ライフサイエンスコーパス: vascular malformation

1 ut the presumed etiology was an unidentified vascular malformation.

2 ts a vascular neoplasm, vascular anomaly, or vascular malformation.

3 to our knowledge, have not been described in vascular malformations.

4 There were 49 hemangiomas and 38 vascular malformations.

5 re performed in three patients with low-flow vascular malformations.

6 giectasia (HHT1), a disease characterized by vascular malformations.

7 ins were widely patent without thrombosis or vascular malformations.

8 hways also contribute to atherosclerosis and vascular malformations.

9 d its involvement in two, if not more, human vascular malformations.

10 as (CHs) account for 5% to 12% of all spinal vascular malformations.

11 nomalies, differentiating high- and low-flow vascular malformations.

12 a potential strategy to treat patients with vascular malformations.

13 tracranial tumors, functional disorders, and vascular malformations.

14 uctive pulmonary disease, cancers, and brain vascular malformations.

15 eds produced CNS-specific hyperproliferative vascular malformations.

16 rment after surgery for epilepsy, tumours or vascular malformations.

17 to oxygen-induced remodeling without causing vascular malformations.

18 Tie-2 in blue rubber bleb nevus and sporadic vascular malformations.

19 yrAkt led to embryonic lethality, edema, and vascular malformations.

20 p53 plays a direct role in formation of the vascular malformations.

21 d is frequently associated with intracranial vascular malformations.

22 lastoma multiforme and some other tumors and vascular malformations.

23 1), a disease characterised by bleeding from vascular malformations.

24 oplasms, surgeries nearby sinuses and orbit, vascular malformations, acute sinusitis, systemic abnorm

25 S can be used to distinguish hemangioma from vascular malformation and detect arterial flow.

26 rain vascular innervation, contribute to the vascular malformation and its consequences.

27 levels reached 82.4%, accompanied by severe vascular malformation and steatosis in the liver.

28 ORC1 signaling in endothelial cells promotes vascular malformation and suggest that mTORC1 inhibitors

29 cidate the molecular pathogenesis of hepatic vascular malformation and the safety of therapeutics inh

30 Given links between vascular malformations and angiosarcoma with activated R

31 ciency of HIF-1alpha resulted in cardiac and vascular malformations and embryonic lethality at E10.5.

32 e and prevented vessel maturation leading to vascular malformations and endotheliomas.

33 significantly higher for AVM than for other vascular malformations and hemangioma.

34 ents with HHT associated with severe hepatic vascular malformations and high cardiac output, administ

35 S patients, include Hashimoto's thyroiditis, vascular malformations and mental retardation.

36 None of 154 other vascular malformations and tumors harbored an IDH1 R132C

37 gnosis and topographical characterization of vascular malformations and tumors of cervicofacial area

38 stem causing hemorrhage-prone multiple lumen vascular malformations and very severe neurological cons

39 atic seizures after presentation, ICH due to vascular malformation, and elevated intracranial pressur

40 cal issues for patients with hemangiomas and vascular malformations, and (4) the elucidation of seque

41 ns that underlie the formation of many human vascular malformations are known, the extent to which ab

42 Vascular malformations are linked to mutations in RAS p2

43 Vascular malformations are non-neoplastic expansions of

44 Dural vascular malformations are often elusive on all cross-se

45 In addition, many vascular malformations are related to deregulation of TG

46 Congenital vascular malformations are tumour-like, non-neoplastic l

47 Vascular malformations, arterial aneurysms and dissectio

48 Viewing atherosclerosis and vascular malformations as instances of pathological morp

49 ) may represent a hyperplastic response to a vascular malformation, but the precise etiology remains

50 ascular development and to prevent postnatal vascular malformations, but its molecular effectors are

51 Human vascular malformations cause disease as a result of chan

52 ral cavernous malformations (CCMs) are human vascular malformations caused by mutations in three gene

53 One prevalent form of these vascular malformations, cerebral cavernous malformation,

54 All targeted vascular malformation compartments were filled with scle

55 r, and its deregulation is associated with a vascular malformation consistent with Klippel-Trenaunay

56 coding SMAD4) or BMPR1A, and the latter is a vascular malformation disorder caused by mutations in EN

57 diologists must identify the MRI features of vascular malformations for better diagnosis and classifi

58 Furthermore, enlarged vessels and vascular malformations form in either the presence or ab

59 or T2-weighted imaging for low-grade tumors, vascular malformations, gliosis after infarction, inflam

60 potential therapeutic targets against these vascular malformations identified so far, as well as the

61 This vascular malformation, if undetected, can lead to seriou

62 genesis may contribute to the development of vascular malformation in IUGR, but in vitro these change

63 us malformations (CCMs) are a common type of vascular malformation in the brain that are a major caus

64 beta-catenin transcription activity, reduce vascular malformations in endothelial CCM3-deficient mic

65 he Id1-Id3 double knockout mice also display vascular malformations in the forebrain and an absence o

66 atients; mean age, 32.9 years +/- 14.1) with vascular malformations in the head and neck (n = 64), sp

67 rapping around VEGF-producing fibers, and of vascular malformations in the muscle at high levels, did

68 a scintigraphic image of familial congenital vascular malformations in two sisters.

69 els, defective angiogenic remodeling, severe vascular malformations including arterio-venous malforma

70 Vascular malformations, including angiodysplasia and Die

71 bral haemorrhage resulting from intracranial vascular malformation, intracranial venous thrombosis, h

72 dothelium-selective Grk2 ablation had marked vascular malformations involving impaired recruitment of

73 umor cells and also seen in two benign human vascular malformations, juvenile angiofibromas and infan

74 cavernous malformation (CCM) is a disease of vascular malformations known to be caused by mutations i

75 redictor for differentiating hemangioma from vascular malformation (likelihood ratio test = 109.8, P

76 Alk1-conditional deletion resulted in severe vascular malformations mimicking all pathologic features

77 rogenic procedures (n = 14, 16%), congenital vascular malformations (n = 13, 15%), tumor (n = 13, 15%

78 n of both normal retinal anatomy, as well as vascular malformations, nonperfusion, and neovasculariza

79 th headache, scalp defects and structural or vascular malformations of the brain.

80 deafness, facial weakness, hypoventilation, vascular malformations of the internal carotid arteries

81 ipal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early

82 ignificantly greater compared with the other vascular malformations (P < .001 in each case).

83 Vascular malformations pose a diagnostic and therapeutic

84 other cellular properties in hemangiomas and vascular malformations relevant to vascular development,

85 mportant in experimental stroke and cerebral vascular malformation research.

86 dilated and fragile blood vessels similar to vascular malformations seen in HHT patients.

87 temic thrombolysis in a patient with a known vascular malformation should be individualized.

88 agnosed disorders related to the presence of vascular malformations should undergo periodic follow-up

89 rmed, and genomic DNA was extracted from the vascular malformation specimen and normal skin.

90 the cerebral vasculature, such as congenital vascular malformations, stroke and tumors, compromise ne

91 ibromatosis (NF1), nor is it associated with vascular malformations, such as in the recently reported

92 The genetic basis for a variety of vascular malformation syndromes have been described, wit

93 Genes responsible for familial vascular malformation syndromes have increasingly been s

94 ity pathways are good candidates for causing vascular malformation syndromes.

95 cyte protein of 76 kDa (SLP76) resulted in a vascular malformation that directed blood flow through m

96 Here, we focus on two of the most studied vascular malformations that are induced by deregulation

97 pathological angiogenesis is angiodysplasia, vascular malformations that cause severe gastrointestina

98 ons (CCMs) are common inherited and sporadic vascular malformations that cause strokes and seizures i

99 Vascular malformations that occur inside bone tissue are

100 llary beds, and the formation of hemorrhagic vascular malformations that remain adherent to the menin

101 Congenital cardio-vascular malformations, the most frequent birth defect,

102 ed to endothelial proliferative lesions from vascular malformations to vascular tumors in adult mice.

103 ve therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, p

104 and miR-155 knock-out in mice causes retinal vascular malformations typical of faulty maturation, mim

105 meruloid microvascular proliferations (GMP), vascular malformations (VM), feeding arteries (FA), and

106 usative for autosomal-recessive intraosseous vascular malformation (VMOS) in five different families.

107 Staged surgical excision of the vascular malformation was performed, and genomic DNA was

108 an adaptor protein whose mutation results in vascular malformations, we have found that it is involve

109 (<1 year), venous or orthopedic surgery, or vascular malformations were clinically stratified for CV

110 In static and whole-body examinations vascular malformations were visualised in the area of th

111 rteriovenous malformations (AVMs) are common vascular malformations, which may result in hemorrhagic

112 tinterventional perfusion changes within the vascular malformation with calculation of changes in con

113 nd without complications by filling targeted vascular malformations with sclerosing agent.

114 ial Notch1 from birth led to similar hepatic vascular malformations within 2 weeks.

115 tion of hemangiomas (48 of 49) compared with vascular malformations (zero of 38) consisted of a solid