| pubmed-article:2902315 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2902315 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:2902315 | lifeskim:mentions | umls-concept:C0014544 | lld:lifeskim |
| pubmed-article:2902315 | lifeskim:mentions | umls-concept:C0205234 | lld:lifeskim |
| pubmed-article:2902315 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:2902315 | lifeskim:mentions | umls-concept:C1149380 | lld:lifeskim |
| pubmed-article:2902315 | pubmed:issue | 8616 | lld:pubmed |
| pubmed-article:2902315 | pubmed:dateCreated | 1988-11-10 | lld:pubmed |
| pubmed-article:2902315 | pubmed:abstractText | Ten patients with partial epilepsy and five healthy controls had positron emission tomography (PET) of the brain after intravenous administration of the 11C-labelled benzodiazepine (BZ) receptor ligand 'Ro-15 1788'. In all ten patients BZ receptor binding was significantly lower in the epileptic focus than in the contralateral homotopic reference region and the remaining neocortex. No asymmetries in BZ receptor binding were observed between homotopic reference regions in the controls or the non-epileptic regions of patients. These results demonstrate the potential of the BZ receptor as a biochemical marker for display of epileptic foci by PET, and also strengthen the hypothesis that inhibitory mechanisms are disturbed in the epileptic focus. | lld:pubmed |
| pubmed-article:2902315 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2902315 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2902315 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:2902315 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2902315 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2902315 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:2902315 | pubmed:issn | 0140-6736 | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:PerssonAA | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:SedvallGG | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:WidénLL | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:RolandPP | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:PauliSS | lld:pubmed |
| pubmed-article:2902315 | pubmed:author | pubmed-author:SavioEE | lld:pubmed |
| pubmed-article:2902315 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2902315 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:2902315 | pubmed:volume | 2 | lld:pubmed |
| pubmed-article:2902315 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2902315 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2902315 | pubmed:pagination | 863-6 | lld:pubmed |
| pubmed-article:2902315 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:2902315 | pubmed:meshHeading | pubmed-meshheading:2902315-... | lld:pubmed |
| pubmed-article:2902315 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2902315 | pubmed:articleTitle | In-vivo demonstration of reduced benzodiazepine receptor binding in human epileptic foci. | lld:pubmed |
| pubmed-article:2902315 | pubmed:affiliation | Department of Clinical Neurophysiology, Karolinska Hospital, Stockholm, Sweden. | lld:pubmed |
| pubmed-article:2902315 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2902315 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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