Source:http://linkedlifedata.com/resource/pubmed/id/20665726
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003062,
umls-concept:C0026336,
umls-concept:C0031809,
umls-concept:C0032743,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0040053,
umls-concept:C0205178,
umls-concept:C0205263,
umls-concept:C0205365,
umls-concept:C0475224,
umls-concept:C0521390,
umls-concept:C1883709,
umls-concept:C2603343
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pubmed:issue |
3
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pubmed:dateCreated |
2010-12-30
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pubmed:abstractText |
We evaluated sequential changes in rat brain function up to 14 days after focal ischemic insult with a small animal positron emission tomography (PET). Unilateral focal ischemic cerebral damage was induced by left middle cerebral artery occlusion with a photochemically induced thrombosis (PIT) method. PET scans were conducted with [(11)C](R)-PK11195 ([(11)C](R)-PK) for peripheral benzodiazepine receptor (PBR), [(11)C]flumazenil ([(11)C]FMZ) for central benzodiazepine receptor (CBR), and [(18)F]fluoro-2-deoxy-D-glucose ([(18)F]FDG) for glucose metabolism at before (as "Normal") and after PIT. At 1 and 3 days after PIT, [(18)F]FDG indicated lower uptake in the infarct area. Interestingly, unexpectedly high-[(18)F]FDG uptake was observed in the peri-infarct area surrounding the infarct area at day 7. The high-[(18)F]FDG uptake region completely overlapped with the high-[(11)C](R)-PK uptake region at day 7, which resulted in the underestimation of neuronal damage. Immunohistochemical data also suggested that the high-[(18)F]FDG uptake peak at day 7 was caused by inflammation including microglial cell activation. In contrast, imaging with [(11)C]FMZ indicated cortical neuronal damage on days 7 and 14 without any disturbance by microglial formation. These results indicated that [(18)F]FDG might not be a suitable ligand for ischemic neuronal damage detection from acute to subacute phases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Radioisotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorodeoxyglucose F18,
http://linkedlifedata.com/resource/pubmed/chemical/Isoquinolines,
http://linkedlifedata.com/resource/pubmed/chemical/PK 11195,
http://linkedlifedata.com/resource/pubmed/chemical/Radiopharmaceuticals
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1098-2396
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pubmed:author | |
pubmed:copyrightInfo |
2010 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
65
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
207-14
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pubmed:meshHeading |
pubmed-meshheading:20665726-Animals,
pubmed-meshheading:20665726-Carbon Radioisotopes,
pubmed-meshheading:20665726-Fluorodeoxyglucose F18,
pubmed-meshheading:20665726-Immunohistochemistry,
pubmed-meshheading:20665726-Infarction, Middle Cerebral Artery,
pubmed-meshheading:20665726-Isoquinolines,
pubmed-meshheading:20665726-Neurons,
pubmed-meshheading:20665726-Positron-Emission Tomography,
pubmed-meshheading:20665726-Radiopharmaceuticals,
pubmed-meshheading:20665726-Rats
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pubmed:year |
2011
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pubmed:articleTitle |
Multiparametric assessment of acute and subacute ischemic neuronal damage: a small animal positron emission tomography study with rat photochemically induced thrombosis model.
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pubmed:affiliation |
Central Research Laboratory, Hamamatsu Photonics K.K., Hamamatsu, Shizuoka 434-8601, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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