| pubmed-article:7706468 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0439660 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0005821 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0016011 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0001459 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C1458140 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0439855 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
| pubmed-article:7706468 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
| pubmed-article:7706468 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:7706468 | pubmed:dateCreated | 1995-5-9 | lld:pubmed |
| pubmed-article:7706468 | pubmed:abstractText | Much discussion has concerned the central role of ADP in platelet aggregation. We now describe a patient (M.L.) with an inherited bleeding disorder whose specific feature is that ADP induces a limited and rapidly reversible platelet aggregation even at high doses. Platelet shape change and other hemostatic parameters were unmodified. A receptor defect was indicated, for, while epinephrine normally lowered cAMP levels of PGE1-treated (M.L.) platelets, ADP was without effect. The binding of [3H]2-methylthio-ADP decreased from 836 +/- 126 molecules/platelet for normals to 30 +/- 17 molecules/platelet for the patient. Flow cytometry confirmed that ADP induced a much lower fibrinogen binding to (M.L.) platelets. Nonetheless, the binding in whole blood of activation-dependent monoclonal antibodies showed that some activation of GP IIb-IIIa complexes by ADP was occurring. Platelets of a patient with type I Glanzmann's thrombasthenia bound [3H]2-methylthio-ADP and responded normally to ADP in the presence of PGE1. Electron microscopy showed that ADP-induced aggregates of (M. L.) platelets were composed of loosely bound shape-changed platelets with few contact points. Thus this receptor defect has a direct influence on the capacity of platelets to bind to each other in response to ADP. | lld:pubmed |
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| pubmed-article:7706468 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7706468 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7706468 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:7706468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:7706468 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7706468 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:7706468 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:HeilmannEE | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:SawaII | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:NurdenAA | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:MaffrandJ PJP | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:HerbertJ MJM | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:BihourCC | lld:pubmed |
| pubmed-article:7706468 | pubmed:author | pubmed-author:NurdenPP | lld:pubmed |
| pubmed-article:7706468 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7706468 | pubmed:volume | 95 | lld:pubmed |
| pubmed-article:7706468 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7706468 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7706468 | pubmed:pagination | 1612-22 | lld:pubmed |
| pubmed-article:7706468 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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