1
40
3
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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.0038359" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0038359</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
13-13
Issue
5
Volume
7
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Performance of Repetitive Tasks Induces Decreased Grip Strength and Increased Fibrogenic Proteins in Skeletal Muscle: Role of Force and Inflammation
Publisher
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PLOS ONE
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-05
Subject
The topic of the resource
carpal-tunnel-syndrome; factor gene-expression; flexor tendon cells; in-vivo; lengthening contractions; necrosis-factor-alpha; rat model; Science & Technology - Other Topics; strain injury; tissue growth-factor; tnf-alpha
Creator
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Abdelmagid S M; Barr A E; Rico M; Amin M; Litvin J; Popoff S N; Safadi F; Barbe M F
Description
An account of the resource
Background: This study elucidates exposure-response relationships between performance of repetitive tasks, grip strength declines, and fibrogenic-related protein changes in muscles, and their link to inflammation. Specifically, we examined forearm flexor digitorum muscles for changes in connective tissue growth factor (CTGF; a matrix protein associated with fibrosis), collagen type I (Col1; a matrix component), and transforming growth factor beta 1 (TGFB1; an upstream modulator of CTGF and collagen), in rats performing one of two repetitive tasks, with or without anti-inflammatory drugs. Methodology/Results: To examine the roles of force versus repetition, rats performed either a high repetition negligible force food retrieval task (HRNF), or a high repetition high force handle-pulling task (HRHF), for up to 9 weeks, with results compared to trained only (TR-NF or TR-HF) and normal control rats. Grip strength declined with both tasks, with the greatest declines in 9-week HRHF rats. Quantitative PCR (qPCR) analyses of HRNF muscles showed increased expression of Col1 in weeks 3-9, and CTGF in weeks 6 and 9. Immunohistochemistry confirmed PCR results, and also showed greater increases of CTGF and collagen matrix in 9-week HRHF rats than 9-week HRNF rats. ELISA, and immunohistochemistry revealed greater increases of TGFB1 in TR-HF and 6-week HRHF, compared to 6-week HRNF rats. To examine the role of inflammation, results from 6-week HRHF rats were compared to rats receiving ibuprofen or anti-TNF-alpha treatment in HRHF weeks 4-6. Both treatments attenuated HRHF-induced increases in CTGF and fibrosis by 6 weeks of task performance. Ibuprofen attenuated TGFB1 increases and grip strength declines, matching our prior results with anti-TNF alpha. Conclusions/Significance: Performance of highly repetitive tasks was associated with force-dependent declines in grip strength and increased fibrogenic-related proteins in flexor digitorum muscles. These changes were attenuated, at least short-term, by anti-inflammatory treatments.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0038359" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0038359</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Abdelmagid S M
Amin M
Barbe M F
Barr A E
carpal-tunnel-syndrome
factor gene-expression
flexor tendon cells
in-vivo
Journal Article or Conference Abstract Publication
lengthening contractions
Litvin J
necrosis-factor-alpha
PloS one
Popoff S N
rat model
Rico M
Safadi F
Science & Technology - Other Topics
strain injury
tissue growth-factor
TNF-alpha
-
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/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-015-0399-0</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
13-13
Volume
12
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Early pro-inflammatory cytokine elevations in the DBA/2J mouse model of glaucoma
Publisher
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Journal of Neuroinflammation
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
Aging; axonal-transport; axoplasmic-transport; Cytokines; fibroblast-growth-factor; gene-expression; glaucoma; Immunology; inflammation; Intraocular pressure; Intraocular pressure; necrosis-factor-alpha; neurodegeneration; Neurosciences & Neurology; ocular hypertension; optic-nerve head; retinal ganglion-cells; tnf-alpha
Creator
An entity primarily responsible for making the resource
Wilson G N; Inman D M; Denger-Crish C M; Smith M A; Crish S D
Description
An account of the resource
Background: Neuroinflammation-astrogliosis, microglial activation, and changes in cytokine signaling-is a prominent feature of neurodegenerative disorders. Glaucoma is a group of chronic neurodegenerative conditions that make up the leading cause of irreversible blindness worldwide. Neuroinflammation has been postulated to play a significant role in the pathogenesis and progression of glaucomatous neurodegeneration. Though much is known regarding inflammation in the eye in glaucoma, little is known about cytokine activity outside of the retina where pathologies develop early. Methods: We traced the primary visual projection from the eye to the superior colliculus (SC) in DBA/2J and DBA/2J. Gpnmb(+) (control) mice using the anterograde tracer cholera toxin-B (CTB) to assay axonal transport deficits. Forty-eight hours later, visual structures were microdissected from fresh tissue based on transport outcome. Using magnetic bead multiplexing assays, we measured levels of 20 cytokines in the retina, proximal and distal optic nerves, CTB-positive and negative SC subdivisions, cerebellum, and serum at different ages representing different stages of pathology. Results: Pro-and anti-inflammatory cytokine levels in mice often changed in the same direction based on strain, age, and tissue. Significant elevations in retinal pro-inflammatory cytokines were observed in young DBA/2J mice compared to controls, followed by an age-dependent decrease in the DBA/2J mice. Proximal optic nerve of young DBA/2J mice showed a 50 % or greater decrease in levels of certain cytokines compared to older DBA/2J cohorts and controls, while both proximal and distal optic nerve of DBA/2Js showed elevations in IL-1 beta at all ages compared to controls. Pro-inflammatory cytokine IL-6 levels varied in accordance with transport outcome in the SC: IL-6 was elevated 44-80 % in glaucomatous DBA/2J collicular regions deficient in anterograde transport from retinal ganglion cells (RGCs) compared to areas with intact transport. Conclusion: Dysregulation of cytokine signaling in the RGC projection of DBA/2J mice was evident early in distal retinal targets, well before intraocular pressure elevation or axonal degeneration begins.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">10.1186/s12974-015-0399-0</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2015
Aging
axonal-transport
axoplasmic-transport
Crish S D
Cytokines
Denger-Crish C M
Department of Pharmaceutical Sciences
fibroblast-growth-factor
gene-expression
Glaucoma
Immunology
Inflammation
Inman D M
Intraocular Pressure
Journal Article
Journal of neuroinflammation
necrosis-factor-alpha
NEOMED College of Pharmacy
Neurodegeneration
Neurosciences & Neurology
Ocular Hypertension
optic-nerve head
retinal ganglion-cells
Smith M A
TNF-alpha
Wilson G 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/10.1074/jbc.M113.512269" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M113.512269</a>
Pages
6877–6885
Issue
10
Volume
289
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
Modulation of ten-eleven translocation 1 (TET1), Isocitrate Dehydrogenase (IDH) expression, alpha-Ketoglutarate (alpha-KG), and DNA hydroxymethylation levels by interleukin-1beta in primary human chondrocytes.
Publisher
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The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-03
Subject
The topic of the resource
*DNA Methylation; *Epigenesis; 5-hmC; 5-Methylcytosine/analogs & derivatives; Chondrocytes; Chondrocytes/chemistry/*metabolism; Cytokine; Cytosine/*analogs & derivatives/analysis/metabolism; Dioxygenase; DNA Methylation; DNA-Binding Proteins/*biosynthesis/genetics; Epigenetics; Genetic; Humans; IL-1; Interleukin-1beta/pharmacology/*physiology; Isocitrate Dehydrogenase/*biosynthesis/genetics; Ketoglutaric Acids/*metabolism; Messenger/biosynthesis/genetics; Mixed Function Oxygenases; Primary Cell Culture; Proto-Oncogene Proteins/*biosynthesis/genetics; RNA; TNF-alpha; Tumor Necrosis Factor-alpha/pharmacology/physiology
Creator
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Haseeb Abdul; Makki Mohammad Shahidul; Haqqi Tariq M
Description
An account of the resource
5-Hydroxymethylcytosine (5-hmC) generated by ten-eleven translocation 1-3 (TET1-3) enzymes is an epigenetic mark present in many tissues with different degrees of abundance. IL-1beta and TNF-alpha are the two major cytokines present in arthritic joints that modulate the expression of many genes associated with cartilage degradation in osteoarthritis. In the present study, we investigated the global 5-hmC content, the effects of IL-1beta and TNF-alpha on 5-hmC content, and the expression and activity of TETs and isocitrate dehydrogenases in primary human chondrocytes. The global 5-hmC content was found to be approximately 0.1% of the total genome. There was a significant decrease in the levels of 5-hmC and the TET enzyme activity upon treatment of chondrocytes with IL-1beta alone or in combination with TNF-alpha. We observed a dramatic (10-20-fold) decrease in the levels of TET1 mRNA expression and a small increase (2-3-fold) in TET3 expression in chondrocytes stimulated with IL-1beta and TNF-alpha. IL-1beta and TNF-alpha significantly suppressed the activity and expression of IDHs, which correlated with the reduced alpha-ketoglutarate levels. Whole genome profiling showed an erasure effect of IL-1beta and TNF-alpha, resulting in a significant decrease in hydroxymethylation in a myriad of genes including many genes that are important in chondrocyte physiology. Our data demonstrate that DNA hydroxymethylation is modulated by pro-inflammatory cytokines via suppression of the cytosine hydroxymethylation machinery. These data point to new mechanisms of epigenetic control of gene expression by pro-inflammatory cytokines in human chondrocytes.
Identifier
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<a href="http://doi.org/10.1074/jbc.M113.512269" target="_blank" rel="noreferrer noopener">10.1074/jbc.M113.512269</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).
*DNA methylation
*Epigenesis
2014
5-hmC
5-Methylcytosine/analogs & derivatives
Chondrocytes
Chondrocytes/chemistry/*metabolism
Cytokine
Cytosine/*analogs & derivatives/analysis/metabolism
Department of Anatomy & Neurobiology
Dioxygenase
DNA Methylation
DNA-Binding Proteins/*biosynthesis/genetics
Epigenetics
Genetic
Haqqi Tariq M
Haseeb Abdul
Humans
IL-1
Interleukin-1beta/pharmacology/*physiology
Isocitrate Dehydrogenase/*biosynthesis/genetics
Ketoglutaric Acids/*metabolism
Makki Mohammad Shahidul
Messenger/biosynthesis/genetics
Mixed Function Oxygenases
NEOMED College of Medicine
Primary Cell Culture
Proto-Oncogene Proteins/*biosynthesis/genetics
RNA
The Journal of biological chemistry
TNF-alpha
Tumor Necrosis Factor-alpha/pharmacology/physiology