:A Case Study
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概要
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A 9 years old Japanese non-albino girl has presented with mild to moderate nosebleed. Routine studies revealed normal counts and sizes of the patient's platelets and normal coagulation tests but prolonged bleeding times (over 12min). The platelets showed normal shape change in response to ADP. Aggregations of the platelets by ADP and collagen were significantly delayed in onset and weaker than controls, while aggregation/agglutination by epinephrine, thrombin, A23187 or ristocetin were normal, suggesting that the patient's platelets are abnormal only in ADP-induced activation. The platelet ATP secretion by 20μg/ml collagen was about half of controls by a Lumi-aggregometer. 3H-ADP binding to the patient's platelets as well as Ca2+ influx and mobilization induced by ADP were normal, suggesting a normal quantity of three ADP receptors and a normal function of P2X1, a component of the receptors. Immunoblots revealed that Giα subunit, a G-protein associated with P2Yac that is the second component of the receptors, was decreased in the patient's platelets than controls, but Gqα subunit, a G-protein associated with P2Y1 that is the third component of the receptors, was normal in the patient's platelets. Stimulation of PGE1-pretreated platelets by 10μM ADP or 10μM epinephrine reduced the cAMP levels in the patient's platelets to the same extent as in control platelets, indicating a normal function of P2Yac in spite of the decreased Giα subunit. The patient's platelet abnormality characterized with defective activation induced by ADP appears to originate from defective coordination between decreased Giαsubunit and other ADP receptors.
- 一般社団法人 日本血栓止血学会の論文
一般社団法人 日本血栓止血学会 | 論文
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