurodegenerative diseases worldwide. While AD is notorious for destroying memory and cognition, dementia patients also experience greater incidence of bone loss and skeletal fracture than age-matched neurotypical individuals, greatly impacting their quality of life. Despite the significance of this comorbidity, there is no solid understanding of the mechanisms driving early bone loss in AD. Here, we review studies that have evaluated many of the obvious risk factors shared by dementia and osteoporosis, and illuminate emerging work investigating covert pathophysiological mechanisms shared between the disorders that may have potential as new risk biomarkers or therapeutic targets in AD. Conclusions: Skeletal deficits emerge very early in clinical Alzheimer's progression, and cannot be explained by coincident factors such as aging, female sex, mobility status, falls, or genetics. While research in this area is still in its infancy, studies implicate several potential mechanisms in disrupting skeletal homeostasis that include direct effects of amyloid-beta pathology on bone cells, neurofibrillary tau-induced damage to neural centers regulating skeletal remodeling, and/or systemic Wnt/Beta-catenin signaling deficits. Data from an increasing number of studies substantiate a role for the newly discovered "exercise hormone" irisin and its protein precursor FNDC5 in bone loss and AD-associated neurodegeneration. We conclude that the current status of research on bone loss in AD is insufficient and merits critical attention because this work could uncover novel diagnostic and therapeutic opportunities desperately needed to address AD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/03008207.2019.1624734" target="_blank" rel="noreferrer noopener">10.1080/03008207.2019.1624734</a>
2019
Aging
Alzheimer’s
Bone Density
Bretland Katie A
Connective tissue research
dementia
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Frame Gabrielle
June 2019 Update
NEOMED College of Pharmacy
Osteoporosis
-
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/10.1080/03008207.2019.1624734" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/03008207.2019.1624734</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
1-15
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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
A name given to the resource
Mechanistic complexities of bone loss in Alzheimer's disease: a review.
Publisher
An entity responsible for making the resource available
Connective Tissue Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Aging; Alzheimer’s; bone density; dementia; osteoporosis
Creator
An entity primarily responsible for making the resource
Frame Gabrielle; Bretland Katie A; Dengler-Crish Christine M
Description
An account of the resource
Purpose/Aim: Alzheimer's disease (AD), the primary cause of dementia in the elderly, is one of the leading age-related neurodegenerative diseases worldwide. While AD is notorious for destroying memory and cognition, dementia patients also experience greater incidence of bone loss and skeletal fracture than age-matched neurotypical individuals, greatly impacting their quality of life. Despite the significance of this comorbidity, there is no solid understanding of the mechanisms driving early bone loss in AD. Here, we review studies that have evaluated many of the obvious risk factors shared by dementia and osteoporosis, and illuminate emerging work investigating covert pathophysiological mechanisms shared between the disorders that may have potential as new risk biomarkers or therapeutic targets in AD. Conclusions: Skeletal deficits emerge very early in clinical Alzheimer's progression, and cannot be explained by coincident factors such as aging, female sex, mobility status, falls, or genetics. While research in this area is still in its infancy, studies implicate several potential mechanisms in disrupting skeletal homeostasis that include direct effects of amyloid-beta pathology on bone cells, neurofibrillary tau-induced damage to neural centers regulating skeletal remodeling, and/or systemic Wnt/Beta-catenin signaling deficits. Data from an increasing number of studies substantiate a role for the newly discovered "exercise hormone" irisin and its protein precursor FNDC5 in bone loss and AD-associated neurodegeneration. We conclude that the current status of research on bone loss in AD is insufficient and merits critical attention because this work could uncover novel diagnostic and therapeutic opportunities desperately needed to address AD.;
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/03008207.2019.1624734" target="_blank" rel="noreferrer noopener">10.1080/03008207.2019.1624734</a>
2019
Aging
Alzheimer’s
Bone Density
Bretland Katie A
Connective tissue research
dementia
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Frame Gabrielle
NEOMED College of Pharmacy
Osteoporosis
September 2019 Update
-
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/10.1074/jbc.RA119.007743" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.RA119.007743</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).
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
A name given to the resource
Defining α-synuclein species responsible for Parkinson disease phenotypes in mice
Publisher
An entity responsible for making the resource available
The Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Subject
The topic of the resource
alpha-synuclein (a-synuclein); amyloid; cytotoxicity; fibril; Lewy Body; motor behavior defect; neurodegenerative disease; oligomer; Parkinson disease; protein aggregation
Creator
An entity primarily responsible for making the resource
Froula Jessica M; Castellana-Cruz Marta; Anabtawi Nadia M; Camino José D; Chen Serene W; Thrasher Drake R; Freire Jennifer; Yazdi Allen A; Fleming Sheila; Dobson Christopher M; Kumita Janet R; Cremades Nunilo; Volpicelli-Daley Laura A
Description
An account of the resource
Parkinson disease (PD) is a neurodegenerative disorder characterized by fibrillar neuronal inclusions composed of aggregated α-synuclein. These inclusions are associated with behavioral and pathological PD phenotypes. One strategy for therapeutic interventions is to prevent the formation of these inclusions in order to halt disease progression. α-Synuclein exists in multiple structural forms, including disordered, non-amyloid oligomers, ordered amyloid oligomers, and fibrils. It is critical to understand which conformers contribute to specific PD phenotypes. Here, we utilized a mouse model to explore the pathological effects of stable amyloid β-sheet oligomers compared with those of fibrillar α-synuclein. We biophysically characterized these species with transmission EM, atomic-force microscopy, CD spectroscopy, FTIR spectroscopy, analytical ultracentrifugation, and thioflavin T assays. We then injected these different α-synuclein forms into the mouse striatum to determine their ability to induce PD-related phenotypes. We found that β-sheet oligomers produce a small but significant loss of dopamine neurons in the substantia nigra pars compacta (SNc). Injection of small β-sheet fibril fragments, however, produced the most robust phenotypes, including reduction of striatal dopamine terminals, SNc loss of dopamine neurons, and motor behavior defects. We conclude that although the β-sheet oligomers cause some toxicity, the potent effects of the short fibrillar fragments can be attributed to their ability to recruit monomeric α-synuclein and spread in vivo and hence contribute to the development of PD-like phenotypes. These results suggest that strategies to reduce the formation and propagation of β-sheet fibrillar species could be an important route for therapeutic intervention in PD and related disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.RA119.007743" target="_blank" rel="noreferrer noopener">10.1074/jbc.RA119.007743</a>
2019
alpha-synuclein (a-synuclein)
amyloid
Anabtawi Nadia M
Camino José D
Castellana-Cruz Marta
Chen Serene W
Cremades Nunilo
cytotoxicity
Department of Pharmaceutical Sciences
Dobson Christopher M
fibril
Fleming Sheila
Freire Jennifer
Froula Jessica M
June 2019 Update
Kumita Janet R
Lewy Body
motor behavior defect
NEOMED College of Pharmacy
neurodegenerative disease
oligomer
Parkinson Disease
Protein Aggregation
The Journal of biological chemistry
Thrasher Drake R
Volpicelli-Daley Laura A
Yazdi Allen A
-
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/10.1074/jbc.ra119.007743" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.ra119.007743</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
10392-10406
Issue
27
Volume
294
Search for Full-text
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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
A name given to the resource
Defining α-synuclein species responsible for Parkinson's disease phenotypes in mice.
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-07
Subject
The topic of the resource
DOPAMINERGIC neurons; FOURIER transform infrared spectroscopy; MOUSE diseases; PARKINSON'S disease; SPECIES; SUBSTANTIA nigra
Creator
An entity primarily responsible for making the resource
Froula Jessica M; Castellana-Cruz Marta; Anabtawi Nadia M; Camino José D; Chen Serene W; Thrasher Drake R; Freire Jennifer; Yazdi Allen A; Fleming Sheila; Dobson Christopher M; Kumita Janet R; Cremades Nunilo; Volpicelli-Daley Laura A
Description
An account of the resource
Parkinson's disease (PD) is a neurodegenerative disorder characterized by fibrillar neuronal inclusions composed of aggregatedβ-synuclein (β-syn). These inclusions are associated with behavioral and pathological PD phenotypes. One strategy for therapeutic interventions is to prevent the formation of these inclusions to halt disease progression. β-Synuclein exists in multiple structural forms, including disordered, nonamyloid oligomers, ordered amyloid oligomers, and fibrils. It is critical to understand which conformers contribute to specific PD phenotypes. Here, we utilized a mouse model to explore the pathological effects of stable α-amyloid-sheet oligomers compared with those of fibrillar β-synuclein. We biophysically characterized these species with transmission EM, atomic-force microscopy, CD spectroscopy, FTIR spectroscopy, analytical ultracentrifugation, and thioflavin T assays. We then injected these different β-synuclein forms into the mouse striatum to determine their ability to induce PD-related phenotypes. We found thatα-sheet oligomers produce a small but significant loss of dopamine neurons in the substantia nigra pars compacta (SNc). Injection of small α-sheet fibril fragments, however, produced the most robust phenotypes, including reduction of striatal dopamine terminals, SNc loss of dopamine neurons, and motor-behavior defects. We conclude that although theα-sheet oligomers cause some toxicity, the potent effects of the short fibrillar fragments can be attributed to their ability to recruit monomeric β-synuclein and spread in vivo and hence contribute to the development of PD-like phenotypes. These results suggest that strategies to reduce the formation and propagation ofα-sheet fibrillar species could be an important route for therapeutic intervention in PD and related disorders. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.ra119.007743" target="_blank" rel="noreferrer noopener">10.1074/jbc.ra119.007743</a>
2019
Anabtawi Nadia M
Camino José D
Castellana-Cruz Marta
Chen Serene W
Cremades Nunilo
Department of Pharmaceutical Sciences
Dobson Christopher M
DOPAMINERGIC neurons
Fleming Sheila
FOURIER transform infrared spectroscopy
Freire Jennifer
Froula Jessica M
Journal of Biological Chemistry
Kumita Janet R
MOUSE diseases
NEOMED College of Pharmacy
Parkinson's disease
September 2019 Update
SPECIES
SUBSTANTIA nigra
Thrasher Drake R
Volpicelli-Daley Laura A
Yazdi Allen A
-
Text
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<a href="http://doi.org/10.1093/toxsci/kfz090" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfz090</a>
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Title
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Society of Toxicology Develops Learning Framework for Undergraduate Toxicology Courses Following the Vision and Change Core Concepts Model.
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Toxicological sciences : an official journal of the Society of Toxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-04
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Gray Joshua P; Curran Christine P; Fitsanakis Vanessa A; Ray Sidhartha; Stine Karen E; Eidemiller Betty J
Description
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The Society of Toxicology announces the development of a Learning Framework (https://www.toxicology.org/education/docs/SOT-Toxicology-Learning-Objectives.pdf ) for undergraduate toxicology that will facilitate the development and sharing of evidence-based teaching materials for undergraduate toxicology educators throughout the world. This Learning Framework was modeled on the "Vision and Change Report" (www.visionandchange.org), an effort of the National Science Foundation and American Association for the Advancement of Science defining Core Concepts and Core Competencies to inform undergraduate biology course design. Vision and Change (V&C) has gained national acceptance, becoming a foundation for 14 upper-level courses designed by professional life science scientific societies. The undergraduate toxicology Learning Framework includes five Core Concepts aligned with V&C that encompass the discipline of toxicology: Evolution; Biological Information, Risk and Risk; Management; Systems Toxicology; and Pathways and Transformations for Energy and Matter. Underpinning the Core Concepts are Level Two Toxicology Concepts, which are broad disciplinary categories, Level Three Learning Objectives, which address specific learning goals, and Level Four Example Learning Objectives and Case Studies, which provide examples of how content might be taught. Syllabi from more than 20 undergraduate toxicology courses and several undergraduate toxicology textbooks were surveyed to determine toxicology-related Learning Objectives. From these, undergraduate educators can design courses tailored to their institutional needs by selecting a subset of Learning Objectives. Publication of a Learning Framework for toxicology will enable integration into other disciplines and facilitate the development and sharing of evidenced-based teaching materials for toxicology to educators in allied disciplines. Ultimately this will expand toxicology's impact to a broader audience.
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<a href="http://doi.org/10.1093/toxsci/kfz090" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfz090</a>
2019
Curran Christine P
Department of Pharmaceutical Sciences
Eidemiller Betty J
Fitsanakis Vanessa A
Gray Joshua P
NEOMED College of Pharmacy
Ray Sidhartha
Stine Karen E
Toxicological sciences : an official journal of the Society of Toxicology
-
Text
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URL Address
<a href="http://doi.org/10.2174/1389200220666191003161114" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1389200220666191003161114</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).
ISSN
1875-5453
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Recognition Sites for Cancer-Targeting Durg Delivery Systems
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Current Drug Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10-03
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Nanoparticles; tumor; ligand; Recognition sites; targeted drug delivery system
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Guan Siyu; Zhang Qianqian; Bao Jianwei; Hu Rongfeng; Czech Tori; Tang Jihui
Description
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BACKGROUND: Target-homing drug delivery systems are now gaining significant traction for use as novel therapeutic approaches in antitumor targeting for cancer therapy. Numerous targeted drug delivery systems have been designed to improve the targeting effects because these systems can display a range of favorable properties. Thus, providing suitable characteristics for clinical applicability of anticancer drugs, such as increasing the solubility, and improving the drug distribution at target sites. The majority of these targeting systems are designed with respect to differences between cancerous and normal tissues, for instance, the low pH of tumor tissues or overexpressed receptors on tumor cell membranes. Because of the growing number of targeting possibilities, it is important to know the tumor-specific recognition strategies for designing novel, targeted, drug delivery systems. Herein, we will identify and summarize literature pertaining to various recognition sites for optimizing the design of targeted drug delivery systems to augment current chemotherapeutic approaches. OBJECTIVE: This review focuses on identification of the recognition sites for developing targeted drug delivery systems for use in cancer therapeutics. METHOD: We have reviewed and compiled cancer-specific recognition sites and their abnormal characteristics within tumor tissues (low pH, high glutathione, targetable receptors, etc.), tumor cells (receptor overexpression or tumor cell membrane changes) and tumor cell organelles (nuclear and endoplasmic reticular dysregulation) utilizing existing scientific literature. Moreover, we have highlighted the design of some targeted drug delivery systems that can be used as homing tools for these recognition sites. RESULTS AND CONCLUSION: Targeted drug delivery systems are a promising therapeutic approach for tumor chemotherapy. Additional research focused on finding novel recognition sites, and subsequent development of targeting moieties for use with drug delivery systems will aid in the evaluation and clinical application of new and improved chemotherapeutics.
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<a href="http://doi.org/10.2174/1389200220666191003161114" target="_blank" rel="noreferrer noopener">10.2174/1389200220666191003161114</a>
PMID: 31580248
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Anhui Medical University
Bao Jianwei
Current Drug Metabolism
Czech Tori
Department of Pharmaceutical Sciences
Guan Siyu
Hu Rongfeng
Journal Article
ligand
Nanoparticles
NEOMED College of Pharmacy
NEOMED College of Pharmacy Student
November 2019 Update
Recognition sites
Tang Jihui
targeted drug delivery system
Tumor
Zhang Qianqian
-
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/10.1080/02713683.2018.1516783" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/02713683.2018.1516783</a>
Pages
34–45
Issue
1
Volume
44
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Alpha 2-Adrenergic Receptor Agonist Brimonidine Stimulates ERK1/2 and AKT Signaling via Transactivation of EGF Receptors in the Human MIO-M1 Muller Cell Line.
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Current eye research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01
Subject
The topic of the resource
adrenergic receptors; AKT pathway; and Src-kinase; brimonidine; EGF receptor; ERK1/2; matrix metalloproteinases; Muller cell
Creator
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Harun-Or-Rashid Mohammad; Hallbook Finn
Description
An account of the resource
PURPOSE: Alpha 2-adrenergic receptor (alpha2-ADR) agonists are used clinically for a range of indications including reducing elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Animal experiments show that alpha2-ADR agonists attenuate the injury-induced Muller cell dedifferentiation by a mechanism that involves activation and regulation of extracellular signal-regulated kinase (ERK) 1/2 leading to transactivation of epidermal growth factor receptors (EGFRs). The purpose of this study was to study and corroborate the activation of this system in human cells. MATERIAL AND METHODS: The human Muller cell line MIO-M1 was treated with the alpha2A-ADR agonist brimonidine in combination with inhibitors for Src-kinase, EGFR-kinase, matrix metalloproteinase (MMP) as well as small interfering RNAs (siRNAs) for the EGFR. The cells were analyzed using immunocytochemistry, quantitative PCR and western blot techniques. RESULTS: Our results show that human MIO-M1 cells express alpha2A-ADRs and that stimulation of these receptors caused a robust increase of ERK1/2 and protein kinase B (PKB/AKT) (Thr-308) phosphorylation in
Identifier
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<a href="http://doi.org/10.1080/02713683.2018.1516783" target="_blank" rel="noreferrer noopener">10.1080/02713683.2018.1516783</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).
2019
adrenergic receptors
AKT pathway
and Src-kinase
brimonidine
Current eye research
Department of Pharmaceutical Sciences
EGF receptor
ERK1/2
Hallbook Finn
Harun-Or-Rashid Mohammad
matrix metalloproteinases
Muller cell
NEOMED College of Pharmacy
-
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/kfy238" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfy238</a>
Pages
249–257
Issue
1
Volume
167
Dublin Core
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Title
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Regional Susceptibility to ER Stress and Protection by Salubrinal Following a Single Exposure to Deltamethrin.
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Toxicological sciences : an official journal of the Society of Toxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01
Creator
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Hossain Muhammad M; Sivaram Ganeshraj; Richardson Jason R
Description
An account of the resource
Endoplasmic reticulum (ER) stress is a significant contributor to neurodegeneration and cognitive dysfunction. Recently, we reported that repeated exposure to the pyrethroid insecticide deltamethrin caused ER stress in the hippocampus of adult mice, which was accompanied by deficits in learning (Hossain et al., 2015). Here, we investigated regional susceptibility to ER stress and the ability of salubrinal, an inhibitor of ER stress, to reduce apoptosis following a single oral administration of deltamethrin (6 mg/kg). Deltamethrin significantly increased the ER stress marker C/EBP-homologous protein (CHOP) in the hippocampus by 148% at 24 and 48 h compared with age-matched controls. In contrast, CHOP was increased by 146% in the frontal cortex only at 48 h after deltamethrin exposure. Similarly, the level of GRP-78 was increased by 314% and 262% in the hippocampus at 24 and 48 h, whereas the same factors were increased by 178% at 24 h and 139% at 48 h in the frontal cortex. These changes were accompanied by increased levels of activated caspase-12, caspase-3, and TUNEL-positive cells in both brain regions, with the hippocampus showing a more robust response. Pre-treatment of mice with the eIf2alpha inhibitor salubrinal prevented deltamethrin-induced caspase-3 activation and attenuated the number of TUNEL-positive cells. These data demonstrate that the hippocampus appears to be particularly vulnerable to deltamethrin exposure in adult animals, which may contribute to observed effects of deltamethrin on cognitive function.
Identifier
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<a href="http://doi.org/10.1093/toxsci/kfy238" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfy238</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).
2019
Department of Pharmaceutical Sciences
Hossain Muhammad M
NEOMED College of Pharmacy
Richardson Jason R
Sivaram Ganeshraj
Toxicological sciences : an official journal of the Society of Toxicology
-
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/10.1021/acs.analchem.9b02757" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/acs.analchem.9b02757</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).
Pages
14340-14351
Issue
22
Volume
91
ISSN
1520-6882
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Title
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Calculation of the Protein Turnover Rate Using the Number of Incorporated 2H Atoms and Proteomics Analysis of a Single Labeled Sample
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Analytical Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-11-19
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Ilchenko Serguei; Haddad Andrew; Sadana Prabodh; Recchia Fabio A; Sadygov Rovshan G; Kasumov Takhar
Description
An account of the resource
Rate constant estimation with heavy water requires a long-term experiment with data collection at multiple time points (3-4 weeks for mitochondrial proteome dynamics in mice and much longer in other species). When tissue proteins are analyzed, this approach requires euthanizing animals at each time point or multiple tissue biopsies in humans. Although short-term protocols are available, they require knowledge of the maximum number of isotope labels (N) and accurate quantification of observed 2H-enrichment in the peptide. The high-resolution accurate mass spectrometers used for proteome dynamics studies are characterized by a systematic spectral error that compromises these measurements. To circumvent these issues, we developed a simple algorithm for the rate constant calculation based on a single labeled sample and comparable unlabeled (time 0) sample. The algorithm determines N for all proteogenic amino acids from a long-term experiment to calculate the predicted plateau 2H-labeling of peptides for a short-term protocol and estimates the rate constant based on the measured baseline and the predicted plateau 2H-labeling of peptides. The method was validated based on the rate constant estimation in a long-term experiment in mice and dogs. The improved 2 time-point method enables the rate constant calculation with less than 10% relative error compared to the bench-marked multi-point method in mice and dogs and allows us to detect diet-induced subtle changes in ApoAI turnover in mice. In conclusion, we have developed and validated a new algorithm for protein rate constant calculation based on 2-time point measurements that could also be applied to other biomolecules.
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<a href="http://doi.org/10.1021/acs.analchem.9b02757" target="_blank" rel="noreferrer noopener">10.1021/acs.analchem.9b02757</a>
PMID: 31638786
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Analytical Chemistry
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Haddad Andrew
Ilchenko Serguei
Journal Article
Kasumov Takhar
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
November 2019 Update
Recchia Fabio A
Sadana Prabodh
Sadygov Rovshan G
-
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/10.1167/iovs.18-24977" target="_blank" rel="noreferrer noopener">http://doi.org/10.1167/iovs.18-24977</a>
Pages
1–15
Issue
1
Volume
60
Dublin Core
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Title
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Evidence of Hypoxic Glial Cells in a Model of Ocular Hypertension.
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Investigative ophthalmology & visual science
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01
Creator
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Jassim Assraa H; Inman Denise M
Description
An account of the resource
Purpose: Reoxygenation after hypoxia can increase reactive oxygen species and upregulate autophagy. We determined, for the first time, the impact of elevated IOP on hypoxia induction, superoxide accumulation, and autophagy in a bead model of glaucoma. Method: Ocular hypertension was achieved with magnetic bead injection into the anterior chamber. Before mice were killed, they were injected with pimonidazole for hypoxia detection and dihydroethidium (DHE) for superoxide detection. Total retinal ganglion cells (RGCs) and optic nerve (ON) axons were quantified, total glutathione (GSH) was measured, and retinal and ON protein and mRNA were analyzed for hypoxia (Hif-1alpha and Hif-2alpha), autophagy (LC3 and p62), and SOD2. Results: With IOP elevation (P \textless 0.0001), the retina showed significantly (P \textless 0.001) decreased GSH compared with control, and a significant decrease (P \textless 0.01) in RGC density compared with control. Pimonidazole-positive Muller glia, microglia, astrocytes, and RGCs were present in the retinas after 4 weeks of ocular hypertension but absent in both the control and after only 2 weeks of ocular hypertension. The ON showed significant axon degeneration (P \textless 0.0001). The mean intensity of DHE in the ganglion cell layer and ON significantly increased (P \textless 0.0001). The ratio of LC3-II to LC3-I revealed a significant increase (P \textless 0.05) in autophagic activity in hypertensive retinas compared with control. Conclusions: We report a novel observation of hypoxia and a significant decrease in GSH, likely contributing to superoxide accumulation, in the retinas of ocular hypertensive mice. The significant increase in the ratio of
Identifier
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<a href="http://doi.org/10.1167/iovs.18-24977" target="_blank" rel="noreferrer noopener">10.1167/iovs.18-24977</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).
2019
Department of Pharmaceutical Sciences
Inman Denise M
Investigative ophthalmology & visual science
Jassim Assraa H
NEOMED College of Pharmacy
-
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/10.1007/s12035-019-1576-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s12035-019-1576-4</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).
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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
A name given to the resource
Higher Reliance on Glycolysis Limits Glycolytic Responsiveness in Degenerating Glaucomatous Optic Nerve.
Publisher
An entity responsible for making the resource available
Molecular neurobiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-04
Subject
The topic of the resource
Glaucoma; Mitochondria; DBA/2J; Fluorocitrate; Optic nerve; Seahorse analyzer
Creator
An entity primarily responsible for making the resource
Jassim Assraa Hassan; Coughlin Lucy; Harun-Or-Rashid Mohammad; Kang Patrick T; Chen Yeong-Renn; Inman Denise M
Description
An account of the resource
Metabolic dysfunction accompanies neurodegenerative disease and aging. An important step for therapeutic development is a more sophisticated understanding of the source of metabolic dysfunction, as well as to distinguish disease-associated changes from aging effects. We examined mitochondrial function in ex vivo aging and glaucomatous optic nerve using a novel approach, the Seahorse Analyzer. Optic nerves (ON) from the DBA/2J mouse model of glaucoma and the DBA/2-Gpnmb(+) control strain were isolated, and oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), the discharge of protons from lactate release or byproducts of substrate oxidation, were measured. The glial-specific aconitase inhibitor fluorocitrate was used to limit the contribution of glial mitochondria to OCR and ECAR. We observed significant decreases in maximal respiration, ATP production, and spare capacity with aging. In the presence of fluorocitrate, OCR was higher, with more ATP produced, in glaucoma compared to aged ON. However, glaucoma ON showed lower maximal respiration. In the presence of fluorocitrate and challenged with ATPase inhibition, glaucoma ON was incapable of further upregulation of glycolysis to compensate for the loss of oxidative phosphorylation. Inclusion of 2-deoxyglucose as a substrate during ATPase inhibition indicated a significantly higher proportion of ECAR was derived from TCA cycle substrate oxidation than glycolysis in glaucoma ON. These data indicate that glaucoma axons have limited ability to respond to increased energy demand given their lower maximal respiration and inability to upregulate glycolysis when challenged. The higher ATP output from axonal mitochondria in glaucoma optic nerve compensates for this lack of resiliency but is ultimately inadequate for continued function.
Identifier
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<a href="http://doi.org/10.1007/s12035-019-1576-4" target="_blank" rel="noreferrer noopener">10.1007/s12035-019-1576-4</a>
2019
Chen Yeong-Renn
Coughlin Lucy
DBA/2J
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Fluorocitrate
Glaucoma
Harun-Or-Rashid Mohammad
Inman Denise M
Jassim Assraa Hassan
Kang Patrick T
Mitochondria
Molecular neurobiology
NEOMED College of Medicine
NEOMED College of Pharmacy
optic nerve
Seahorse analyzer
-
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="https://iovs.arvojournals.org/article.aspx?articleid=2741311" target="_blank" rel="noreferrer noopener">https://iovs.arvojournals.org/article.aspx?articleid=2741311</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).
Issue
9
Volume
60
ISSN
0146-0404
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Title
A name given to the resource
Pre-degenerative Accumulation of Superoxide and Hydroxide in a Chronic Mouse Model of Glaucoma
Publisher
An entity responsible for making the resource available
Investigative Ophthalmology & Visual Science
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-07
Creator
An entity primarily responsible for making the resource
Jassim Assraa Hassan; Inman Denise M
Identifier
An unambiguous reference to the resource within a given context
<a href="https://iovs.arvojournals.org/article.aspx?articleid=2741311" target="_blank" rel="noreferrer noopener">https://iovs.arvojournals.org/article.aspx?articleid=2741311</a>
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The file format, physical medium, or dimensions of the resource
Journal Article
2019
Department of Pharmaceutical Sciences
Inman Denise M
Investigative ophthalmology & visual science
Jassim Assraa Hassan
Journal Article
NEOMED College of Graduate Studies
NEOMED College of Graduate Studies Student
NEOMED College of Pharmacy
November 2019 Update
-
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/10.1002/osp4.309" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/osp4.309</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).
Pages
36-45
Issue
1
Volume
5
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
A name given to the resource
A systematic review: the appraisal of the effects of metformin on lipoprotein modification and function.
Publisher
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Obesity science & practice
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Lipoproteins; Type II diabetes; Gycation; Metformin
Creator
An entity primarily responsible for making the resource
Kheniser K G; Kashyap S R; Kasumov T
Description
An account of the resource
Aims: Metformin is a commonly prescribed anti-hyperglycaemic pharmacological agent, and it remains a staple in the management of type II diabetes. In addition to metformin's glucose lowering effects, research has indicated that metformin inhibits glycation-mediated and oxidative modification of lipoprotein residues. The purpose was to discuss the effects of metformin as it relates to high-density lipoprotein (HDL) and low-density lipoprotein (LDL) modification. Materials and methods: The purpose was to conduct a narrative and pragmatic review on the effects of metformin as it pertains to HDL and LDL modification. Results: High-density lipoprotein (HDL) concentration is a quantitative measure and therefore does not provide insight into its function, which is a qualitative property. Dysfunctional HDLs are unable to carry out functions normally associated with HDL because they can be modified by glycating agents. Metformin may counteract HDL dysfunction by abating HDL modification. Reductions in HDL modification may improve reverse cholesterol transport ability and thus possibly diminish cardiovascular risk. Similarly, metformin-mediated attenuations in LDL modification may reduce their atherogenic potency. Conclusion: Metformin may partially ameliorate HDL dysfunction and reduce LDL modification by inhibiting alpha-dicarbonyl-mediated modification of apolipoprotein residues; consequently, the results are salient because cardiovascular disease incidence may be reduced given that reverse cholesterol transport activity predicts risk, and modified LDL are proatherogenic.
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<a href="http://doi.org/10.1002/osp4.309" target="_blank" rel="noreferrer noopener">10.1002/osp4.309</a>
2019
Department of Pharmaceutical Sciences
Gycation
Kashyap S R
Kasumov T
Kheniser K G
Lipoproteins
metformin
NEOMED College of Pharmacy
Obesity science & practice
Type II diabetes
-
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/10.1002/osp4.309" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/osp4.309</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).
Pages
36-45
Issue
1
Volume
5
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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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A Systematic Review: The Appraisal Of The Effects Of Metformin On Lipoprotein Modification And Function
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Obesity Science & Practice
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
a-i; cardiovascular-disease; cholesterol; Endocrinology & Metabolism; expression; glycation end-products; Gycation; high-density-lipoprotein; increases; Lipoproteins; metformin; methylglyoxal; oxidative stress; Type II diabetes; type-2
Creator
An entity primarily responsible for making the resource
Kheniser K G; Kashyap S R; Kasumov T
Description
An account of the resource
Aims Metformin is a commonly prescribed anti-hyperglycaemic pharmacological agent, and it remains a staple in the management of type II diabetes. In addition to metformin's glucose lowering effects, research has indicated that metformin inhibits glycation-mediated and oxidative modification of lipoprotein residues. The purpose was to discuss the effects of metformin as it relates to high-density lipoprotein (HDL) and low-density lipoprotein (LDL) modification. Materials and methods The purpose was to conduct a narrative and pragmatic review on the effects of metformin as it pertains to HDL and LDL modification. Results High-density lipoprotein (HDL) concentration is a quantitative measure and therefore does not provide insight into its function, which is a qualitative property. Dysfunctional HDLs are unable to carry out functions normally associated with HDL because they can be modified by glycating agents. Metformin may counteract HDL dysfunction by abating HDL modification. Reductions in HDL modification may improve reverse cholesterol transport ability and thus possibly diminish cardiovascular risk. Similarly, metformin-mediated attenuations in LDL modification may reduce their atherogenic potency. Conclusion Metformin may partially ameliorate HDL dysfunction and reduce LDL modification by inhibiting alpha-dicarbonyl-mediated modification of apolipoprotein residues; consequently, the results are salient because cardiovascular disease incidence may be reduced given that reverse cholesterol transport activity predicts risk, and modified LDL are proatherogenic.
Identifier
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<a href="http://doi.org/10.1002/osp4.309" target="_blank" rel="noreferrer noopener">10.1002/osp4.309</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2019
a-i
cardiovascular-disease
Cholesterol
Department of Pharmaceutical Sciences
Endocrinology & Metabolism
expression
glycation end-products
Gycation
high-density-lipoprotein
increases
Journal Article or Conference Abstract Publication
Kashyap S R
Kasumov T
Kheniser K G
Lipoproteins
metformin
methylglyoxal
NEOMED College of Pharmacy
Obesity science & practice
Oxidative Stress
Type II diabetes
type-2
-
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/10.1111/jphp.13138" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/jphp.13138</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
1421-1428
Issue
9
Volume
71
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Title
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AMPK‐SIRT1‐independent inhibition of ANGPTL3 gene expression is a potential lipid‐lowering mechanism of metformin.
Publisher
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Journal of Pharmacy & Pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
angiopoietin‐like 3; diabetes; dyslipidaemia; lipoprotein lipase; metformin
Creator
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Lin Li; Burke Jamie; Venkatesh Sahana; Sadana Prabodh
Description
An account of the resource
Objectives: Hypertriglyceridaemia enhances cardiovascular disease risk in patients with diabetes. Lipoprotein lipase (LPL) regulates plasma triglyceride levels by hydrolysing chylomicrons and very‐low‐density lipoprotein (VLDL). Metformin, an antidiabetic drug, improves plasma lipids including triglycerides. We examined metformin's regulation of angiopoietin‐like 3 (ANGPTL3), a liver‐derived secretory protein with LPL inhibitory property. Methods: Using HepG2 cells, a human hepatocyte cell line, the effects of metformin on ANGPTL3 gene and protein expression were determined. The role of AMPK‐SIRT1 pathway in metformin regulation of ANGPTL3 was determined using pharmacological, RNAi and reporter assays. Metformin regulation of ANGPTL3 expression was also examined in sodium palmitate‐induced insulin resistance. Key findings: Metformin and pharmacological activators of AMPK and SIRT1 inhibited the expression of ANGPTL3 in HepG2 cells. Pharmacological or RNAi‐based antagonism of AMPK or SIRT1 failed to affect metformin inhibition of ANGPTL3. AMPK‐SIRT1 activators and metformin exhibited distinct effects on the expression of ANGPTL3 gene luciferase reporter. Sodium palmitate‐induced insulin resistance in cells resulted in increased ANGPTL3 gene expression which was suppressed by pretreatment with metformin. Conclusions: Metformin inhibits ANGPTL3 expression in the liver in an AMPK‐SIRT1‐independent manner as a potential mechanism to regulate LPL and lower plasma lipids. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1111/jphp.13138" target="_blank" rel="noreferrer noopener">10.1111/jphp.13138</a>
2019
angiopoietin‐like 3
Burke Jamie
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Diabetes
dyslipidaemia
Journal of Pharmacy & Pharmacology
Lin Li
Lipoprotein lipase
metformin
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Sadana Prabodh
September 2019 Update
Venkatesh Sahana
-
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/10.1016/j.nano.2019.102107" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nano.2019.102107</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
102107
Volume
23
ISSN
1549-9642
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.nano.2019.102107" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.nano.2019.102107</a>
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Title
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Nose-to-brain co-delivery of repurposed simvastatin and BDNF synergistically attenuates LPS-induced neuroinflammation
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Nanomedicine: Nanotechnology, Biology, And Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10-23
Subject
The topic of the resource
Microglia; Nanoparticles; Drug repurposing; Polymersomes; Intranasal delivery
Creator
An entity primarily responsible for making the resource
Manickavasagam Dharani; Lin Li; Oyewumi Moses O
Description
An account of the resource
A therapeutic strategy that can combat the multifaceted nature of neuroinflammation pathology was investigated. Thus, we fabricated PEG-PdLLA polymersomes and evaluated the efficacy in co-delivery of simvastatin (Sim, as a repurposed anti-inflammatory agent) with brain derived neurotrophic factor (BDNF, as an exogeneous trophic factor supplementation). Using LPS model of neuroinflammation, intranasal administration of combination drug-loaded polymersomes (containing both Sim and BDNF; Sim-BDNF-Ps) markedly down-regulated brain levels of cytokines compared to free drug and single-drug-loaded polymersomes. Further, Sim-BDNF-Ps effectively replenished brain level of BDNF that was depleted following neuroinflammation, resulting in a 2-fold BDNF increase versus untreated LPS control group. We found out that the efficiency of the combination drug-loaded polymersomes to suppress microglia activation in brain regions followed the order: frontal cortex > striatum > hippocampus. Our findings indicated that Sim-BDNF-Ps could effectively inhibit microglial-mediated inflammation as well as potentially resolve the neurotoxic microenvironment that is often associated with neuroinflammation.
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<a href="http://doi.org/10.1016/j.nano.2019.102107" target="_blank" rel="noreferrer noopener">10.1016/j.nano.2019.102107</a>
PMID: 31655202
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
And Medicine
Biology
Department of Pharmaceutical Sciences
Drug repurposing
Intranasal delivery
Journal Article
Lin Li
Manickavasagam Dharani
Microglia
Nanomedicine: Nanotechnology
Nanomedicine: Nanotechnology, Biology, And Medicine
Nanoparticles
NEOMED College of Pharmacy
NEOMED College of Pharmacy Student
NEOMED Student Publications
November 2019 Update
Oyewumi Moses O
polymersomes
-
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/10.1016/j.ijpharm.2019.118690" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijpharm.2019.118690</a>
Pages
118690-118690
Volume
570
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Title
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Internalization of particulate delivery systems by activated microglia influenced the therapeutic efficacy of simvastatin repurposing for neuroinflammation
Publisher
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International Journal of Pharmaceutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
Brain; Drug delivery; Drug repurposing; PEG-PdLLA; Polymersomes
October 2019 Update
Creator
An entity primarily responsible for making the resource
Manickavasagam Dharani; Oyewumi Moses O
Description
An account of the resource
We recently evaluated the suitability of polymersome delivery systems in simvastatin repurposing for treating neuroinflammation. The goal of the current study is to elucidate the therapeutic impact of particulate internalization by activated microglia on the resultant anti-inflammatory properties. Thus, we investigated the endocytic mechanism(s) involved in uptake and transport of simvastatin-loaded polymersomes by BV2 microglia cells coupled with delineation of the intracellular pathway(s) involved in regulating anti-inflammatory effects. Our data indicated that internalization of polymersome delivery systems by activated microglial BV2 cells was important in the suppression of nitric oxide (NO), TNF-α and IL-6 production. Further, we observed that the lipid raft/caveolae pathway had the most influential effect on polymersome internalization by microglia cells while clathrin-mediated endocytosis did not play a major role. Enhancement of anti-inflammatory effects of simvastatin could be attributed to inhibition of ERK1/2, JNK and AKT signaling pathways and internalization of polymersome delivery systems in activated microglia. Taken together, our data provided insights into how the intracellular trafficking of delivery systems by microglial could be a useful tool in modulating the desired anti-inflammatory effects of drugs.
Identifier
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<a href="http://doi.org/10.1016/j.ijpharm.2019.118690" target="_blank" rel="noreferrer noopener">10.1016/j.ijpharm.2019.118690</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).
2019
Brain
Department of Pharmaceutical Sciences
Drug delivery
Drug repurposing
International Journal of Pharmaceutics
Manickavasagam Dharani
NEOMED College of Pharmacy
October 2019 Update
Oyewumi Moses O
PEG-PdLLA
polymersomes
-
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/10.1152/ajpendo.00193.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpendo.00193.2019</a>
Search for Full-text
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Title
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HDL Flux is Higher in Patients with Nonalcoholic Fatty Liver Disease
Publisher
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American Journal of Physiology. Endocrinology and Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
haevy water; HDL; NAFLD; NASH; proteomics
October 2019 Update
Creator
An entity primarily responsible for making the resource
McCullough Arthur; Previs Stephen F; Dasarathy Jaividhya; Lee Kwangwon; Osme Abdullah; Kim Chunki; Ilchenko Serguei; Lorkowski Shuhui W; Smith Jonathan D; Dasarathy Srinivasan; Kasumov Takhar
Description
An account of the resource
Altered lipid metabolism and inflammation are involved in the pathogenesis of both non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). Even though high-density lipoprotein (HDL), a CVD protective marker, is decreased, whether HDL metabolism and function are perturbed in NAFLD are currently unknown. We examined the effect of NAFLD and disease severity on HDL metabolism and function in patients with biopsy-proven simple steatosis (SS), nonalcoholic steatohepatitis (NASH), and healthy controls. HDL turnover and HDL proteins dynamics in SS (n=7), NASH patients (n=8), and healthy controls (n=9) were studied in vivo. HDL maturation and remodeling, anti-oxidant, cholesterol efflux properties, and activities of lecithin cholesterol ester acyl transferase (LCAT) and cholesterol ester transfer protein (CETP) were quantified using in vitro assays. All NAFLD patients had increased turnover of both HDL cholesterol (HDLc, 0.16±0.09 vs. 0.34±0.18 day-1, P<0.05) and ApoAI (0.26±0.04 vs. 0.34±0.06 day-1, P<0.005) compared to healthy controls. The fractional catabolic rates (FCR) of other HDL proteins, including ApoAII (and ApoAIV were higher (P<0.05) in NAFLD patients who also had higher CETP activity, ApoAI/HDLc ratio (P<0.05). NAFLD-induced alterations were associated with lower antioxidant (114.2±46.6 vs 220.5±48.2 nml/ml●min) but higher total efflux properties of HDL (23.4±1.3 vs. 25.5±2.3 %) (both P<0.05) which was more pronounced in individuals with NASH. However, no differences were observed in either HDL turnover, antioxidant and cholesterol efflux functions of HDL or HDL proteins' turnover between SS and NASH subjects. Thus, HDL metabolism and function are altered in NAFLD without any significant differences between SS and NASH.
Identifier
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<a href="http://doi.org/10.1152/ajpendo.00193.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpendo.00193.2019</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).
2019
American journal of physiology. Endocrinology and metabolism
Dasarathy Jaividhya
Dasarathy Srinivasan
Department of Pharmaceutical Sciences
haevy water
HDL
Ilchenko Serguei
Kasumov Takhar
Kim Chunki
Lee Kwangwon
Lorkowski Shuhui W
McCullough Arthur
NAFLD
NASH
NEOMED College of Pharmacy
October 2019 Update
Osme Abdullah
Previs Stephen F
proteomics
Smith Jonathan D
-
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/10.1016/j.bbr.2019.112456" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbr.2019.112456</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
112456
Volume
381
ISSN
1872-7549
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Update Year & Number
January 2020 Update
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
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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Sex differences in cognitive performance and alcohol consumption in High Alcohol-Drinking (HAD-1) rats
Publisher
An entity responsible for making the resource available
Behavioural Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-12-28
Subject
The topic of the resource
Alcohol use disorders; Attention; Exploratory behavior; Novel object recognition; Object recognition test; Selectively bred high alcohol-drinking rats
Creator
An entity primarily responsible for making the resource
Mittal N; Fleming S M; Martinez A; Thakore N; Bell R L; Maddox W T; Schallert T; Duvauchelle C L
Description
An account of the resource
Excessive alcohol (ethanol) consumption negatively impacts social, emotional, as well as cognitive function and well-being. Thus, identifying behavioral and/or biological predictors of excessive ethanol consumption is important for developing prevention and treatment strategies against alcohol use disorders (AUDs). Sex differences in alcohol consumption patterns are observed in humans, primates, and rodents. Selectively bred high alcohol-drinking rat lines, such as the "HAD-1" lines are recognized animal models of alcoholism. The present work examined sex differences in alcohol consumption, object recognition, and exploratory behavior in male and female HAD-1 rats. Naïve male and female HAD-1 rats were tested in an object recognition test (ORT) prior to a chronic 24 h intermittent ethanol access procedure for five weeks. Object recognition parameters measured included exploratory behavior, object investigation, and time spent near objects. During the initial training trial, rearing, active object investigation and amount of time spent in the object-containing section was significantly greater in female HAD-1 rats compared to their male counterparts. During the subsequent testing trial, time spent in the object-containing section was greater in female, compared to male, rats; but active object investigation and rearing did not statistically differ between females and males. In addition, female HAD-1 rats consumed significantly more ethanol than their male counterparts, replicating previous findings. Moreover, across all animals there was a significant positive correlation between exploratory behavior in ORT and ethanol consumption level. These results indicate there are significant sex differences in cognitive performance and alcohol consumption in HAD-1 rats, which suggests neurobiological differences as well.
Identifier
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<a href="http://doi.org/10.1016/j.bbr.2019.112456" target="_blank" rel="noreferrer noopener">10.1016/j.bbr.2019.112456</a>
PMID: 31891743
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Alcohol use disorders
Attention
Behavioural brain research
Bell R L
Department of Pharmaceutical Sciences
Duvauchelle C L
Exploratory behavior
Fleming S M
January 2020 Update
Journal Article
Maddox W T
Martinez A
Mittal N
NEOMED College of Pharmacy
Novel object recognition
Object recognition test
Schallert T
Selectively bred high alcohol-drinking rats
Thakore N
-
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/10.1002/cne.24610" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cne.24610</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
1179-1195
Issue
7
Volume
527
Dublin Core
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Title
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Astrocytic changes with aging and Alzheimer's disease-type pathology in chimpanzees
Publisher
An entity responsible for making the resource available
The Journal of Comparative Neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Subject
The topic of the resource
Aging; Alzheimer's disease; astrocytes; cerebral cortex; chimpanzees; hippocampus; prefrontal cortex; RRID: AB2109645; RRID: AB223647; RRID: AB2313952; RRID: AB2314223; stereology
Creator
An entity primarily responsible for making the resource
Munger Emily L; Edler Melissa K; Hopkins William D; Ely John J; Erwin Joseph M; Perl Daniel P; Mufson Elliott J; Hof Patrick R; Sherwood Chet C; Raghanti Mary Ann
Description
An account of the resource
Astrocytes are the main homeostatic cell of the central nervous system. In addition, astrocytes mediate an inflammatory response when reactive to injury or disease known as astrogliosis. Astrogliosis is marked by an increased expression of glial fibrillary acidic protein (GFAP) and cellular hypertrophy. Some degree of astrogliosis is associated with normal aging and degenerative conditions such as Alzheimer's disease (AD) and other dementing illnesses in humans. The recent observation of pathological markers of AD (amyloid plaques and neurofibrillary tangles) in aged chimpanzee brains provided an opportunity to examine the relationships among aging, AD-type pathology, and astrocyte activation in our closest living relatives. Stereologic methods were used to quantify GFAP-immunoreactive astrocyte density and soma volume in layers I, III, and V of the prefrontal and middle temporal cortex, as well as in hippocampal fields CA1 and CA3. We found that the patterns of astrocyte activation in the aged chimpanzee brain are distinct from humans. GFAP expression does not increase with age in chimpanzees, possibly indicative of lower oxidative stress loads. Similar to humans, chimpanzee layer I astrocytes in the prefrontal cortex are susceptible to AD-like changes. Both prefrontal cortex layer I and hippocampal astrocytes exhibit a high degree of astrogliosis that is positively correlated with accumulation of amyloid beta and tau proteins. However, unlike humans, chimpanzees do not display astrogliosis in other cortical layers. These results demonstrate a unique pattern of cortical aging in chimpanzees and suggest that inflammatory processes may differ between humans and chimpanzees in response to pathology.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/cne.24610" target="_blank" rel="noreferrer noopener">10.1002/cne.24610</a>
2019
Aging
Alzheimer's disease
Astrocytes
cerebral cortex
chimpanzees
Department of Pharmaceutical Sciences
Edler Melissa K
Ely John J
Erwin Joseph M
Hippocampus
Hof Patrick R
Hopkins William D
June 2019 Update
Mufson Elliott J
Munger Emily L
NEOMED College of Pharmacy
Perl Daniel P
prefrontal cortex
Raghanti Mary Ann
RRID: AB2109645
RRID: AB223647
RRID: AB2313952
RRID: AB2314223
Sherwood Chet C
Stereology
The Journal of comparative neurology
-
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="https://iovs.arvojournals.org/article.aspx?articleid=2741271" target="_blank" rel="noreferrer noopener">https://iovs.arvojournals.org/article.aspx?articleid=2741271</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).
Issue
9
Volume
60
ISSN
0146-0404
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Dublin Core
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Title
A name given to the resource
Upregulation of monocarboxylate transporter 2 protects retinal ganglion cells in glaucoma
Publisher
An entity responsible for making the resource available
Investigative Ophthalmology & Visual Science
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-07
Creator
An entity primarily responsible for making the resource
Pappenhagen Nate; Harun-Or-Rashid Mohammad; Jaboori Assraa Jassim; Inman Denise M
Identifier
An unambiguous reference to the resource within a given context
<a href="https://iovs.arvojournals.org/article.aspx?articleid=2741271" target="_blank" rel="noreferrer noopener">https://iovs.arvojournals.org/article.aspx?articleid=2741271</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Department of Pharmaceutical Sciences
Harun-Or-Rashid Mohammad
Inman Denise M
Investigative ophthalmology & visual science
Jaboori Assraa Jassim
Journal Article
NEOMED College of Graduate Studies
NEOMED College of Graduate Studies Student
NEOMED Student Publications
November 2019 Update
Pappenhagen Nate
-
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/10.1016/j.nbd.2019.104525" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2019.104525</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
104525-104525
Volume
130
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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
A name given to the resource
Time course and magnitude of alpha-synuclein inclusion formation and nigrostriatal degeneration in the rat model of synucleinopathy triggered by intrastriatal α-synuclein preformed fibrils
Publisher
An entity responsible for making the resource available
Neurobiology of Disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10
Subject
The topic of the resource
Alpha-Synuclein; PARKINSON'S disease; Preformed fibrils; Synucleinopathy
Creator
An entity primarily responsible for making the resource
Patterson Joseph R; Duffy Megan F; Kemp Christopher J; Howe Jacob W; Collier Timothy J; Stoll Anna C; Miller Kathryn M; Patel Pooja; Levine Nathan; Moore Darren J; Luk Kelvin C; Fleming Sheila M; Kanaan Nicholas M; Paumier Katrina L; El-Agnaf Omar M A; Sortwell Caryl E
Description
An account of the resource
Animal models that accurately recapitulate the accumulation of alpha-synuclein (α-syn) inclusions, progressive neurodegeneration of the nigrostriatal system and motor deficits can be useful tools for Parkinson's disease (PD) research. The preformed fibril (PFF) synucleinopathy model in rodents generally displays these PD-relevant features, however, the magnitude and predictability of these events is far from established. We therefore sought to optimize the magnitude of α-syn accumulation and nigrostriatal degeneration, and to understand the time course of both. Rats were injected unilaterally with different quantities of α-syn PFFs (8 or 16 μg of total protein) into striatal sites selected to concentrate α-syn inclusion formation in the substantia nigra pars compacta (SNpc). Rats displayed an α-syn PFF quantity-dependent increase in the magnitude of ipsilateral SNpc inclusion formation at 2 months and bilateral loss of nigral dopamine neurons at 6 months. Unilateral 16 μg PFF injection also resulted in modest sensorimotor deficits in forelimb adjusting steps associated with degeneration at 6 months. Bilateral injection of 16 μg α-syn PFFs resulted in symmetric bilateral degeneration equivalent to the ipsilateral nigral degeneration observed following unilateral 16 μg PFF injection (~50% loss). Bilateral PFF injections additionally resulted in alterations in several gait analysis parameters. These α-syn PFF parameters can be applied to generate a reproducible synucleinopathy model in rats with which to study pathogenic mechanisms and vet potential disease-modifying therapies.
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<a href="http://doi.org/10.1016/j.nbd.2019.104525" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2019.104525</a>
2019
Alpha-synuclein
Collier Timothy J
Department of Family & Community Medicine
Department of Pharmaceutical Sciences
Duffy Megan F
El-Agnaf Omar M A
Fleming Sheila M
Howe Jacob W
Kanaan Nicholas M
Kemp Christopher J
Levine Nathan
Luk Kelvin C
Miller Kathryn M
Moore Darren J
NEOMED College of Medicine
NEOMED College of Pharmacy
Neurobiology of disease
Parkinson's disease
Patel Pooja
Patterson Joseph R
Paumier Katrina L
Preformed fibrils
September 2019 Update
Sortwell Caryl E
Stoll Anna C
Synucleinopathy
-
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/10.1016/j.ymgme.2018.12.295" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ymgme.2018.12.295</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).
Pages
S116-S116
Issue
2
Volume
126
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Title
A name given to the resource
Intravenous infusion of iPSC-derived neural progenitors expressing GCase ameliorates alpha-synuclein aggregates in a mouse model of Gaucher disease
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Molecular Genetics and Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
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Endocrinology & Metabolism; Genetics & Heredity; medicine; Research & Experimental
Creator
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Peng Y Y; Liou B; Inskeep V; Blackwood R; Fleming S; Mayhew C N; Sun Y
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<a href="http://doi.org/10.1016/j.ymgme.2018.12.295" target="_blank" rel="noreferrer noopener">10.1016/j.ymgme.2018.12.295</a>
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The file format, physical medium, or dimensions of the resource
Journal Article
2019
Blackwood R
Department of Pharmaceutical Sciences
Endocrinology & Metabolism
Fleming S
Genetics & Heredity
Inskeep V
Journal Article
Liou B
Mayhew C N
Medicine
Molecular Genetics and Metabolism
NEOMED College of Pharmacy
Peng Y Y
Research & Experimental
Sun Y
-
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="https://iovs.arvojournals.org/article.aspx?articleid=2741309">https://iovs.arvojournals.org/article.aspx?articleid=2741309</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).
Issue
9
Volume
60
ISSN
0146-0404
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Glaucoma-associated E50K-optineurin mutation impairs mitochondrial-derived vesicle trafficking
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Investigative Ophthalmology & Visual Science
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-07
Creator
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Powers James; Trautman-Buckley Kayla; Sun Emily; Chen Charlaine; Inman Denise M; Tseng Henry
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<a href="https://iovs.arvojournals.org/article.aspx?articleid=2741309">https://iovs.arvojournals.org/article.aspx?articleid=2741309</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Chen Charlaine
Department of Pharmaceutical Sciences
Inman Denise M
Investigative ophthalmology & visual science
Journal Article
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED College of Pharmacy
NEOMED Student Publications
November 2019 Update
Powers James
Sun Emily
Trautman-Buckley Kayla
Tseng Henry
-
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/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</a>
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Title
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Neurotoxicity of pesticides
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Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; Fungicide; Glyphosate; iPSC; Microelectrode array; Mitochondrial Complex I; Neurodegeneration; Neurotoxicity; Organochlorine; Organophosphate; Paraquat; Pesticide; Pyrethroid; Pyridaben; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans.
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<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
Department of Pharmaceutical Sciences
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
Fitsanakis Vanessa
Fungicide
Glyphosate
IPSC
June 2019 Update
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
NEOMED College of Pharmacy
Neurodegeneration
Neurotoxicity
Organochlorine
Organophosphate
Paraquat
Pesticide
Pyrethroid
Pyridaben
Richardson Jason R
Rotenone
Westerink Remco H S
Zebrafish
-
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/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</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
343-362
Issue
3
Volume
138
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Title
A name given to the resource
Neurotoxicity of pesticides.
Publisher
An entity responsible for making the resource available
Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
activity; cell-culture; developmental; Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; exposure; Fungicide; Glyphosate; glyphosate-based herbicide; induced oxidative stress; iPSC; Microelectrode array; Mitochondrial Complex I; mitochondrial complex-i; Neurodegeneration; neuronal network; Neurosciences & Neurology; Neurotoxicity; Neurotoxicity; nigrostriatal dopamine system; Organochlorine; Organophosphate; Paraquat; parkinsons-disease; Pathology; Pesticide; Pyrethroid; pyrethroid insecticides; Pyridaben; reproduces features; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
activity
cell-culture
Department of Pharmaceutical Sciences
Developmental
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
exposure
Fitsanakis Vanessa
Fungicide
Glyphosate
glyphosate-based herbicide
induced oxidative stress
IPSC
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
mitochondrial complex-i
NEOMED College of Pharmacy
Neurodegeneration
neuronal network
Neurosciences & Neurology
Neurotoxicity
nigrostriatal dopamine system
Organochlorine
Organophosphate
Paraquat
parkinsons-disease
Pathology
Pesticide
Pyrethroid
pyrethroid insecticides
Pyridaben
reproduces features
Richardson Jason R
Rotenone
September 2019 Update
Westerink Remco H S
Zebrafish
-
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/10.4088/JCP.18m12588" target="_blank" rel="noreferrer noopener">http://doi.org/10.4088/JCP.18m12588</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).
Issue
4
Volume
80
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
A name given to the resource
Prevalence and Predictors of Benzodiazepine Monotherapy in Patients With Depression: A National Cross-Sectional Study
Publisher
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The Journal of Clinical Psychiatry
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Creator
An entity primarily responsible for making the resource
Soric Mate M; Paxos Chris; Dugan Sara E; Fosnight Susan M; Turosky Jodie Z; Sadana Prabodh; Emshoff Jessica B; Everly Lukas; Snyder Brittany M; Mistry Bhavin K; Bhat Shubha; Unruh Amy E; Safi Ismail M
Description
An account of the resource
OBJECTIVE: Depression guidelines discourage benzodiazepine monotherapy and limit use to short-term adjunctive therapy with antidepressants; however, patients with depression continue to receive benzodiazepine monotherapy. The prevalence and predictors of this prescribing pattern have not been described previously and are warranted to assist clinicians in identifying patients at highest risk of receiving benzodiazepine monotherapy. METHODS: A national, cross-sectional analysis of the National Ambulatory Medical Care Survey from 2012 to 2015 was performed for adults treated for depression. Depression was identified using a survey item specifically assessing the presence of depression. Office visits involving patients with bipolar disorder, schizoaffective disorder, or pregnancy were identified by ICD-9 code or specific survey item and were excluded. The primary endpoint was benzodiazepine monotherapy prescribing rate defined as initiation or continuation of a benzodiazepine in the absence of any antidepressant agent. A multivariate logistic regression model was created to identify variables associated with benzodiazepine monotherapy. RESULTS: In total, 9,426 unweighted visits were eligible for inclusion. Benzodiazepine monotherapy was identified in 9.3% of patients treated for depression (95% CI, 8.2%-10.6%). Predictors of benzodiazepine monotherapy included age of 45-64 years (OR = 1.39; 95% CI, 1.01-1.91), epilepsy-related office visit (OR = 5.34; 95% CI, 1.39-20.44), anxiety-related office visit (OR = 1.67; 95% CI, 1.23-2.27), underlying pulmonary disease (OR = 1.43; 95% CI, 1.09-1.87), and concomitant opiate prescribing (OR = 2.86; 95% CI, 2.01-4.06). Psychiatrists were less likely to prescribe benzodiazepine monotherapy than were other providers (OR = 0.42; 95% CI, 0.29-0.61). CONCLUSIONS: Benzodiazepine monotherapy is utilized in nearly 1 in 10 patients treated for depression. Adults aged 45 to 65 years, patients prescribed opioids, patients seen by primary care providers, and those with underlying anxiety, epilepsy, or pulmonary disorders are at highest risk.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4088/JCP.18m12588" target="_blank" rel="noreferrer noopener">10.4088/JCP.18m12588</a>
2019
Bhat Shubha
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Dugan Sara E
Emshoff Jessica B
Everly Lukas
Fosnight Susan M
June 2019 Update
Mistry Bhavin K
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED College of Pharmacy
Paxos Chris
Sadana Prabodh
Safi Ismail M
Snyder Brittany M
Soric Mate M
The Journal of clinical psychiatry
Turosky Jodie Z
Unruh Amy E
-
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
n/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
850A
Issue
1
Volume
70
ISSN
0270-9139
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A name given to the resource
ABLATION OF CISD2 IN HEPATOCYTES PROTECTS MICE FROM ETHANOL-INDUCED LIVER DAMAGE
Publisher
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Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10
Creator
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Stahl Zachary; Li Yun; Buehler Brian; You Min
Identifier
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n/a
Format
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Journal Article
2019
Buehler Brian
Department of Pharmaceutical Sciences
Hepatology
Journal Article
Li Yun
NEOMED College of Pharmacy
November 2019 Update
Stahl Zachary
You Min
-
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 class="epub-doi" href="https://doi.org/10.1111/acer.14060">https://doi.org/10.1111/acer.14060</a>
Pages
277A–277A
Volume
43
ISSN
0145-6008
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Title
A name given to the resource
ADIPOSE‐SPECIFIC LIPIN‐1 OVEREXPRESSION DISRUPTS HEPATIC ADIPONECTIN SIGNALING AND AGGRAVATES ALCOHOLIC STEATOHEPATITIS IN MICE
Publisher
An entity responsible for making the resource available
Alcoholism-Clinical and Experimental Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Substance Abuse
Creator
An entity primarily responsible for making the resource
You M
Identifier
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<a class="epub-doi" href="https://doi.org/10.1111/acer.14060">https://doi.org/10.1111/acer.14060</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).
Description
An account of the resource
Lipin‐1 is a pivotal regulator of lipid metabolism and inflammation and is involved in adipocyte development and maturation. Adiponectin is a hormone largely secreted by adipocytes. In adipocytes, lipin‐1 and adiponectin exhibit cross‐regulation. In the present study, we investigated whether and how adipose lipin‐1‐adiponectin axis contributes to the development and progression of alcoholic steatohepatitis. The effects of ethanol on adipose lipin‐1 and experimental alcoholic steatohepatitis were assessed in cultured 3T3‐L1 adipocytes and in transgenic mice overexpressing lipin‐1 in adipose (LPIN1‐Tg). In cultured 3T3‐adipocytes, ethanol exposure perturbed lipin‐1 signaling by inhibiting lipin‐1 expression, interfering lipin‐1 pre‐mRNA splicing and inducing nucleocytoplasmic shuttling of lipin‐1. Furthermore, secretion of adiponectin into 3T3‐L1 adipocytes culture medium was markedly enhanced by overexpression of lipin‐1. Consistent with the in vitro cell culture findings, feeding LPIN1‐Tg mice with an ethanol‐containing liquid diet resulted in substantial increases in serum concentrations of total and HMW adiponectin compared to ethanol‐fed WT mice. Surprisingly, despite drastically elevated circulating adiponectin levels, ethanol‐fed LPIN1‐Tg mice showed the rapid onset and progression of steatosis, inflammation, hepatobiliary damage and mild liver fibrosis. Further mechanistic studies revealed that adipose‐specific lipin‐1 overexpression exacerbated ethanol‐mediated inhibitory effects on mRNA abundance of hepatic adiponectin receptors in mice. Concurrently, adipose‐specific lipin‐1 overexpression severely suppressed protein expression of sirtuin (Sirt) 1, one of the critical components in mediating hepatic adiponectin signaling, in mice after ethanol administration. Altogether, our findings suggest that adipose‐specific lipin‐1 overexpression may in whole or in part cause disruption of hepatic adiponectin‐Sirt1 signaling routes and ultimately exacerbate alcoholic steatohepatitis in mice.
2019
Alcoholism-Clinical and Experimental Research
Department of Pharmaceutical Sciences
June 2019 Update
NEOMED College of Pharmacy
Substance Abuse
You M
-
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/10.1016/j.jhep.2018.10.037" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jhep.2018.10.037</a>
Pages
237–248
Issue
2
Volume
70
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
A name given to the resource
Effect of ethanol on lipid metabolism.
Publisher
An entity responsible for making the resource available
Journal of hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Alcohol-related liver disease; Lipid homeostasis; Metabolism; Steatosis
Creator
An entity primarily responsible for making the resource
You Min; Arteel Gavin E
Description
An account of the resource
Hepatic lipid metabolism is a series of complex processes that control influx and efflux of not only hepatic lipid pools, but also organismal pools. Lipid homeostasis is usually tightly controlled by expression, substrate supply, oxidation and secretion that keep hepatic lipid pools relatively constant. However, perturbations of any of these processes can lead to lipid accumulation in the liver. Although it is thought that these responses are hepatic arms of the 'thrifty genome', they are maladaptive in the context of chronic fatty liver diseases. Ethanol is likely unique among toxins, in that it perturbs almost all aspects of hepatic lipid metabolism. This complex response is due in part to the large metabolic demand placed on the organ by alcohol metabolism, but also appears to involve more nuanced changes in expression and substrate supply. The net effect is that steatosis is a rapid response to alcohol abuse. Although transient steatosis is largely an inert pathology, the chronicity of alcohol-related liver disease seems to require steatosis. Better and more specific understanding of the mechanisms by which alcohol causes steatosis may therefore translate into targeted therapies to treat alcohol-related liver disease and/or prevent its progression.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jhep.2018.10.037" target="_blank" rel="noreferrer noopener">10.1016/j.jhep.2018.10.037</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2019
Alcohol-related liver disease
Arteel Gavin E
Department of Pharmaceutical Sciences
Journal of hepatology
Lipid homeostasis
Metabolism
NEOMED College of Pharmacy
Steatosis
You Min
-
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/10.1016/S0618-8278(19)30550-X" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/S0618-8278(19)30550-X</a>
Pages
E287–E287
Volume
70
ISSN
0168-8278
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Title
A name given to the resource
FGF15 deficiency aggregates experimental alcoholic steatohepatitis in mice: A critical role for lipocalin 2 signaling
Publisher
An entity responsible for making the resource available
Journal of Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-04
Subject
The topic of the resource
Gastroenterology & Hepatology
Creator
An entity primarily responsible for making the resource
Zhou Z; Ye T J; DeCaro E; Buehler B; Stahl Z; Bonavita G; You M
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/S0618-8278(19)30550-X" target="_blank" rel="noreferrer noopener">10.1016/S0618-8278(19)30550-X</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2019
Bonavita G
Buehler B
DeCaro E
Department of Pharmaceutical Sciences
Gastroenterology & Hepatology
Journal of hepatology
June 2019 Update
NEOMED College of Pharmacy
Stahl Z
Ye T J
You M
Zhou Z
-
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/10.1016/S0618-8278(19)30551-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/S0618-8278(19)30551-1</a>
Pages
E287–E287
Volume
70
ISSN
0168-8278
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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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Hepatocyte-specific deletion of splicing factor SRSF3 exacerbates experimental alcoholic steatohepatitis in mice
Publisher
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Journal of Hepatology
Date
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2019
2019-04
Subject
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Gastroenterology & Hepatology
Creator
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Zhou Z; Ye T J; DeCaro E; Buehler B; Stahl Z; Bonavita G; You M
Identifier
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<a href="http://doi.org/10.1016/S0618-8278(19)30551-1" target="_blank" rel="noreferrer noopener">10.1016/S0618-8278(19)30551-1</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).
2019
Bonavita G
Buehler B
DeCaro E
Department of Pharmaceutical Sciences
Gastroenterology & Hepatology
Journal of hepatology
June 2019 Update
NEOMED College of Pharmacy
Stahl Z
Ye T J
You M
Zhou Z
-
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/10.1002/hep4.1333" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1333</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
656-669
Issue
5
Volume
3
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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Adipose‐Specific Lipin‐1 Overexpression Renders Hepatic Ferroptosis and Exacerbates Alcoholic Steatohepatitis in Mice.
Publisher
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Hepatology Communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Subject
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APOPTOSIS; FATTY liver; PROTEIN expression
Creator
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Zhou Zhou; Ye Ting Jie; Bonavita Gregory; Daniels Michael; Kainrad Noah; Jogasuria Alvin; You Min
Description
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Lipin‐1 is a Mg2+‐dependent phosphatidic acid phosphohydrolase involved in the generation of diacylglycerol during synthesis of phospholipids and triglycerides. Ethanol‐mediated inhibitory effects on adipose‐specific lipin‐1 expression were associated with experimental steatohepatitis in rodents. In the present study, using an adipose‐specific lipin‐1 overexpression transgenic (Lpin1‐Tg) mouse model, we tested a hypothesis that adipose‐specific lipin‐1 overexpression in mice might dampen ethanol‐induced liver damage. Experimental alcoholic steatohepatitis was induced by pair‐feeding ethanol to Lpin1‐Tg and wild‐type (WT) mice using the chronic‐plus‐binge ethanol feeding protocol. Unexpectedly, following the chronic‐plus‐binge ethanol challenge, Lpin1‐Tg mice exhibited much more pronounced steatosis, exacerbated inflammation, augmented elevation of serum liver enzymes, hepatobiliary damage, and fibrogenic responses compared with the WT mice. Mechanistically, overexpression of adipose lipin‐1 in mice facilitated the onset of hepatic ferroptosis, which is an iron‐dependent form of cell death, and subsequently induced ferroptotic liver damage in mice under ethanol exposure. Concurrently, adipose lipin‐1 overexpression induced defective adiponectin signaling pathways in ethanol‐fed mice. Conclusion: We identified ferroptosis as a mechanism in mediating the detrimental effects of adipose‐specific lipin‐1 overexpression in mice under chronic‐plus‐binge ethanol exposure. Our present study sheds light on potential therapeutic approaches for the prevention and treatment of human alcoholic steatohepatitis. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1002/hep4.1333" target="_blank" rel="noreferrer noopener">10.1002/hep4.1333</a>
2019
Apoptosis
Bonavita Gregory
Daniels Michael
Department of Pharmaceutical Sciences
Fatty Liver
Hepatology communications
Jogasuria Alvin
June 2019 Update
Kainrad Noah
NEOMED College of Pharmacy
PROTEIN expression
Ye Ting Jie
You Min
Zhou Zhou
-
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/10.1016/j.ajpath.2019.09.012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2019.09.012</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).
ISSN
1525-2191
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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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Intestinal SIRT1 Deficiency Protects Mice from Ethanol-Induced Liver Injury by Mitigating Ferroptosis
Publisher
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The American Journal Of Pathology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10-11
Creator
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Zhou Zhou; Ye Ting Jie; DeCaro Elizabeth; Buehler Brian; Stahl Zachary; Bonavita Gregory; Daniels Michael; You Min
Description
An account of the resource
Aberrant liver sirtuin 1 (SIRT1), a mammalian NAD+-dependent protein deacetylase, is implicated in the pathogenesis of alcoholic liver disease. However, the role of intestinal SIRT1 in alcoholic liver disease is presently unknown. This study investigated the involvement of intestine-specific SIRT1 in ethanol-induced liver dysfunction in mice. Ethanol feeding studies were performed on knockout mice with intestinal-specific SIRT1 deletion [SIRT1i knockout (KO)] and flox control [wild-type (WT)] mice with a chronic-plus-binge ethanol feeding protocol. After ethanol administration, hepatic inflammation and liver injury were substantially attenuated in the SIRT1iKO mice compared with the WT mice, suggesting that intestinal SIRT1 played a detrimental role in the ethanol-induced liver injury. Mechanistically, the hepatic protective effect of intestinal SIRT1 deficiency was attributable to ameliorated dysfunctional iron metabolism, increased hepatic glutathione contents, and attenuated lipid peroxidation, along with normalization of a panel of genes implicated in the ferroptosis process in the livers of ethanol-fed mice. This study demonstrates that ablation of intestinal SIRT1 protected mice from the ethanol-induced inflammation and liver damage. The protective effects of intestinal SIRT1 deficiency are mediated, at least partially, by mitigating hepatic ferroptosis. Targeting intestinal SIRT1 or dampening hepatic ferroptosis signaling may have therapeutic potential for alcoholic liver disease in humans.
Identifier
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<a href="http://doi.org/10.1016/j.ajpath.2019.09.012" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2019.09.012</a>
PMID: 31610175
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Journal Article
2019
Bonavita Gregory
Buehler Brian
Daniels Michael
DeCaro Elizabeth
Department of Pharmaceutical Sciences
Journal Article
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
November 2019 Update
Stahl Zachary
The American journal of pathology
Ye Ting Jie
You Min
Zhou Zhou