ライフサイエンスコーパス: thrombasthenia

1 show symptoms of both LAD-I and Glanzmann's thrombasthenia.

2 use the bleeding disorder termed Glanzmann's thrombasthenia.

3 tegrin cause the bleeding disorder Glanzmann thrombasthenia.

4 erious bleeding disorder, known as Glanzmann thrombasthenia.

5 ion and a bleeding tendency termed Glanzmann thrombasthenia.

6 ins of alphaIIb in 2 patients with Glanzmann thrombasthenia.

7 SLP-76 and in patients with type I Glanzmann thrombasthenia.

8 ally distinct families affected by Glanzmann thrombasthenia.

9 s on the platelet surface produces Glanzmann thrombasthenia.

10 white man was diagnosed as having Glanzmann thrombasthenia.

11 alphaIIbbeta3 from a patient with Glanzmann thrombasthenia.

12 ent platelets from patients with Glanzmann's thrombasthenia.

13 ntal treatment of a patient with Glanzmann's thrombasthenia.

14 ptake and the pathophysiology of Glanzmann's thrombasthenia.

15 served in either von Willebrand's disease or thrombasthenia.

16 evelop methods for gene therapy of Glanzmann thrombasthenia, a murine leukemia virus (MuLV)-derived v

17 Glanzmann thrombasthenia, an inherited bleeding disorder, can be c

18 in a noncompliant patient having Glanzmann's thrombasthenia and briefly discusses other hereditary bl

19 The severity of bleeding is unpredictable in thrombasthenia and does not correlate with the severity

20 ent with clinical features of both Glanzmann thrombasthenia and leukocyte adhesion deficiency-1.

21 s with bleeding similar to that in Glanzmann thrombasthenia and platelet dysfunction in addition to i

22 e ex vivo phenotypic correction of Glanzmann thrombasthenia and support the potential use of hematopo

23 ccurring mutations responsible for Glanzmann thrombasthenia and to point mutations that affect ligand

24 ta, and delta storage pool deficiency (SPD), thrombasthenia, and in two new patients with isolated de

25 mechanisms of mutagenesis causing Glanzmann thrombasthenia, and our findings will be valuable for su

26 e parallel alterations in these responses in thrombasthenia, as in SPD, further show the close associ

27 of China was diagnosed as having Glanzmann's thrombasthenia based on (1) nearly a lifelong history of

28 sic insights resulting in improved Glanzmann thrombasthenia carrier detection and prenatal diagnosis,

29 othrombinase responses were also observed in thrombasthenia, depending on the agonist and stirring co

30 m of the human bleeding disorder Glanzmann's thrombasthenia, fails to rescue beta 3(-/-) osteoclasts

31 The human bleeding disorder Glanzmann thrombasthenia (GT) can result from defects in the genes

32 reported as being associated with Glanzmann thrombasthenia (GT), 20 associated with alloimmune throm

33 Glanzmann thrombasthenia (GT), an autosomal recessive bleeding dis

34 SCs derived from two patients with Glanzmann thrombasthenia (GT), an inherited platelet disorder caus

35 re example of a platelet disorder, Glanzmann thrombasthenia (GT), is characterized by life-long morbi

36 f the inherited platelet disorder, Glanzmann thrombasthenia (GT), mutant alpha(IIb)beta(3) may intera

37 mplified by the bleeding disorder, Glanzmann thrombasthenia (GT), where abnormalities of the platelet

38 vere combined immune deficiency, Glanzmann's thrombasthenia, Hermansky-Pudlak syndrome, May-Hegglin a

39 studies of the molecular basis of Glanzmann thrombasthenia in a child of mixed Caucasian background

40 We report a case of Glanzmann thrombasthenia in a Pakistani child whose platelets expr

41 other thrombotic diseases whereas Glanzmann thrombasthenia, in which platelet aggregation is reduced

42 d on platelets from a patient with Glanzmann thrombasthenia, indicating that alphaII(b)beta3 is not r

43 ion, known to cause a variant of Glanzmann's thrombasthenia, inhibits the ability of the beta3 cytopl

44 Glanzmann's thrombasthenia is a qualitative platelet disorder charac

45 Glanzmann thrombasthenia is an inherited bleeding disorder charact

46 Glanzmann thrombasthenia is an inherited bleeding disorder charact

47 Glanzmann thrombasthenia is an inherited bleeding disorder due to

48 Thrombasthenia is clinically characterized by mucocutane

49 d kindlin-3 deficiency, but not in Glanzmann thrombasthenia lacking the platelet pool of fibrinogen a

50 f the ligand binding domain by the Glanzmann thrombasthenia mutation beta3-D119Y constitutively aboli

51 sease in humans, manifesting by neutropenia, thrombasthenia, myelofibrosis, and progressive bone marr

52 Patients with Glanzmann thrombasthenia or Leukocyte Adhesion Deficiency-III synd

53 sponsible for the genetic disorder Glanzmann thrombasthenia Paris I did not inhibit cell adhesion of

54 a3 expression and/or function in Glanzmann's thrombasthenia patients, platelet dysfunction can be a r

55 cy was not as severe as in other Glanzmann's thrombasthenia patients.

56 ro mutation appears to produce the Glanzmann thrombasthenia phenotype by both qualitative and quantit

57 Similar results were obtained with Glanzmann thrombasthenia platelets.

58 ear-old female with a history of Glanzmann's thrombasthenia presented for periodontal therapy for spo

59 m a patient with a variant form of Glanzmann thrombasthenia that expressed normal levels of FcgammaRI

60 The bleeding seen in Glanzmann's thrombasthenia usually includes bruising, epistaxis, gin

61 Studies of thrombasthenia variants have facilitated identification

62 platelets from three patients with Glanzmann thrombasthenia, who lacked GPIIb/IIIa receptors but had

63 ral blood CD34(+) cells from 2 patients with thrombasthenia with defects in the beta(3) gene.