ライフサイエンスコーパス: cavernous

1 review the neuroophthalmic manifestations of cavernous and posterior communicating artery aneurysms a

2 The natural history of cavernous aneurysms has recently been systematically fol

3 sions in 44 patients with inoperable carotid cavernous aneurysms or head and neck tumours to examine

4 a large white kindred with familial cerebral cavernous angioma and confirm the mapping to 7q11-22, in

5 It lacks the "hemosiderin rim" of cavernous angioma and demonstrates increased susceptibil

6 f the candidate region for familial cerebral cavernous angioma and facilitate the search for the gene

7 the region containing the familial cerebral cavernous angioma gene.

8 ly, a gene responsible for familial cerebral cavernous angioma in a large Hispanic kindred was mapped

9 Familial cerebral cavernous angioma occurs as an autosomal dominant disord

10 arched for the terms cavernous malformation, cavernous angioma, and cavernoma.

11 Cerebral cavernous angiomas are collections of closely clustered

12 Two patients had multiple classic cerebral cavernous angiomas.

13 grew rapidly and were devoid of the typical cavernous architecture of slow-growing Ang2-expressing h

14 ation from the proximal sites of both of the cavernous arteries and a right cavernosal artery pseudoa

15 r with a high-velocity shunt between the two cavernous arteries.

16 rature made us conclude that embolization of cavernous artery by means of an autologous clot is a ver

17 mic acid residues that extend outward from a cavernous cleft.

18 Schnabel cavernous degeneration (SCD) has been observed in eyes w

19 Schnabel cavernous degeneration was seen in 17 (0.9%) UM eyes, 9

20 esent, with these channels coalescing into a cavernous, endothelium-lined blood pool resembling a hem

21 showed significant thrombosis of the carotid cavernous fistula and no intervention was warranted.

22 d spontaneous partial closure of the carotid cavernous fistula and the procedure was aborted.

23 have undergone apparent closure of a carotid cavernous fistula be carefully monitored for worsening o

24 nts after spontaneous closure of her carotid cavernous fistula had been noted.

25 e in blood flow, an indirect sign of carotid cavernous fistula.

26 with subretinal fluid secondary to a carotid cavernous fistula.

27 described as a rare complication of carotid cavernous fistula.

28 a small indirect Barrow type D right carotid cavernous fistula.

29 wo months subsequent to closure of a carotid cavernous fistula.

30 Carotid-cavernous fistulas are abnormal communications between t

31 Carotid cavernous fistulas are abnormal communications between t

32 Although rare, closure of carotid cavernous fistulas can lead to immediate ocular complica

33 11 pseudoaneurysms, 17 thromboses, 4 carotid cavernous fistulas, and 1 transected internal carotid ar

34 o occur immediately after closure of carotid cavernous fistulas, but not over months as in our patien

35 doaneurysms, visceral aneurysms, and carotid-cavernous fistulas.

36 cinoma (n = 23), cholangiocarcinoma (n = 6), cavernous hemangioma (n = 4), focal nodular hyperplasia

37 rl showed increased uptake in a subcutaneous cavernous hemangioma, which should be added to the list

38 Cavernous hemangiomas (CHs) account for 5% to 12% of all

39 ce heterozygous for the 1-lox allele develop cavernous hemangiomas of the liver, a rare manifestation

40 locator (Arnt) genes in a VHL mouse model of cavernous liver hemangiomas and polycythemia.

41 Cerebral cavernous malformation (CCM) is a common autosomal domin

42 Cerebral cavernous malformation (CCM) is a common vascular dyspla

43 Cerebral cavernous malformation (CCM) is a disease of the central

44 Cerebral cavernous malformation (CCM) is a disease of vascular ma

45 Cerebral cavernous malformation (CCM) is a disease that affects b

46 Cerebral cavernous malformation (CCM) is a Mendelian model of str

47 The prevalence of cerebral cavernous malformation (CCM) is unknown.

48 ining the mechanism of formation of cerebral cavernous malformation (CCM) lesions.

49 The cerebral cavernous malformation (CCM) pathway is required in endo

50 The cerebral cavernous malformation (CCM) signaling pathway utilizes

51 CCM3 mutations are associated with cerebral cavernous malformation (CCM), a disease affecting 0.1-0.

52 Cerebral cavernous malformation (CCM), a disease associated with

53 evelopment of the vascular disorder Cerebral Cavernous Malformation (CCM).

54 patients with sporadic, nonfamilial cerebral cavernous malformation (CCM).

55 ations are the most common cause of cerebral cavernous malformation (CCM).

56 emorrhagic telangiectasia (HHT) and cerebral cavernous malformation (CCM).

57 The Heart of Glass-Cerebral Cavernous Malformation (Heg-CCM) pathway is essential fo

58 a cells via an interaction with the cerebral cavernous malformation 2 (CCM2) protein.

59 Krev1 interaction trapped (KRIT1), Cerebral cavernous malformation 2 (CCM2), and Programmed cell dea

60 Loss of function of cerebral cavernous malformation 3 (CCM3) results in an autosomal

61 GCKIIIs are effectors of Cerebral cavernous malformation 3 (CCM3), a protein mutated in va

62 Virtually all cases of familial and sporadic cavernous malformation among Hispanic Americans of Mexic

63 ce to mutation screening efforts in cerebral cavernous malformation and may contribute to our underst

64 ion of genetic markers and clinical cases of cavernous malformation in Hispanic-American kindreds wit

65 proteins (ccm3Delta) known to cause cerebral cavernous malformation in humans confers cardiovascular

66 o compared the alleles for markers linked to cavernous malformation in patients with familial and spo

67 Cerebral cavernous malformation is a common human vascular diseas

68 Cerebral cavernous malformation is a vascular disease of the brai

69 spanic Americans have a higher prevalence of cavernous malformation than do other ethnic groups, rais

70 reds with familial disease showed linkage of cavernous malformation to a short segment of chromosome

71 case has been found with KRIT1, the cerebral cavernous malformation type 1 (CCM1) gene.

72 The CCM (cerebral cavernous malformation) family of proteins (KRIT1 (Krev-

73 ein whose loss of function leads to cerebral cavernous malformation, a cerebrovascular dysplasia occu

74 action trapped gene 1 (KRIT1) cause cerebral cavernous malformation, an autosomal dominant disease fe

75 and MRI reports were searched for the terms cavernous malformation, cavernous angioma, and cavernoma

76 rm of these vascular malformations, cerebral cavernous malformation, is characterized by thin-walled

77 ped 1), a defective gene product in cerebral cavernous malformation, was cloned from a HeLa cell cDNA

78 l alleles for up to 15 markers linked to the cavernous-malformation gene, demonstrating that they had

79 0.52%), six pituitary adenomas (0.16%), five cavernous malformations (0.14%), eight vascular stenoses

80 Cerebral cavernous malformations (CCM) are congenital vascular an

81 Cerebral cavernous malformations (CCM) are irregularly shaped and

82 Cerebral cavernous malformations (CCM) are vascular lesions causi

83 Cerebral cavernous malformations (CCM) consist of clusters of abn

84 r mechanism for the pathogenesis of cerebral cavernous malformations (CCM) resulting from loss of CCM

85 For cerebral cavernous malformations (CCM), the lesions are grossly-d

86 aptor proteins CCM2 or CCM3 lead to cerebral cavernous malformations (CCM), vascular lesions that mos

87 nd biochemically and are mutated in cerebral cavernous malformations (CCM).

88 of the inherited vascular disorder cerebral cavernous malformations (CCM1).

89 The products of genes that cause cerebral cavernous malformations (CCM1/KRIT1, CCM2, and CCM3) phy

90 Cerebral cavernous malformations (CCMs) affect 0.1-0.5% of the po

91 Cerebral cavernous malformations (CCMs) are a cause of stroke and

92 Cerebral cavernous malformations (CCMs) are a common type of vasc

93 Cerebral cavernous malformations (CCMs) are common inherited and

94 Cerebral cavernous malformations (CCMs) are common vascular anoma

95 Cerebral cavernous malformations (CCMs) are congenital vascular a

96 Cerebral cavernous malformations (CCMs) are human vascular malfor

97 Familial cerebral cavernous malformations (CCMs) are predominantly neurova

98 Cerebral cavernous malformations (CCMs) are prone to bleeding but

99 Cerebral cavernous malformations (CCMs) are sporadically acquired

100 o test the hypothesis that sporadic cerebral cavernous malformations (CCMs) are systematically associ

101 Cerebral cavernous malformations (CCMs) are vascular abnormalitie

102 Cerebral cavernous malformations (CCMs) are vascular anomalies of

103 Cerebral cavernous malformations (CCMs) are vascular lesions affe

104 Cerebral cavernous malformations (CCMs) are vascular lesions of t

105 The reported effects of treating cerebral cavernous malformations (CCMs) by neurosurgical excision

106 Cerebral cavernous malformations (CCMs) can cause symptomatic int

107 Familial cerebral cavernous malformations (CCMs) in humans result from mut

108 ns for various disorders, including cerebral cavernous malformations (CCMs) in which focal vascular l

109 oximately 40% of autosomal-dominant cerebral cavernous malformations (CCMs), a disease occurring in u

110 CCM genes are responsible for human cerebral cavernous malformations (CCMs), which are characterized

111 y (CT) are associated with familial cerebral cavernous malformations (fCCMs) in carriers of the CCM1

112 ree intracellular adaptor proteins, cerebral cavernous malformations 1 protein (CCM1), CCM2, and CCM3

113 Cerebral cavernous malformations 2 (CCM2) loss is associated with

114 v interaction trapped 1 (KRIT1) and cerebral cavernous malformations 2 (CCM2), respectively) directly

115 causes autosomal dominant familial cerebral cavernous malformations and disrupts cardiovascular deve

116 logy, including arteriovenous malformations, cavernous malformations and moyamoya disease, coupled wi

117 Cavernous malformations are characterized by enlarged va

118 To test the hypothesis that growth of cavernous malformations depends on somatic loss of heter

119 CM3, a causative genetic defect for cerebral cavernous malformations in humans.

120 xpression of CCM1 in adulthood suggests that cavernous malformations may be the result of primary neu

121 Our studies suggest that cavernous malformations result from primary vascular rat

122 mic adaptor protein associated with cerebral cavernous malformations, has previously been shown to in

123 of CCM2 predisposes individuals to cerebral cavernous malformations, vascular abnormalities that cau

124 of 20 heterozygous mice failed to detect any cavernous malformations.

125 causes autosomal dominant familial cerebral cavernous malformations.

126 ar anomalies in the brain, known as cerebral cavernous malformations.

127 ctomy leads to Wallerian degeneration of the cavernous nerve (CN) and erectile dysfunction (ED).

128 s) elicited by electrical stimulation of the cavernous nerve (ES) and to recombinant human VEGF165.

129 Both electrical stimulation of the cavernous nerve and direct intracavernosal injection of

130 The dorsal nerve of the clitoris and the cavernous nerve both innervate the distal urethra and th

131 injection, or augmented by forskolin during cavernous nerve electrical stimulation, is prevented by

132 y initiated by electrical stimulation of the cavernous nerve in wild-type but not Mc4r-null mice; (ii

133 Erectile responses to both cavernous nerve stimulation and intracavernosal injectio

134 Moreover, cavernous nerve stimulation was associated with a marked

135 ure (MAP) upon electrical stimulation of the cavernous nerve.

136 opathologically the lesions were composed of cavernous or telangiectatic channels; 1 showed advanced

137 geometry dramatizes the significance of the cavernous primary specificity site, pointing the way for

138 ry to a traumatic dissecting aneurysm in the cavernous segment of internal carotid artery (ICA) is a

139 t of ICA, and the dissecting aneurysm of the cavernous segment was successfully managed with a stent-

140 ) together with a dissecting aneurysm in the cavernous segment.

141 a (n = 2), parapharyngeal space (n = 1), and cavernous sinus (n = 1).

142 cluding tumour activity, relationship to the cavernous sinus and patient predisposition to headache.

143 ulas are abnormal communications between the cavernous sinus and the external or internal carotid art

144 bers that terminate in the trabeculae of the cavernous sinus as an ending that resembles a Golgi tend

145 tion of OCTA in a patient with dural carotid-cavernous sinus fistula (CCF), which was complicated by

146 t or in certain cases as primary treatment), cavernous sinus fistulae, parasellar syndromes, and pitu

147 superior orbital fissure, orbital apex, and cavernous sinus have been used to define the anatomic lo

148 tal invasion in 4 cases and paranasal and/or cavernous sinus invasion in 3 cases.

149 Cavernous sinus invasion was present in the minority of

150 These areas include cavernous sinus lesions and sellar lesions (for which ra

151 iographically proved dural AV fistula of the cavernous sinus were retrospectively reviewed.

152 ns a compelling treatment for lesions of the cavernous sinus, pineal, and sellar regions and offers i

153 In cases of severe dural AV fistula in the cavernous sinus, the pituitary gland is enlarged, which

154 nications between the carotid system and the cavernous sinus.

155 icular and spiny endings at the level of the cavernous sinus.

156 vibrissae capsule, adjacent to the ring and cavernous sinuses (the areas adjacent to blood and lymph

157 t structures, including the optic nerves and cavernous sinuses, and may result in more profound visua

158 Narial blood supply and cavernous tissue corroborate the rostral position in din

159 bi resolved in five patients, progression to cavernous transformation occurred in one patient, and pa

160 e-thrombosis (MPV and other), 17 (17.3%) had cavernous transformation of portal vein, and 3 (3.1%) ha

161 al portal venous flow, Budd-Chiari syndrome, cavernous transformation of the portal vein, ovarian mas

162 Eleven patients (31%) had cavernous transformation of the PV; eight (23%), a cordl

163 PV occlusion of greater than 1 year with cavernous transformation seems to be a factor causing te

164 Cavernous transformation, calcifications of the venous w

165 traosseous vascular lesions resemble orbital cavernous venous malformations (not true hemangiomas), e

166 by excessive fusion of capillary plexes into cavernous vessels and hyperdilation of large vessels.

167 a subset of the endothelial cells lining the cavernous vessels and not in interstitial lesion cells.