1
40
77
-
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.jid.2017.08.034" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jid.2017.08.034</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
219-227
Issue
1
Volume
138
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
Glycoprotein Nonmelanoma Clone B Regulates the Crosstalk between Macrophages and Mesenchymal Stem Cells toward Wound Repair.
Publisher
An entity responsible for making the resource available
The Journal of investigative dermatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
Humans; Male; Animals; Mice; Cell Differentiation; Wound Healing/*physiology; Macrophages/*physiology; Diabetes Mellitus; Cells; Cultured; Inbred C57BL; Animal; Disease Models; Administration; Cutaneous; Cell Communication/*physiology; Eye Proteins/administration & dosage/genetics/*physiology; Membrane Glycoproteins/administration & dosage/genetics/*physiology; Mesenchymal Stem Cells/*physiology; Recombinant Proteins/administration & dosage/genetics/metabolism; Skin/*injuries/metabolism; Type 2/complications/pathology
Creator
An entity primarily responsible for making the resource
Yu Bing; Alboslemy Talib; Safadi Fayez; Kim Min-Ho
Description
An account of the resource
The process of wound repair requires the coordinated participation of multiple types of cells, which are sequentially recruited during the healing process. In response to tissue injury, both macrophages and mesenchymal stem cells (MSCs) are recruited to the site of injury, where they participate in the repair process. Despite considerable understanding of the role of each cell type in the process of wound repair, the nature of the dynamic interplay between these two cell types and how this interaction influences the process of wound repair are not well understood. Here, using an in vivo model of cutaneous wound healing in mice, we provide evidence that GPNMB is functionally important in promoting the recruitment of MSCs to the site of skin injury, which in turn modulates inflammatory responses by directing the M2 polarization of macrophages in acute wound healing. Furthermore, we show that GPNMB activity is impaired in a diabetic wound environment, which is associated with impaired MSC recruitment that is reversed by the topical administration of recombinant GPNMB protein to the wounds of diabetic mice. Our study provides important insight into the crosstalk between macrophages and endogenous MSCs toward wound repair.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jid.2017.08.034" target="_blank" rel="noreferrer noopener">10.1016/j.jid.2017.08.034</a>
2018
Administration
Alboslemy Talib
Animal
Animals
Cell Communication/*physiology
Cell Differentiation
Cells
Cultured
Cutaneous
Diabetes Mellitus
Disease Models
Eye Proteins/administration & dosage/genetics/*physiology
Humans
Inbred C57BL
Kim Min-Ho
Macrophages/*physiology
Male
Membrane Glycoproteins/administration & dosage/genetics/*physiology
Mesenchymal Stem Cells/*physiology
Mice
Recombinant Proteins/administration & dosage/genetics/metabolism
Safadi Fayez
Skin/*injuries/metabolism
The Journal of investigative dermatology
Type 2/complications/pathology
Wound Healing/*physiology
Yu Bing
-
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/hep.29857" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.29857</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
1574-1588
Issue
4
Volume
68
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
Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism.
Publisher
An entity responsible for making the resource available
Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-10
Subject
The topic of the resource
Male; Animals; Mice; Random Allocation; Sensitivity and Specificity; *Signal Transduction; Lipid Metabolism; Bile Acids and Salts/*metabolism; GTP-Binding Proteins/*metabolism; Receptors; Inbred C57BL; Animal; Disease Models; G-Protein-Coupled/*metabolism; Gastrointestinal Microbiome/*drug effects; Glucagon-Like Peptide 1/metabolism; Cytoplasmic and Nuclear/*antagonists & inhibitors/pharmacology
Creator
An entity primarily responsible for making the resource
Pathak Preeti; Xie Cen; Nichols Robert G; Ferrell Jessica M; Boehme Shannon; Krausz Kristopher W; Patterson Andrew D; Gonzalez Frank J; Chiang John Y L
Description
An account of the resource
Bile acids activate farnesoid X receptor (FXR) and G protein-coupled bile acid receptor-1 (aka Takeda G protein-coupled receptor-5 [TGR5]) to regulate bile acid metabolism and glucose and insulin sensitivity. FXR and TGR5 are coexpressed in the enteroendocrine L cells, but their roles in integrated regulation of metabolism are not completely understood. We reported recently that activation of FXR induces TGR5 to stimulate glucagon-like peptide-1 (GLP-1) secretion to improve insulin sensitivity and hepatic metabolism. In this study, we used the intestine-restricted FXR agonist fexaramine (FEX) to study the effect of activation of intestinal FXR on the gut microbiome, bile acid metabolism, and FXR and TGR5 signaling. The current study revealed that FEX markedly increased taurolithocholic acid, increased secretion of fibroblast growth factors 15 and 21 and GLP-1, improved insulin and glucose tolerance, and promoted white adipose tissue browning in mice. Analysis of 16S ribosomal RNA sequences of the gut microbiome identified the FEX-induced and lithocholic acid-producing bacteria Acetatifactor and Bacteroides. Antibiotic treatment completely reversed the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.29857" target="_blank" rel="noreferrer noopener">10.1002/hep.29857</a>
*Signal Transduction
2018
Animal
Animals
Bile Acids and Salts/*metabolism
Boehme Shannon
Chiang John Y L
Cytoplasmic and Nuclear/*antagonists & inhibitors/pharmacology
Department of Integrative Medical Sciences
Disease Models
Ferrell Jessica M
G-Protein-Coupled/*metabolism
Gastrointestinal Microbiome/*drug effects
Glucagon-Like Peptide 1/metabolism
Gonzalez Frank J
GTP-Binding Proteins/*metabolism
Hepatology (Baltimore, Md.)
Inbred C57BL
Krausz Kristopher W
Lipid Metabolism
Male
Mice
NEOMED College of Medicine
Nichols Robert G
Pathak Preeti
Patterson Andrew D
Random Allocation
Receptors
Sensitivity and Specificity
Xie Cen
-
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.
Pages
628–632
Issue
6
Volume
19
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
Origins of spondyloarthropathy in Perissodactyla.
Publisher
An entity responsible for making the resource available
Clinical and experimental rheumatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-12
Subject
The topic of the resource
Animals; *Fossils; *Paleopathology; *Perissodactyla; Horse Diseases/history/*pathology; Horses; North America; Sacroiliac Joint/pathology; Spine/pathology; History; Ancient; Animal; Disease Models; Spondylitis; Ankylosing/history/*pathology
Creator
An entity primarily responsible for making the resource
Rothschild B M; Prothero D R; Rothschild C
Description
An account of the resource
OBJECTIVE: Spondyloarthropathy has clearly been documented as not limited in occurrence to humans. Transmammalian in nature, it is of interest to understand the antiquity, and perhaps the origins, of this disorder in animal groups sufficiently represented in the skeletal record. METHODS: Fossil and recent skeletons of perissodactylae from North America were systematically examined to determine the occurrence and population frequency of spondyloarthropathy. RESULTS: Spondyloarthropathy was the most common form of arthritis recognized in the extant and fossil records. Common in extinct families such as Brontotheriidae and Chalicotheriidae, a progressive increase in the frequency of spondyloarthropathy was observed through geologic time in Equidae and Rhinocerotidae. CONCLUSION: Erosive arthritis of the spondyloarthropathy variety is now documented as not only persisting in Perissodactyla, but as actually increasing significantly in frequency (3-6 fold). Given the unusual evolutionary penetrance of this "disease," the possibility must be considered that its persistence provides evidence for some unknown benefit to the affected host.
Rights
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).
*Fossils
*Paleopathology
*Perissodactyla
2001
Ancient
Animal
Animals
Ankylosing/history/*pathology
Clinical and experimental rheumatology
Disease Models
History
Horse Diseases/history/*pathology
Horses
North America
Prothero D R
Rothschild B M
Rothschild C
Sacroiliac Joint/pathology
Spine/pathology
Spondylitis
-
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.
Pages
157–172
Issue
2
Volume
25
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
Sex steroid induction of gallstones in the male Syrian hamster.
Publisher
An entity responsible for making the resource available
Journal of submicroscopic cytology and pathology
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
1993-04
Subject
The topic of the resource
Male; Animals; Body Weight; Organ Size; Cricetinae; Drug Combinations; Estradiol/*pharmacology; Mesocricetus; Medroxyprogesterone/*pharmacology; Cholelithiasis/*etiology; Endoplasmic Reticulum/drug effects/ultrastructure; Gallbladder/*drug effects/ultrastructure; Golgi Apparatus/drug effects/ultrastructure; Animal; Disease Models
Creator
An entity primarily responsible for making the resource
Gilloteaux J; Kosek E; Kelly T R
Description
An account of the resource
Light (LM), transmission (TEM) and scanning (SEM) electron microscopic techniques were used to characterize morphologic changes induced in the gallbladder of Syrian hamsters following a one-month estradiol (E) and estradiol + medroxyprogesterone (E+MP) treatment. The TEM results were correlated with the SEM findings. Compared to control (C), E-treated surface epithelial cells contain abundant RER, enlarged Golgi, multivesicular (foamy-heterophagosomes) bodies or lipofuscin inclusions. A 10-day E treatment showed large vesicles develop and, after longer E treatment, they could coalesce and create some of the large multivesicular bodies. Interestingly, E+MP epithelia are characterized by distinct bulging apices where a large number of apical granules accumulate, and contain an anionic mucous core. After a 4-week E+MP treatment, even though all the hamsters were fed a diet with trace cholesterol, significant increase in hamster liver weight, serum level of cholesterol and HDL were measured and, correspondingly, gallstones were found exclusively in E+MP-treated hamsters. Our results showed that not only does the Syrian hamster provide an appropriate model to study experimental lithogenesis without manipulating the diet. In addition, MP appears to induce morphologic changes associated with the formation of gallstones.
Rights
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).
1993
Animal
Animals
Body Weight
Cholelithiasis/*etiology
Cricetinae
Disease Models
Drug Combinations
Endoplasmic Reticulum/drug effects/ultrastructure
Estradiol/*pharmacology
Gallbladder/*drug effects/ultrastructure
Gilloteaux J
Golgi Apparatus/drug effects/ultrastructure
Journal of submicroscopic cytology and pathology
Kelly T R
Kosek E
Male
Medroxyprogesterone/*pharmacology
Mesocricetus
Organ Size
-
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.
Pages
36–42
Issue
6
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
A name given to the resource
Gender differences in neurotoxicity of the nigrostriatal dopaminergic system: implications for Parkinson's disease.
Publisher
An entity responsible for making the resource available
The journal of gender-specific medicine : JGSM : the official journal of the Partnership for Women's Health at Columbia
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
2000-10
Subject
The topic of the resource
Female; Humans; Male; Sex Factors; Sex Distribution; Estrogens/*pharmacology; Dopamine/metabolism; Postmenopause; Corpus Striatum/pathology/*physiopathology; Neurotoxins/*antagonists & inhibitors; Parkinson Disease/metabolism/pathology/*physiopathology; Substantia Nigra/pathology/*physiopathology; Animal; Disease Models
Creator
An entity primarily responsible for making the resource
Dluzen D E; McDermott J L
Description
An account of the resource
This article describes the progression of steps followed to demonstrate a gender difference associated with Parkinson's disease (PD) and to gain an understanding of the basis, mechanisms, and implications of this gender specificity. First, a review of the literature on PD shows a greater incidence in men. Next, data are presented from a series of laboratory studies in animal models of PD that suggest a basis for this gender difference: estrogen appears to act as a neuroprotectant of the striatal dopaminergic system. One mechanism for this effect may be that estrogen inhibits the uptake of neurotoxins capable of producing degeneration within dopaminergic neurons. Finally, some of the potential neurologic implications of manipulating estrogen in premenopausal and postmenopausal women are considered.
Rights
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).
2000
Animal
Corpus Striatum/pathology/*physiopathology
Disease Models
Dluzen D E
Dopamine/metabolism
Estrogens/*pharmacology
Female
Humans
Male
McDermott J L
Neurotoxins/*antagonists & inhibitors
Parkinson Disease/metabolism/pathology/*physiopathology
Postmenopause
Sex Distribution
Sex Factors
Substantia Nigra/pathology/*physiopathology
The journal of gender-specific medicine : JGSM : the official journal of the Partnership for Women's Health at Columbia
-
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.
Pages
340–344
Issue
2
Volume
767
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
Estrogen decreases corpus striatal neurotoxicity in response to
Publisher
An entity responsible for making the resource available
Brain research
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
1997-09
Subject
The topic of the resource
Female; Animals; Rats; Corpus Striatum/*drug effects; Dopamine/metabolism; Neurotoxins/*toxicity; Estradiol/*pharmacology; Oxidopamine/*toxicity; Parkinson Disease/*physiopathology; Sprague-Dawley; Animal; Disease Models; 3; 4-Dihydroxyphenylacetic Acid/metabolism
Creator
An entity primarily responsible for making the resource
Dluzen D
Description
An account of the resource
Ovariectomized rats treated or not with an estradiol pellet were subjected to an unilateral intrastriatal infusion of 6-hydroxydopamine (6-OHDA). Various parameters of nigrostriatal dopaminergic function as derived from measurements of dopamine and dihydroxyphenylacetic acid (DOPAC) concentrations were determined from the 6-OHDA lesioned and non-lesioned sides of the corpus striatum in these animals. Dopamine concentrations within the 6-OHDA lesioned striatum of estrogen-treated rats were significantly greater than non-estrogen-treated rats. There were no differences in striatal dopamine concentrations between estrogen- versus non-estrogen-treated rats on their non-lesioned side. In contrast to that of dopamine, no differences in DOPAC concentrations between estrogen and non-estrogen-treated rats were obtained within the 6-OHDA-lesioned side. The DOPAC concentrations on the non-lesioned side of the striatum were significantly greater in the non-estrogen-treated rats. These results demonstrate that estrogen significantly diminishes the depletion of striatal dopamine resulting from the neurotoxin 6-OHDA. The data obtained from the DOPAC determinations imply that this capacity of estrogen may be exerted through actions upon uptake processes of striatal dopaminergic neurons. Such findings suggest that estrogen may function as an important modulatory factor capable of attenuating degeneration within the corpus striatum, and in this way serve as a neuroprotectant of the nigrostriatal dopaminergic system.
Rights
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).
1997
3
4-Dihydroxyphenylacetic Acid/metabolism
Animal
Animals
Brain research
Corpus Striatum/*drug effects
Disease Models
Dluzen D
Dopamine/metabolism
Estradiol/*pharmacology
Female
Neurotoxins/*toxicity
Oxidopamine/*toxicity
Parkinson Disease/*physiopathology
Rats
Sprague-Dawley
-
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.
Pages
3843–3853
Issue
5
Volume
73
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
Intrastrain variants of herpes simplex virus type 1 isolated from a neonate with fatal disseminated infection differ in the ICP34.5 gene, glycoprotein processing, and neuroinvasiveness.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-05
Subject
The topic of the resource
Humans; Male; Animals; Mice; Amino Acid Sequence; *Genetic Variation; Base Sequence; Molecular Sequence Data; Polymerase Chain Reaction/methods; DNA; Deoxyribonuclease BamHI; Deoxyribonuclease EcoRI; Glycoproteins/metabolism; Viral Envelope Proteins/analysis; Viral Proteins/*genetics; Genes; Viral; Animal; Disease Models; Herpesvirus 1; Inbred BALB C; Amino Acid; Sequence Homology; Sequence Analysis; Nucleic Acid; Polymorphism; *Protein Processing; Post-Translational; Human/*genetics/growth & development/isolation & purification; Restriction Fragment Length
Creator
An entity primarily responsible for making the resource
Bower J R; Mao H; Durishin C; Rozenbom E; Detwiler M; Rempinski D; Karban T L; Rosenthal K S
Description
An account of the resource
Two intrastrain variants of herpes simplex virus type 1 (HSV-1) were isolated from a newborn with fatal disseminated infection. A small-plaque-producing variant (SP7) was the predominant virus (\textgreater99%) in the brain, and a large-plaque-producing variant (LP5) was the predominant virus (\textgreater99%) in the lung and gastrointestinal tract. EcoRI and BamHI restriction fragment patterns indicated that SP7 and LP5 are related strains. The large-plaque variants produced plaques similar in size to those produced by HSV-1 KOS. Unlike LP5 or KOS, SP7 was highly cell associated and processing of glycoprotein C and glycoprotein D was limited to precursor forms in infected Vero cells. The large-plaque phenotype from KOS could be transferred into SP7 by cotransfection of plasmids containing the EK or JK EcoRI fragment or a 3-kb plasmid with the UL34.5 gene of HSV-1 KOS together with SP7 DNA. PCR analysis using primers from within the ICP34.5 gene indicated differences for SP7, LP5, and KOS. Sequencing data indicated two sets of deletions in the UL34.5 gene that distinguish SP7 from LP5. Both SP7 and LP5 variants were neurovirulent (lethal following intracranial inoculation of young BALB/c mice); however, the LP5 variant was much less able to cause lethal neuroinvasive disease (footpad inoculation) whereas KOS caused no disease. Passage of SP7 selected for viruses (SLP-5 and SLP-10) which were attenuated for lethal neuroinvasive disease, were not cell-associated, and differed in the UL34.5 gene. UL34.5 from SLP-5 or SLP-10 resembled that of KOS. These findings support a role for UL34.5 in promoting virus egress and for neuroinvasive disease.
Rights
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).
*Genetic Variation
*Protein Processing
1999
Amino Acid
Amino Acid Sequence
Animal
Animals
Base Sequence
Bower J R
Deoxyribonuclease BamHI
Deoxyribonuclease EcoRI
Detwiler M
Disease Models
DNA
Durishin C
Genes
Glycoproteins/metabolism
Herpesvirus 1
Human/*genetics/growth & development/isolation & purification
Humans
Inbred BALB C
Journal of virology
Karban T L
Male
Mao H
Mice
Molecular Sequence Data
Nucleic Acid
Polymerase Chain Reaction/methods
Polymorphism
Post-Translational
Rempinski D
Restriction Fragment Length
Rosenthal K S
Rozenbom E
Sequence Analysis
Sequence Homology
Viral
Viral Envelope Proteins/analysis
Viral Proteins/*genetics
-
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/10.5966/sctm.2013-0157" target="_blank" rel="noreferrer noopener">http://doi.org/10.5966/sctm.2013-0157</a>
Pages
760–767
Issue
6
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
A name given to the resource
Functional outcome after anal sphincter injury and treatment with mesenchymal stem cells.
Publisher
An entity responsible for making the resource available
Stem cells translational medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-06
Subject
The topic of the resource
Female; Time Factors; Animals; Rats; Mesenchymal stem cells; Transfection; Recovery of Function; Fibrosis; *Mesenchymal Stem Cell Transplantation; *Regeneration; Anal Canal/injuries/metabolism/pathology/physiopathology/*surgery; Anal pressures; Anal sphincter; Fecal incontinence; Green Fluorescent Proteins/biosynthesis/genetics; i.v. infusion; Mesenchymal Stem Cells/metabolism; Pressure; Injections; Intralesional; Sprague-Dawley; Cells; Cultured; Animal; Disease Models; Infusions; Intravenous
Creator
An entity primarily responsible for making the resource
Salcedo Levilester; Penn Marc; Damaser Margot; Balog Brian; Zutshi Massarat
Description
An account of the resource
This research demonstrates the regenerative effects of mesenchymal stem cells (MSCs) on the injured anal sphincter by comparing anal sphincter pressures following intramuscular and serial intravascular MSC infusion in a rat model of anal sphincter injury. Fifty rats were divided into injury (n = 35) and no injury (NI; n = 15) groups. Each group was further divided into i.m., serial i.v., or no-treatment (n = 5) groups and followed for 5 weeks. The injury consisted of an excision of 25% of the anal sphincter complex. Twenty-four hours after injury, 5 x 10(5) green fluorescent protein-labeled MSCs in 0.2 ml of phosphate-buffered saline (PBS) or PBS alone (sham) were injected into the anal sphincter for i.m. treatment; i.v. and sham i.v. treatments were delivered daily for 6 consecutive days via the tail vein. Anal pressures were recorded before injury and 10 days and 5 weeks after treatment. Ten days after i.m. MSC treatment, resting and peak pressures were significantly increased compared with those in sham i.m. treatment (p \textless .001). When compared with the NI group, the injury groups had anal pressures that were not significantly different 5 weeks after i.m./i.v. treatment. Both resting and peak pressures were also significantly increased after i.m./i.v. MSC treatment compared with treatment with PBS (p \textless .001), suggesting recovery. Statistical analysis was done using paired t test with Bonferroni correction. Marked decrease in fibrosis and scar tissue was seen in both MSC-treated groups. Both i.m. and i.v. MSC treatment after injury caused an increase in anal pressures sustained at 5 weeks, although fewer cells were injected i.m. The
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.5966/sctm.2013-0157" target="_blank" rel="noreferrer noopener">10.5966/sctm.2013-0157</a>
Rights
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).
*Mesenchymal Stem Cell Transplantation
*Regeneration
2014
Anal Canal/injuries/metabolism/pathology/physiopathology/*surgery
Anal pressures
Anal sphincter
Animal
Animals
Balog Brian
Cells
Cultured
Damaser Margot
Disease Models
Fecal incontinence
Female
Fibrosis
Green Fluorescent Proteins/biosynthesis/genetics
i.v. infusion
Infusions
Injections
Intralesional
Intravenous
Mesenchymal stem cells
Mesenchymal Stem Cells/metabolism
Penn Marc
Pressure
Rats
Recovery of Function
Salcedo Levilester
Sprague-Dawley
Stem cells translational medicine
Time Factors
Transfection
Zutshi Massarat
-
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/10.3233/JAD-160658" target="_blank" rel="noreferrer noopener">http://doi.org/10.3233/JAD-160658</a>
Pages
1605–1619
Issue
4
Volume
55
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
Early Evidence of Low Bone Density and Decreased Serotonergic Synthesis in the Dorsal Raphe of a Tauopathy Model of Alzheimer's Disease.
Publisher
An entity responsible for making the resource available
Journal of Alzheimer's disease : JAD
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
Female; Male; Animals; Mice; *Alzheimer's disease; Body Weight; Body Composition; Age Factors; Body Weight/genetics; Phosphorylation; Bone Density/*physiology; *Alzheimer Disease/complications/genetics/pathology; *bone density; *microtubule-associated protein; *serotonin; *tau proteins; *tauopathies; Body Composition/genetics; Bone Diseases/*etiology; Dorsal Raphe Nucleus/*pathology; Neurons/metabolism/pathology; Serotonin/*metabolism; tau Proteins/*genetics/metabolism; Tauopathies/complications/genetics; Tryptophan Hydroxylase/metabolism; Biological; Models; Inbred C57BL; Animal; Disease Models; Transgenic; Nerve Tissue Proteins; Neurodegenerative Diseases; Animal Studies; Alzheimer's Disease; Bone Density – Physiology; Nerve Tissue Proteins – Metabolism; Neurodegenerative Diseases – Complications; Alzheimer's Disease – Complications; Alzheimer's Disease – Pathology; Bone Diseases – Etiology; Brain Stem – Pathology; Neurons – Metabolism; Neurons – Pathology; Oxidoreductases – Metabolism; Serotonin – Metabolism
Creator
An entity primarily responsible for making the resource
Dengler-Crish Christine M; Smith Matthew A; Wilson Gina N
Description
An account of the resource
Reduced bone mineral density (BMD) and its clinical sequelae, osteoporosis, occur at a much greater rate in patients with Alzheimer's disease (AD), often emerging early in the disease before significant cognitive decline is seen. Reduced BMD translates to increased bone fracture risk, decreased quality of life, and increased mortality for AD patients. However, the mechanism responsible for this observation is unclear. We hypothesize that bone loss is an additional component of an AD prodrome-changes that emerge prior to dementia and are mediated by dysfunction of the central serotonergic pathways. We characterized the skeletal phenotype of htau mice that express human forms of the microtubule-associated protein tau that become pathologically hyperphosphorylated in AD. Using radiographic densitometry, we measured BMD in female and male htau mice from 2-6 months of age-time-points prior to the presence of significant tauopathy in the hippocampal/entorhinal regions characteristic of this model. We found a significantly reduced BMD phenotype in htau mice that was most pronounced in males. Using western blotting and immunofluorescence, we showed overall reduced tryptophan hydroxylase (TPH) protein in htau brainstem and a 70% reduction in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3233/JAD-160658" target="_blank" rel="noreferrer noopener">10.3233/JAD-160658</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).
*Alzheimer Disease/complications/genetics/pathology
*Alzheimer's disease
*bone density
*microtubule-associated protein
*serotonin
*tau proteins
*tauopathies
2017
Age Factors
Alzheimer's disease
Alzheimer's Disease – Complications
Alzheimer's Disease – Pathology
Animal
Animal Studies
Animals
Biological
Body Composition
Body Composition/genetics
Body Weight
Body Weight/genetics
Bone Density – Physiology
Bone Density/*physiology
Bone Diseases – Etiology
Bone Diseases/*etiology
Brain Stem – Pathology
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Disease Models
Dorsal Raphe Nucleus/*pathology
Female
Inbred C57BL
Journal of Alzheimer's disease : JAD
Male
Mice
Models
NEOMED College of Pharmacy
Nerve Tissue Proteins
Nerve Tissue Proteins – Metabolism
Neurodegenerative Diseases
Neurodegenerative Diseases – Complications
Neurons – Metabolism
Neurons – Pathology
Neurons/metabolism/pathology
Oxidoreductases – Metabolism
Phosphorylation
Serotonin – Metabolism
Serotonin/*metabolism
Smith Matthew A
tau Proteins/*genetics/metabolism
Tauopathies/complications/genetics
Transgenic
Tryptophan Hydroxylase/metabolism
Wilson Gina 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/10.3109/10837450.2011.647035" target="_blank" rel="noreferrer noopener">http://doi.org/10.3109/10837450.2011.647035</a>
Pages
957–962
Issue
4
Volume
18
Dublin Core
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Title
A name given to the resource
Thermoreversible gel for delivery of activin receptor-like kinase 5 inhibitor
Publisher
An entity responsible for making the resource available
Pharmaceutical development and technology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
Time Factors; Animals; Body Temperature; *Drug Delivery Systems; Temperature; Rabbits; Benzodioxoles/*administration & dosage/pharmacokinetics/toxicity; Delayed-Action Preparations; Drug Carriers/chemistry/toxicity; Fibroblasts/drug effects/metabolism; Filtering Surgery/*methods; Gels; Glaucoma/*surgery; Imidazoles/*administration & dosage/pharmacokinetics/toxicity; Poloxamer/chemistry/toxicity; Protein-Serine-Threonine Kinases/antagonists & inhibitors; Pyridines/*administration & dosage/pharmacokinetics/toxicity; Viscosity; Receptors; Receptor; Animal; Disease Models; Transforming Growth Factor-beta Type I; Transforming Growth Factor beta/antagonists & inhibitors
Creator
An entity primarily responsible for making the resource
Sutariya Vijaykumar; Miladore Nicholas; Geldenhuys Werner; Bhatia Deepak; Wehrung Daniel; Nakamura Hiroshi
Description
An account of the resource
The purpose of this study is to investigate a thermoreversible gel using Pluronic
Identifier
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<a href="http://doi.org/10.3109/10837450.2011.647035" target="_blank" rel="noreferrer noopener">10.3109/10837450.2011.647035</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).
*Drug Delivery Systems
2013
Animal
Animals
Benzodioxoles/*administration & dosage/pharmacokinetics/toxicity
Bhatia Deepak
Body Temperature
Delayed-Action Preparations
Disease Models
Drug Carriers/chemistry/toxicity
Fibroblasts/drug effects/metabolism
Filtering Surgery/*methods
Geldenhuys Werner
Gels
Glaucoma/*surgery
Imidazoles/*administration & dosage/pharmacokinetics/toxicity
Miladore Nicholas
Nakamura Hiroshi
Pharmaceutical development and technology
Poloxamer/chemistry/toxicity
Protein-Serine-Threonine Kinases/antagonists & inhibitors
Pyridines/*administration & dosage/pharmacokinetics/toxicity
Rabbits
Receptor
Receptors
Sutariya Vijaykumar
Temperature
Time Factors
Transforming Growth Factor beta/antagonists & inhibitors
Transforming Growth Factor-beta Type I
Viscosity
Wehrung Daniel
-
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/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0166560</a>
Pages
e0166560–e0166560
Issue
11
Volume
11
Dublin Core
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Title
A name given to the resource
Salvianolic Acid B Alleviates Heart Failure by Inactivating ERK1/2/GATA4 Signaling Pathway after Pressure Overload in Mice.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016
Subject
The topic of the resource
Male; Animals; Mice; Phosphorylation/drug effects; Signal Transduction/*drug effects; Rats; Cell Line; Proto-Oncogene Proteins c-akt/metabolism; Benzofurans/chemistry/*pharmacology; Blood Pressure/drug effects; GATA4 Transcription Factor/metabolism; Heart Failure/metabolism/*pathology; Heart Ventricles/diagnostic imaging; Mitogen-Activated Protein Kinase 1/metabolism; Mitogen-Activated Protein Kinase 3/metabolism; Myocardium/metabolism/pathology; Drugs; Inbred C57BL; Animal; Disease Models; Myocytes; Aorta; Brain/blood; Natriuretic Peptide; Cardiac/cytology/drug effects/metabolism; Chinese Herbal/chemistry/pharmacology; Thoracic/surgery
Creator
An entity primarily responsible for making the resource
Yu Juan; Chen Renshan; Tan Yafang; Wu Jiashin; Qi Jianyong; Zhang Minzhou; Gu Weiwang
Description
An account of the resource
BACKGROUND: Heart failure(HF) is a dangerous disease that affects millions of patients. Radix Salvia is widely used in Chinese clinics to treat heart diseases. Salvianolic acid B(SalB) is the major active component of Radix Salvia. This study investigated the mechanisms of action and effects of SalB on HF in an experimental mouse model of HF. METHODS: We created a mouse model of HF by inducing pressure overload with transverse aortic constriction(TAC) surgery for 2 weeks and compared among 4 study groups: SHAM group (n = 10), TAC group (n = 9), TAC+MET group (metprolol, positive drug treatment, n = 9) and TAC+SalB group (SalB, 240 mg*kg-1*day-1, n = 9). Echocardiography was used to evaluate the dynamic changes in cardiac structure and function in vivo. Plasma brain natriuretic peptide (BNP) concentration was detected by Elisa method. In addition, H9C2 rat cardiomyocytes were cultured and Western blot were implemented to evaluate the phosphorylation of ERK1/2, AKT, and protein expression of GATA4. RESULTS: SalB significantly inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, but not Ser473 site of AKT, subsequently inhibited protein expression of GATA4 and plasma BNP(P \textless 0.001), and then inhibited HF at 2 weeks after TAC surgery. CONCLUSIONS: Our data provide a mechanism of inactivating the ERK1/2/GATA4 signaling pathway for SalB inhibition of the TAC-induced HF.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0166560" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0166560</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).
2016
Animal
Animals
Aorta
Benzofurans/chemistry/*pharmacology
Blood Pressure/drug effects
Brain/blood
Cardiac/cytology/drug effects/metabolism
Cell Line
Chen Renshan
Chinese Herbal/chemistry/pharmacology
Disease Models
Drugs
GATA4 Transcription Factor/metabolism
Gu Weiwang
Heart Failure/metabolism/*pathology
Heart Ventricles/diagnostic imaging
Inbred C57BL
Male
Mice
Mitogen-Activated Protein Kinase 1/metabolism
Mitogen-Activated Protein Kinase 3/metabolism
Myocardium/metabolism/pathology
Myocytes
Natriuretic Peptide
Phosphorylation/drug effects
PloS one
Proto-Oncogene Proteins c-akt/metabolism
Qi Jianyong
Rats
Signal Transduction/*drug effects
Tan Yafang
Thoracic/surgery
Wu Jiashin
Yu Juan
Zhang Minzhou
-
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/10.1359/JBMR.050108" target="_blank" rel="noreferrer noopener">http://doi.org/10.1359/JBMR.050108</a>
Pages
987–993
Issue
6
Volume
20
Dublin Core
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Title
A name given to the resource
Growth hormone injections improve bone quality in a mouse model of osteogenesis imperfecta.
Publisher
An entity responsible for making the resource available
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-06
Subject
The topic of the resource
Humans; Time Factors; Animals; Mice; Phenotype; Heterozygote; Body Weight/drug effects; Biomechanical Phenomena; Mutation; Bone and Bones/drug effects; Collagen Type I; Collagen/genetics; Densitometry; Femur/drug effects/pathology; Growth Hormone/*therapeutic use; Lumbar Vertebrae/drug effects; Osteoblasts/*drug effects/metabolism; Osteogenesis Imperfecta/*drug therapy; Inbred C57BL; Animal; Disease Models; Transgenic; Fractures; Bone/prevention & control
Creator
An entity primarily responsible for making the resource
King Donna; Jarjoura David; McEwen Heather A; Askew Michael J
Description
An account of the resource
UNLABELLED: Systemic growth hormone injections increased spine and femur length in a mouse model of OI. Femur BMC, cross-sectional area, and BMD were increased. Smaller gains were produced in vertebral BMC and cross-sectional area. Biomechanical testing showed improvements to structural and material properties in the femur midshaft, supporting expanded testing of growth hormone therapy in children with OI. INTRODUCTION: Osteoblasts in heterozygous Cola2oim mutant mice produce one-half the normal amounts of the alpha2 strand of type I procollagen. The mice experience a mild osteogenesis imperfecta (OI) phenotype, with femurs and vertebrae that require less force than normal to break in a biomechanical test. MATERIALS AND METHODS: Subcutaneous injections of recombinant human growth hormone (rhGH) or saline were given 6 days per week to oim/+ mice between 3 and 12 weeks of age, in a protocol designed to simulate a trial on OI children. RESULTS: rhGH injections promoted significant weight gain and skeletal growth compared with saline-treated control animals. Femur and spine lengths were increased significantly. Significant increases at the femur midshaft in cortical BMD (2.2%), BMC (15.5%), and cross-sectional area (13%) were produced by rhGH treatment. Increases in the same cortical bone parameters were measured in the metaphyseal region of the femur and in tail vertebrae, but lumbar vertebrae showed significant increases in BMC (9.6%) and cross-sectional area (10.1%) of trabecular bone. Three-point bending testing documented functional improvements to the femur mid-shafts. GH treatment produced significant increases in bone stiffness (23.7%), maximum load (30.8%), the energy absorbed by the femurs to the point of maximum load (44.5%), and the energy to actual fracture (40.4%). The ultimate stress endured by the bone material was increased by 14.1%. CONCLUSIONS: Gains in bone length, cross-sectional area, BMD, BMC, structural biomechanical properties, and strength were achieved without directly addressing the genetic collagen defect in the mice. Results support expanded clinical testing of GH injections in children with OI.
Identifier
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<a href="http://doi.org/10.1359/JBMR.050108" target="_blank" rel="noreferrer noopener">10.1359/JBMR.050108</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).
2005
Animal
Animals
Askew Michael J
Biomechanical Phenomena
Body Weight/drug effects
Bone and Bones/drug effects
Bone/prevention & control
Collagen Type I
Collagen/genetics
Densitometry
Department of Family & Community Medicine
Disease Models
Femur/drug effects/pathology
Fractures
Growth Hormone/*therapeutic use
Heterozygote
Humans
Inbred C57BL
Jarjoura David
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
King Donna
Lumbar Vertebrae/drug effects
McEwen Heather A
Mice
Mutation
NEOMED College of Medicine
Osteoblasts/*drug effects/metabolism
Osteogenesis Imperfecta/*drug therapy
Phenotype
Time Factors
Transgenic
-
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/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M064709</a>
Pages
1144–1154
Issue
7
Volume
57
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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Cholesterol 7alpha-hydroxylase-deficient mice are protected from high-fat/high-cholesterol diet-induced metabolic disorders.
Publisher
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Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-07
Subject
The topic of the resource
*bile acids and salt/metabolism; *cholesterol/diet; *lipids; *liver; Animal; Animals; Bile Acids and Salts/genetics/metabolism; Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism; Cholesterol/*metabolism; Diet; Disease Models; Exhalation/genetics; Glucose/metabolism; High-Fat; Homeostasis; Humans; Lipid Metabolism/genetics; Liver/enzymology/pathology; Metabolic Diseases/*genetics/metabolism; Mice
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Boehme Shannon; Li Feng; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) is the first and rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver. In addition to absorption and digestion of nutrients, bile acids play a critical role in the regulation of lipid, glucose, and energy homeostasis. We have backcrossed Cyp7a1(-/-) mice in a mixed B6/129Sv genetic background to C57BL/6J mice to generate Cyp7a1(-/-) mice in a near-pure C57BL/6J background. These mice survive well and have normal growth and a bile acid pool size approximately 60% of WT mice. The expression of the genes in the alternative bile acid synthesis pathway are upregulated, resulting in a more hydrophilic bile acid composition with reduced cholic acid (CA). Surprisingly, Cyp7a1(-/-) mice have improved glucose sensitivity with reduced liver triglycerides and fecal bile acid excretion, but increased fecal fatty acid excretion and respiratory exchange ratio (RER) when fed a high-fat/high-cholesterol diet. Supplementing chow and Western diets with CA restored bile acid composition, reversed the glucose tolerant phenotype, and reduced the RER. Our current study points to a critical role of bile acid composition, rather than bile acid pool size, in regulation of glucose, lipid, and energy metabolism to improve glucose and insulin tolerance, maintain metabolic homeostasis, and prevent high-fat diet-induced metabolic disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">10.1194/jlr.M064709</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).
*bile acids and salt/metabolism
*cholesterol/diet
*Lipids
*Liver
2016
Animal
Animals
Bile Acids and Salts/genetics/metabolism
Boehme Shannon
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism
Cholesterol/*metabolism
Department of Integrative Medical Sciences
Diet
Disease Models
Exhalation/genetics
Ferrell Jessica M
Glucose/metabolism
High-Fat
Homeostasis
Humans
Journal of lipid research
Li Feng
Lipid Metabolism/genetics
Liver/enzymology/pathology
Metabolic Diseases/*genetics/metabolism
Mice
NEOMED College of Medicine
-
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/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M015859</a>
Pages
1561–1568
Issue
8
Volume
52
Dublin Core
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Title
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Aldo-keto reductase 1B7 is a target gene of FXR and regulates lipid and glucose homeostasis.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
*Aldehyde Reductase/genetics/metabolism; Adenoviridae; Animal; Animals; Blood Glucose/*metabolism; Cholesterol/analysis; Cytoplasmic and Nuclear/genetics/*metabolism; Diabetes Mellitus/genetics/*metabolism/physiopathology; Disease Models; Fatty Liver/genetics/*metabolism/physiopathology; Gene Expression; Genetic Vectors; Gluconeogenesis/genetics; Homeostasis; Humans; Liver/*metabolism/physiopathology; Malondialdehyde/blood; Mice; Polymerase Chain Reaction; Receptors; Transfection; Transgenic; Triglycerides/analysis
Creator
An entity primarily responsible for making the resource
Ge Xuemei; Yin Liya; Ma Huiyan; Li Tiangang; Chiang John Y L; Zhang Yanqiao
Description
An account of the resource
Aldo-keto reductase 1B7 (AKR1B7) is proposed to play a role in detoxification of by-products of lipid peroxidation. In this article, we show that activation of the nuclear receptor farnesoid X receptor (FXR) induces AKR1B7 expression in the liver and intestine, and reduces the levels of malondialdehyde (MDA), the end product of lipid peroxidation, in the intestine but not in the liver. To determine whether AKR1B7 regulates MDA levels in vivo, we overexpressed AKR1B7 in the liver. Overexpression of AKR1B7 in the liver had no effect on hepatic or plasma MDA levels. Interestingly, hepatic expression of AKR1B7 significantly lowered plasma glucose levels in both wild-type and diabetic db/db mice, which was associated with reduced hepatic gluconeogenesis. Hepatic expression of AKR1B7 also significantly lowered hepatic triglyceride and cholesterol levels in db/db mice. These data reveal a novel function for AKR1B7 in lipid and glucose metabolism and suggest that AKR1B7 may not play a role in detoxification of lipid peroxides in the liver. AKR1B7 may be a therapeutic target for treatment of fatty liver disease associated with diabetes mellitus.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">10.1194/jlr.M015859</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).
*Aldehyde Reductase/genetics/metabolism
2011
Adenoviridae
Animal
Animals
Blood Glucose/*metabolism
Chiang John Y L
Cholesterol/analysis
Cytoplasmic and Nuclear/genetics/*metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus/genetics/*metabolism/physiopathology
Disease Models
Fatty Liver/genetics/*metabolism/physiopathology
Ge Xuemei
Gene Expression
Genetic Vectors
Gluconeogenesis/genetics
Homeostasis
Humans
Journal of lipid research
Li Tiangang
Liver/*metabolism/physiopathology
Ma Huiyan
Malondialdehyde/blood
Mice
NEOMED College of Medicine
Polymerase Chain Reaction
Receptors
Transfection
Transgenic
Triglycerides/analysis
Yin Liya
Zhang Yanqiao
-
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/10.1186/s13148-017-0416-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s13148-017-0416-5</a>
Pages
117–117
Volume
9
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
Turnover of histones and histone variants in postnatal rat brain: effects of alcohol exposure.
Publisher
An entity responsible for making the resource available
Clinical epigenetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
*2H2O-labeling; *Brain; *Genetic Variation; *Histone; *Mass spectrometry; *Post-translational modifications; *Postnatal alcohol exposure; *Turnover; Acetylation; Animal; Animals; Cell Proliferation; Disease Models; DNA Damage; Epigenesis; Female; Fetal Alcohol Spectrum Disorders/genetics/*metabolism; Genetic; Histones/*genetics/*metabolism; Humans; Post-Translational; Pregnancy; Protein Processing; Proteomics/*methods; Rats; Sprague-Dawley
Creator
An entity primarily responsible for making the resource
Rachdaoui Nadia; Li Ling; Willard Belinda; Kasumov Takhar; Previs Stephen; Sarkar Dipak
Description
An account of the resource
BACKGROUND: Alcohol consumption during pregnancy is a significant public health problem and can result in a continuum of adverse outcomes to the fetus known as fetal alcohol spectrum disorders (FASD). Subjects with FASD show significant neurological deficits, ranging from microencephaly, neurobehavioral, and mental health problems to poor social adjustment and stress tolerance. Neurons are particularly sensitive to alcohol exposure. The neurotoxic action of alcohol, i.e., through ROS production, induces DNA damage and neuronal cell death by apoptosis. In addition, epigenetics, including DNA methylation, histone posttranslational modifications (PTMs), and non-coding RNA, play an important role in the neuropathology of FASD. However, little is known about the temporal dynamics and kinetics of histones and their PTMs in FASD. RESULTS: We examined the effects of postnatal alcohol exposure (PAE), an animal model of human third-trimester equivalent, on the kinetics of various histone proteins in two distinct brain regions, the frontal cortex, and the hypothalamus, using in vivo (2)H2O-labeling combined with mass spectrometry-based proteomics. We show that histones have long half-lives that are in the order of days. We also show that H3.3 and H2Az histone variants have faster turnovers than canonical histones and that acetylated histones, in general, have a faster turnover than unmodified and methylated histones. Our work is the first to show that PAE induces a differential reduction in turnover rates of histones in both brain regions studied. These alterations in histone turnover were associated with increased DNA damage and decreased cell proliferation in postnatal rat brain. CONCLUSION: Alterations in histone turnover might interfere with histone deposition and chromatin stability, resulting in deregulated cell-specific gene expression and therefore contribute to the development of the neurological disorders associated with FASD. Using in vivo (2)H2O-labeling and mass spectrometry-based proteomics might help in the understanding of histone turnover following alcohol exposure and could be of great importance in enabling researchers to identify novel targets and/or biomarkers for the prevention and management of fetal alcohol spectrum disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s13148-017-0416-5" target="_blank" rel="noreferrer noopener">10.1186/s13148-017-0416-5</a>
Rights
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).
*2H2O-labeling
*Brain
*Genetic Variation
*Histone
*Mass spectrometry
*Post-translational modifications
*Postnatal alcohol exposure
*Turnover
2017
Acetylation
Animal
Animals
Cell Proliferation
Clinical epigenetics
Department of Pharmaceutical Sciences
Disease Models
DNA Damage
Epigenesis
Female
Fetal Alcohol Spectrum Disorders/genetics/*metabolism
Genetic
Histones/*genetics/*metabolism
Humans
Kasumov Takhar
Li Ling
NEOMED College of Pharmacy
Post-Translational
Pregnancy
Previs Stephen
Protein Processing
Proteomics/*methods
Rachdaoui Nadia
Rats
Sarkar Dipak
Sprague-Dawley
Willard Belinda
-
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/10.1186/s13024-017-0216-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s13024-017-0216-6</a>
Pages
74–74
Issue
1
Volume
12
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
TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy.
Publisher
An entity responsible for making the resource available
Molecular neurodegeneration
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-10
Subject
The topic of the resource
*Alzheimers disease; *Immunity; *Inflammation; *Tauopathy; *TREM2; Animal; Animals; Disease Models; Humans; Immunologic/*deficiency; Inbred C57BL; Membrane Glycoproteins/*deficiency; Mice; Microglia/metabolism; Protein Kinases/*metabolism; Receptors; Signal Transduction/physiology; tau Proteins/*metabolism; Tauopathies/metabolism/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Bemiller Shane M; McCray Tyler J; Allan Kevin; Formica Shane V; Xu Guixiang; Wilson Gina; Kokiko-Cochran Olga N; Crish Samuel D; Lasagna-Reeves Cristian A; Ransohoff Richard M; Landreth Gary E; Lamb Bruce T
Description
An account of the resource
BACKGROUND: Genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) confer increased risk of developing late-onset Alzheimer's Disease (LOAD) and other neurodegenerative disorders. Recent studies provided insight into the multifaceted roles of TREM2 in regulating extracellular beta-amyloid (Abeta) pathology, myeloid cell accumulation, and inflammation observed in AD, yet little is known regarding the role of TREM2 in regulating intracellular microtubule associated protein tau (MAPT; tau) pathology in neurodegenerative diseases and in AD, in particular. RESULTS: Here we report that TREM2 deficiency leads to accelerated and exacerbated hyperphosphorylation and aggregation of tau in a humanized mouse model of tauopathy. TREM2 deficiency also results, indirectly, in dramatic widespread dysregulation of neuronal stress kinase pathways. CONCLUSIONS: Our results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases. These findings offer new insight into the complex, multiple roles of TREM2 in regulating Abeta and tau pathologies.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s13024-017-0216-6" target="_blank" rel="noreferrer noopener">10.1186/s13024-017-0216-6</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).
*Alzheimers disease
*Immunity
*Inflammation
*Tauopathy
*TREM2
2017
Allan Kevin
Animal
Animals
Bemiller Shane M
Crish Samuel D
Department of Pharmaceutical Sciences
Disease Models
Formica Shane V
Humans
Immunologic/*deficiency
Inbred C57BL
Kokiko-Cochran Olga N
Lamb Bruce T
Landreth Gary E
Lasagna-Reeves Cristian A
McCray Tyler J
Membrane Glycoproteins/*deficiency
Mice
Microglia/metabolism
Molecular neurodegeneration
NEOMED College of Pharmacy
Protein Kinases/*metabolism
Ransohoff Richard M
Receptors
Signal Transduction/physiology
tau Proteins/*metabolism
Tauopathies/metabolism/*pathology
Transgenic
Wilson Gina
Xu Guixiang
-
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/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1346-7</a>
Pages
313–313
Issue
1
Volume
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
Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-11
Subject
The topic of the resource
AMP-activated protein kinase; AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Pathology; Diet; Disease Models; Eye Proteins/genetics; Female; G-Protein-Coupled – Metabolism; G-Protein-Coupled/*metabolism; Glaucoma; Glaucoma – Complications; Glaucoma – Pathology; Glaucoma/*complications/pathology; Impact of Events Scale; Inbred DBA; Inflammation – Etiology; Inflammation – Prevention and Control; Inflammation hydroxycarboxylic acid receptor; Inflammation/*etiology/*prevention & control; Ketogenic diet; Ketogenic/methods; Male; Membrane Glycoproteins; Membrane Glycoproteins/genetics; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia/drug effects/pathology; Models; Mutation; Mutation/genetics; Neuroprotection/drug effects/*physiology; NLR Family; Optic Nerve – Pathology; Optic Nerve/pathology; Phosphotransferases – Metabolism; Proteins; Pyrin Domain-Containing 3 Protein/genetics/metabolism; Receptors; Retina – Drug Effects; Retina – Pathology; Retinal Ganglion Cells/drug effects/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Harun-Or-Rashid Mohammad; Inman Denise M
Description
An account of the resource
BACKGROUND: Glaucoma is a chronic degenerative disease for which inflammation is considered to play a pivotal role in the pathogenesis and progression. In this study, we examined the impact of a ketogenic diet on the inflammation evident in glaucoma as a follow-up to a recent set of experiments in which we determined that a ketogenic diet protected retinal ganglion cell structure and function. METHODS: Both sexes of DBA/2J (D2) mice were placed on a ketogenic diet (keto) or standard rodent chow (untreated) for 8 weeks beginning at 9 months of age. DBA/2J-Gpnmb(+) (D2G) mice were also used as a non-pathological genetic control for the D2 mice. Retina and optic nerve (ON) tissues were micro-dissected and used for the analysis of microglia activation, expression of pro- and anti-inflammatory molecules, and lactate- or ketone-mediated anti-inflammatory signaling. Data were analyzed by immunohistochemistry, quantitative RT-PCR, ELISA, western blot, and capillary tube-based electrophoresis techniques. RESULTS: Microglia activation was observed in D2 retina and ON as documented by intense microglial-specific Iba1 immunolabeling of rounded-up and enlarged microglia. Ketogenic diet treatment reduced Iba1 expression and the activated microglial phenotype. We detected low energy-induced AMP-activated protein kinase (AMPK) phosphorylation in D2 retina and ON that triggered NF-kappaB p65 signaling through its nuclear translocation. NF-kappaB induced pro-inflammatory TNF-alpha,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1346-7</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).
2018
AMP-activated protein kinase
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cells – Drug Effects
Cells – Pathology
Department of Pharmaceutical Sciences
Diet
Disease Models
Eye Proteins/genetics
Female
G-Protein-Coupled – Metabolism
G-Protein-Coupled/*metabolism
Glaucoma
Glaucoma – Complications
Glaucoma – Pathology
Glaucoma/*complications/pathology
Harun-Or-Rashid Mohammad
Impact of Events Scale
Inbred DBA
Inflammation – Etiology
Inflammation – Prevention and Control
Inflammation hydroxycarboxylic acid receptor
Inflammation/*etiology/*prevention & control
Inman Denise M
Journal of neuroinflammation
Ketogenic diet
Ketogenic/methods
Male
Membrane Glycoproteins
Membrane Glycoproteins/genetics
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia/drug effects/pathology
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Neuroprotection/drug effects/*physiology
NLR Family
Optic Nerve – Pathology
Optic Nerve/pathology
Phosphotransferases – Metabolism
Proteins
Pyrin Domain-Containing 3 Protein/genetics/metabolism
Receptors
Retina – Drug Effects
Retina – Pathology
Retinal Ganglion Cells/drug effects/*pathology
Transgenic
-
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/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1310-6</a>
Pages
278–278
Issue
1
Volume
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
Genetically enhancing the expression of chemokine domain of CX3CL1 fails to prevent tau pathology in mouse models of tauopathy.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-09
Subject
The topic of the resource
Alzheimer's disease; Animal; Animals; Antigens; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Metabolism; Cells – Pathology; Chemokine CX3CL1/*genetics/metabolism; Cognition Disorders – Etiology; Cognition Disorders/etiology; CX3CL1; CX3CR1; Cytokines; Cytokines – Metabolism; Cytokines/metabolism; Differentiation/genetics/metabolism; Disease Models; Gene Expression Regulation/drug effects/*genetics; Genes; Genes – Drug Effects; Learning; Lipopolysaccharides; Lipopolysaccharides/toxicity; Maze Learning; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia; Microglia/drug effects/*metabolism/pathology; Models; Mutation; Mutation/genetics; Nerve Tissue Proteins; Nerve Tissue Proteins – Metabolism; Neurodegenerative Diseases; Neurodegenerative Diseases – Complications; Neurodegenerative Diseases – Pathology; Neuroinflammation; Surface; Surface – Metabolism; Tau; tau Proteins/genetics/metabolism; Tauopathies; Tauopathies/complications/genetics/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Bemiller Shane M; Maphis Nicole M; Formica Shane V; Wilson Gina N; Miller Crystal M; Xu Guixiang; Kokiko-Cochran Olga N; Kim Ki-Wook; Jung Steffen; Cannon Judy L; Crish Samuel D; Cardona Astrid E; Lamb Bruce T; Bhaskar Kiran
Description
An account of the resource
BACKGROUND: Fractalkine (CX3CL1) and its receptor (CX3CR1) play an important role in regulating microglial function. We have previously shown that Cx3cr1 deficiency exacerbated tau pathology and led to cognitive impairment. However, it is still unclear if the chemokine domain of the ligand CX3CL1 is essential in regulating neuronal tau pathology. METHODS: We used transgenic mice lacking endogenous Cx3cl1 (Cx3cl1(-/-)) and expressing only obligatory soluble form (with only chemokine domain) and lacking the mucin stalk of CX3CL1 (referred to as Cx3cl1(105Delta) mice) to assess tau pathology and behavioral function in both lipopolysaccharide (LPS) and genetic (hTau) mouse models of tauopathy. RESULTS: First, increased basal tau levels accompanied microglial activation in Cx3cl1(105Delta) mice compared to control groups. Second, increased CD45(+) and F4/80(+) neuroinflammation and tau phosphorylation were observed in LPS, hTau/Cx3cl1(-/-), and hTau/Cx3cl1(105Delta) mouse models of tau pathology, which correlated with impaired spatial learning. Finally, microglial cell surface expression of CX3CR1 was reduced in Cx3cl1(105Delta) mice, suggesting enhanced fractalkine receptor internalization (mimicking Cx3cr1 deletion), which likely contributes to the elevated tau pathology. CONCLUSIONS: Collectively, our data suggest that overexpression of only chemokine domain of CX3CL1 does not protect against tau pathology.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1310-6</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).
2018
Alzheimer's disease
Animal
Animals
Antigens
Bemiller Shane M
Bhaskar Kiran
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cannon Judy L
Cardona Astrid E
Cells – Drug Effects
Cells – Metabolism
Cells – Pathology
Chemokine CX3CL1/*genetics/metabolism
Cognition Disorders – Etiology
Cognition Disorders/etiology
Crish Samuel D
CX3CL1
CX3CR1
Cytokines
Cytokines – Metabolism
Cytokines/metabolism
Department of Pharmaceutical Sciences
Differentiation/genetics/metabolism
Disease Models
Formica Shane V
Gene Expression Regulation/drug effects/*genetics
Genes
Genes – Drug Effects
Journal of neuroinflammation
Jung Steffen
Kim Ki-Wook
Kokiko-Cochran Olga N
Lamb Bruce T
Learning
Lipopolysaccharides
Lipopolysaccharides/toxicity
Maphis Nicole M
Maze Learning
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia
Microglia/drug effects/*metabolism/pathology
Miller Crystal M
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Nerve Tissue Proteins
Nerve Tissue Proteins – Metabolism
Neurodegenerative Diseases
Neurodegenerative Diseases – Complications
Neurodegenerative Diseases – Pathology
Neuroinflammation
Surface
Surface – Metabolism
Tau
tau Proteins/genetics/metabolism
Tauopathies
Tauopathies/complications/genetics/*pathology
Transgenic
Wilson Gina N
Xu Guixiang
-
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/10.1186/1742-2094-5-28" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/1742-2094-5-28</a>
Pages
28–28
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
Suppression of acute proinflammatory cytokine and chemokine upregulation by post-injury administration of a novel small molecule improves long-term neurologic outcome in a mouse model of traumatic brain injury.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-06
Subject
The topic of the resource
Animal; Animals; Brain Injuries/blood/epidemiology/genetics/*physiopathology; Cerebral Cortex/physiopathology; Chemokine CCL2/genetics/physiology; Chemokines/*genetics; Cytokines/*antagonists & inhibitors; Disease Models; Hippocampus/physiopathology; Inflammation/genetics/*physiopathology; Interleukin-1beta/genetics/physiology; Interleukin-6/genetics/physiology; Male; Mice; Tumor Necrosis Factor-alpha/genetics/physiology; United States/epidemiology; Up-Regulation
Creator
An entity primarily responsible for making the resource
Lloyd Eric; Somera-Molina Kathleen; Van Eldik Linda J; Watterson D Martin; Wainwright Mark S
Description
An account of the resource
BACKGROUND: Traumatic brain injury (TBI) with its associated morbidity is a major area of unmet medical need that lacks effective therapies. TBI initiates a neuroinflammatory cascade characterized by activation of astrocytes and microglia, and increased production of immune mediators including proinflammatory cytokines and chemokines. This inflammatory response contributes both to the acute pathologic processes following TBI including cerebral edema, in addition to longer-term neuronal damage and cognitive impairment. However, activated glia also play a neuroprotective and reparative role in recovery from injury. Thus, potential therapeutic strategies targeting the neuroinflammatory cascade must use careful dosing considerations, such as amount of drug and timing of administration post injury, in order not to interfere with the reparative contribution of activated glia. METHODS: We tested the hypothesis that attenuation of the acute increase in proinflammatory cytokines and chemokines following TBI would decrease neurologic injury and improve functional neurologic outcome. We used the small molecule experimental therapeutic, Minozac (Mzc), to suppress TBI-induced up-regulation of glial activation and proinflammatory cytokines back towards basal levels. Mzc was administered in a clinically relevant time window post-injury in a murine closed-skull, cortical impact model of TBI. Mzc effects on the acute increase in brain cytokine and chemokine levels were measured as well as the effect on neuronal injury and neurobehavioral function. RESULTS: Administration of Mzc (5 mg/kg) at 3 h and 9 h post-TBI attenuates the acute increase in proinflammatory cytokine and chemokine levels, reduces astrocyte activation, and the longer term neurologic injury, and neurobehavioral deficits measured by Y maze performance over a 28-day recovery period. Mzc-treated animals also have no significant increase in brain water content (edema), a major cause of the neurologic morbidity associated with TBI. CONCLUSION: These results support the hypothesis that proinflammatory cytokines contribute to a glial activation cycle that produces neuronal dysfunction or injury following TBI. The improvement in long-term functional neurologic outcome following suppression of cytokine upregulation in a clinically relevant therapeutic window indicates that selective targeting of neuroinflammation may lead to novel therapies for the major neurologic morbidities resulting from head injury, and indicates the potential of Mzc as a future therapeutic for TBI.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/1742-2094-5-28" target="_blank" rel="noreferrer noopener">10.1186/1742-2094-5-28</a>
Rights
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).
2008
Animal
Animals
Brain Injuries/blood/epidemiology/genetics/*physiopathology
Cerebral Cortex/physiopathology
Chemokine CCL2/genetics/physiology
Chemokines/*genetics
Cytokines/*antagonists & inhibitors
Disease Models
Hippocampus/physiopathology
Inflammation/genetics/*physiopathology
Interleukin-1beta/genetics/physiology
Interleukin-6/genetics/physiology
Journal of neuroinflammation
Lloyd Eric
Male
Mice
Somera-Molina Kathleen
Tumor Necrosis Factor-alpha/genetics/physiology
United States/epidemiology
Up-Regulation
Van Eldik Linda J
Wainwright Mark S
Watterson D Martin
-
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/10.1164/ajrccm.158.3.9802031" target="_blank" rel="noreferrer noopener">http://doi.org/10.1164/ajrccm.158.3.9802031</a>
Pages
760–768
Issue
3
Volume
158
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
Adrenal epinephrine increases alveolar liquid clearance in a canine model of neurogenic pulmonary edema.
Publisher
An entity responsible for making the resource available
American journal of respiratory and critical care medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
1998
1998-09
Subject
The topic of the resource
Adrenal Glands/*metabolism; Adrenalectomy; Adrenergic beta-Agonists/blood/*pharmacology/therapeutic use; Adrenergic beta-Antagonists/therapeutic use; Amiloride/therapeutic use; Animal; Animals; Blood; Blood Pressure; Brain Diseases/chemically induced/*complications; Central Nervous System Agents/adverse effects; Cisterna Magna; Disease Models; Diuretics/therapeutic use; Dogs; Epinephrine/blood/*physiology/therapeutic use; Extravascular Lung Water/chemistry/*metabolism; Female; Hypertension; Injections; Male; Propanolamines/therapeutic use; Proteins/analysis; Pulmonary Alveoli/*metabolism; Pulmonary Artery; Pulmonary Edema/etiology/*metabolism/prevention & control; Pulmonary/prevention & control; Sodium Channel Blockers; Veratrine/adverse effects
Creator
An entity primarily responsible for making the resource
Lane S M; Maender K C; Awender N E; Maron M B
Description
An account of the resource
Case reports of neurogenic pulmonary edema (NPE) often indicate that the edema resolves quickly. Because plasma epinephrine concentration may be elevated in NPE, and epinephrine has been shown to increase the rate of alveolar liquid clearance (ALC), we determined if ALC was increased in a canine model of NPE produced by the intracisternal administration of veratrine. ALC was determined by instilling autologous plasma into a lower lung lobe and using the increase in instillate protein concentration after 4 h to calculate the volume of fluid cleared from the airspaces by mass balance. To prevent pulmonary hypertension and edema, which would confound the mass balance analysis, carotid arterial blood was allowed to drain into a reservoir as pulmonary arterial pressure started to rise after veratrine administration. ALC in animals administered veratrine (n = 6) was 30.4 +/- 1.6 (SE)% of the instilled volume compared with 14.1 +/- 2.1% observed in control animals. The increase in ALC could be inhibited by adrenalectomy, beta2-adrenergic blockade using ICI 118,551, or sodium channel blockade using amiloride and could be duplicated by infusing epinephrine to increase plasma epinephrine concentration to levels observed in NPE. These data indicate that the increased ALC was mediated by adrenal epinephrine and suggest that edema resolution in patients with NPE might be accelerated by endogenous epinephrine.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1164/ajrccm.158.3.9802031" target="_blank" rel="noreferrer noopener">10.1164/ajrccm.158.3.9802031</a>
Rights
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).
1998
Adrenal Glands/*metabolism
Adrenalectomy
Adrenergic beta-Agonists/blood/*pharmacology/therapeutic use
Adrenergic beta-Antagonists/therapeutic use
American journal of respiratory and critical care medicine
Amiloride/therapeutic use
Animal
Animals
Awender N E
Blood
Blood Pressure
Brain Diseases/chemically induced/*complications
Central Nervous System Agents/adverse effects
Cisterna Magna
Disease Models
Diuretics/therapeutic use
Dogs
Epinephrine/blood/*physiology/therapeutic use
Extravascular Lung Water/chemistry/*metabolism
Female
Hypertension
Injections
Lane S M
Maender K C
Male
Maron M B
Propanolamines/therapeutic use
Proteins/analysis
Pulmonary Alveoli/*metabolism
Pulmonary Artery
Pulmonary Edema/etiology/*metabolism/prevention & control
Pulmonary/prevention & control
Sodium Channel Blockers
Veratrine/adverse effects
-
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/10.1161/CIRCRESAHA.111.252734" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.252734</a>
Pages
851–856
Issue
6
Volume
110
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
Absence of type VI collagen paradoxically improves cardiac function, structure, and remodeling after myocardial infarction.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-03
Subject
The topic of the resource
Animal; Animals; Apoptosis/physiology; Cardiac/pathology/physiology; Collagen Type VI/*genetics/*metabolism; Disease Models; Echocardiography; Extracellular Matrix/metabolism/pathology; Fibrosis/genetics/pathology/physiopathology; Knockout; Male; Mice; Myocardial Infarction/diagnostic imaging/*genetics/*physiopathology; Myocytes; Ventricular Remodeling/*physiology
Creator
An entity primarily responsible for making the resource
Luther Daniel J; Thodeti Charles K; Shamhart Patricia E; Adapala Ravi K; Hodnichak Cheryl; Weihrauch Dorothee; Bonaldo Paolo; Chilian William M; Meszaros J Gary
Description
An account of the resource
RATIONALE: We previously reported that type VI collagen deposition increases in the infarcted myocardium in vivo. To date, a specific role for this nonfibrillar collagen has not been explored in the setting of myocardial infarction (MI). OBJECTIVE: To determine whether deletion of type VI collagen in an in vivo model of post-MI wound healing would alter cardiac function and remodeling in the days to weeks after injury. METHODS AND RESULTS: Wild-type and Col6a1(-/-) mice were subjected to MI, followed by serial echocardiographic and histological assessments. At 8 weeks after MI, infarct size was significantly reduced, ejection fraction was significantly preserved (43.9% +/- 3.3% versus 29.1% +/- 4.3% for wild-type), and left ventricular chamber dilation was attenuated in the Col6a1(-/-) MI group (25.8% +/- 7.9% increase versus 62.6% +/- 16.5% for wild-type). The improvement in cardiac remodeling was evident as early as 10 days after MI in the Col6a1(-/-) mice. Myocyte apoptosis within the infarcted zones was initially greater in the Col6a1(-/-) group 3 days after MI, but by day 14 this was significantly reduced. Collagen deposition also was reduced in the infarcted and remote areas of the Col6a1(-/-) hearts. The reductions in chronic myocyte apoptosis and fibrosis are critical events leading to improved long-term remodeling and functional outcomes. CONCLUSIONS: These unexpected results demonstrate for the first time that deletion of type VI collagen in this knockout model plays a critical protective role after MI by limiting infarct size, chronic apoptosis, aberrant remodeling, and fibrosis, leading to preservation of cardiac function.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.252734" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.252734</a>
Rights
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).
2012
Adapala Ravi K
Animal
Animals
Apoptosis/physiology
Bonaldo Paolo
Cardiac/pathology/physiology
Chilian William M
Circulation research
Collagen Type VI/*genetics/*metabolism
Department of Integrative Medical Sciences
Disease Models
Echocardiography
Extracellular Matrix/metabolism/pathology
Fibrosis/genetics/pathology/physiopathology
Hodnichak Cheryl
Knockout
Luther Daniel J
Male
Meszaros J Gary
Mice
Myocardial Infarction/diagnostic imaging/*genetics/*physiopathology
Myocytes
NEOMED College of Medicine
Shamhart Patricia E
Thodeti Charles K
Ventricular Remodeling/*physiology
Weihrauch Dorothee
-
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/10.1161/CIRCRESAHA.111.250126" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.250126</a>
Pages
241–252
Issue
2
Volume
110
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
Induction of vascular progenitor cells from endothelial cells stimulates coronary collateral growth.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
*Collateral Circulation; *Coronary Circulation; Animal; Animals; Biomarkers/metabolism; Cell Differentiation; Cell Lineage; Cells; Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery; Coronary Vessels/metabolism/pathology/*physiopathology; Cultured; Developmental; Disease Models; Endothelial Cells/metabolism/pathology/*transplantation; Epigenesis; Gene Expression Profiling; Gene Expression Regulation; Genetic; Induced Pluripotent Stem Cells/metabolism/*transplantation; Mice; Muscle; Myocytes; Neovascularization; Physiologic; Rats; Regenerative Medicine/methods; Regional Blood Flow; Reverse Transcriptase Polymerase Chain Reaction; SCID; Smooth; Smooth Muscle/metabolism/pathology/*transplantation; Sprague-Dawley; Teratoma/metabolism/pathology; Time Factors; Transcription Factors/genetics/metabolism; Transduction; Vascular/metabolism/pathology/*physiopathology
Creator
An entity primarily responsible for making the resource
Yin Liya; Ohanyan Vahagn; Pung Yuh Fen; Delucia Angelo; Bailey Erin; Enrick Molly; Stevanov Kelly; Kolz Christopher L; Guarini Giacinta; Chilian William M
Description
An account of the resource
RATIONALE: A well-developed coronary collateral circulation improves the morbidity and mortality of patients following an acute coronary occlusion. Although regenerative medicine has great potential in stimulating vascular growth in the heart, to date there have been mixed results, and the ideal cell type for this therapy has not been resolved. OBJECTIVE: To generate induced vascular progenitor cells (iVPCs) from endothelial cells, which can differentiate into vascular smooth muscle cells (VSMCs) or endothelial cells (ECs), and test their capability to stimulate coronary collateral growth. METHODS AND RESULTS: We reprogrammed rat ECs with the transcription factors Oct4, Klf4, Sox2, and c-Myc. A population of reprogrammed cells was derived that expressed pluripotent markers Oct4, SSEA-1, Rex1, and AP and hemangioblast markers CD133, Flk1, and c-kit. These cells were designated iVPCs because they remained committed to vascular lineage and could differentiate into vascular ECs and VSMCs in vitro. The iVPCs demonstrated better in vitro angiogenic potential (tube network on 2-dimensional culture, tube formation in growth factor reduced Matrigel) than native ECs. The risk of teratoma formation in iVPCs is also reduced in comparison with fully reprogrammed induced pluripotent stem cells (iPSCs). When iVPCs were implanted into myocardium, they engrafted into blood vessels and increased coronary collateral flow (microspheres) and improved cardiac function (echocardiography) better than iPSCs, mesenchymal stem cells, native ECs, and sham treatments. CONCLUSIONS: We conclude that iVPCs, generated by partially reprogramming ECs, are an ideal cell type for cell-based therapy designed to stimulate coronary collateral growth.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.250126" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.250126</a>
Rights
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).
*Collateral Circulation
*Coronary Circulation
2012
Animal
Animals
Bailey Erin
Biomarkers/metabolism
Cell Differentiation
Cell Lineage
Cells
Chilian William M
Circulation research
Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery
Coronary Vessels/metabolism/pathology/*physiopathology
Cultured
Delucia Angelo
Department of Integrative Medical Sciences
Developmental
Disease Models
Endothelial Cells/metabolism/pathology/*transplantation
Enrick Molly
Epigenesis
Gene Expression Profiling
Gene Expression Regulation
Genetic
Guarini Giacinta
Induced Pluripotent Stem Cells/metabolism/*transplantation
Kolz Christopher L
Mice
Muscle
Myocytes
NEOMED College of Medicine
Neovascularization
Ohanyan Vahagn
Physiologic
Pung Yuh Fen
Rats
Regenerative Medicine/methods
Regional Blood Flow
Reverse Transcriptase Polymerase Chain Reaction
SCID
Smooth
Smooth Muscle/metabolism/pathology/*transplantation
Sprague-Dawley
Stevanov Kelly
Teratoma/metabolism/pathology
Time Factors
Transcription Factors/genetics/metabolism
Transduction
Vascular/metabolism/pathology/*physiopathology
Yin Liya
-
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/10.1161/CIRCEP.114.001578" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCEP.114.001578</a>
Pages
1181–1188
Issue
6
Volume
7
Dublin Core
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Title
A name given to the resource
Isolation of canine coronary sinus musculature from the atria by radiofrequency catheter ablation prevents induction of atrial fibrillation.
Publisher
An entity responsible for making the resource available
Circulation. Arrhythmia and electrophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-12
Subject
The topic of the resource
*Catheter Ablation; Acetylcholine; Action Potentials; Animal; Animal Studies; Animals; Artificial; atrial fibrillation; Atrial Fibrillation – Etiology; Atrial Fibrillation – Physiopathology; Atrial Fibrillation – Prevention and Control; Atrial Fibrillation/etiology/physiopathology/*prevention & control; Biological; Body Surface Potential Mapping; Cardiac Pacing; catheter ablation; Catheter Ablation; coronary sinus; Coronary Sinus/physiopathology/*surgery; Coronary Vessels – Physiopathology; Coronary Vessels – Surgery; Disease Models; Dogs; Heart Atria/physiopathology/surgery; Heart Atrium – Physiopathology; Heart Atrium – Surgery; Male; Models; optical Vm mapping; Time Factors
Creator
An entity primarily responsible for making the resource
Morita Hiroshi; Zipes Douglas P; Morita Shiho T; Wu Jiashin
Description
An account of the resource
BACKGROUND: The junction between the coronary sinus (CS) musculature and both atria contributes to initiation of atrial tachyarrhythmias. The current study investigated the effects of CS isolation from the atria by radiofrequency catheter ablation on the induction and maintenance of atrial fibrillation (AF). METHODS AND RESULTS: Using an optical mapping system, we mapped action potentials at 256 surface sites in 17 isolated and arterially perfused canine atrial tissues containing the entire musculature of the CS, right atrial septum, posterior left atrium, left inferior pulmonary vein, and vein of Marshal. Rapid pacing from each site before and after addition of acetylcholine (0.5 mumol/L) was applied to induce AF. Epicardial radiofrequency catheter ablation at CS-atrial junctions isolated the CS from the atria. Rapid pacing induced sustained AF in all tissues after acetylcholine. Microreentry within the CS drove AF in 88% of preparations. Reentries associated with the vein of Marshall (29%), CS-atrial junctions (53%), right atrium (65%), and pulmonary vein (76%) (frequently with 2-4 simultaneous circuits) were additional drivers of AF. Radiofrequency catheter ablation eliminated AF in 13 tissues before acetylcholine (P\textless0.01) and in 5 tissues after acetylcholine. Radiofrequency catheter ablation also abbreviated the duration of AF in 12 tissues (P\textless0.01). CONCLUSIONS: CS and its musculature developed unstable reentry and AF, which were prevented by isolation of CS musculature from atrial tissue. The results suggest that CS can be a substrate of recurrent AF in patients after pulmonary vein isolation and that CS isolation might help prevent recurrent AF.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCEP.114.001578" target="_blank" rel="noreferrer noopener">10.1161/CIRCEP.114.001578</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).
*Catheter Ablation
2014
Acetylcholine
Action Potentials
Animal
Animal Studies
Animals
Artificial
Atrial fibrillation
Atrial Fibrillation – Etiology
Atrial Fibrillation – Physiopathology
Atrial Fibrillation – Prevention and Control
Atrial Fibrillation/etiology/physiopathology/*prevention & control
Biological
Body Surface Potential Mapping
Cardiac Pacing
Catheter Ablation
Circulation. Arrhythmia and electrophysiology
coronary sinus
Coronary Sinus/physiopathology/*surgery
Coronary Vessels – Physiopathology
Coronary Vessels – Surgery
Disease Models
Dogs
Heart Atria/physiopathology/surgery
Heart Atrium – Physiopathology
Heart Atrium – Surgery
Male
Models
Morita Hiroshi
Morita Shiho T
optical Vm mapping
Time Factors
Wu Jiashin
Zipes Douglas P
-
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/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.113.301591</a>
Pages
1911–1919
Issue
8
Volume
33
Dublin Core
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Title
A name given to the resource
Mitochondrial oxidative stress corrupts coronary collateral growth by activating adenosine monophosphate activated kinase-alpha signaling.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Body Weight/physiology; Cells; collateral circulation; coronary circulation; Coronary Vessels/cytology/*enzymology; Cultured; Disease Models; Endothelial Cells/cytology/*enzymology; Humans; Inbred WKY; Ischemia/metabolism/pathology; mitochondria; Mitochondria/drug effects/*metabolism; Myocardium/enzymology/pathology; Oxidative Stress/*physiology; Rats; reactive oxygen species; Rotenone/pharmacology; Signal Transduction/*physiology; TOR Serine-Threonine Kinases/metabolism; Uncoupling Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Stevanov Kelly; Enrick Molly; Chen Chwen-Lih; Kolz Christopher; Thakker Prashanth; Hardwick James P; Chen Yeong-Renn; Dyck Jason R B; Yin Liya; Chilian William M
Description
An account of the resource
OBJECTIVE: Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart. APPROACH AND RESULTS: Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/mL vascular endothelial growth factor, 1 micromol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (P\textless0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-alpha and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-alpha suggested impairments in energy production, which was reflected by decrease in O2 consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-alpha (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-alpha. Conversely, expression of a constitutively active AMPK-alpha blocked tube formation. CONCLUSIONS: We conclude that activation of AMPK-alpha during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.113.301591</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).
2013
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Body Weight/physiology
Cells
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Collateral Circulation
Coronary Circulation
Coronary Vessels/cytology/*enzymology
Cultured
Department of Integrative Medical Sciences
Disease Models
Dyck Jason R B
Endothelial Cells/cytology/*enzymology
Enrick Molly
Hardwick James P
Humans
Inbred WKY
Ischemia/metabolism/pathology
Kolz Christopher
Mitochondria
Mitochondria/drug effects/*metabolism
Myocardium/enzymology/pathology
NEOMED College of Medicine
Oxidative Stress/*physiology
Pung Yuh Fen
Rats
reactive oxygen species
Rotenone/pharmacology
Sam Wai Johnn
Signal Transduction/*physiology
Stevanov Kelly
Thakker Prashanth
TOR Serine-Threonine Kinases/metabolism
Uncoupling Agents/pharmacology
Yin Liya
-
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/10.1161/ATVBAHA.111.241802" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.111.241802</a>
Pages
325–334
Issue
2
Volume
32
Dublin Core
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Title
A name given to the resource
Resolution of mitochondrial oxidative stress rescues coronary collateral growth in Zucker obese fatty rats.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-02
Subject
The topic of the resource
Animal; Animals; Antioxidants/*pharmacology; Collateral Circulation/*drug effects/physiology; Coronary Vessels/drug effects/*growth & development; Disease Models; Heart/*drug effects/physiology; Lipid Peroxidation/drug effects/physiology; Lipid Peroxides/metabolism; Male; Metabolic Syndrome/*metabolism/physiopathology; Mitochondria; Mitochondrial Proteins/metabolism; Obesity/*metabolism/physiopathology; Organophosphorus Compounds/pharmacology; Oxidative Stress/*drug effects/physiology; Piperidines/pharmacology; Rats; Reactive Oxygen Species/metabolism; Ubiquinone/pharmacology; Zucker
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Rocic Petra; Murphy Michael P; Smith Robin A J; Hafemeister Jennifer; Ohanyan Vahagn; Guarini Giacinta; Yin Liya; Chilian William M
Description
An account of the resource
OBJECTIVE: We have previously found abrogated ischemia-induced coronary collateral growth in Zucker obese fatty (ZOF) rats compared with Zucker lean (ZLN) rats. Because ZOF rats have structural abnormalities in their mitochondria suggesting dysfunction and also show increased production of O(2), we hypothesized that mitochondrial dysfunction caused by oxidative stress impairs coronary collateral growth in ZOF. METHODS AND RESULTS: Increased levels of reactive oxygen species were observed in aortic endothelium and smooth muscle cells in ZOF rats compared with ZLN rats. Reactive oxygen species levels were decreased by the mitochondria-targeted antioxidants MitoQuinone (MQ) and MitoTempol (MT) as assessed by MitoSox Red and dihydroethidine staining. Lipid peroxides (a marker of oxidized lipids) were increased in ZOF by approximately 47% compared with ZLN rats. The elevation in oxidative stress was accompanied by increased antioxidant enzymes, except glutathione peroxidase-1, and by increased uncoupling protein-2 in ZOF versus ZLN rats. In addition, elevated respiration rates were also observed in the obese compared with lean rats. Administration of MQ significantly normalized the metabolic profiles and reduced lipid peroxides in ZOF rats to the same level observed in lean rats. The protective effect of MQ also suppressed the induction of uncoupling protein-2 in the obese rats. Resolution of mitochondrial oxidative stress by MQ or MT restored coronary collateral growth to the same magnitude observed in ZLN rats in response to repetitive ischemia. CONCLUSIONS: We conclude that mitochondrial oxidative stress and dysfunction play a key role in disrupting coronary collateral growth in obesity and the metabolic syndrome, and elimination of the mitochondrial oxidative stress with MQ or MT rescues collateral growth.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.111.241802" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.111.241802</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).
2012
Animal
Animals
Antioxidants/*pharmacology
Arteriosclerosis, thrombosis, and vascular biology
Chilian William M
Collateral Circulation/*drug effects/physiology
Coronary Vessels/drug effects/*growth & development
Department of Integrative Medical Sciences
Disease Models
Guarini Giacinta
Hafemeister Jennifer
Heart/*drug effects/physiology
Lipid Peroxidation/drug effects/physiology
Lipid Peroxides/metabolism
Male
Metabolic Syndrome/*metabolism/physiopathology
Mitochondria
Mitochondrial Proteins/metabolism
Murphy Michael P
NEOMED College of Medicine
Obesity/*metabolism/physiopathology
Ohanyan Vahagn
Organophosphorus Compounds/pharmacology
Oxidative Stress/*drug effects/physiology
Piperidines/pharmacology
Pung Yuh Fen
Rats
Reactive Oxygen Species/metabolism
Rocic Petra
Smith Robin A J
Ubiquinone/pharmacology
Yin Liya
Zucker
-
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/10.1161/ATVBAHA.107.154294" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.107.154294</a>
Pages
61–67
Issue
1
Volume
28
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
The mechanistic basis for the disparate effects of angiotensin II on coronary collateral growth.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-01
Subject
The topic of the resource
Angiotensin; Angiotensin II/*physiology; Animal; Animals; Coronary Occlusion/drug therapy/*physiopathology; Disease Models; Hemorheology; Ischemia/drug therapy/*physiopathology; Male; Neovascularization; Oxidative Stress/*physiology; Physiologic/*physiology; Rats; Reactive Oxygen Species/adverse effects/metabolism; Receptor; Type 1/*drug effects/physiology; Vasoconstrictor Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Reed Ryan; Kolz Christopher; Potter Barry; Rocic Petra
Description
An account of the resource
OBJECTIVE: We hypothesize that controversial effects of angiotensin II (Ang II) are attributable to its regulation of reactive oxygen species (ROS) and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.107.154294" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.107.154294</a>
Rights
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).
2008
Angiotensin
Angiotensin II/*physiology
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Coronary Occlusion/drug therapy/*physiopathology
Disease Models
Hemorheology
Ischemia/drug therapy/*physiopathology
Kolz Christopher
Male
Neovascularization
Oxidative Stress/*physiology
Physiologic/*physiology
Potter Barry
Rats
Reactive Oxygen Species/adverse effects/metabolism
Receptor
Reed Ryan
Rocic Petra
Type 1/*drug effects/physiology
Vasoconstrictor Agents/pharmacology
-
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/10.1155/2017/3613505" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2017/3613505</a>
Pages
3613505–3613505
Volume
2017
Dublin Core
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Title
A name given to the resource
LEAPS Vaccine Incorporating HER-2/neu Epitope Elicits Protection That Prevents and Limits Tumor Growth and Spread of Breast Cancer in a Mouse Model.
Publisher
An entity responsible for making the resource available
Journal of immunology research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
*Cancer Vaccines/genetics/immunology/therapeutic use; Animal; Animals; Breast Neoplasms/genetics/immunology/prevention & control/therapy; CD8-Positive T-Lymphocytes/immunology; Cell Line; Cytotoxic/immunology; Disease Models; Disease Progression; Epitopes; erbB-2; Experimental/immunology/pathology/*prevention & control/*therapy; Female; Genes; Immunoglobulin G/blood; Inbred BALB C; Mammary Neoplasms; Mice; Neoplasm Metastasis/prevention & control; Proof of Concept Study; T-Lymphocyte/immunology; T-Lymphocytes; Tumor
Creator
An entity primarily responsible for making the resource
Rosenthal Ken S; Stone Sarah; Koski Gary; Zimmerman Daniel H
Description
An account of the resource
The prototype J-LEAPS T cell vaccine for HER-2/neu breast cancer (J-HER) consists of the murine HER-2/neu66-74 H-2(d) CD8 T cell epitope covalently attached through a triglycine linker to the J-immune cell binding ligand (ICBL) (human beta2 microglobulin38-50 peptide). The J-ICBL was chosen for its potential to promote Th1/Tc1 responses. In this proof-of-concept study, the ability of J-HER to prevent or treat cancer was tested in the TUBO cell-challenged BALB/c mouse model for HER-2/neu-expressing tumors. The J-HER vaccine was administered as an emulsion in Montanide ISA-51 without the need for a more potent adjuvant. When administered as a prophylactic vaccination before tumor challenge, J-HER protected against tumor development for at least 48 days. Despite eliciting protection, antibody production in J-HER-immunized, TUBO-challenged mice was less than that in unimmunized mice. More importantly, therapeutic administration of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2017/3613505" target="_blank" rel="noreferrer noopener">10.1155/2017/3613505</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).
*Cancer Vaccines/genetics/immunology/therapeutic use
2017
Animal
Animals
Breast Neoplasms/genetics/immunology/prevention & control/therapy
CD8-Positive T-Lymphocytes/immunology
Cell Line
Cytotoxic/immunology
Disease Models
Disease Progression
Epitopes
erbB-2
Experimental/immunology/pathology/*prevention & control/*therapy
Female
Genes
Immunoglobulin G/blood
Inbred BALB C
Journal of immunology research
Koski Gary
Mammary Neoplasms
Mice
Neoplasm Metastasis/prevention & control
Proof of Concept Study
Rosenthal Ken S
Stone Sarah
T-Lymphocyte/immunology
T-Lymphocytes
Tumor
Zimmerman Daniel H
-
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/10.1155/2014/643457" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2014/643457</a>
Pages
643457–643457
Volume
2014
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
Weighted Lin-Wang tests for crossing hazards.
Publisher
An entity responsible for making the resource available
Computational and mathematical methods in medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-07
Subject
The topic of the resource
*Survival Analysis; Algorithms; Animal; Animals; Computer Simulation; Data Interpretation; Disease Models; Humans; Kaplan-Meier Estimate; Leukemia/drug therapy; Mice; Models; Reproducibility of Results; Statistical
Creator
An entity primarily responsible for making the resource
Koziol James A; Jia Zhenyu
Description
An account of the resource
Lin and Wang have introduced a quadratic version of the logrank test, appropriate for situations in which the underlying survival distributions may cross. In this note, we generalize the Lin-Wang procedure to incorporate weights and investigate the performance of Lin and Wang's test and weighted versions in various scenarios. We find that weighting does increase statistical power in certain situations; however, none of the procedures was dominant under every scenario.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2014/643457" target="_blank" rel="noreferrer noopener">10.1155/2014/643457</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).
*Survival Analysis
2014
Algorithms
Animal
Animals
Computational and mathematical methods in medicine
Computer Simulation
Data Interpretation
Disease Models
Humans
Jia Zhenyu
Kaplan-Meier Estimate
Koziol James A
Leukemia/drug therapy
Mice
Models
Reproducibility of Results
Statistical
-
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/jappl.1990.68.3.912" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jappl.1990.68.3.912</a>
Pages
912–918
Issue
3
Volume
68
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
Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema.
Publisher
An entity responsible for making the resource available
Journal of applied physiology (Bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
1990-03
Subject
The topic of the resource
Animal; Animals; Catecholamines/physiology; Disease Models; Dogs; Female; Hypertension; In Vitro Techniques; Male; Perfusion; Pulmonary Circulation/drug effects/*physiology; Pulmonary Edema/chemically induced/*physiopathology; Pulmonary/chemically induced/physiopathology; Splenectomy; Sympathetic Nervous System/drug effects/physiopathology; Vasoconstriction/drug effects/*physiology; Veratrine
Creator
An entity primarily responsible for making the resource
Maron M B
Description
An account of the resource
The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL) perfusion of seven splenectomized (to keep hematocrit and blood viscosity constant) dogs was isolated so the LLL could be perfused at constant flow and outflow pressure with blood pumped from the pulmonary artery. The LLL was denervated by removing it from the dog. Veratrine (40-160 micrograms/kg) increased LLL arterial pressure by 39.2% and produced large increases in plasma catecholamine concentrations. The double-occlusion technique indicated that 74% of the increase in the LLL arteriovenous pressure gradient was due to an increase in venous tone. This pattern of vasoconstriction was similar to that previously observed during the infusion of exogenous catecholamines and suggested that catecholamines mediated the LLL response. The more severe degree of PH observed in the intact animal in NPE, however, suggests that passive rather than active changes in pulmonary hemodynamics are predominantly responsible for the development of PH in this disorder.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.1990.68.3.912" target="_blank" rel="noreferrer noopener">10.1152/jappl.1990.68.3.912</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).
1990
Animal
Animals
Catecholamines/physiology
Disease Models
Dogs
Female
Hypertension
In Vitro Techniques
Journal of applied physiology (Bethesda, Md. : 1985)
Male
Maron M B
Perfusion
Pulmonary Circulation/drug effects/*physiology
Pulmonary Edema/chemically induced/*physiopathology
Pulmonary/chemically induced/physiopathology
Splenectomy
Sympathetic Nervous System/drug effects/physiopathology
Vasoconstriction/drug effects/*physiology
Veratrine
-
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/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.01330.2006</a>
Pages
H2729–2736
Issue
6
Volume
292
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
Optimal reactive oxygen species concentration and p38 MAP kinase are required for coronary collateral growth.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-06
Subject
The topic of the resource
*Collateral Circulation/drug effects; *Coronary Circulation/drug effects; *MAP Kinase Signaling System/drug effects; Acetophenones/pharmacology; Animal; Animals; Blood Flow Velocity; Cells; Coronary Vessels/surgery; Cultured; Disease Models; Ditiocarb/pharmacology; Endothelial Cells/drug effects/enzymology/*metabolism; Enzyme Inhibitors/pharmacology; Humans; Imidazoles/pharmacology; Inbred WKY; Ligation; Male; Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology; NADPH Oxidases/antagonists & inhibitors/metabolism; Neovascularization; Onium Compounds/pharmacology; Oxygenases/antagonists & inhibitors/metabolism; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism; Physiologic; Pyridines/pharmacology; Rats; Reactive Oxygen Species/*metabolism; Superoxide Dismutase/antagonists & inhibitors/metabolism; Vascular Endothelial Growth Factor A/metabolism
Creator
An entity primarily responsible for making the resource
Rocic Petra; Kolz Christopher; Reed Ryan; Potter Barry; Chilian William M
Description
An account of the resource
Reactive oxygen species (ROS) are implicated in coronary collateral growth (CCG). We evaluated the requirement for ROS in human coronary artery endothelial cell (HCAEC) tube formation, CCG in vivo, and signaling (p38 MAP kinase) by which ROS may stimulate vascular growth. The flavin-containing oxidase inhibitor diphenyleneiodonium (DPI) or the superoxide dismutase inhibitor diethyldithiocarbamate (DETC) blocked vascular endothelial growth factor-induced HCAEC tube formation in Matrigel. We assessed the effect of DPI and DETC on CCG in a rat model of repetitive ischemia (RI) (40 s left anterior descending coronary artery occlusion every 20 min for 2 h 20 min, 3 times/day, 10 days). DPI or DETC was given intraperitoneally, or the NAD(P)H oxidase inhibitor apocynin was given in drinking water. Collateral-dependent flow (measured by using microspheres) was expressed as a ratio of normal and ischemic zone flows. In sham-operated rats, collateral flow in the ischemic zone was 18 +/- 6% of normal zone; in the RI group, collateral flow in the ischemic zone was 83 +/- 5% of normal zone. DPI prevented the increase in collateral flow after RI (25 +/- 4% of normal zone). Similar results were obtained with apocynin following RI (32 +/- 7% of that in the normal zone). DETC achieved similar results (collateral flow after RI was 21 +/- 2% of normal zone). DPI and DETC blocked RI-induced p38 MAP kinase activation in response to vascular endothelial growth factor and RI. These results demonstrate a requirement for optimal ROS concentration in HCAEC tube formation, CCG, and p38 MAP kinase activation. p38 MAP kinase inhibition prevented HCAEC tube formation and partially blocked RI-induced CCG (42 +/- 7% of normal zone flow), indicating that p38 MAP kinase is a critical signaling mediator of CCG.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.01330.2006</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).
*Collateral Circulation/drug effects
*Coronary Circulation/drug effects
*MAP Kinase Signaling System/drug effects
2007
Acetophenones/pharmacology
American journal of physiology. Heart and circulatory physiology
Animal
Animals
Blood Flow Velocity
Cells
Chilian William M
Coronary Vessels/surgery
Cultured
Department of Integrative Medical Sciences
Disease Models
Ditiocarb/pharmacology
Endothelial Cells/drug effects/enzymology/*metabolism
Enzyme Inhibitors/pharmacology
Humans
Imidazoles/pharmacology
Inbred WKY
Kolz Christopher
Ligation
Male
Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology
NADPH Oxidases/antagonists & inhibitors/metabolism
NEOMED College of Medicine
Neovascularization
Onium Compounds/pharmacology
Oxygenases/antagonists & inhibitors/metabolism
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
Physiologic
Potter Barry
Pyridines/pharmacology
Rats
Reactive Oxygen Species/*metabolism
Reed Ryan
Rocic Petra
Superoxide Dismutase/antagonists & inhibitors/metabolism
Vascular Endothelial Growth Factor A/metabolism
-
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/ajpheart.00653.2016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00653.2016</a>
Pages
H541–H545
Issue
3
Volume
312
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
The JCR:LA-cp rat: a novel rodent model of cystic medial necrosis.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
*Rats; Animal; Animals; Aortic Aneurysm; Atherosclerosis/pathology; Blood Glucose/metabolism; Blood Vessels/pathology; Body Weight; Collagen/biosynthesis; Cysts/*genetics/pathology; Disease Models; hypoxia; Hypoxia; Inbred Strains; leptin; Lipids/blood; Male; metabolic syndrome; Metabolic Syndrome/*genetics/pathology; Necrosis; Proteoglycans/biosynthesis; Rats; rodent model; Thoracic/*genetics/pathology
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Chilian William M; Bennett Martin R; Figg Nichola; Kamarulzaman Mohd Hamzah
Description
An account of the resource
Although there are multiple rodent models of the metabolic syndrome, very few develop vascular complications. In contrast, the JCR:LA-cp rat develops both metabolic syndrome and early atherosclerosis in predisposed areas. However, the pathology of the normal vessel wall has not been described. We examined JCR:LA control (+/+) or cp/cp rats fed normal chow diet for 6 or 18 mo. JCR:LA-cp rats developed multiple features of advanced cystic medial necrosis including "cysts," increased collagen formation and proteoglycan deposition around cysts, apoptosis of vascular smooth muscle cells, and spotty medial calcification. These appearances began within 6 mo and were extensive by 18 mo. JCR:LA-cp rats had reduced medial cellularity, increased medial thickness, and vessel hypoxia that was most marked in the adventitia. In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia.NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00653.2016" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00653.2016</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).
*Rats
2017
American journal of physiology. Heart and circulatory physiology
Animal
Animals
Aortic Aneurysm
Atherosclerosis/pathology
Bennett Martin R
Blood Glucose/metabolism
Blood Vessels/pathology
Body Weight
Chilian William M
Collagen/biosynthesis
Cysts/*genetics/pathology
Department of Integrative Medical Sciences
Disease Models
Figg Nichola
hypoxia
Inbred Strains
Kamarulzaman Mohd Hamzah
leptin
Lipids/blood
Male
Metabolic syndrome
Metabolic Syndrome/*genetics/pathology
Necrosis
NEOMED College of Medicine
Proteoglycans/biosynthesis
Pung Yuh Fen
Rats
rodent model
Thoracic/*genetics/pathology
-
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/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00449.2015</a>
Pages
H20–28
Issue
1
Volume
310
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
Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
alpha Subunit/metabolism; Amino Acids; Animal; Animals; Apoptosis/drug effects; Cardiotonic Agents/*pharmacology; Cell Hypoxia; Cell Line; CXCR4/deficiency/genetics/*metabolism; Dicarboxylic/*pharmacology; Disease Models; Enzyme Inhibitors/pharmacology; hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism; Inbred C57BL; Knockout; Left/*drug effects; Mice; myocardial infarction; Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology; Myocardium/*metabolism/pathology; Rats; Receptors; Recovery of Function; Signal Transduction/drug effects; stem cells; Stem Cells/drug effects/metabolism; Stroke Volume/drug effects; Time Factors; Up-Regulation; Ventricular Function
Creator
An entity primarily responsible for making the resource
Mayorga Mari; Kiedrowski Matthew; Shamhart Patricia; Forudi Farhad; Weber Kristal; Chilian William M; Penn Marc S; Dong Feng
Description
An account of the resource
The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to engage the SDF-1:CXCR4 axis and improve cardiac repair. The effects of the hypoxia inducible factor (HIF) hydroxylase inhibitor dimethyloxalylglycine (DMOG) on CXCR4 expression was tested on H9c2 cells. In mice a myocardial infarction (MI) was produced in CM-CXCR4 null and wild-type controls. Mice were randomized to receive injection of DMOG (DMOG group) or saline (Saline group) into the border zone after MI. Protein and mRNA expression of CM-CXCR4 were quantified. Echocardiography was used to assess cardiac function. During hypoxia, DMOG treatment increased CXCR4 expression of H9c2 cells by 29 and 42% at 15 and 24 h, respectively. In vivo DMOG treatment increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00449.2015</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).
2016
alpha Subunit/metabolism
American journal of physiology. Heart and circulatory physiology
Amino Acids
Animal
Animals
Apoptosis/drug effects
Cardiotonic Agents/*pharmacology
Cell Hypoxia
Cell Line
Chilian William M
CXCR4/deficiency/genetics/*metabolism
Department of Integrative Medical Sciences
Dicarboxylic/*pharmacology
Disease Models
Dong Feng
Enzyme Inhibitors/pharmacology
Forudi Farhad
hypoxia
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism
Inbred C57BL
Kiedrowski Matthew
Knockout
Left/*drug effects
Mayorga Mari
Mice
myocardial infarction
Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Penn Marc S
Rats
Receptors
Recovery of Function
Shamhart Patricia
Signal Transduction/drug effects
stem cells
Stem Cells/drug effects/metabolism
Stroke Volume/drug effects
Time Factors
Up-Regulation
Ventricular Function
Weber Kristal
-
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/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00082.2011</a>
Pages
H1135–1142
Issue
3
Volume
301
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
Endothelin-mediated in vivo pressor responses following TRPV1 activation.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-09
Subject
The topic of the resource
*Blood Pressure/drug effects; *Vasoconstriction/drug effects; Adrenergic alpha-Agonists/administration & dosage; Analysis of Variance; Animal; Animals; Azepines/administration & dosage; Biphenyl Compounds/administration & dosage; Capsaicin/administration & dosage; Cells; Cultured; Diabetes Mellitus; Diabetic Angiopathies/genetics/*metabolism/physiopathology; Dipeptides/administration & dosage; Disease Models; Dose-Response Relationship; Drug; Endothelial Cells/metabolism; Endothelin A Receptor Antagonists; Endothelin A/metabolism; Endothelin B Receptor Antagonists; Endothelin B/metabolism; Endothelin-1/*metabolism; Enzyme-Linked Immunosorbent Assay; Femoral Artery/drug effects/*metabolism/physiopathology; Inbred C57BL; Indoles/administration & dosage; Infusions; Intravenous; Knockout; Male; Mice; Phenylephrine/administration & dosage; Receptor; TRPV Cation Channels/agonists/deficiency/genetics/*metabolism; Type 2/genetics/*metabolism/physiopathology; Vasoconstrictor Agents/administration & dosage
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn A; Guarini Giacinta; Thodeti Charles K; Talasila Phani K; Raman Priya; Haney Rebecca M; Meszaros J Gary; Damron Derek S; Bratz Ian N
Description
An account of the resource
Transient receptor potential vanilliod 1 (TRPV1) channels have recently been postulated to play a role in the vascular complications/consequences associated with diabetes despite the fact that the mechanisms through which TRPV1 regulates vascular function are not fully known. Accordingly, our goal was to define the mechanisms by which TRPV1 channels modulate vascular function and contribute to vascular dysfunction in diabetes. We subjected mice lacking TRPV1 [TRPV1((-/-))], db/db, and control C57BLKS/J mice to in vivo infusion of the TRPV1 agonist capsaicin or the alpha-adrenergic agonist phenylephrine (PE) to examine the integrated circulatory actions of TRPV1. Capsaicin (1, 10, 20, and 100 mug/kg) dose dependently increased MAP in control mice (5.7 +/- 1.6, 11.7 +/- 2.1, 25.4 +/- 3.4, and 51.6 +/- 3.9%), which was attenuated in db/db mice (3.4 +/- 2.1, 3.9 +/- 2.1, 7.0 +/- 3.3, and 17.9 +/- 6.2%). TRPV1((-/-)) mice exhibited no changes in MAP in response to capsaicin, suggesting the actions of this agonist are specific to TRPV1 activation. Immunoblot analysis revealed decreased aortic TRPV1 protein expression in db/db compared with control mice. Capsaicin-induced responses were recorded following inhibition of endothelin A and B receptors (ET(A) /ET(B)). Inhibition of ET(A) receptors abolished the capsaicin-mediated increases in MAP. Combined antagonism of ET(A) and ET(B) receptors did not further inhibit the capsaicin response. Cultured endothelial cell exposure to capsaicin increased endothelin production as shown by an endothelin ELISA assay, which was attenuated by inhibition of TRPV1 or endothelin-converting enzyme. TRPV1 channels contribute to the regulation of vascular reactivity and MAP via production of endothelin and subsequent activation of vascular ET(A) receptors. Impairment of TRPV1 channel function may contribute to vascular dysfunction in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00082.2011</a>
Rights
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).
*Blood Pressure/drug effects
*Vasoconstriction/drug effects
2011
Adrenergic alpha-Agonists/administration & dosage
American journal of physiology. Heart and circulatory physiology
Analysis of Variance
Animal
Animals
Azepines/administration & dosage
Biphenyl Compounds/administration & dosage
Bratz Ian N
Capsaicin/administration & dosage
Cells
Cultured
Damron Derek S
Department of Integrative Medical Sciences
Diabetes Mellitus
Diabetic Angiopathies/genetics/*metabolism/physiopathology
Dipeptides/administration & dosage
Disease Models
Dose-Response Relationship
Drug
Endothelial Cells/metabolism
Endothelin A Receptor Antagonists
Endothelin A/metabolism
Endothelin B Receptor Antagonists
Endothelin B/metabolism
Endothelin-1/*metabolism
Enzyme-Linked Immunosorbent Assay
Femoral Artery/drug effects/*metabolism/physiopathology
Guarini Giacinta
Haney Rebecca M
Inbred C57BL
Indoles/administration & dosage
Infusions
Intravenous
Knockout
Male
Meszaros J Gary
Mice
NEOMED College of Medicine
Ohanyan Vahagn A
Phenylephrine/administration & dosage
Raman Priya
Receptor
Talasila Phani K
Thodeti Charles K
TRPV Cation Channels/agonists/deficiency/genetics/*metabolism
Type 2/genetics/*metabolism/physiopathology
Vasoconstrictor Agents/administration & dosage
-
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/10.1128/IAI.00369-17" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/IAI.00369-17</a>
Issue
11
Volume
85
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
Impairment of Hematopoietic Precursor Cell Activation during the Granulopoietic Response to Bacteremia in Mice with Chronic-Plus-Binge Alcohol Administration.
Publisher
An entity responsible for making the resource available
Infection and immunity
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-11
Subject
The topic of the resource
*Alcohol; *bacteremia; *cell signaling; *granulocytes; *granulopoietic response; *stem cells; Animal; Animals; Antigens; Bacteremia/genetics/*immunology/pathology; Binge Drinking/genetics/*immunology/pathology; Bone Marrow Cells/drug effects/immunology/pathology; CCAAT-Enhancer-Binding Protein-beta/genetics/immunology; Cyclin D1/genetics/immunology; Disease Models; Escherichia coli Infections/genetics/*immunology/pathology; Escherichia coli/growth & development/immunology; Ethanol/*pharmacology; Gene Expression Regulation/*drug effects/immunology; Granulocytes/drug effects/immunology/pathology; Hematopoiesis/*drug effects/genetics/immunology; Inbred BALB C; Ly/genetics/immunology; Male; Membrane Proteins/genetics/immunology; Mice; Mitogen-Activated Protein Kinase 1/genetics/immunology; Mitogen-Activated Protein Kinase 3/genetics/immunology; Nucleotidyltransferases/deficiency/genetics/immunology; Proto-Oncogene Proteins c-kit/genetics/immunology; Signal Transduction/*drug effects/immunology; Toll-Like Receptor 4/genetics/immunology
Creator
An entity primarily responsible for making the resource
Shi Xin; Lin Yuan-Ping; Gao Bin; Zhang Ping
Description
An account of the resource
Alcohol abuse impairs immune defense. To study the effect of chronic-plus-binge alcohol exposure on the granulopoietic response, acute alcohol intoxication (intraperitoneal injection of 5 g alcohol/kg body weight) was introduced to mice chronically fed on the Lieber-DeCarli low-fat liquid alcohol diet for 5 weeks. Bacteremia was induced by intravenous injection of Escherichia coli Bacteremia caused a remarkable increase in marrow lin(-) c-kit(+) Sca-1(+) cells. Activation of cell proliferation supported the increase in marrow lin(-) c-kit(+) Sca-1(+) cells. Alcohol administration inhibited this activation of lin(-) c-kit(+) Sca-1(+) cells. The bone marrow of pair-fed control mice receiving intraperitoneal saline stored a large number of mature granulocytes expressing a high level of Gr1 (Gr1(hi) cells). The proportion of Gr1(hi) cells and the total number of Gr1(+) cells were markedly reduced in the bone marrow, along with an increase in the ratio of Gr1(+) granulocytes in peripheral white blood cells following bacteremia. E. coli infection stimulated proliferation of granulopoietic precursor cells, resulting in a marked increase in the ratio of immature Gr1(lo) cells in the bone marrow. Alcohol administration itself triggered marrow release of Gr1(+) cells, resulting in reduction of the marrow granulocyte reserve with an elevation of granulocytes in the circulation. Alcohol also impaired activation of granulopoietic precursor proliferation following bacteremia. Alcohol disrupted lipopolysaccharide (LPS)-TLR4-ERK1/2-cyclin D1 signaling and inhibited upregulation of Sca-1 and C/EBPbeta expression by lineage-negative marrow cells in response to bacteremia. These results indicate that chronic-plus-binge alcohol exposure inhibits the granulopoietic response by disrupting key cell signaling for hematopoietic precursor cell activation and commitment to granulocyte lineage development.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/IAI.00369-17" target="_blank" rel="noreferrer noopener">10.1128/IAI.00369-17</a>
Rights
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).
*alcohol
*bacteremia
*cell signaling
*granulocytes
*granulopoietic response
*Stem cells
2017
Animal
Animals
Antigens
Bacteremia/genetics/*immunology/pathology
Binge Drinking/genetics/*immunology/pathology
Bone Marrow Cells/drug effects/immunology/pathology
CCAAT-Enhancer-Binding Protein-beta/genetics/immunology
Cyclin D1/genetics/immunology
Department of Integrative Medical Sciences
Disease Models
Escherichia coli Infections/genetics/*immunology/pathology
Escherichia coli/growth & development/immunology
Ethanol/*pharmacology
Gao Bin
Gene Expression Regulation/*drug effects/immunology
Granulocytes/drug effects/immunology/pathology
Hematopoiesis/*drug effects/genetics/immunology
Inbred BALB C
Infection and immunity
Lin Yuan-Ping
Ly/genetics/immunology
Male
Membrane Proteins/genetics/immunology
Mice
Mitogen-Activated Protein Kinase 1/genetics/immunology
Mitogen-Activated Protein Kinase 3/genetics/immunology
NEOMED College of Medicine
Nucleotidyltransferases/deficiency/genetics/immunology
Proto-Oncogene Proteins c-kit/genetics/immunology
Shi Xin
Signal Transduction/*drug effects/immunology
Toll-Like Receptor 4/genetics/immunology
Zhang Ping
-
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/j.1440-1681.2007.04616.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1440-1681.2007.04616.x</a>
Pages
555–565
Issue
7
Volume
34
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
Oestrogen and nigrostriatal dopaminergic neurodegeneration: animal models and clinical reports of Parkinson's disease.
Publisher
An entity responsible for making the resource available
Clinical and experimental pharmacology & physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-07
Subject
The topic of the resource
Animal; Animals; Basal Ganglia/drug effects/*metabolism/pathology; Disease Models; Dopamine/*metabolism; Estrogens/*metabolism/pharmacology/therapeutic use; Humans; Nerve Degeneration/drug therapy/*metabolism/pathology; Neurons/metabolism/pathology; Neuroprotective Agents/*metabolism/pharmacology/therapeutic use; Parkinson Disease/drug therapy/*metabolism/pathology; Parkinsonian Disorders/drug therapy/*metabolism/pathology; Substantia Nigra/drug effects/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Liu Bin; Dluzen Dean E
Description
An account of the resource
1. The exact nature of oestrogen (positive, negative or no effect) in the dopaminergic neurodegenerative disorder Parkinson's disease is controversial. 2. In the present review, we summarize the data on oestrogen and nigrostriatal dopaminergic neurodegeneration in animal models and clinical reports of Parkinson's disease. 3. Most animal studies support the ability of oestrogen to function as a neuroprotectant against neurotoxins that target the nigrostriatal dopaminergic system. 4. Retrospective and prospective clinical studies generally support the findings from animal studies that oestrogen exerts a positive, or, at worst, no effect, in Parkinson's disease. 5. Oestrogen was chosen as one of the 12 neuroprotective compounds to be attractive candidates for further clinical trials (Phase II or III) in 2003.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1440-1681.2007.04616.x" target="_blank" rel="noreferrer noopener">10.1111/j.1440-1681.2007.04616.x</a>
Rights
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).
2007
Animal
Animals
Basal Ganglia/drug effects/*metabolism/pathology
Clinical and experimental pharmacology & physiology
Disease Models
Dluzen Dean E
Dopamine/*metabolism
Estrogens/*metabolism/pharmacology/therapeutic use
Humans
Liu Bin
Nerve Degeneration/drug therapy/*metabolism/pathology
Neurons/metabolism/pathology
Neuroprotective Agents/*metabolism/pharmacology/therapeutic use
Parkinson Disease/drug therapy/*metabolism/pathology
Parkinsonian Disorders/drug therapy/*metabolism/pathology
Substantia Nigra/drug effects/*metabolism/pathology
-
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/10.1097/RHU.0000000000000279" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/RHU.0000000000000279</a>
Pages
296–299
Issue
6
Volume
21
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
Intestinal Flora Modification of Arthritis Pattern in Spondyloarthropathy.
Publisher
An entity responsible for making the resource available
Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-09
Subject
The topic of the resource
*Bacteria/classification/genetics/isolation & purification; *Diarrhea/complications/microbiology; *Gastrointestinal Microbiome; *Spondylarthropathies/diagnosis/etiology/physiopathology; 16S/analysis; Animal; Animals; Disease Models; Gastrointestinal Tract/*microbiology; Gorilla gorilla; Humans; Pan troglodytes; Protective Factors; Ribosomal; RNA
Creator
An entity primarily responsible for making the resource
Rothschild Bruce M
Description
An account of the resource
BACKGROUND: The reactive form of spondyloarthropathy appears inducible by exposure to agents of infectious diarrhea, but do those organisms represent the tip of the iceberg, as indicated by renewed interest in gastrointestinal flora? Prevalence of spondyloarthropathy (20% of chimpanzees [Pan] and 28% of gorillas) is independent of subspecies and species, respectively. However, there are major differences in arthritis patterns, a characteristic shared with humans. OBJECTIVES: Do patterns of arthritis correlate with gastrointestinal flora? Could such associated modifications be in the form of disease induction or represent protective effectors (at least against the extent of peripheral arthritis)? METHODS: The skeletons of 2 chimpanzee subspecies (79 Pan troglodytes troglodytes and 26 Pan troglodytes schweinfurthii) and 2 gorilla species (99 Gorilla gorilla and 38 Gorilla beringei) adults were examined, and arthritis pattern noted. Feces of Eastern (P. schweinfurthii and G. beringei) and Western (great apes collected in their normal ranges) apes were assessed for 16S rRNA c and its character. RESULTS: Patterns of arthritis recognized on examination of skeletons showed geographic variation in skeletal distribution. East African apes (P. troglodytes schweinfurthii and G. beringei) had pauciarticular arthritis and frequent sacroiliac disease, whereas West African apes (P. troglodytes troglodytes and G. gorilla) had polyarticular peripheral joint disease with minimal sacroiliac involvement. DNA evidence revealed that Corynebactericeae were prominently represented in great apes with polyarticular disease, whereas Dietzia and Bifidobacterium exposure correlated with reduced peripheral joint arthritis distribution. CONCLUSIONS: Suggestions of a protective effect (in this case, limiting extent of peripheral arthritis, but not the disease itself) offered by these organisms are well represented by documented effects in other diseases (eg, tuberculosis) in the zoologic record. Perhaps it is this disease-modifying character that reduces the extent of the peripheral erosive disease, while increasing propensity to axial (sacroiliac) disease. A potential role for probiotic organisms in management of arthritis in humans is suggested, as has been documented for tuberculosis, gastrointestinal disorders, and food allergies.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/RHU.0000000000000279" target="_blank" rel="noreferrer noopener">10.1097/RHU.0000000000000279</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).
*Bacteria/classification/genetics/isolation & purification
*Diarrhea/complications/microbiology
*Gastrointestinal Microbiome
*Spondylarthropathies/diagnosis/etiology/physiopathology
16S/analysis
2015
Animal
Animals
Disease Models
Gastrointestinal Tract/*microbiology
Gorilla gorilla
Humans
Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases
Pan troglodytes
Protective Factors
Ribosomal
RNA
Rothschild Bruce 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/10.1097/01.brs.0000168550.65726.cb" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/01.brs.0000168550.65726.cb</a>
Pages
1491–1495
Issue
13
Volume
30
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
Effects of growth hormone transgene expression on vertebrae in a mouse model of osteogenesis imperfecta.
Publisher
An entity responsible for making the resource available
Spine
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-07
Subject
The topic of the resource
Animal; Animals; Biomechanical Phenomena; Bone Density; Disease Models; Female; Gene Expression; Genetic Therapy/*methods; Heterozygote; Human Growth Hormone/*genetics; Humans; Inbred C57BL; Male; Mice; Osteogenesis Imperfecta/pathology/physiopathology/*therapy; Spine/pathology/*physiology; Tail; Transgenic
Creator
An entity primarily responsible for making the resource
King Donna; Chase Jeff; Havey Robert M; Voronov Leonard; Sartori Mark; McEwen Heather A; Beamer Wesley G; Patwardhan Avinash G
Description
An account of the resource
STUDY DESIGN: A human growth hormone transgene was bred into mice of the Cola2oim (oim) lineage. Caudal (tail) vertebrae from male and female mice at early skeletal maturity and at midlife were evaluated for physical and biomechanical properties. OBJECTIVE: To test whether constant low-level growth hormone expression within the marrow could improve structural or material properties of caudal vertebrae in oim mice. SUMMARY OF BACKGROUND DATA: A spontaneous genetic defect in a type I procollagen gene created the oim mouse model for osteogenesis imperfecta. Bones of heterozygous oim mice are biomechanically inferior to wild-type controls. Bone marrow expression of human growth hormone was demonstrated previously to enhance bone deposition and structural biomechanical properties in caudal vertebrae of transgenic mice. METHODS: Compression tests were performed individually on three caudal vertebrae (Ca4, 5, and 6) from each mouse to determine their structural biomechanical properties. Volumetric and mineral content measurements were also made. In a subset of vertebrae, the ashing measurements were confirmed and extended by peripheral quantitative tomographic scanning, which also allowed calculation of the failure stress. RESULTS: Heterozygous oim mouse vertebrae had structural and material properties inferior to the wild-type controls. Growth hormone transgene expression increased the size and mineral content of the vertebrae from mutant mice, and increased biomechanical structural values for maximum load and energy to failure. Failure stress was not improved. CONCLUSIONS: Growth hormone stimulation of size and bone mineral content of osteogenesis imperfecta mutant mouse caudal vertebrae contributed to their improved performance in axial compression. There was no evidence for improved material properties, however.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/01.brs.0000168550.65726.cb" target="_blank" rel="noreferrer noopener">10.1097/01.brs.0000168550.65726.cb</a>
Rights
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).
2005
Animal
Animals
Beamer Wesley G
Biomechanical Phenomena
Bone Density
Chase Jeff
Department of Family & Community Medicine
Disease Models
Female
Gene Expression
Genetic Therapy/*methods
Havey Robert M
Heterozygote
Human Growth Hormone/*genetics
Humans
Inbred C57BL
King Donna
Male
McEwen Heather A
Mice
NEOMED College of Medicine
Osteogenesis Imperfecta/pathology/physiopathology/*therapy
Patwardhan Avinash G
Sartori Mark
Spine
Spine/pathology/*physiology
Tail
Transgenic
Voronov Leonard
-
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/rheumatology/kel263" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/rheumatology/kel263</a>
Pages
246–249
Issue
2
Volume
46
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
Lack of bone stiffness/strength contribution to osteoarthritis–evidence for primary role of cartilage damage.
Publisher
An entity responsible for making the resource available
Rheumatology (Oxford, England)
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-02
Subject
The topic of the resource
Animal; Animals; Articular/physiopathology; Biomechanical Phenomena; Bird Diseases/*physiopathology; Birds; Bone and Bones/*physiopathology; Cartilage; Disease Models; Mechanical; Osteoarthritis/*physiopathology/*veterinary; Species Specificity; Stress
Creator
An entity primarily responsible for making the resource
Rothschild B M; Panza R K
Description
An account of the resource
OBJECTIVES: This study was performed to assess osseous contributions to osteoarthritis, obviating the analysis challenges presented by confounding factors in humans and rarity of osteoarthritis in free-ranging mammals. METHODS: Frequency of osteoarthritis in 21 bird species was examined and contrasted with measures of afflicted element bone stiffness and strength and compression/tension-resistant characteristics. RESULTS: Osteoarthritis was present in the ankle of 0-16% of bird species analysed, independent of bone laminarity, cortical thickness, circularity, polarization, cross-sectional diameter, length and pneumatization. CONCLUSIONS: No correlation of frequency of osteoarthritis with parameters of bone strength and biomechanical parameters was found, suggesting that bone is only secondarily affected in osteoarthritis and that cartilage is the initial target of the disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/rheumatology/kel263" target="_blank" rel="noreferrer noopener">10.1093/rheumatology/kel263</a>
Rights
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).
2007
Animal
Animals
Articular/physiopathology
Biomechanical Phenomena
Bird Diseases/*physiopathology
Birds
Bone and Bones/*physiopathology
Cartilage
Disease Models
Mechanical
Osteoarthritis/*physiopathology/*veterinary
Panza R K
Rheumatology (Oxford, England)
Rothschild B M
Species Specificity
Stress
-
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/hmg/ddw322" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/hmg/ddw322</a>
Pages
5126–5141
Issue
23
Volume
25
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
Modulating ryanodine receptors with dantrolene attenuates neuronopathic phenotype in Gaucher disease mice.
Publisher
An entity responsible for making the resource available
Human molecular genetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
Animal; Animals; Calcium Signaling/genetics; Dantrolene/*administration & dosage; Disease Models; Gaucher Disease/*drug therapy/genetics/physiopathology; Humans; Mice; Mitochondria/*drug effects/genetics/pathology; Neurons/drug effects/pathology; Neuroprotective Agents/administration & dosage; Ryanodine Receptor Calcium Release Channel/*genetics/metabolism
Creator
An entity primarily responsible for making the resource
Liou Benjamin; Peng Yanyan; Li Ronghua; Inskeep Venette; Zhang Wujuan; Quinn Brian; Dasgupta Nupur; Blackwood Rachel; Setchell Kenneth D R; Fleming Sheila; Grabowski Gregory A; Marshall John; Sun Ying
Description
An account of the resource
Neuronopathic Gaucher disease (nGD) manifests as severe neurological symptoms in patients with no effective treatment available. Ryanodine receptors (Ryrs) are a family of calcium release channels on intracellular stores. The goal of this study is to determine if Ryrs are potential targets for nGD treatment. A nGD cell model (CBE-N2a) was created by inhibiting acid beta-glucosidase (GCase) in N2a cells with conduritol B epoxide (CBE). Enhanced cytosolic calcium in CBE-N2a cells was blocked by either ryanodine or dantrolene, antagonists of Ryrs and by Genz-161, a glucosylceramide synthase inhibitor, suggesting substrate-mediated
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/hmg/ddw322" target="_blank" rel="noreferrer noopener">10.1093/hmg/ddw322</a>
Rights
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).
2016
Animal
Animals
Blackwood Rachel
Calcium Signaling/genetics
Dantrolene/*administration & dosage
Dasgupta Nupur
Department of Pharmaceutical Sciences
Disease Models
Fleming Sheila
Gaucher Disease/*drug therapy/genetics/physiopathology
Grabowski Gregory A
Human molecular genetics
Humans
Inskeep Venette
Li Ronghua
Liou Benjamin
Marshall John
Mice
Mitochondria/*drug effects/genetics/pathology
NEOMED College of Pharmacy
Neurons/drug effects/pathology
Neuroprotective Agents/administration & dosage
Peng Yanyan
Quinn Brian
Ryanodine Receptor Calcium Release Channel/*genetics/metabolism
Setchell Kenneth D R
Sun Ying
Zhang Wujuan
-
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/10.1089/neu.2015.3970" target="_blank" rel="noreferrer noopener">http://doi.org/10.1089/neu.2015.3970</a>
Pages
625–640
Issue
7
Volume
33
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
Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.
Publisher
An entity responsible for making the resource available
Journal of neurotrauma
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-04
Subject
The topic of the resource
Alzheimer Disease/etiology/*metabolism/pathology; Alzheimer's disease; Amyloid beta-Peptides/*metabolism; Animal; Animal/physiology; Animals; Behavior; Blotting; Brain Injuries; Brain/*metabolism/pathology; Disease Models; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Humans; Immunohistochemistry; Inbred C57BL; Inflammation/*metabolism/pathology; macrophage; Mice; neuroinflammation; Transgenic; traumatic brain injury; Traumatic/complications/*metabolism/*pathology; Western
Creator
An entity primarily responsible for making the resource
Kokiko-Cochran Olga N; Ransohoff Lena; Veenstra Mike; Lee Sungho; Saber Maha; Sikora Matt; Teknipp Ryan; Xu Guixiang; Bemiller Shane M; Wilson Gina; Crish Samuel; Bhaskar Kiran; Lee Yu-Shang; Ransohoff Richard M; Lamb Bruce T
Description
An account of the resource
Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. The R1.40 mouse model of cerebral amyloidosis was used, with a focus on time points well before robust AD pathologies. Unexpectedly, in R1.40 mice, the acute neuroinflammatory response to TBI was strikingly muted, with reduced numbers of CNS myeloid cells acquiring a macrophage phenotype and decreased expression of inflammatory cytokines. At chronic time points, macrophage activation substantially declined in non-Tg TBI mice; however, it was relatively unchanged in R1.40 TBI mice. The persistent inflammatory response coincided with significant tissue loss between 3 and 120 days post-injury in R1.40 TBI mice, which was not observed in non-Tg TBI mice. Surprisingly, inflammatory cytokine expression was enhanced in R1.40 mice compared with non-Tg mice, regardless of injury group. Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1089/neu.2015.3970" target="_blank" rel="noreferrer noopener">10.1089/neu.2015.3970</a>
Rights
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).
2016
Alzheimer Disease/etiology/*metabolism/pathology
Alzheimer's disease
Amyloid beta-Peptides/*metabolism
Animal
Animal/physiology
Animals
Behavior
Bemiller Shane M
Bhaskar Kiran
Blotting
Brain Injuries
Brain/*metabolism/pathology
Crish Samuel
Department of Pharmaceutical Sciences
Disease Models
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Humans
Immunohistochemistry
Inbred C57BL
Inflammation/*metabolism/pathology
Journal of neurotrauma
Kokiko-Cochran Olga N
Lamb Bruce T
Lee Sungho
Lee Yu-Shang
macrophage
Mice
NEOMED College of Pharmacy
Neuroinflammation
Ransohoff Lena
Ransohoff Richard M
Saber Maha
Sikora Matt
Teknipp Ryan
Transgenic
Traumatic brain injury
Traumatic/complications/*metabolism/*pathology
Veenstra Mike
Western
Wilson Gina
Xu Guixiang