ライフサイエンスコーパス: platelet dysfunction

1 Crimean-Congo haemorrhagic fever relates to platelet dysfunction.

2 ing with thrombocytopenia and/or evidence of platelet dysfunction.

3 ions as an important mechanism for inherited platelet dysfunction.

4 of platelet aggregates for the detection of platelet dysfunction.

5 ve been associated with thrombocytopenia and platelet dysfunction.

6 n the presence of thrombocytopenia or severe platelet dysfunction.

7 S and assessed the effect of GT treatment on platelet dysfunction.

8 une system, as well as thrombocytopenia with platelet dysfunction.

9 gical postcardiopulmonary bypass bleeding is platelet dysfunction.

10 oderate thrombocytopenia in combination with platelet dysfunction.

11 classical EDS to characterize the extent of platelet dysfunction.

12 at severe allergic inflammation is linked to platelet dysfunction.

13 with moderate to severe thrombocytopenia and platelet dysfunction.

14 unction, culminating in thrombocytopenia and platelet dysfunction.

15 NS1 Ab-mediated endothelial cell damage and platelet dysfunction.

16 nistic insights explaining dasatinib-related platelet dysfunction and bleeding.

17 emostasis, and granule biology, in line with platelet dysfunction and bleedings.

18 The existence of animal models of platelet dysfunction and currently used antiplatelet the

19 s, hemodialysis is associated with transient platelet dysfunction and decreased membrane expression o

20 ited in the perioperative setting because of platelet dysfunction and gastrointestinal toxicity.

21 s characterized by the presence of albinism, platelet dysfunction and pulmonary fibrosis.

22 urring TxA(2)R variant to be associated with platelet dysfunction and the first in which loss of rece

23 ombosis during hemodialysis (HD), subsequent platelet dysfunction and tissue dysregulation are less u

24 (FPDMM), characterized by thrombocytopenia, platelet dysfunction, and a predisposition to hematologi

25 is characterized by oculocutaneous albinism, platelet dysfunction, and in some patients, pulmonary fi

26 s associated with familial thrombocytopenia, platelet dysfunction, and predisposition to acute leukem

27 bg mutation is characterized by NK cell and platelet dysfunction, and systemic treatment of WT mice

28 , MLC phosphorylation, thrombocytopenia, and platelet dysfunction associated with RUNX1 mutations.

29 tic peptide, in the mouse model of inherited platelet dysfunction because of mutation of the myosin 9

30 Abs can lead to endothelial cell damage and platelet dysfunction by antigenic cross-reactivity.

31 N substitution causes clinically significant platelet dysfunction by reducing ligand binding establis

32 tion in Glanzmann's thrombasthenia patients, platelet dysfunction can be a result of genetic variabil

33 stemic features, including renal disease and platelet dysfunction, caused by the defect in a conserve

34 ry phenotype in these individuals, including platelet dysfunction, dysregulated fibrinolysis, and enh

35 proposed mechanisms that induce TIC, such as platelet dysfunction, endogenous anticoagulation, endoth

36 understanding of TIC, including the role of platelet dysfunction, endothelial activation, and fibrin

37 GRP2 that account for bleeding diathesis and platelet dysfunction in 2 unrelated families.

38 ilar to that in Glanzmann thrombasthenia and platelet dysfunction in addition to impaired leukocyte a

39 Platelet dysfunction in CF could contribute to pulmonary

40 Contrary to the historical view that platelet dysfunction in cirrhosis might be responsible f

41 oaches that can advance our understanding of platelet dysfunction in CKD are needed, and studies that

42 this study was to elucidate the mechanism of platelet dysfunction in critically injured patients.

43 Platelet dysfunction in DKO mice is revealed by prolonge

44 Our findings suggest that platelet dysfunction in EDS is an outcome of reduced int

45 Collectively, our data indicate that platelet dysfunction in EDS is likely contributing to he

46 otential mechanistic link between uremia and platelet dysfunction in ESKD, we used liquid chromatogra

47 However, the impact of insulin therapy on platelet dysfunction in patients treated with P2Y12 anta

48 cular explanation for the universally severe platelet dysfunction in this disease, and the cumulative

49 Platelet dysfunction includes impaired contractility, wh

50 Platelet dysfunction is a common cause of bleeding after

51 Platelet dysfunction is a major cause of excessive micro

52 In this study, we uncovered evidence that platelet dysfunction is a third possible mechanism for b

53 Platelet dysfunction is common.

54 present study indicate that diabetes-induced platelet dysfunction is mediated largely by calpain acti

55 Whereas platelet dysfunction is severe and consistent, immune de

56 by virus-induced IFN-alpha/beta that causes platelet dysfunction, mucocutaneous blood loss and suppr

57 However, the molecular mechanism for platelet dysfunction observed in patients with diabetes

58 ide generation may play an important role in platelet dysfunction observed in patients with diabetes.

59 ), carriage of haemophilia-A gene (one), and platelet dysfunction (one).

60 ndrome is an autosomal recessive disorder of platelet dysfunction presenting with mild thrombocytopen

61 disorder characterized by thrombocytopenia, platelet dysfunction, splenomegaly, reticulocytosis, and

62 ts who had undergone cardiopulmonary bypass, platelet dysfunction strongly correlated with the need f

63 Although the transient platelet dysfunction that occurs after platelet contact

64 Platelet dysfunction was apparent after completion of th

65 The observed platelet dysfunction was associated with reduced express

66 Platelet dysfunction was independent of glycemic control

67 ion to inflammatory response, and increasing platelet dysfunction with blood flow rate (BFR) and Vint