1
40
2
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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/10.1182/blood-2007-10-118497" target="_blank" rel="noreferrer noopener">http://doi.org/10.1182/blood-2007-10-118497</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
256-263
Issue
2
Volume
112
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Scavenging roles of chemokine receptors: chemokine receptor deficiency is associated with increased levels of ligand in circulation and tissues
Publisher
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Blood
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-07
Subject
The topic of the resource
in-vitro; central-nervous-system; Hematology; blood-brain-barrier; ccx-ckr; cutting edge; d6; dendritic cell; experimental autoimmune encephalomyelitis; immune-response; sjogrens-syndrome
Creator
An entity primarily responsible for making the resource
Cardona A E; Sasse M E; Liu L P; Cardona S M; Mizutani M; Savarin C; Hu T; Ransohoff R M
Description
An account of the resource
In vitro studies have implicated chemokine receptors in consumption and clearance of specific ligands. We studied the role that various signaling chemokine receptors play during ligand homeostasis in vivo. We examined the levels of ligands in serum and CNS tissue in mice lacking chemokine receptors. Compared with receptor-sufficient controls, Cx3cr1(-/-) mice exhibited augmented levels of CX3CL1 both in serum and brain, and circulating levels of CXCL1 and CXCL2 were increased in Cxcr2(-/-) mice. CCR2-deficient mice showed significantly increased amounts of circulating CCL2 compared with wild-type mice. Cxcr3(-/-) mice revealed increased levels of circulating and brain CXCL10 after experimental autoimmune encephalomyelitis (EAE) induction. CCR2-deficient peripheral blood and resident peritoneal cells exhibited reduced binding capacity and biologic responses to the CCR1 ligand CCL3, suggesting that elevated levels of CCR2 ligands had down-regulated CCR1. The results indicate that signaling chemokine receptors clear chemokines from circulation and tissues. These homeostatic functions of signaling chemokine receptors need to be integrated into safety and efficacy calculations when considering therapeutic receptor blockade.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1182/blood-2007-10-118497" target="_blank" rel="noreferrer noopener">10.1182/blood-2007-10-118497</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2008
Blood
blood-brain-barrier
Cardona A E
Cardona S M
ccx-ckr
central-nervous-system
cutting edge
d6
dendritic cell
experimental autoimmune encephalomyelitis
Hematology
Hu T
immune-response
in-vitro
Journal Article or Conference Abstract Publication
Liu L P
Mizutani M
Ransohoff R M
Sasse M E
Savarin C
sjogrens-syndrome
-
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/s0378-5955(01)00326-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s0378-5955(01)00326-4</a>
Pages
117–124
Issue
1
Volume
159
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
Auditory nerve fiber differences in the normal and neurofilament deficient Japanese quail.
Publisher
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Hearing research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-09
Subject
The topic of the resource
*Mutation; Animals; Auditory; Axons/ultrastructure; Brain Stem; Cochlear Nerve/*pathology/*physiopathology; Coturnix/genetics; Electron; Evoked Potentials; Microscopy; Myelin Sheath/ultrastructure; Nerve Fibers/pathology/physiology; Neurofilament Proteins/*deficiency/*genetics
Creator
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Sheykholeslami K; Kaga K; Mizutani M
Description
An account of the resource
A primary axonal disease affecting the central and peripheral nervous system was discovered in a mutant strain of the Japanese quail, named quiver (Quv). We have previously demonstrated altered auditory evoked potentials in the neurofilament (NF) deficient quail. In this current study we attempt to find relationships between the auditory evoked potential results and the histo-pathological abnormalities of the auditory neurons. No abnormalities in the external auditory meatus and tympanic cavity were observed in either Quv or control quails and the ganglion cell bodies and their nuclei appeared normal by light microscopy. The myelin staining pattern was found to be similar in both strains with hematoxylin and eosin and Kluver-Barrera staining. The frequency histograms of fiber and axonal diameters of myelinated fibers showed an unimodal pattern in both strains. In Quv quails myelinated fibers and their axoplasm were smaller in diameter than in controls resulting in smaller neural tissue mass. In electron microscopic observation the axons of the Quv quail were composed of mitochondria and microtubules and smooth endoplasmic reticuli. In Quv quail electron micrographs of cochlear nerve myelinated fibers NFs were not seen in the axons and the neuronal cell bodies. Our current findings indicate that the previously reported reduction of conduction velocity of auditory evoked potentials may be due to smaller fiber and/or axonal diameter. The g-ratio, myelin thickness and fiber circularity were found to be the same for both strains. In conclusion, loss of axonal cytoskeletal elements (NFs) correlates well with our electrophysiological findings. Reduced conduction velocity and severely distorted auditory evoked potentials in NF deficient quails seem to be primarily due to axonal hypotrophy.
Identifier
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<a href="http://doi.org/10.1016/s0378-5955(01)00326-4" target="_blank" rel="noreferrer noopener">10.1016/s0378-5955(01)00326-4</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Mutation
2001
Animals
Auditory
Axons/ultrastructure
Brain Stem
Cochlear Nerve/*pathology/*physiopathology
Coturnix/genetics
Electron
Evoked Potentials
Hearing research
Kaga K
Microscopy
Mizutani M
Myelin Sheath/ultrastructure
Nerve Fibers/pathology/physiology
Neurofilament Proteins/*deficiency/*genetics
Sheykholeslami K